Doctors of Seattle Children’s Hospital (SCH), who are also professors of the University of Washington, poisoned an infant patient with formulas in 2013 after their cover-up of his metabolic condition. It would have connected the disastrous injuries to their negligence, which was failing to check his blood glucose in the PICU for over 40 hours (PDF) when the patient was put on fasting. Let’s start with two urine organic acids lab cover-ups.
On Apr. 09, 2013, a normally healthy, six-month old infant was referred to SCH for full body swelling with a fever. The patient was diagnosed with acute liver failure (ALF) the next morning without an etiology. Then he had critically low glucose again* at 5:00AM on Apr. 12th after fasting. The overnight hypoglycemia (low glucose) indicated a metabolic condition: fatty acid oxidation disorder (FAOD). The SCH pediatric intensive care unit (PICU) ordered both urine organic acids and plasma acylcarnitine profiles to investigate the possibility of an FAOD, following the algorithm in the textbook edited by [glossary]Jerry J Zimmerman, MD, PhD[/glossary], who was the patient’s attending physician and the SCH PICU director.
1. However, the only urine organic acids lab after the critical event, ordered on Apr. 12, 2013, was cancelled by [glossary]Rhona Jack, PhD[/glossary] of the SCH biochemical lab 6 days later, when the lab should have been completed.
* This was the 2nd hypoglycemia in 3 days. The ED cancelled his glucose lab to hide the 1st hypoglycemia, resulting in acute liver failure (ALF).
2. The SCH biochemical lab made up an excuse to hide the diagnosis that can be found using another urine organic acids lab (PDF) with a specimen collected eight hours before the critical event. The elevated dicarboxylic acids are indicative of FAOD. However, the lab report, signed by [glossary]Rhona Jack, PhD[/glossary], attributed the elevations to dietary MCT while the formula that the patient was given, NUTRAMIGEN, has no MCT (PDF).
This lab pointed to the patient’s secondary FAOD, ACAD9 deficiency, which was confirmed by another source. Both BCM and CCHMC refused to release the raw data.
The SCH PICU also ordered a plasma acylcarnitine profiles lab for the cover-up only. Instead of asking for the Newborn Screening (NBS) values, every baby’s first lab, which are acylcarnitine profiles READY for interpretation from the Washington state Department of Health (DOH), they collected a specimen NOT during the critical event, but when his glucose had been CORRECTED for more than four hours.
In the same textbook by [glossary]Jerry J Zimmerman, MD, PhD[/glossary], he wrote, “Diagnostic metabolic laboratory studies are most likely to provide definitive information if performed on clinical samples obtained at initial presentation and before any therapy is initiated. Failure to obtain the necessary specimens at this time may miss an important diagnostic window of opportunity.” The SCH PICU delayed the speciment timing to be four hours after the treatment to hide the diagnosis.
1. SCH used a specimen taken NOT during the critical event at 5:00 AM, but at 10:25 AM by nurse Talia Osurman when the glucose had been corrected for 4.5 hours. (Order information – below, the lab report – right.)
2. There was a blood specimen from the critical event, but this was not used and later destroyed.
3. SCH withheld the urine organic acids and acylcarnitine profile reports from the patient’s family and Best Doctors –a review service- for 8 months (PDF), telling the parents that both results were normal.
Although the glucose had been corrected, the C16, still elevated, pointed to the patient’s primary fatty acid oxidation disorder (FAOD): either CPT-II or CACT deficiency.
The PICU stopped the request for newborn screening (NBS) values and continued to give the patient the harmful formula, Nutramigen.
On a baby’s NBS - an acylcarnitine profile using blood spots on Guthrie card, there are two reports: a regular report and a report with analyte values. When a patient shows symptoms, doctors should interpret the values using acylcarnitine reference ranges instead of checking a regular report, which only screens a few diseases. (WA doesn’t screen CPT-II deficiency.)
Information released by WA Department of Health (DOH) shows that SCH did request NBS, TWICE on Apr. 10 2013.
The TWO requests showed that SCH knew that a NBS can be used for diagnosis (PDF).
Unfortunately, the 1st RECEIVED NBS was a regular report (on right). PICU asked again and received the same report.
1. On the night of Apr. 11, the father heard and saw that a male PICU staff member wrote down a request by Dr. Laura Chen, a resident doctor, asking for a NBS with values, not a regular report, to be requested from the DOH the first thing next morning. This request was evidently stopped as the DOH did not receive any more after Apr. 11.
The patient was put on fasting by resident doctors based on a normal regular report when his attending physician on Apr 10, [glossary]Lincoln S. Smith, MD[/glossary] was absent.
2. After the SCH PICU stopped the NBS request and manipulated the acylcarnitine lab, they continued to give the patient Nutramigen formula, which derives 50% of its total calories from long chain triglycerides (LCT). However, the WA DOH requires
3. The harm caused by the formula was stopped by the parents around 11:45pm on Apr 13 when they practically commanded the PICU to replace Nutramigen with IV glucose after Dr. Zimmerman did not show up for 7 hours to address the formula issue. (PICU has up to 60 hours over weekends, not 12 overnight, to harm a patient as shown on the right.)
This action against the doctor’s order was not documented by Dr. Zimmerman. He did not speak to the family during his 3-day service. The patient’s family calls [glossary]Jerry J Zimmerman, MD, PhD[/glossary] the 1st murderer in Seattle Children Hospital and the University of Washington.
The next morning, Apr 14, the parents asked SCH PICU to investigate FAOD before considering any other diseases and shared with them one paper. The parents also shared it with the new metabolic doctor, [glossary]Sihoun Hahn, MD, PhD[/glossary], who documented this (PDF). The PICU asked the parents to wait for [glossary]Simon P. Horslen, MD[/glossary].
Uncertain about the patient’s condition, the parents took his GI doctor’s advice, giving him EleCare, a formula that derives 30% of its total calories from LCT. The patient’s ammonia slowly climbed to 128, ~4x the normal maximum (33 mcmol/L), before a liver biopsy on Apr 18th.
Dr. Horslen, the ALF expert of SCH, promised that the biopsy would give an answer. He assured the parents that SCH’s most experienced pathologist would review the biopsy on Apr 15.
The CPT-II deficiency, based on the NBS marker C16, was confirmed by CPT-II enzyme activity values. Opinions of multiple professionals will be presented together.
The SCH pathology lab cover-up was the most notorious because many SCH doctors, who were also UW professors, were involved.
“13.2 Handling a Liver Biopsy Specimen for Suspected Metabolic Disease
At least two cores of liver tissue should be obtained. … Freeze one core of liver tissue or one slice of a surgical biopsy specimen in anticipation of need for biochemical or genetic analysis.”
“13.6.3 Diagnosis (of FAOD)
Diagnosis is usually based upon a characteristic abnormal urine acylcarnitine profile … and plasma acylcarnitine profile … from Guthrie card bloodspots, organic acid profiles, and studies of fatty acid processing performed on cultured fibroblasts. Mutation analysis is available for the most common mutations in MCAD.”
1. One of the two cores, intended for biochemical or genetic analysis, was missing. The surgeon, [glossary]Patrick J. Healey, MD[/glossary], told the parents that he took two good specimens. (As shown in the picture on right.)
2. The parents were told that the patient’s original pathologist was replaced. In the 2nd page of the pathology report, [glossary]Erin R. Rudzinski, MD[/glossary] wrote, “Preliminary findings were reviewed with Dr. Simon Horslen on 4/19/13 at approximately 14:30h”. Dr. Healey told the parents in the 4/18 afternoon that the report should have been out when he delivered the picture. Who was the ORIGINAL pathologist?
3. The urine organic acids lab was cancelled at 10:11 AM, 27 minutes after the surgery procedure finished at 9:44 AM. It means that the lab was cancelled after [glossary]Simon P. Horslen, MD[/glossary] had seen the injuries.
4. Many other cover-ups are marked in the pathology reports (right): 1 – no clinical history for a patient with a 10-day stay; 2 – there was a 3rd pathologist, with initial [MA] which is identical to the initial of SCH lab director, [glossary]Michael Lee Astion, MD, PhD[/glossary]; etc. Three pathologists, one hepatologist, and one surgeon were involved in this fraud. At least two were medical directors. (PDF)
[MA] and Dr. Horslen used Dr. Erin R. Rudzinski, who only worked at SCH for 3 months, to sign the report hiding the diagnoses: liver injuries from acute starvation and FAOD.
SCH did not treat the patient’s partially recoverable acute injuries: fatty change. Instead, they put him on the UNOS transplant waiting list to control him; then tested him PRECISELY for the purpose of poisoning him by overloading his liver with a formula with too much fat.
The treatments of FAOD infants include avoiding fasting and low fat diets: formulas with 10% LCT calories, high carbohydrate foods and MCT supplements.
1. On Apr 22, SCH put the patient on the transplantation waiting list. They did nothing to treat the patient’s acute injuries for FOUR DAYS after his biopsy on April 18. As soon as his father signed the transplant paperwork at around 10:40, they changed the patient’s formula.
2. They actually did a comparison without telling the parents. First, they gave the patient Pregestimil – which has 20% LCT, plus polycose - a carbohydrate for FAOD patients, reducing his ammonia from 105 to 53 in one day. Then, they gave him Pregestimil ONLY, which increased ammonia to a stable 62, ~2x of the normal max, in two days. The 2nd one is obviously harmful, but the parents did not know until they saw the Nutrition Progress Note years later.
3. On Apr 25, 2013, SCH discharged the patient with a diagnosis of End Stage Liver Disease (ESLD) of unknown etiology (reason of disease). SCH prescribed Pregestimil to the patient, without the beneficial polycose*.
4. Dr. Simon P. Horslen told the father that the liver was 90% permanently injured and he expected a transplant within 30 days. The parents asked about the patient’s new liver cells as he was just an infant, but Dr. Horslen said the bridging fibrosis left no room for new cells to grow. They would die outside the liver in lumps (as shown above – not the patient’s picture). Dr. Horslen explained more below in his email in red, and denied FAOD (PDF).
The patient’s family calls Dr. Simon P. Horslen the 2nd murderer of SCH and UW.
*If they had not changed the formula, the patient would have died in hospital and lawyers may have taken this case. SCH’s plan was to murder him slowly.
One year of care at SCH was one year of crimes. Former CHP hepatologist, [glossary]Benjamin L Shneider, MD[/glossary], was the 1st doctor to refuse to cover for SCH.
The graph below is the timeline of the patient’s ammonia levels* and diets. Green boxes on top are diets, the line shows the ammonia levels, and blue boxes on bottom are major events.
The graph shows that ammonia increased whenever the patient was given formulas. It decreased when he was given glucose (D5, D10) or a low fat diet.
The parents did the right thing after the discharge; they gave him a low-fat diet, considering his liver cirrhosis. His ammonia dropped to 25 in a month.
The transplant did not happen as SCH said it would, so the parents became concerned about the unknown etiology. They asked Best Doctors to review his case. Though MGH brought up about 10x more steatosis – fatty change, UCSF Benioff and Lurie Children’s doctors offered little help. The family quickly fell in the trap as SCH introduced more fat in his diet as often as possible.
1. In Aug 2013, when the father asked [glossary]Karen F. Murray, MD[/glossary] about the patient’s thinning limb muscles, reddening hair, fishy odor, large belly and significant weight loss - the symptoms from protein-energy malnutrition (PEM) - she neither addressed his questions nor documented them (PDF), likely because his PEM was caused by the SCH acute starvation. (PDF) However, the acute starvation caused his body weight to drop from 50 percentile to less than 5 percentile as shown in the growth chart. Instead of correcting the excessive protein in the patient’s diet then by adding carbohydrates, she took this chance to increase Pregestimil intake by 20%. The patient became weak and lethargic. His ammonia slowly climbed in the next several months before a terrible incident happened (below). Considering she was the GI head, the parents thought that she knew the diagnosis and made this suggestion to harm the patient on purpose.
2. In Dec 2013, [glossary]Simon P. Horslen, MD[/glossary] convinced the father that his son did not have an FAOD by using a genetic report (PDF) from Baylor College of Medicine (BCM), signed by [glossary]Christine M. Eng, MD[/glossary] and [glossary]Yaping Yang, PhD[/glossary]. The parents then gave the patient full eggs, and did not notice that he got sick quickly from egg yolk. Soon, he was getting worse and looked like he was dying on New Year’s Eve. This near-death experience convinced the parents that their son had an FAOD and changed his diet immediately. His GFR was still critically low at 44 (normal > 120) a week later, meaning his kidney was losing its function. (PDF) His ammonia returned to normal range after 3 months. However, SCH continued denying his FAOD and making harmful suggestions. (PDF) In July 2014, the parents took their son to Children’s Hospital of Pittsburgh (CHP) of UPMC.
July 2014, CHP of UPMC
[glossary]Areeg Hassan El-Gharbawy, MD[/glossary], a genetic doctor who took this case from the department chief [glossary]Gerard Vockley, MD[/glossary], denied the patient’s FAOD as a representative of the CHP genetics department. She sent everything to Dr. Vockley. (PDF)
[glossary]Benjamin L Shneider, MD[/glossary], the director of pediatric hepatology, told the parents, “You will never get a diagnosis in US.”, “A diagnosis is just an opinion.”, and “Find a lawyer.” Dr. Shneider declined to make comments on the patient’s metabolic condition.
Dr. Shneider said that the SCH biopsy showed that permanent injuries were around 5% at the moment of biopsy, no more than 10%. Compared to being told 90% was permanently injured, the parents realized SCH’s crimes. Dr. Shneider said that the other injuries were acute and partially recoverable.
Dr. Shneider promised not to discuss this visit with SCH. (PDF) He left several months later for Texas Children’s.
*SCH doctors closely monitored the poisoning by testing ammonia regularly. None of the hepatologists of CHP, OHSU, and CCHMC tested the patient’s ammonia.
WA state CPS and DOH helped SCH cover their crimes. The CPS and hospitals’ cover-ups put the family in a difficult position*.
The parents decided to take the patient to Oregon, not staying with SCH transplant program. However, WA Children Protective Service (CPS) visited the night before their OHSU appointment.
Whoever made the false report was attempting a medical kidnapping!
([glossary]Evelyn Kanyu Hsu, MD[/glossary]: PDF1 on diagnosis miss, and PDF2 on CPS)
Thankfully, the WA CPS cleared the parents, finding the claim “Unfounded”. US hospitals often divert the parents’ anger to CPS through medical kidnapping: all beginning from the doctors’ false accusation of the parents’ negligence. National media demonize CPS so that the parents become protective. Some children are taken away by the CPS. And often times, these children die under foster care (PDF). Thus, hospitals escape their responsibility. Watch shocking videos below:
Nancy Schaefer Memorial
WA state DOH covers for SCH by claiming that the ordeal with the patient’s pathology lab was a normal practice and refusing to investigate the patient’s diagnosis. On the contrary, the DOH will punish any staff who causes a hospital loss. A former SCH nurse, MS Kimberly Hiatt, committed suicide (PDF) after she was punished by the DOH when she admitted her negligence to a co-worker.
Back to the visit in Oct 2014. [glossary]Yasemen Eroglu, MD[/glossary] of OHSU found that the patient’s pancreas was injured as well.
She consulted an OHSU metabolic doctor and then made the suggestion to use medicine to absorb long chain fat. It was an inevitable treatment after three hospitals denied the patient’s FAOD condition. WA DOH, CPS, SCH, CHP, and OHSU put the parents in a difficult position*. But Dr. Eroglu kindly offered the parents another choice, “I will refer you to any doctor you choose if you still have a concern!”
The parents chose [glossary]William F. Balistreri, MD[/glossary] of Cincinnati Children's Hospital Medical Center (CCHMC).
*The parents had to either follow the order to poison their son or possibly let him be taken away by the CPS for NOT GIVING HIM ENOUGH long chain fat.
[glossary]William F. Balistreri, MD[/glossary] was the only doctor who did a thorough examination on the patient (PDF). He also ordered a MetaboSeq Fatty Acid Oxidation Defects Panel. He, [glossary]Amy T Sheil, MD[/glossary]*, and [glossary]Kevin E. Bove, MD[/glossary] wrote: “metabolic”, “collapse”, and “not ESLD” after reviewing SCH biopsy slides.
On March 4, 2015, the parents took the patient and his elder brother to CCHMC:
1. [glossary]James E. Squires, MD[/glossary], Dr. Balistreri’s student, said that both brothers had a similar metabolic condition because both showed elevated CPK. (Click here for all labs.) They would work on the patient since he had severe organ injuries.
2. Dr. Balistreri said that for some infants with certain diseases, their organs will be permanently injured if they are put on fasting for more than 12 hours.
3. Dr. Balistreri ordered MetaboSeq Fatty Acid Oxidation Defects Panel after he reviewed the hypoglycemia, acylcarnitine profile, and urine organic acids from SCH.
4. The NBS and the pathology report were not discussed due to lack of time.
Later, [glossary]William F. Balistreri, MD[/glossary], [glossary]Amy T Sheil, MD[/glossary], and her mentor [glossary]Kevin E. Bove, MD[/glossary] reviewed SCH slides together. They reported that it was metabolic, featured collapse, remotely related to FAOD, survived an insult, but NOT ESLD. We will explain two below:
5. “the blue staining is not intense, but rather lighter, suggestive of collapse.” Collapse is severe acute hepatocyte injuries exceeding the capacity of the liver cells’ regenerative capacity. (PDF on the injuries process.)
6. “A FAOD may also be a remote possibility.” FAODs will not cause organ injuries when treated properly, such as in the patient’s brother. The patient’s injuries were from the wrong treatment - prolonged fasting without monitoring. (PDF of Intake Record.)
Pathway for mitochondrial fatty acid beta-oxidation: the letters represent key enzymes that use long chain fatty acid to generate glucose.
The perfect visit was tarnished by a CCHMC lab fraud from [glossary]Arnold W. Strauss, MD[/glossary], CCHMC’s former chief medical officer. Of the 11 mutations on ACAD9, only one was reported. The parents were told the exome sequencing should not fail IF both brothers have the same disease, it may reveal the trick that hospitals use: ClinVar to track patients (PDF). Their requests of sequencing data were declined by both BCM and CCHMC.
However, one other lab done by the Center of Inherited Disorders of Energy Metabolism (CIDEM) of Case Western Reserve University (CWRU) before this visit explained everything.
*[glossary]Amy T Sheil, MD[/glossary], the only doctor who told us that the NBS can be used for diagnosis, left CCHMC after signing the patient’s pathology report. (Click to read her email.)
The enzyme activity reports based on NBS confirmed CPT-II deficiency and nationwide lab frauds. It also explained how the patient landed in SCH after a fever and why he survived.
Hinted by [glossary]Benjamin L Shneider, MD[/glossary]-"You will never get a diagnosis in US.", the parents changed the patient’s PCP and took him to University Hospitals on Dec. 03, 2014. They told [glossary]Jirair Bedoyan, MD[/glossary] the complete medical history but changed the location to China, and then presented him the patient’s NBS values. He immediately pointed out it was CPT-II deficiency, not CPT-I, and needed to be differentiated with CACT deficiency. (ACMG Algorithm PDF)
Dr. Bedoyan ordered both CACT and CPT(s) labs
The CACT activities are normal using a T-75 test vs T-75 reference (PDF). CPT-II deficiency was denied by using T-75 test vs T-25 reference, a factor of 3x in size. After using the CPT-I to CPT-II ratio, which is not affected by the flask sizes, the increased CPT-I becomes normal and the normal CPT-II becomes deficient. We explain more details below:
1. In L#06, the CPT-I sensitive forward reaction are 3.5, 3.6, vs 3.0 (new reference), indicating normal CPT-I.
2. In the “Control” Column (red box), L#02 and L#06 show very close values, 3.7 vs 3.6, indicating that CPT-II is not effective at all. This severe infantile form explains how the patient landed in SCH ED after a fever.
3. In L#02, the values shows apparent deficiency (4.5 vs 8.7) with some residue (not so low as 3.7). It is adult form CPT-II deficiency. It explains why he survived.
The differences are called thermolability (sensitivity to temperature). It is typically measured at 37 degrees C and 41 degrees C respectively.
This is the most useful lab report, but it is still a fraud.
CPT-II (aka CPT2) deficiency is the most common muscular metabolic condition. There are 3 phenotypes (PDF):
1. Lethal neonatal form: is almost invariably death regardless of intervention. (Activities,
Click to read the SCH transplant team’s plan and the GI’s last notes:
SCH underestimated his enzyme activities at normal temperature.
Just like Dr. Balistreri, Dr. Bedoyan spent more time on the patient than scheduled. He and his student, Dr. William Hannah spent their lunch time helping the patient with the skin biopsy. They are great doctors. After discovering the mistake, the parents asked CIDEM about the T-25 reference. [glossary]Charles Hoppel, MD[/glossary] claimed that the T-25 was a typo. It should be T-75, but the interpretation stays the same. (PDF – CPT-II and replies.)
Petition to Washington, Ohio, Texas, Pennsylvania, and the US Federal Government
The patient deserves an honest diagnosis of his metabolic condition and etiology of his multiple organ injuries through government investigations to put his care on track as soon as possible, instead of his endless suffering and being cheated for years by the US healthcare system (right) which is turning many doctors to cheats and criminals.
- How much exactly are the activity levels of the patient’s two FAOD enzymes – CPT-II and ACAD9 at 37 degrees C and 41 degrees C respectively compared to those of a normal person? Are they deficient?
- How were the patient’s liver and pancreas injured? (Plus possible heart, brain, and muscle injuries.)
- The family requests that BCM and CCHMC release the patient’s sequencing data, their lab references and standards, and report all mutations related to fat metabolism to the family and doctors. They also request CWRU to release CPT-I/CPT-II ratio at 37 degrees C and 41 degrees C respectively compared to those of a normal person, which are not affected by flask sizes. Did these expensive labs meet American clinical lab standards (PDF)?
Every year, hundreds of kids die under foster care. Some die after they were taken away for medical neglect (PDF). Unlike tragic Alfie Evans (PDF), this patient’s survival gives the corrupted US government and the evil US health care system a chance to make America a safe place to raise kids, please investigate:
- Are the following SCH actions intentional cover-ups for this infant patient’s metabolic condition: cancelling the urine organic acids lab, evading the FAOD diagnosis using the MCT excuse, manipulating the blood timing for plasma acylcarnitine profile lab, stopping the request of the newborn screening (NBS) analyte values to the DOH, and a pathology lab with numerous problems – including a missing core specimen and changing pathologists? What did his original pathologist do on Apr. 18, 2013?
- For an infant with acute liver failure and FAOD, SCH transplant program doctors prescribed a formula with more fat than WA state standard, PICU, GI, and metabolic doctors used every chance to introduce more fat in his diet, and they monitored toxic ammonia at the same time. How does the WA DOH handle these SCH crimes?
- Who reported that the parents were not giving their son enough protein? If it is a doctor, how can the DOH prevent doctors from abusing Children Protective Service (CPS)?
- Sedgwick, a 3rd party hired by SCH, denied all claims without interviewing any doctor they asked for (PDF). Please release all the investigation documents.
- The American Medical Genetics failed on the patient, even with all the labs and doctors. Please investigate the cover-up by the division of medical genetics at CHP of UPMC.
- Why did the SCH PICU, transplant, and GI directors fail one after another? Were there any higher authorities involved?
The family would like to share all the records they have received, the genetic data, and anything necessary to assist the investigations. These professionals are critical for investigations:
Doctors that helped the family: SCH – Dr. Laura Chen, [glossary]Jorge D. Reyes, MD[/glossary]; CHP – [glossary]Benjamin L Shneider, MD[/glossary]; OHSU – [glossary]Yasemen Eroglu, MD[/glossary]; UHs – [glossary]Jirair Bedoyan, MD[/glossary], CWRU – [glossary]Charles Hoppel, MD[/glossary], CCHMC – [glossary]William F. Balistreri, MD[/glossary], [glossary]Amy T Sheil, MD[/glossary], [glossary]Jorge A. Bezerra, MD[/glossary], and [glossary]Kevin E. Bove, MD[/glossary].
Doctors that ignored the patient’s health, some of which harmed the patient on purpose: SCH – [glossary]Jerry J Zimmerman, MD, PhD[/glossary], [glossary]Simon P. Horslen, MD[/glossary], [glossary]Karen F. Murray, MD[/glossary], [glossary]Sihoun Hahn, MD, PhD[/glossary], [glossary]Lawrence Merritt, MD[/glossary], [glossary]Evelyn Kanyu Hsu, MD[/glossary], [glossary]Erin R. Rudzinski, MD[/glossary], Pathologist [MA], [glossary]Rhona Jack, PhD[/glossary]; CHP – [glossary]Areeg Hassan El-Gharbawy, MD[/glossary], [glossary]Gerard Vockley, MD[/glossary]; BCM - [glossary]Christine M. Eng, MD[/glossary], [glossary]Yaping Yang, PhD[/glossary]; CCHMC – [glossary]Arnold W. Strauss, MD[/glossary]; UCSF Benioff – [glossary]Philip Rosenthal, MD[/glossary]; CHC – [glossary]Barbara K. Burton, MD[/glossary]; SCH nurse – MS. Talia Osurman, who told a resident doctor that she knew it was wrong, but she was told to do so around 10:25, Apr 12, 2013.
Please watch the videos below.
Every year, hundreds of kids die in foster care in the United States, many of them taken from their parents through medical kidnapping (PDF, Link). Our story told you what happened in Seattle Children’s Hospital before an attempted medical kidnapping, which started when a doctor filed a false claim against the parents (PDF). Watch the videos below which explain the harsh reality:
A medically kidnapped child, also a Washington state resident, died under foster care. (PDF on the filmmaker and his unfinished film, Youtube)
A society will be judged on the basis of how it treats its weakest members, or children. - from Nancy Schaefer Memorial 2017: A Fathers Plea.(Youtube)
The cruel crimes in Seattle Children’s Hospital should inspire Americans to save lives by preventing hospitals from abusing the CPS to cover their crimes.