Did Bryant Arroyo Kill Baby Jordan Anthony Shenk,
As Alleged by the Commonwealth Of Pennsylvania?

Mohammed Ali Al-Bayati PhD, DABT, DABVT
Toxicologist & Pathologist, Toxi-Health International
150 Bloom Dr. Dixon, CA 95620 Phone: (707) 678-4484 Fax: (707) 678-8505

Table of Contents

Section III.
Review of The Medical Examiner’s Autopsy and Pathology Report,
and Interpretation of Results

Jordan Anthony Shenk was pronounced dead at 0340 on 25 September 1994 in the Lancaster General Hospital. Dr. Wayne K. Ross, forensic pathologist of Lancaster County, Pennsylvania performed the autopsy at about 0800 [Autopsy No: A94-347 (LC94-265)]. The objectives of Dr. Ross’s autopsy were to identify the cause and the manner of death. Assistant District Attorney Randy Miller, Officer Roland L. Buch, and Detective Allen W. Leed from the Manheim Township Police Department were present with Dr. Ross and observed the autopsy.

Prior to autopsy, full-body x-rays were performed on Jordan, showing no evidence of acute or healing trauma. Dr. Boal, pediatric radiologist, also reviewed these x-rays and did not observe any significant abnormalities. In addition, Dr. Ross examined Jordan’s body and observed no evidence of injuries caused by trauma in the scalp, mouth, back, and upper and lower extremities [2].

Dr. Ross took tissue samples from selected organs and lesions at the time of autopsy. He submitted them to Harrisburg Hospital to process them for histological evaluation. Dr. Ross examined the H & E stained tissue sections of the samples that he received from Harrisburg Hospital at a later date. He found significant abnormalities in several organs as described below in Section III-A [2].

Dr. Ross went to Manheim Township Police Department on 25 September after he finished his autopsy on Jordan and met with officers and Detectives. He informed them that Jordan died due to complications from blunt trauma to the chest and abdomen and that the manner of death was homicide. He also provided the same information to Mr. Miller in the district attorney’s office [9, 11, 12].

Dr. Ross stated in his autopsy report [2], “After autopsy and review of the history, it is my opinion that the cause of death is complications of blunt chest and abdominal trauma. The manner of death is homicide. The blunt chest and abdominal trauma is due to a severe, repetitive beating. Multiple bruises are seen on/in the skin. In addition, multiple hemorrhages on the liver, in the liver, in the gallbladder, and in the mesentery of the bowel as well as in the outer portions of the bowel itself. The beating is most probably due to being repetitively hit with knuckles from a fist, but could be from holding the abdomen with severe pressure, kicking with toes, or the beatings from the hands.”

I am very surprised to learn that Dr. Ross declared the cause and the manner of death in this case prior to examining the tissues microscopically to see if Jordan was suffering from acute and/or chronic illnesses that led to his cardiac arrest and bleedings. In addition, he did not perform differential diagnosis to consider all possible causes of the bleedings and inflammation in tissues observed in this case.

My review of Dr. Ross’ autopsy and pathology report and other medical evidence pertinent to this case revealed that Jordan suffered from chronic and acute health problems that led to cardiac arrest and bleedings. He had serious brain disease (spongiosis of the cerebral cortex and white matter and focal Purkinje cell dropout in the cerebellum); aspiration pneumonitis; sepsis; inflammation of the liver, gallbladder, and the mesentery; thymus atrophy; and weight loss [2].

Dr. Ross examined Jordan's H & E stained tissue sections microscopically and found brain spongiosis; aspiration pneumonitis; and inflammation of the liver, mesentery, and gallbladder [2]. However, he did not consider these serious illnesses in his evaluation of the cause of bleedings and death. In addition, Dr. Ross testified in court in October of 1994 and May of 1995 concerning Jordan’s case, but did not reveal to the court that the baby had brain spongiosis, Purkinje cell dropout in the cerebellum, and aspiration pneumonitis [11, 12]. These are the factual causes of death.

My investigation of the medical literature revealed that babies who had propionic acidemia and other metabolic problems involving branched amino acids developed brain spongiosis, aspiration pneumonia, thymus atrophy, sepsis, and weight loss, as did Jordan. These babies also had severe thrombocytopenia that led to bleedings. Also, severe liver inflammation usually caused reduction in the synthesis of clotting factors, with enhanced bleedings, as also happened in Jordan’s case.

Furthermore, the literature reveals that bruises on skin and damage to lungs, liver, and gastrointestinal tract have been reported in children and adults who received cardiac pulmonary resuscitation (CPR). Bryant, a police officer, and the paramedics performed CPR on Jordan. Jordan’s mother stated that Bryant caused bruises on her son’s chest when he performed CPR. The medical evidence below shows that CPR was the likely cause of the bruises and marks observed on Jordan’s lower chest and upper abdomen.

The paramedics observed eleven bruises on the lower chest and upper abdomen. The largest one was 1/8 inch in diameter. However, Dr. Ross counted sixteen bruises in these areas, with the largest being 1/2 inch in diameter—an increase of 400%. Also, five new bruises appeared on Jordan’ lower chest area following the time that the baby was transported from his house by the paramedics. Dr. Ross did not consider these medical data in his evaluation, which clearly indicate that CPR and medical intervention were the probable causes of the bruises observed on the baby’s skin on the chest and abdomen.

Below are detailed descriptions of Dr. Ross’ autopsy and histopathology findings and the pertinent medical evidence. These data clearly 1) invalidate Dr. Ross's conclusions that Jordan died as a result of blunt trauma to the chest and abdomen and that the manner of death was homicide; 2) show that Dr. Ross did not follow standard medical procedures to perform the required medical tests and to interpret medical data correctly; 3) show that Dr. Ross rushed to judgment in accusing Bryant in Jordan's death. Furthermore, these data explain the factual causes of death and bleedings in this case.

III-A. Spongiosis of the cerebrum,
Purkinje cell dropout in cerebellum, and brain edema

Dr. Ross examined Jordan’s brain grossly at the time of autopsy on 25 September and observed severe cerebral edema. The weight of the brain was 900 gm. His microscopic examination of the H & E stained sections of the brain at a later date revealed serious chronic brain lesions (spongiosis of the cerebral cortex and white matter, and focal Purkinje cell dropout in the cerebellum) [2]. These lesions indicate a serious, chronic neurological problem. However, Dr. Ross did not consider these lesions in his evaluation of the cause of death. In addition, he did not reveal these crucial medical findings in court when he testified in October of 1994 and May of 1995 [11, 12]. Below are the questions that were presented to Dr. Ross in court by the defense lawyer, and Dr. Ross's answers.

Defense lawyer: Did you notice anything unusual about anything else within the body?
Dr. Ross: No [11, page 42].
Defense lawyer: Dr. Ross, have you prepared an autopsy report in this matter?
Dr. Ross: Yes.
Defense lawyer: And have you testified from that report today?
Dr. Ross: Yes, I have [11, page 51].

Dr. Ross’ answers in court clearly contradict the histology findings described in his autopsy report: that Jordan had spongiosis of the cerebrum and focal Purkinje cell dropout in the cerebellum [2: page 10]. These lesions indicate serious metabolic and neurological problems that led to weight loss; thymus atrophy; aspiration pneumonitis; bleedings in the lungs and other tissues; sepsis; inflammation of the liver, gallbladder, and mesentery; and cardiac arrest.

Spongiosis of the brain, pulmonary infection, atrophy of the thymus, thrombocytopnea, and loss of weight have been described in children who suffered from propionic acidemia and other metabolic diseases as shown by the published medical studies described below.

Propionic acidemia (PA) is a genetic disorder of branched amino acid and odd-chain fatty acid metabolism. It is caused by an inhibition of the activity of propionyl coenzyme A carboxylase and the accumulation of propionyl-CoA. The main sources of propionyl-CoA are isoleucine, valine, methionine, and cholesterol. Odd-chain and branched odd-chain fatty acids are also significant contributors. The propionyl-CoA is known to inhibit several key enzymes (such as pyruvate dehydrogenase) as well as fatty acid oxidation. It also inhibits N-acetylglutamate, which might account for impaired ureogenesis and hyperammonia [13, 14, 15].

The clinical features of PA typically begin shortly after birth, but in some cases present in young adulthood. The symptoms and lesions of this disorder may include dehydration, lethargy, nausea, vomiting, generalized hypotonia and muscle weakness, thrombocytopenia, neutropenia, intercurrent infections, and neurological problems [14-17]. The symptoms of PA with onset in late infancy or early childhood are usually identical to those of the neonatal-onset disorder.

The onset of acute PA may be precipitated by upper respiratory tract or gastrointestinal infections, or possibly severe constipation. Many children who survive severe or prolonged metabolic disturbances sustain brain damage. Seizures are common in patients with propionic acidemia [16]. In neonates and older children, the neuropathologic findings in propionic acidemia may include spongiosis of the cerebrum (white matter and/or gray matter) and Purkinje cell dropout in the cerebellar cortex [13-16, 18, 19]. Dr. Ross observed these serious lesions in Jordan’s brain.

The diagnosis of PA is readily achieved by urine gas chromatography/mass spectrometry (GC/MS), by tandem mass spectrometry (MS/MS), or by enzyme analysis of fibroblasts. Dr. Ross did not perform these clinical tests to exclude propionic acidemia from his findings.

The following are descriptions of published studies describing cases of children who suffered from PA. These children developed symptoms and lesions in brain and other tissues identical to those observed in Jordan’s case. Some of these children also had bleedings resulting from thrombocytopenia.

1) Asconape et al. described pathologic changes in the brain of a five-and-a-half-month-old male infant who died of PA. These changes included spongy degeneration of the white matter and marked diffuse atrophy with early loss of the external granular layer of the cerebellum [19].

2) Feliz, Witt, and Harris reported a case of a 4-year-old girl with PA from infancy who died from multiorganism bronchopneumonia after a protracted clinical course. She was neutropenic (white blood cell count 0.9 x 103/µL; normal range, 4.3-10.8 x 103/µL) and thrombocytopenic (platelet count 0.9 x 103/µL; normal range, 150-300 x 103/µL). Their postmortem neuropathology examination revealed widespread gray matter vacuolization. The cerebellar cortex showed a patchy dropout of Purkinje cells and a proliferation of Bergmann glia [14].

3) Steinman et al. found spongiform changes in the white matter of the cerebrum in an infant who died as result of PA [18].

4) Ozand et al. studied twenty-five cases of neonates and infants with PA, and most of these children had acute or chronic encephalopathy with or without acidosis [15]. In fourteen patients, PA presented acutely with acidosis, hyperammonemia, and thrombocytopenia. Five infants presented encephalopathy with acidosis, and four infants showed a progressive encephalopathy without acidosis. In addition, three infants showed immune deficiency. The prognosis in PA remained grave despite rigorous treatment. Only seven of the 25 PA patients recovered to have a normal lifestyle, while eight patients expired [15].

The clinical picture of PA in these patients included severe hypotonia with diminished reflexes and vomiting. During acute metabolic crisis, PA usually, but not always, causes acidosis, accumulation of ketone bodies and lactic acid in body fluids, hyperammonemia in the range of 200-800 µM, and at times hypoglycemia. Characteristically, organic acids and organic acid esters are excreted in the urine [15].

Severe thrombocytopenia is the hallmark of the metabolic crisis. Severe and sustained thrombocytopenia is almost pathognomonic of propionic acidemia. Intracranial hemorrhage was observed in four patients with PA, and in three of them the intracranial bleeding caused death. Thrombocytopenia is encountered in other organic acidurias. Isovaleric acidemia can also cause severe thrombocytopenia during a metabolic event [15].

The immune suppressive action of PA can be so severe that the thymus gland may become atrophic. A thymic biopsy was obtained from a patient with PA, which showed depletion of lymphocytes from thymic cortex, with no differentiation between cortex and medulla, and with numerous epithelioid cells. Also the numbers of Hassall’s corpuscles are reduced [15].

Repeated infections might be the only presenting symptom of the disease, with other signs of PA being less apparent or initially absent. The acute attacks are accompanied by mild neutropenia and by recurrent severe infections. Postmortem blood culture of one patient grew Klebsiella pneumonia and coagulase-positive Staphylococcus aureus. In a second patient, Pseudomonas aeruginosa and Staphylococcus aureus were isolated from blood culture and her symptoms were attributed to sepsis. In a third patient, blood culture grew coagulase-negative Staphylococcus aureus [15].

5) Hamilton et al. reported neuropathologic findings in two patients with PA who were diagnosed in infancy and survived 35 months and 9 years, respectively [13]. Examination of the brain of the 35-month-old boy showed vascular and parenchymal mineralization, focal pallor and spongy change, and foci of acute neuronal injury.

The 9-year-old girl was in good metabolic control when she died. She was found at autopsy to have acute hemorrhagic lesions in the caudate, putamen, and globus pallidus bilaterally and in the left ventral thalamus. There was also focal neuronal loss. Vascular proliferation and swollen endothelial cells were seen in the basal ganglia, thalamus and substantia nigra of the brain. Electron microscopy showed swelling of endothelial cells with viable adjacent brain parenchyma. The endothelial changes suggest a breakdown of the blood-brain barrier [13].

6) Nyhan et al. evaluated two children with propionic acidemia who suffered from prominent neurological disease without the life-threatening episodes of ketoacidosis. Their prominent features were hypotonia followed by spastic quadriparesis, and both had seizures. One patient was mildly mentally retarded but grew normally physically. The other had profound mental retardation and failure to thrive [20].

7) Akman et al. evaluated a neonate with propionic acidemia who had prominent neurological problems but without ketoacidosis. The baby had a serum ammonia level of 3,500 micrograms/dL. He developed Candida albicans, peritonitis, and sepsis, and died of cardiorespiratory failure [21].

III-B. Jordan's weight loss.

At autopsy on 25 September 1994, Dr. Ross reported Jordan’s weight as 15 lb, 10 oz. However, Jordan's weight on 12 August was also 15 lb, 10 oz. These data indicate that the baby did not gain any weight during the 43-day-prior to his cardiac arrest. Jordan’s clinical chart showed that he was given about 410 ml of fluid IV, which weighs about a pound, by the paramedics and in the hospital following his cardiac arrest on 25 September. These data indicate that the baby lost about one pound during the forty-three days prior to his cardiac arrest.

The average body weight and the 10th percentile weight for infants at nine months of age in the USA were reported as 19.6 lb (8.91 kg) and 17.82 (8.1 kg), respectively, [22]. It seems that Jordan’s weight at the time of autopsy was about 2 to 3 lb less than babies of that age who have body weight at the 10th percentile. These data indicate that Jordan was suffering from serious weight loss.

III-C. Jordan's thymus atrophy

Dr. Ross stated that Jordan’s thymus weight was 13 g and that its external and sectioned surfaces were unremarkable [2]. The average thymus weight (g) in a white male infant at six to nine months of age was found to be 25 g [22]. Jordan’s age at the time of autopsy was eight-and-a-half months. It seems that Jordan’s thymus weight was about 52% of normal. In addition, at Jordan’s age, thymus weight is usually equal to the spleen weight. Jordan's spleen weight was 33 grams. These data indicate that Jordan suffered from thymus atrophy and contradict Dr. Ross’s claim that Jordan had normal thymus size.

Furthermore, Dr. Ross did not take tissue samples from Jordan’s thymus for histological evaluation. His conclusion that Jordan’s thymus was normal is not scientifically valid. Reportedly, babies who suffered from spongiosis of the brain and propionic acidemia (PA) also had thymus atrophy, as observed in Jordan’s case. A thymus biopsy obtained from a patient with PA showed depletion of lymphocytes from the thymic cortex with no differentiation between cortex and medulla. It also showed numerous epithelioid cells and clear reduction in the numbers of Hassall’s corpuscles [15].

III-D. Jordan's aspiration pneumonitis

Dr. Ross examined Jordan’s lungs grossly at the time of the autopsy on 25 September 1994. He stated that the lung parenchyma showed diffuse and severe pulmonary edema and congestion. He also observed petechial hemorrhages in lung parenchyma and hemorrhages in the alveoli in multiple areas. The total lung weight was 128 grams [2].

Furthermore, Dr. Ross examined the H & E stained tissue sections of Jordan’s lungs microscopically at a later date. He found that the baby had aspiration pneumonitis, bleedings, and pulmonary edema [2: page 10]. Dr. Ross testified in court in October of 1994 and May of 1995 concerning the cause of Jordan’s death. However, he did not reveal to the court that the baby had aspiration pneumonitis [11, 12]. Below are the questions that were presented to Dr. Ross in court by the defense lawyer and his answers [11:pages 42-51].

Defense lawyer: Did you notice anything unusual about anything else within the body?
Dr. Ross: No.
Defense Lawyer: Lungs?
Dr. Ross: There is bleeding inside the lungs.
Defense lawyer: Dr. Ross, have you prepared an autopsy report in this matter?
Dr. Ross: Yes.
Defense lawyer: And have you testified from that report today?
Dr. Ross: Yes, I have.

Aspiration pneumonitis is mentioned in Dr. Ross’ autopsy report [2: page 10] but he did not mention it in court. It is usually caused by a foreign substance (food and/or secretions) and microorganisms entering the lung causing inflammation. The severity of the lung’s injury after an aspiration incident is determined by pH of the aspirated material and presence of pathogenic bacteria. Very low pH or extremely high pH will cause a significant inflammatory response. Children at highest risk are children with poor airway reflexes or gastroesophageal reflux, or both [23: page 1213]. Jordan had serious neurological problems that caused poor airway and gastroesophageal reflexes, namely spongiosis of the cerebral cortex and white matter and focal Purkinje cell dropout in the cerebellum [2: page 10].

Inflammation of the lungs due to the aspiration of foreign substance and bacteria can explain Jordan’s bleedings and edema of the lungs. Streptococcus pneumoniae is normally present in the nasopharynx. Frequently, this pneumonia follows viral infections of the upper respiratory tract. The bronchial secretions stimulated by the viral infection provide a hospitable environment for the proliferation of S. pneumoniae organisms. The thin, watery secretions carry the organisms into the alveoli, thereby initiating an inflammatory response [24].

Jordan’s mother and his babysitter stated that Jordan had a cold during the week preceding his cardiac arrest. Jordan’s cold and his neurological problems are important factors in causing the inflammation of the lungs by bacteria. In the earliest stage of pneumococcal pneumonia, protein-rich edema fluid containing numerous organisms usually fills the alveoli. The lesions include marked congestion of the capillaries, massive infiltration of polymorphonuclear leukocytes, and intra-alveolar hemorrhage. On gross examination, the lungs of patients who die of streptococcal pneumonia are heavy and display bloody edema [24: pages 567 and 569]. Dr. Ross observed these lesions in Jordan’s lungs [2].

Aspiration pneumonitis can also be caused by microorganisms other than S. pneumoniae, such as fusobacteria and other Bacteroides species. Pneumonia due to anaerobes is an especially likely outcome if the aspirated material is large in volume or contains virulent components of the anaerobic microbrial flora or foreign bodies, such as aspirated food or necrotic tissue. Impairment of the cough reflex increases the risk of pneumonia, as does mucociliary or alveolar macrophage dysfunction [24: page 569, 25: page 1776]. Schmidt reviewed the data of 98 children for foreign body aspiration. In this data review, 78% of the children were younger than 2 years. Predominant clinical features were fever (46%), pneumonia (39%), and coughing (29%) [26].

I am very surprised to learn that Dr. Ross used a theory to explain the causes of bleeding in Jordan’s lungs rather than citing aspiration pneumonitis. Dr. Ross stated that when you hit the abdomen or the chest, you produce various waves—shock and shear waves, which were responsible for Jordan’s bleeding in the lungs [12: page 95]. It is very obvious to me that aspiration pneumonitis was the actual cause of the bleeding and edema.

Furthermore, aspiration pneumonitis can also cause asphyxia, as was described in Jordan’s case. Delmonte and Capelozzi observed signs of asphyxia in thirty-five victims who died as a result of aspiration pneumonitis. Autopsies revealed that the lungs of these victims had congestion, septal hemorrhage, and foreign bodies, as observed in Jordan [27].

III-E. Causes of the marks observed
on Jordan’s lower chest and upper abdomen

Dr. Ross examined Jordan's body at about 0800 on 25 September 1994. He observed sixteen brownish/purplish circular contusions of various sizes (1/8-1/2 inch in diameter) on the lower anterior chest wall and upper abdomen [2]. He alleged that these were bruises caused by repetitive beatings of the chest and abdomen by knuckles and/or fists or by kicking [11: page 9]. He stated that the injuries observed in Jordan were equivalent to those caused by the impact of a car moving at 20-26 miles per hour.

Furthermore, Dr. Ross excluded cardiopulmonary resuscitation (CPR) as the cause of injuries. He stated that Jordan’s injuries were severe and showed inflammatory reactions as indicated by the presences of white blood cells. Dr. Ross concluded that Jordan died within hours after receiving the injuries, and this allowed enough time to cause an inflammatory response [11, 12].

My review of the medical evidence in this case revealed that Dr. Ross based his conclusions on a theory and not on medical facts. The following is a list of medical facts that invalidate Dr. Ross’s conclusions. They also clearly show that CPR was the likely cause of the marks observed on Jordan’s lower chest and upper abdomen.

1) The paramedics examined Jordan prior to transporting him to Lancaster General Hospital at 0305 on 25 September and observed only eleven brownish/purplish circular marks on his lower chest and upper abdomen. The sizes of the marks were approximately 1/8 inch in diameter. In addition, the physician who examined Jordan at the hospital’s emergency room estimated the sizes of the marks to be about a half centimeter in diameter (1/5 inch). However, Dr. Ross stated that he found 16 bruises and that the sizes of these bruises were 1/8-1/12 inch in diameter.

These observations indicate that five of the sixteen bruises observed by Dr. Ross occurred after the baby was transported to the hospital. Also, the sizes of the bruises increased by 400% from the time the paramedics transported the baby at 0305 until the time of autopsy at 0800.

2) Dr. Ross examined the H & E stained tissue sections of the bruises on Jordan’s chest, including muscle, and found fresh hemorrhage without the presence of a significant white blood cell infiltration. These observations contradict Dr. Ross’s conclusion that the bruises on the chest occurred when the baby was alive because the injury triggered inflammatory response.

3) Dr. Ross examined the H & E stained tissue section from the marks on Jordan’s upper abdomen and observed only congested blood vessels with no obvious hemorrhage or inflammatory reactions. These findings contradict Dr. Ross statements that he found bruises on the upper abdomen, that these marks were caused by hitting the baby with a strong force, and that the marks occurred prior to the baby’s death.

4) Jordan’s mother stated that the bruises on Jordan’s chest were caused by Bryant’s attempts to do CPR.

5) Jordan had brain spongiosis and aspiration pneumonitis. Severe thrombocytopenia has been reported in children with sepsis and brain spongiosis. Patients with thrombocytopenia are susceptible to bruising and bleedings.

6) Various types of injuries in the chest and abdomen areas have been reported in patients receiving CPR. These injuries are more severe than those reported in Jordan’s case. For example, complications caused by cardiopulmonary resuscitation (CPR) were reviewed by analyzing the autopsy protocols of 25 patients who died after receiving standard CPR. Rib fractures were detected in 28%, and sternal fractures in 16% [28].

In addition, Sokolove reported a case of a 61-year-old woman in whom cardiopulmonary resuscitation (CPR) was unsuccessful. While the patient was initially resuscitated from the primary cardiac arrest, with evidence of neurologic recovery, she ultimately succumbed to injuries resulting directly from CPR. Autopsy revealed multiple rib fractures, a sternal fracture, pulmonary laceration, and cardiac rupture [29]. Also, costochondritis resulting from resuscitation was described in another patient [30].

III-F. Causes of the inflammation and bleedings in Jordan’s liver

Dr. Ross examined Jordan’s liver at autopsy on 25 September 1994 and observed subcapsular hemorrhage, bruises, and bleedings in multiple areas of the left and right lobes of the liver. In addition, he examined the H & E stained tissue sections of the liver at a later date and found edema, fresh hemorrhage, and blood clotting. In addition, the entire liver was infiltrated primarily with polymorphonuclear cells, but macrophages also [2].

Dr. Ross concluded that the injuries observed in Jordan’s liver were caused by blunt trauma to the abdomen. He also excluded CPR as a factor in causing these injuries. Furthermore, Dr. Ross stated that the type of injuries observed in Jordan’s liver usually occurred in people hit by a car moving at approximately 26 miles per hour [12:page 236]. I found Dr. Ross’ conclusions invalid, based on the following medical facts:

1) The presence of the polymorphonuclear neutrophils (PMN) and macrophages throughout Jordan’s liver indicates an inflammation that started about 24 hours prior to death. PMN usually enter the inflammatory site in 6 to 12 hours after the initial injury, while macrophages enter the site at the later time, usually after 24 hours. [23:page 220; 24:page 49].

2) Bacterial infection was the likely cause of the inflammation observed in Jordan’s liver, because he had aspiration pneumonitis. Bacteria can travel via blood to infect the liver and other organs. In addition, Jordan had thymus atrophy, which predisposed him to infection.

3) The bleedings and bruises observed in Jordan’s liver likely resulted from the synergistic actions of the following factors:

a. Jordan had sepsis and brain spongiosis, which were probably caused by propionic acidemia. Reportedly, babies who suffered from these illnesses also developed thrombocytopenia and bleedings;

b. Inflammation of the liver usually causes deficiency of clotting factors. Blood clotting factors, except factor VIII, are made exclusively in hepatocytes. The serum half-lives of the clotting factors range from 6 hours for factor VII to 5 days for fibrinogen [25:page 1714];

c. Severe liver damage has been reported in people receiving CPR. For example, Adler et al. treated two patients with laceration of the liver precipitated by cardiopulmonary resuscitation (CPR) and recognized ante mortem [31]. These patients had excruciating abdominal pain and bled massively, which led to the development of hypovolemic shock. The authors stated that when severe abdominal pain associated with hypovolemic shock occurs in a patient who has received CPR, hepatic laceration, hematoma, or both, should be considered [31].

In addition, Druwe et al. reported a patient with an acute myocardial infarction who had to be resuscitated due to recurring ventricular fibrillation. Fourteen hours later, clinical signs of hemoperitoneum developed and the diagnosis of liver rupture was made [32]. Also Reinartz reported a case of a combined manifold rupture of the liver and spleen occurring after the individual received cardiopulmonary resuscitation [33].

4) Dr. Ross examined the H & E stained tissue section from the marks on the skin in the abdominal area and observed only congested blood vessels with no obvious hemorrhage or inflammatory reactions. These findings contradict Dr. Ross's statement that the baby was hit by a strong force equivalent to a car driving 26 miles per hour, or by any significant force that causes internal bleedings.

III-G. Causes of the inflammation and necrosis in Jordan’s gallbladder

Dr. Ross examined Jordan’s gallbladder at autopsy and observed hemorrhage in the perigallbladder region and on the wall inside the gallbladder. He also found early necrosis associated with edema in the gallbladder wall. In addition, he examined the H & E stained tissue sections of the gallbladder microscopically and observed blood clot, autolysis of the epithelium, and subepithelial hemorrhages with early infiltration by polymorphonuclear cells. Dr. Ross concluded that the lesions in Jordan’s gallbladder were caused by blunt trauma and that it occurred within 20 minutes to two hours prior to the baby's death. I found these conclusions by Dr. Ross’s scientifically invalid.

It takes about three to four hours for the gallbladder necrosis to become apparent to the naked eye. In addition, the autolysis of epithelium occurred after the death of cells and the release of the lysosomal enzymes. The autolysis observed in this case occurred prior to the death of the child because the wall of the gallbladder was infiltrated by white blood cells. Dead cells usually evoke an inflammatory reaction that brings leukocytes to the area [23, 24].

Furthermore, infection with microorganisms was the likely cause of the inflammation and the necrosis of Jordan’s gallbladder, because the baby had aspiration pneumonitis and liver inflammation. Microorganisms can travel via blood to infect the gallbladder and other organs. The baby also had thymus atrophy, which predisposed him to infections. In addition, the bleeding in Jordan’s gallbladder likely resulted from the synergistic actions of several factors, as described above in the liver section. Briefly, these include thrombocytopenia, sepsis, metabolic problems, and liver inflammation that led to reduction in the synthesis of clotting factors.

III-H. Causes of the bleedings in Jordan’s intestine and mesentery

Dr. Ross examined Jordan’s gastrointestinal tract and abdominal cavity at autopsy and observed fresh bleedings in multiple areas of the mesentery, pericolonic region, serosa of small intestine, and ascending colon. He collected 200 ml of bloody fluid from the abdominal cavity. At a later date, Dr. Ross examined the H & E stained tissue sections of the mesentery and intestines and found a fresh hemorrhage with inflammation in the mesentery and fresh hemorrhage and edema in the wall of the ascending colon. The mesentery was infiltrated primarily with polymorphonuclear cells, but some macrophages were noted also. No significant abnormalities were observed in the small intestine.

Dr. Ross concluded that the injuries of the mesentery and the intestine in Jordan’s case were caused by blunt trauma applied to the upper abdomen and the lower anterior chest. He also stated that the injuries observed in Jordan’s case usually occur in people hit by a car moving at approximately a 26 miles per hour, and that these injuries cannot be caused by somebody performing CPR [12: page 236]. The following is a list of medical facts that invalidate Dr. Ross’s conclusions concerning the cause of injuries observed in Jordan’s intestine and mesentery.

1) The presence of the polymorphonuclear neutrophils (PMN) and macrophages in the mesenteric tissue indicates that Jordan’s mesentery was inflamed and that the inflammation was about 24 hours old or older, as shown by the presence of macrophages. Macrophages usually enter the site of inflammation after 24 hours [23, 24].

2) Bacterial infection was the likely cause of the inflammation of the mesentery in Jordan’s case because he had aspiration pneumonitis and inflammation of the liver and gallbladder. Microorganisms can travel from infected organs via blood to the mesentery and other organs. Jordan’s immune function was also depressed because of the thymus atrophy.

3) The bleedings in the mesentery and the intestines arose from the synergistic actions of several factors, as described in the liver section (III F). These include thrombocytopenia, sepsis, liver inflammation, and CPR. Severe damage of gastrointestinal tract has been reported in people receiving CPR. For example, Aguilar reviewed 16 patients with documented gastric trauma resulting from cardiopulmonary resuscitation [34].

In addition, Waldman evaluated a case of a child in which conventional CPR was augmented with interposed abdominal compressions. In this case, intraperitoneal visceral injury was noticed in the form of blood within the stomach and small intestine and parenchymal hemorrhage within the pancreas [35]. In addition, McGrath reported a case of fatal gastrointestinal hemorrhage from gastric mucosal lacerations related to closed-chest cardiac compression of CPR [36]. Also, previous autopsy series suggest that gastroesophageal lacerations may occur in 12 percent of cases not surviving CPR [36].

Also, three cases of gastric trauma following cardiopulmonary resuscitation were
reported by Hulewicz [37]. In two cases, full-thickness lacerations were observed in the gastric wall, resulting in pneumoperitoneum. In the third case, gastric hemorrhage resulting from gastric mucosal lacerations was described. Reiger et al. also reported two patients who developed gastric rupture after successful standard CPR [38]. Furthermore, McDonnell et al. observed at autopsy two patients in whom clinically significant gastrointestinal bleeding occurred from gastric mucosal tears following closed-chest cardiac massage [39].

In addition, Bedell and Fulton studied autopsy findings of 130 patients who died after attempted CPR. Twenty-one percent of these patients had at least one CPR-related complication. Patients resuscitated in the wards were more likely to have a complication than those treated in the intensive care unit. This suggests that more proficient technique in CPR may reduce morbidity from this procedure [40].

4) As previously stated in this report, Dr. Ross examined the H & E stained tissue section from the marks on the skin in the abdominal area, observing only congested blood vessels and no obvious hemorrhage or inflammatory reactions. These findings contradict Dr. Ross's statement that the baby was hit by a strong force equivalent to a car moving 26 miles per hour.

III-I. Likely causes of Jordan’s petechial hemorrhages

Dr. Ross examined Jordan’s body at autopsy and observed petechial hemorrhage at various sites of his body. These sites include upper and lower lips, gums, distal end of tongue, sclera, eyelids, mucosa of the trachea, and the thymus.

Petechiae in tissues have been observed in patients in whom cardiopulmonary resuscitation has reestablished blood flow. The increase in the blood pressure in small vessels already damaged by hypoxia can result in the formation of petechiae [41, 42]. Jordan had anoxia because he was not breathing. In addition to CPR, Jordan was given 410 mL of fluid, which increased his blood volume by 100%. Jordan's weight was about 7 kg. His total blood volume was about 420 mL (60 mL per Kg). Injecting a relatively large volume of fluid in leaky blood vessels can cause petechiae.

Maxeiner and Winklhofer analyzed 474 autopsies. Resuscitation efforts (RES) were done in 144 cases (31%). Nineteen percent of these victims presented with petechial bleedings, predominantly in the conjunctivae, compared to only 11% in the non-RES group. The analysis revealed an influence of the following factors in the development of petechial bleedings: cause of death, age of the person, and the body mass of the person [42].

Furthermore, the frequency and density of intrathoracic and subconjunctival petechiae were studied in 250 cases of sudden infant death syndrome (SIDS) and 69 controls. Intrathoracic petechiae were found significantly more frequently in the SIDS group (91.2% SIDS; 42% controls; p < 0.001) and were present at a higher density (p < 0.001). In addition, subpericardial and thymic petechiae were detected at high density in older SIDS infants [43].