Court Opinion

ID: 7801095
Source: CourtListenerOpinion
Date Created: 2022-08-16 21:01:49.501192+00
Date Added: 2024-06-11T16:29:14.225023
License: Public Domain

In the United States Court of Federal Claims
                                  OFFICE OF SPECIAL MASTERS
                                        Filed: July 29, 2022

* * * * * * * * * * * * * * * *                   *
CARLA ADAL and MATTHEW SHIEL,                     *      No. 15-1496V
as parents, next of kin, and on behalf of         *
Z.S., a deceased minor,                           *      Special Master Sanders
                                                  *
              Petitioners,                        *
                                                  *      Denial of Entitlement; Pneumo-
v.                                                *      coccal Conjugate Vaccine (“PCV”);
                                                  *      Haemophilus B Conjugate Vaccine
SECRETARY OF HEALTH                               *      (“HiB-OMP”); Diphtheria-Tetanus-
AND HUMAN SERVICES,                               *      Acellular-Pertussis Hepatitis B
                                                  *      Inactivated Polio Vaccine (“DTaP-
              Respondent.                         *      HepB-IPV”); Table Encephalopathy;
* * * * * * * * * * * * * * * *                   *      Death.
Russell W. Lewis, IV, Johnson Law Group, Nashville, TN, for Petitioner.
Naseem Kourosh, United States Department of Justice, Washington, DC, for Respondent.

                                  DECISION ON ENTITLEMENT 1

        On December 10, 2015, Carla Adal and Matthew Shiel (“Petitioners”) filed a petition for
compensation under the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10
to -34 (2012). 2 (“Vaccine Act” or “Program”). Petitioners alleged that Z.S., Petitioners’ minor
child, received pneumococcal conjugate (“PCV13”), haemophilus B conjugate (“HiB-OMP”), and
diphtheria-tetanus-acellular-pertussis, hepatitis B, and inactivated polio (“DTaP-HepB-IPV”)
vaccines on November 18, 2014, and thereafter died on November 19, 2014, and that said death
was “caused in fact” by the vaccinations. Pet. at 1, ECF No. 1. Petitioners did not file an amended
petition. However, in their post-hearing briefs, Petitioners clarified that “[f]or the reasons argued
at the hearing and in [P]etitioners’ pre- and post-hearing submissions, [P]etitioners request that the
Court find [P]etitioners entitled to compensation based on the existence of a Vaccine Table
encephalopathy.” 3 Pet’r’s Post-Hrg. Br. at 30, ECF No. 67. After carefully analyzing and weighing
1
  This Decision shall be posted on the United States Court of Federal Claims’ website, in accordance with
the E-Government Act of 2002, 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of
Electronic Government Services). In accordance with Vaccine Rule 18(b), a party has 14 days to identify
and move to delete medical or other information that satisfies the criteria in § 300aa-12(d)(4)(B). Further,
consistent with the rule requirement, a motion for redaction must include a proposed redacted Decision. If,
upon review, I agree that the identified material fits within the requirements of that provision, such material
will be withheld from public access.
2
  National Childhood Vaccine Injury Act of 1986, Pub.L. No. 99–660, 100 Stat. 3755. Hereinafter, for ease
of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa
(2012).
3
  Encephalopathy is generally defined as “any degenerative disease of the brain.” Dorland’s Illustrated
Medical Dictionary 1, 614 (32nd ed. 2012) [hereinafter “Dorland’s”].
the evidence presented in this case in accordance with the applicable legal standards, 4 I find
that Petitioners have not presented preponderant evidence that Z.S. suffered from a Table
encephalopathy or that her vaccinations were the cause-in-fact of her death.5 Accordingly,
Petitioners’ case is dismissed.

    I.      Procedural History

        On December 10, 2015, Petitioners filed a petition for compensation on behalf of Z.S. Pet.
Petitioners allege the pneumococcal, HiB-OMP, and DTaP-HepB-IPV vaccines Z.S. received on
November 18, 2014, caused her death. Id. Medical records and affidavits from Petitioners were
filed along with the petition. Pet’r’s Exs. 1–14, ECF Nos. 1-2–1-15. Petitioners filed a statement
of completion on December 17, 2015. ECF No. 8. On February 3, 2016, Petitioners filed additional
records, including VAERS and fire and police department reports, and an amended statement of
completion. Pet’r’s Exs. 15–17, ECF Nos. 11–12.

        On March 8, 2016, Respondent filed his Rule 4(c) report indicating that this case was not
appropriate for compensation. Resp’t’s Report, ECF No. 13. Thereafter, Petitioners filed an expert
report from Dr. Adel Shaker on July 18, 2016. Pet’r’s Exs. 18–19, ECF Nos. 19-1–19-2. In
response to Petitioners’ expert report, Respondent filed a motion to dismiss or, in the alternative,
for an order requiring Petitioners to file a supplemental expert report from Dr. Shaker that “more
clearly states his theory of causation.” ECF No. 22 at 1. Petitioners filed a response to
Respondent’s motion on September 8, 2016, requesting an opportunity to discuss the deficiencies
in their original report and to file a supplemental expert report. ECF No. 24 at 2. The presiding
special master ordered Petitioners to file a supplemental expert report. ECF No. 25.

        This case was reassigned to me on January 12, 2017. ECF Nos. 26–27. On March 7, 2017,
Petitioners filed a supplemental expert report from Dr. Janice Ophoven. Pet’r’s Exs. 20–21, ECF
Nos. 29-1–29-2. Respondent filed a status report on March 28, 2017, indicating that Petitioners
would provide him with the autopsy slides and copies of the autopsy photographs reviewed by
their expert in her report. ECF No. 31. On June 9, 2017, Respondent filed an unopposed motion
for an extension of time to file his expert reports or, in the alternative, for an order directing
Petitioners to file a supplemental expert report specifying information regarding the autopsy slides
relied on by Petitioners’ experts. ECF No. 32. I granted Respondent’s motion and ordered
Petitioners to file a supplemental expert report with more specificity regarding the autopsy slides.
ECF Nos. 33–34. Petitioners filed a supplemental expert report from Dr. Ophoven on July 12,

4
  While I have reviewed all of the information filed in this case, only those filings and records that are most
relevant to the decision will be discussed. Moriarty v. Sec'y of Health & Hum. Servs., 844 F.3d 1322, 1328
(Fed. Cir. 2016) (“[w]e generally presume that a special master considered the relevant record evidence
even though he does not explicitly reference such evidence in his decision.”) (citation omitted); see also
Paterek v. Sec'y of Health & Hum. Servs., 527 F. App'x 875, 884 (Fed. Cir. 2013) (“[f]inding certain
information not relevant does not lead to—and likely undermines—the conclusion that it was not
considered.”).
5
  Petitioners unequivocally stated that they did not provide, and the record does not show, a biological
mechanism pursuant to Althen prong one. See Pet’r’s Post-Hrg. Br. at 30; Resp’t’s Resp. at 19; Tr. 167–69.
Instead, they wished to proceed on a claim of Table encephalopathy. Therefore, a more thorough discussion
of Petitioners’ causation-in-fact claim is unnecessary.
                                                      2
2017. Pet’r’s Ex. 22, ECF No. 35-1. Respondent provided responsive expert reports from Dr. Sara
Vargas, Dr. Max Wiznitzer, and Dr. Sandra Alexandrescu on August 31, 2017. Resp’t’s Exs. B, B
Tabs 1–3; C–G, ECF Nos. 38-1–38-9. Respondent filed the medical literature referenced in his
reports on September 15, 2017. Resp’t’s Exs. F, Tabs 1–8, ECF Nos. 39-1–39-8.

       I scheduled this matter for an entitlement hearing to take place on May 4–5, 2020. Hrg.
Order, ECF No. 42. Petitioners filed their pre-hearing brief on February 28, 2020. Pet’r’s Br., ECF
No. 46. On March 30, 2020, Respondent submitted his responsive pre-hearing brief. Resp’t’s
Resp., ECF No. 47. I held a status conference with the parties on April 1, 2020, to discuss the
implications of the COVID-19 pandemic. Min. Entry, docketed Apr. 2, 2020. The next day, I
cancelled the entitlement hearing and ordered Petitioners to file a status report indicating how they
wished to proceed. Non-PDF Order, docketed Apr. 2, 2020. Petitioners filed a status report on June
30, 2020, requesting to reschedule the entitlement hearing. ECF No. 51.

        I rescheduled this matter for an entitlement hearing on February 22–23, 2021. Hrg. Order,
ECF No. 54. Respondent resubmitted medical literature and updated curriculum vitae per each
expert on February 16, 2021. Resp’t’s Exs. G–R, ECF Nos. 57-1–57-12. Petitioners resubmitted
highlighted medical literature the same day. Pet’r’s Exs. 23–27, ECF Nos. 59-1–59-5. On February
22, 2021, Petitioners filed an updated medical record. Pet’r’s Ex. 28, ECF No. 60-1. The
entitlement hearing was held as scheduled on February 22–23, 2021. See Min. Entry, docketed
Feb. 23, 2021. Petitioners filed their opening post-hearing brief on June 14, 2021. Pet’r’s Post-
Hrg. Br., ECF No. 67. Respondent filed his responsive post-hearing brief on July 28, 2021.
Resp’t’s Resp., ECF No. 72. On September 1, 2021, Petitioners filed their reply brief. Pet’r’s
Reply, ECF No. 74. This matter is now ripe for consideration.

     II.     Factual History 6

             a. Medical Records

        Z.S. was born healthy on July 23, 2013. Pet’r’s Ex. 3 at 1, ECF No. 1-4. Her medical
records document no relevant medical concerns during her first fifteen months of life. She was
regularly seen for well-baby check-ups with normal, age-appropriate development. See generally
Pet’r’s Ex. 5, ECF No. 1-6. Z.S. received her childhood vaccinations without any reported adverse
effects. See id. Z.S.’s medical records chart her growth from birth:

      Date         Age       Height      Percentile Weight        Percentile        Head          Percentile
                                                                               Circumference
    7-26-2013    1 day      18.5 in.                  6.75 lbs.                [13.19 in.]
                            [46.99 cm]                                         33.5 cm
    7-31-2013    5 days     19.75 in.    25-50th      6.6 lbs.    10-25th      [13.09 in.]        5-10th
                            [50.17 cm]                                         33.25cm
    10-1-2013    2 mos.     23.75 in.    90-95th      12.4 lbs.   10-25th      [14.96 in.]        25-50th
                            [60.33 cm]                                         38cm

6
 Both Petitioners provided affidavits in this case. The affidavits did not contain any new information or
details inconsistent with the narrative provided to police and reflected in the case report. See Pet’r’s Exs.
1–2, ECF Nos. 1-2–1-3.
                                                     3
    8-26-2014    13 mos.     29.75 in.     57th         19 lbs.     12th          [17.13 in.]        8th
                             [75.57 cm]                                           43.5 cm
    11-18-2014   15 mos.     31 in.        58th         20.6 lbs.   11th          [17.52 in.]        12th
                             [78.74 cm]                                           44.5 cm

Pet’r’s Ex. 5 at 7–11.

       On November 18, 2014, Z.S. presented for her fifteen-month well-child check-up. Id. at 3.
During that visit, Z.S. received pneumococcal, HiB-OMP, and DTaP-HepB-IPV vaccines. Id. The
vaccines were administered at approximately 9:30 a.m. Id.; see also Pet’r’s Ex. 1 ¶ 5. The medical
records do not indicate any adverse reaction. See generally Pet’r’s Ex. 5. Petitioners did not submit
additional medical records.

             b. Police and Fire Department Reports

        On November 19, 2014, at 7:36 a.m., Ms. Adal called 911 to report that Z.S. was not
breathing. Pet’r’s Ex. 17 at 3, ECF No. 11-3. Mr. Shiel began CPR per the operator’s instructions,
but upon arrival, EMS found Z.S. unresponsive and with “conclusive signs of death including
dependent lividity 7 and rigor mortis.” 8 Id.; Pet’r’s Ex. 16 at 6, ECF No. 11-2. The police incident
report contained statements from Petitioners. See Pet’r’s Ex. 17. They reported that Z.S. had
received three vaccines in her thighs the morning before, but “t[ook] the shots well.” Id. at 3. Ms.
Adal stated that she did not notice anything out of the ordinary. Id. at 4. She noted Z.S. was
“running warm and it was believed that she might have a fever.” Id. Ms. Adal “went through the
rest of her day holding [Z.S.] to comfort her,” and after dinner, gave Z.S. Children’s Tylenol for
her fever. Id. Ms. Adal reported that at approximately 6:30 p.m., she changed Z.S. and placed her
on her back in her crib. Id. Z.S. reportedly fell asleep without crying. Id.

        The fire department report notes Mr. Shiel “heard [Z.S.] coughing [during the] night.”
Pet’r’s Ex. 16 at 5–6. The police incident report reflects that Petitioners did not hear Z.S. or check
on her during the night. See Pet’r’s Ex. 17 at 4. Mr. Shiel stated that he “assumed [his three
children] were all asleep.” Id. The next morning, Mr. Shiel discovered Z.S. face down, motionless,
and cold. Id. Mr. Shiel told police that he “could see the livor mortis 9 already set and knew that
[Z.S.] was most likely beyond resuscitation.” Id. Despite his fears, he moved her to the master
bedroom and began CPR while Ms. Adal called paramedics. Id.

       Coroner investigator Priscilla Chavez arrived on scene and noted that rigor mortis was
passing and that liver mortis was set. Pet’r’s Ex. 8 at 12, ECF No. 1-9. There were no signs of
outward trauma. Id. Investigator Chavez pronounced Z.S. dead at 9:50 a.m. Id. at 11. There were

7
  Lividity refers to “the quality of being livid; discoloration, as of dependent parts, by the gravitation of the
blood.” Dorland’s at 1069.
8
  Rigor mortis is “the stiffening of a dead body, accompanying the depletion of adenosine triphosphate in
the muscle fibers.” Dorland’s at 1647.
9
  Livor mortis is another word for lividity. It is defined as the “discoloration appearing on dependent parts
of the body after death, as a result of cessation of circulation, stagnation of blood, and settling of the blood
by gravity[.]” Dorland’s at 1069.
                                                       4
no signs of criminal activity. See id. The police investigation was “closed non-criminal.” Pet’r’s
Ex. 17 at 5.

                c. Autopsy

       An autopsy was performed on November 20, 2014. Pet’r’s Ex. 8 at 1. The final pathologic
findings reflected “(I) Moderate cerebral edema;” 10 and “(II) Status post routine childhood
immunizations (A) Reported constitutional symptoms of lethargy, mild temperature elevation,
fussiness; (B) Mild acute inflammation and hemorrhage of injection sites.” Id. The coroner stated:

             This is a 15-month-old female [who] underwent a complete autopsy . . . She
             reportedly had constitutional symptoms following routine childhood immunization
             and was treated with acetaminophen. She was found deceased, prone in her crib,
             the morning following her immunizations. Despite extensive testing, no cause of
             death was identified, and no unequivocal link between her death and immunizations
             was established. For these reasons, the cause and manner of death are listed as
             undetermined.

Id.

        The coroner noted that Z.S.’s bacterial cultures and a metabolic screen were negative but
that her viral screen was positive for rhinovirus/enterovirus. 11 Id. at 8.

      III.      Fact Testimony

                a. Ms. Carla Adal

        Ms. Adal testified at the hearing largely to the same information she provided to the police
on November 19, 2014. See Pet’r’s Ex. 17. She also provided additional details from November
18, 2014, and the morning of November 19, 2014. Ms. Adal testified that following Z.S.’s
vaccinations on November 18, 2014, she put Z.S. down for a nap but noted she “napped longer
than usual.” Tr. 22:2. Ms. Adal said Z.S. was “fussier than normal,” and noted that “[i]t was very
clear [to Ms. Adal] that [Z.S.’s] legs were hurting.” Tr. 23:17, 24:2–3. Ms. Adal described Z.S. as
“extra tired and just lethargic.” Tr. 24:18. Z.S. also did not want to play or eat. Tr. 25:6–7. Ms.
Adal stated that Z.S. “was just blah. Very blah.” Tr. 25:7–8. When compared to Z.S.’s post-
vaccination condition from prior vaccinations, Z.S. “was in a lot more pain,” and “she slept longer
this time.” Tr. 28:18–22.

10
   Cerebral edema is the “excessive accumulation of fluid in the brain substance; causes include trauma,
tumor, and increased permeability of capillaries as a result of anoxia or exposure to toxic substances.”
Dorland’s at 593.
11
   Rhinovirus is “a genus of viruses of the family Picornaviridae that infect the upper respiratory tract and
cause the common cold. Over 100 antigenically distinct types infect humans; bovine and equine
rhinoviruses have also been isolated.” Dorland’s at 1640. Enterovirus is “a genus of viruses of the family
Picornaviridae that preferentially inhabit the intestinal tract. Infection is usually asymptomatic or mild but
may result in a variety of disease syndromes[.]” Id. at 626–27.
                                                      5
        Ms. Adal testified that she did not believe that she heard any sounds from Z.S. on the night
of November 18, 2014, “because normally, she would wake [Ms. Adal] up[,]” but she did not on
that occasion. Tr. 30:12–13.

        On cross-examination, Ms. Adal was asked about her statement to police that she did not
notice Z.S. acting differently after her vaccinations. Tr. 42:9. Ms. Adal stated that originally, she
thought her daughter was just exhibiting the normal level of tiredness from her vaccinations and
was “quieter[.]” Tr. 42:14–19. She noted that since that time, she has had the benefit of hindsight.
Tr. 42:15–16. Ms. Adal confirmed that post vaccination, Z.S. could hear her mother’s voice and
other sounds around her. Tr. 52:24–25, 53:1. Z.S. could also look at objects and she recognized
her mother, father, and brothers. Tr. 53:2–15. Ms. Adal testified that Z.S. did not vomit or indicate
that her head was hurting. Tr. 53:16–22. Ms. Adal did not “witness a seizure” or “notice the loss
of consciousness.” Tr. 54:12–16. She also testified that Z.S. was able to respond to her own name.
Tr. 54:22–23.

            b. Mr. Matthew Shiel

        Mr. Shiel described Z.S. as “kind of floppy” when he came home on the day she received
her vaccinations. Tr. 65:12. He testified that she “was[ not] her usual bouncy, energetic self[]” and
noted that “she seemed weighed down by her own weight.” Tr. 73:12–16. Mr. Shiel agreed that
“[l]ethargic would be a great word” to describe Z.S. Tr. 74:15. He continued, “she was hot, and
she was[ not] her normal self.” Tr. 65:13–14. Mr. Shiel said he was not concerned about Z.S.’s
condition at that time because he is “a firm believer [that his] children are very healthy . . . and the
body normally fixes itself.” Tr. 66:9–12. He noted that Z.S. specifically was “incredibly healthy”
and met her developmental milestones. Tr. 75:20. Z.S. could turn over in her crib if need be. Tr.
76:2–5. Mr. Shiel confirmed that he knew Z.S. was dead when he found her the morning of
November 19, 2014. Tr. 71:13–14. He testified that Z.S. “was perfectly conscious up until the time
she died in her sleep.” Tr. 66:25–67:1. Mr. Shiel expressed frustration about Z.S.’s level of
consciousness. He stated, “she did[ not] have any decreased consciousness until she died in her
sleep in a room by herself.” Tr. 76:16–18. Mr. Shiel did not remember telling the police that he
heard Z.S. coughing during the night. Tr. 82:24. He clarified that “if there had been any type of
noise from [Z.S.] that sounded unusual, then [he] would have responded.” Tr. 83:3–5.

     IV.    Experts 12

            a. Petitioners’ Expert, Janice Ophoven, M.D.

        Dr. Ophoven received her medical degree from the University of Minnesota in 1971.
Pet’r’s Ex. 21 at 1, ECF No. 29-2. Dr. Ophoven completed residencies in pediatrics and anatomic
pathology at the same institution in 1976 and 1979, respectively. Id. She completed a fellowship
in pediatric pathology at the University of Minnesota and Minneapolis Children’s Medical Center
in 1979. Id. In 1980, she completed an additional fellowship in forensic pathology at the Hennepin
County Medical Examiner’s Office in Minneapolis, MN. Id. Dr. Ophoven is board certified in
pathology and forensic pathology. Id. at 1–2. Dr. Ophoven served as the Associate Director, and

12
   Petitioners clarified at the hearing that they would not be relying on Dr. Adel Shaker’s expert report in
this matter and would not be citing to it in any post-hearing briefs that I allow. Tr. 189:11–14.
                                                     6
later the Director, of the St. Paul’s Children’s Hospital Laboratories from 1981–1985 and 1985–
1988, respectively. Id. at 2. She also served as the Deputy Medical Examiner of Hennepin County
from 1989–1992. Id. From 2002–2003, Dr. Ophoven served as a forensic pathologist for several
midwestern counties. Id. She performed the same role at the Minnesota Regional Coroner’s Office
for several other counties from 2003–2012, and simultaneously for the St. Louis County Medical
Examiner’s Office from 2003–2010. Id. Since 1981, Dr. Ophoven has participated in independent
consultations in the field of pediatric forensic pathology. Id. She holds numerous memberships in
several professional and scientific societies and committees. Id. at 3–4. Her curriculum vitae lists
approximately 128 publications, including articles, abstracts, book chapters, and presentations of
which she is a listed author. See id. at 4–12.

        During the hearing, Dr. Ophoven explained that she practices in “the field of injuries in
children . . . especially issues having to do with understanding how children die suddenly and
unexpectedly.” Tr. 90:2–6. Dr. Ophoven asserted that over her approximate forty-year career, she
has “made a significant contribution to not only the body of knowledge having to do with sudden
death in children, but also the principles of forensic pathology applying to sudden death in
childhood.” Tr. 90:25–91:1–3. She noted that during her time as a forensic pathologist, she has
“performed literally hundreds of autopsies on children mostly less than two years of age.” Tr.
93:11–12. Dr. Ophoven testified that she also teaches pediatric pathologists, emergency
physicians, and child abuse center personnel “the pathology and the process of investigating
sudden and unexpected death.” Tr. 93:17–20. Petitioners offered Dr. Ophoven as an expert in
pediatric forensic pathology without objection, and I recognized her as such. Tr. 95:25–96:1–13.

         Dr. Ophoven provided two expert reports in this case and testified at the entitlement
hearing. Pet’r’s Exs. 20, 22, ECF Nos. 29-1, 35-1; Tr. 88–180. Her first report was largely a
recitation of Z.S.’s medical history and the facts surrounding her death. See Pet’r’s Ex. 20. Dr.
Ophoven provided her opinion on the last two pages. Id. at 12–13. She noted the “examiner
identified moderate cerebral edema, with some widening of the gyri13 and narrowing of the
sulci.” 14 Id. at 12. Dr. Ophoven opined that “brain swelling in and of itself constitutes
encephalopathy as broadly defined – a disease, damage or malfunction of the brain.” Id. Dr.
Ophoven reiterated that brain swelling is a “diffuse disease of the brain alteration, pathological
change.” Tr. 153:22–23. She further opined that Z.S.’s condition also meets the definition of a
Vaccine Injury Table encephalopathy. Pet’r’s Ex. 20 at 12–13. She explained “[Z.S.] was too old
for the diagnosis of [sudden infant death syndrome (“SIDS”)]15 or positional asphyxia.”16 Id. at
13. She classified Z.S.’s “death as sudden death in infancy associated with cerebral edema
following triple childhood vaccination.” Id.

13
   Gyri, or singular gyrus, is “one of the convolutions of the surface of the cerebral hemispheres [of the
brain] caused by folding of the cortex[.]” Dorland’s at 813.
14
   Sulci, or singular sulcus, is the “1. anatomic terminology for a long groove or furrow, especially one of
the cerebral sulci. 2. a linear depression or valley in the occlusal surface of a tooth, having sloping sides
that meet at an angle.” Dorland’s at 1797.
15
   Sudden infant death syndrome is “the sudden and unexpected death of an apparently healthy infant,
typically occurring between the ages of 3 weeks and 5 months, and not explained by careful postmortem
studies[.]” Dorland’s at 1850.
16
   Positional asphyxia refers to the “pathologic changes caused by lack of oxygen in respired air, resulting
in hypoxia and hypercapnia[,]” caused by one’s position. See Dorland’s at 166.
                                                     7
        In a supplemental report, Dr. Ophoven asserted that the brevity of her initial report could
be explained by the “straightforward and basic pathological changes characteristic of cerebral
edema observed in the gross examination[,] as well as the microscopic tissue examination[,]” of
Z.S. Pet’r’s Ex. 22 at 1. Dr. Ophoven relied on the autopsy and “the postmortem photographs [that]
show brain swelling.” Id. She noted that her examination “showed a characteristic pathological
change known as spongiosis[,] 17 consisting of widespread vacuolization of cells due to excess
intercellular fluid.” Id. at 2. She asserted that “[f]rankly, no more description is necessary.” Id.
During the hearing, Dr. Ophoven expanded on this idea. Dr. Ophoven defined spongiosis as
vacuolization, or “a change of the cells that shows clearing between the cell membrane and the
nucleus.” Tr. 151:23–25. She testified that she indeed saw evidence of spongiosis on Z.S.’s brain
slides. Tr. 152:13–15.

          Dr. Ophoven’s testimony indicated that unlike a hospital-based autopsy, which
“delineate[s] pretty exhaustively the effects of care,” the forensic autopsy “is actually the proof
that sits underneath the manner and circumstance[,] as well as the cause of death.” Tr. 97:11, 21–
23. She added that the forensic report should also include “the other significant conditions that are
likely to have contributed to or were important to the forensic pathologist in making their opinion.”
Tr. 98:1–4. Forensic pathologists are “taught that the first thing that[ is] on the list should
summarize the most important finding.” Tr. 99:11–13.

        Dr. Ophoven noted two things in this case that the forensic pathologist “considered
important.” Tr. 99:7. Although the cause and manner of death are listed as undetermined,
“moderate cerebral edema and status post childhood immunizations would fit on that line as
important to the case but not necessarily causative of the sudden death.” Tr. 100:8–11. Dr.
Ophoven opined that “the presence of a moderate cerebral edema was not considered secondary
or artifact or [as an] unimportant finding” in this case. Tr. 99:13–15. However, Dr. Ophoven
acknowledged that “the brain swelling, although obviously present, did not have a fatal
consequence attached to it.” Tr. 101:1–3. In cases where brain swelling is the cause of death, there
should be evidence of “pressure at the brainstem.” Tr. 101:4–6. Likewise, Dr. Ophoven noted that
“the timing, of course, is important.” Tr. 99:24–25. And, based on her “review of how this case
was presented, . . . the immunizations had import in determining the circumstances of [Z.S.’s]
death.” Tr. 99:24–25, 100:1–2. Dr. Ophoven also acknowledged that the pathologist reported “no
cause of death identified and no unequivocal link between the death and immunizations.” Tr.
101:14–15. She clarified that “[u]ndetermined does[ not] mean you do[ not] know. It means that
there are multiple circumstances under which the death could have occurred.” Tr. 101:20–22.
Based off the important findings listed in the autopsy report, Dr. Ophoven concluded that the
coroner questioned “whether or not [Z.S.’s] death was because of natural causes or whether or not
it was an accidental complication of the immunization[s].” Tr. 101:24–25, 102:1.

        When asked about SIDS, Dr. Ophoven asserted that “unless there[ is] a recognized
neurologic deficit, a child of this age would not be vulnerable [to the condition] in a face[]down
position.” Tr. 106:7–9. She noted that the autopsy indicated that Z.S. was found face down, but
Dr. Ophoven did not consider “asphyxia, suffocation, anything like that to be a legitimate part of
the differential diagnosis here.” Tr. 106:15–17. She later definitively said that in this case, “the

17
  Spongiosis is the “intercellular edema of the epidermis, giving the tissue a spongelike appearance due to
the formation of micro[-]vesicles.” Dorland’s at 1755.
                                                    8
brain swelling and excessive brain weight excludes [sic] the diagnosis of SIDS.” Tr. 120:16–17.
Dr. Ophoven focused on the moderate cerebral edema documented in Z.S.’s case and noted that
“[b]rain swelling is in the eye of the beholder certainly, but there is a flattening of the surface of
the brain that is appreciated.” Tr. 106:23–25. She explained that “the appearance and texture” and
“the weight of the brain based on the child’s anticipated growth of development really are, at least
according to some references, the gold standard for determining [the] degree of brain swelling.”
Tr. 107:5–10. Dr. Ophoven disagreed with any argument that the swelling in this case occurred
postmortem because the pathologist did not make that indication. Tr. 154:1–14. She also
“disagree[d] that the changes that were seen in this brain are legitimately attributable to
postmortem change because of the extent and the other factors that are present in this case.” Tr.
154:18–21. Dr. Ophoven was unable to explain how to distinguish between premortem and
postmortem edema. She asserted that “[i]f the pathologist believed it to be a postmortem artifact,
they would not have listed it number one on the final diagnosis.” Tr. 156:22–24.

        The finding of brain swelling was supported, in Dr. Ophoven’s opinion, by “some widening
of the gyri and narrowing of the sulci.” Tr. 110:4–5. She explained that “[w]hen the brain swells,
it presses against the cranial vault and it kind of flattens the surface, and it makes the bulges tighter
so that the sulci are narrower.” Tr. 111:2–5. Dr. Ophoven noted that this finding is not
“measurable.” Tr. 111:6. She asserted that “by virtue of experience and age-specific criteria of the
feel, the texture, the consistency of the brain itself, you are able to make a determination that this
brain is swollen compared to a normal child this age.” Tr. 112:2–6. The training and experience of
the examiner are of paramount importance because the examiner has “to have enough experience
examining brains of youngsters to make a distinction between a normal brain and an abnormal
brain and then to pass a judgement.” Tr. 112:10–12. Dr. Ophoven testified that she agreed with the
pathologist’s finding that Z.S.’s brain was abnormal. Tr. 113:6–7.

         Dr. Ophoven counted Z.S.’s measurements from her well-child exams as another key factor
to aid in the examination and interpretation of Z.S.’s brain. She noted that “the child was measured
alive on the day of her immunization, November 18th, [2014,] and she was 31 inches, which
matched her normal growth curve perfectly.” Tr. 121:9–11. Based on this height, Z.S.’s brain
weight at autopsy would have been abnormal. Tr. 122:16. This is more reliable, according to Dr.
Ophoven, than Z.S.’s autopsy height of 33 inches. Tr. 122:4–9. Dr. Ophoven testified that “rigor
mortis was lapsing at the time [Z.S.’s weight] was measured, and the [33 inch] height is [therefore]
unreliable.” Tr. 122:7–9. Dr. Ophoven argued that measuring Z.S.’s brain weight according to the
range for a 33-inch child, which would make her autopsy brain weight normal, “puts her nearly a
year older and provides an inaccurate assessment of what a normal brain would be.” Tr. 122:13–
15.

         Dr. Ophoven described encephalopathy as “a reflection of abnormal brain tissue that is
typically associated with brain swelling,” and diagnosed Z.S.’s brain as encephalopathic. Tr.
114:14–15, 23–24. In support of her diagnosis, Dr. Ophoven relied on the National Institute of
Health’s (“NIH”) description of encephalopathy as “the presence of diffuse disease in the brain
that alters brain function or structure.” Tr. 123:7–9. She reiterated that this conclusion was based
on her training and experience, Z.S.’s brain weight, the pathologist’s observation of brain swelling,
and the presence of water in the brain cells. Tr. 115:1–4.

                                                   9
        When asked about Z.S.’s positive finding for a virus, Dr. Ophoven testified that it was “not
a virulent virus . . . that would be expected to take a child suddenly without any preexisting
symptomology.” Tr. 115:22–25. Dr. Ophoven named myocarditis 18 or encephalitis 19 as examples
of evidence of a fatal viral infection. Tr. 116:3–5. Most importantly, there was no evidence of
bronchitis. 20 Tr. 116:17–20. Dr. Ophoven concluded that the “[b]rain pathology indicating [the]
presence of encephalopathy within 24 hours of triple vaccination with no alternative explanation
for the brain swelling indicates [a] causal connection.” Tr. 124:4–7.

        On cross-examination, Dr. Ophoven admitted that she is not board certified in pediatric
pathology or neuropathology. Tr. 125:4–25. She also admitted that she has been retired since 2010.
Tr. 125:20. Dr. Ophoven was then asked what Z.S.’s brain weight should have been based on the
recorded height at her well-child examination. Tr. 144–45. Dr. Ophoven “would have suggested
that [Z.S.’s] brain weight would have been less than 1,000 grams, perhaps even between 8 and 900
grams based on the other organ weights of her heart and kidneys and so forth.” Tr. 146:6–8. Dr.
Ophoven was then challenged with an approximate average brain weight calculation of 1,050
grams based on a 31-inch child. Tr. 148:5 (citing Pet’r’s Ex. 26 at 2, ECF No. 59-4). 21 She
responded that she also considered other organ weights, “which put[ Z.S.] at a lesser anticipated
brain weight.” Tr. 148:14–15. Dr. Ophoven acknowledged “error in that [she] did[ not] come up
with a maximum anticipated brain weight, but [opined] it would have been less than [Z.S.’s
recorded] 1,059[]” grams. Tr. 148:16–18.

        There was an extensive discussion during cross-examination about how encephalopathic
edema can cause death by asphyxia. Although Dr. Ophoven argued that moderate cerebral edema
is per se encephalopathy, she conceded that “if the edema itself was the trigger [of Z.S.’s death]
then one would expect to see evidence of herniation.” 22 Tr. 158:19–21. She noted that “you would[
not] expect to see significant cytologic changes beyond what we saw here in the timeframe we are
talking about with [Z.S.].” Tr. 159:17–20. Dr. Ophoven further admitted that “there[ is] not a
straight pathway from encephalopathy to death.” Tr. 161:23–24. In cases where edema is fatal,
other complications include intercranial pressure and seizures. Tr. 162:4–8. She explained that
diminished consciousness, responsiveness, or reflexes could also result from edema, but Z.S. was
not at risk for asphyxiation, given her age. Tr. 162:6–8, 20. If, however, Z.S. “was developing
brain swelling and reduced consciousness, then any number of scenarios could have interfered
with her ability to support her life that [] are implicit in the presence of brain swelling.” Tr. 164:16–

18
   Myocarditis is the “inflammation of the muscular walls of the heart.” Dorland’s at 1221.
19
   Encephalitis is generally defined as “inflammation of the brain.” Dorland’s at 612.
20
   Bronchitis is the “inflammation of a bronchus or bronchi; there are both acute and chronic varieties.
Symptoms usually include fever, coughing, and expectoration. Chronic forms may involve secondary
changes to lung tissue.” Dorland’s at 252.
21
   Potter’s Pathology of the Fetus, Infant and Child – Perinatal, fetal, and embryonic autopsy, Ch. 16 (Enid
Gilbert-Barness eds., 2nd ed. 2008).
22
   Herniation is defined as “the abnormal protrusion of an organ or other body structure through a defect or
natural opening in a covering, membrane, muscle, or bone.” Dorland’s at 852. Cerebral herniation refers to
the “protrusion of brain substance through the cranium, through either a cranium bifidum, the foramen
magnum, or the tentorial notch.” Id. at 848.
                                                    10
20. Dr. Ophoven was asked about the finding of Tardieu spots 23 during Z.S.’s autopsy as evidence
of asphyxia. She stated multiple times that “Tardieu spots have nothing to do with asphyxia.” Tr.
165:2–3, 9–10, 20–21. She asserted that “anyone making the comment does[ not] know any
forensic pathology.” Tr. 165:8–9. Z.S. could have suffered from asphyxia “[a]s a secondary
complication of the encephalopathy, [but] she would not have asphyxiated just because she was
face down.” Tr. 165:25, 166:1–2. Dr. Ophoven testified that brain swelling is “enough,” with no
other factors, to conclude that Z.S.’s death was caused by her vaccines. Tr. 167:18–20.

        Dr. Ophoven dismissed evidence of a viral infection. She testified that “there[ is] a positive
culture,” but “no evidence of end organ reactions suggesting [] an upper or lower respiratory viral
infection.” Tr. 169:23–25, 170:1. Dr. Ophoven acknowledged that the lungs were heavy, and
“there was some edema present[;]” but she concluded that in this case it is “not useful.” Tr. 171:2–
5. She then clarified that heavy lungs and a heavy brain are not analogous because “the lungs vary
in weight all the time.” Tr. 172:3. She explained that pulmonary edema means “that[ is] what it is,
there[ is] fluid in the lungs and no pathology, and that has no meaning.” Tr. 171:16–18. In this
case especially, “the [increased] brain weight matches with the microscopic changes and the
observations by the pathologist.” Tr. 171:20–21. Z.S.’s heavy brain weight, “the presence of fluid
in the brain[,] and abnormality seen at autopsy” provided the basis for Dr. Ophoven’s
encephalopathy diagnosis. Tr. 175:9–11. Dr. Ophoven stated that she cannot identify the biological
mechanism that results in encephalopathy and death following vaccination. Tr. 175:3. She opined
that Z.S.’s death was vaccine caused because of the timing between vaccination and the lack of a
“legitimate alternative[]” during that timeframe. Tr. 176:23–24.

           b. Respondent’s Expert, Sara O. Vargas, M.D.

         Dr. Vargas received her medical degree from the University of Vermont College of
Medicine in 1994. Resp’t’s Ex. C at 1, ECF No. 38-5. Dr. Vargas’ post-doctoral training includes
a residency in anatomic and clinical pathology at Brigham and Women’s Hospital in Boston, MA,
completed in 1998. Id. She also completed a fellowship in pediatric pathology at Boston Children’s
Hospital in 1999. Id. Dr. Vargas has been a staff pathologist at Boston Children’s and Brigham
and Women’s Hospitals since 1999. Id. at 2. She has also served as a consultant pathologist at the
Beth-Israel Deaconess Medical Center from 2008–2014. Id. Since 2014, Dr. Vargas has been on
the consulting staff in the Department of Pathology at the Dana-Farber Cancer Institute in Boston.
Id. She has also held academic appointments. Id. at 1. From 2002–2007, Dr. Vargas served as an
assistant professor at Harvard Medical School. Id. Since 2007, she has been an associate professor
at the same institution. Id. She holds numerous editorial roles and has several memberships in
professional and scientific societies and committees. Id. at 3–6. Her curriculum vitae lists over one
hundred publications, including articles, abstracts, book chapters, and presentations of which she
is a listed author. See id. at 9–32.

       During the hearing, Dr. Vargas explained that her pathology training included exposure to
forensic pathology. Tr. 191:10–12. Specifically, she “spent a month in a medical examiner’s office
in Albuquerque, New Mexico . . . two weeks at the San Francisco medical examiner’s office[,] and

23
   Tardieu spots are defined as spots of ecchymosis beneath the pleura, pericardium, and conjunctiva
following death by suffocation. Dorland’s at 1756, 1872. Dorland’s further defines suffocation as
asphyxiation. Id. at 1796.
                                                 11
two weeks at the Boston medical examiner’s office.” Tr. 191:12–16. Within her current clinical
practice at two hospitals, she “do[es] a lot of autopsies.” Tr. 192:18–19. This includes reviewing
autopsies that were done by a state or county medical examiner’s office. Tr. 196:9–20. Dr. Vargas
noted that she is board certified in anatomic, clinical, and pediatric pathology. Tr. 191:22–24.
Respondent offered Dr. Vargas as an expert in general and pediatric pathology without objection,
and I recognized her as such. Tr. 199:8–20.

       Dr. Vargas submitted an expert report and testified at the entitlement hearing in this case.
Resp’t’s Ex. B, ECF No. 38-1; Tr. 190–310. She opined that “[s]ome features seen at [Z.S.’s]
autopsy suggest an asphyxia death.” Resp’t’s Ex. B at 5. She noted “Tardieu spots, thymic
petechia, 24 and epicardial petechiae,” 25 which “are characteristically seen in accidental and
nonaccidental asphyxia.” Id. Dr. Vargas also identified evidence of Z.S.’s viral infection. Id.

        Dr. Vargas could not confirm whether the coroner correctly identified widened gyri and
narrow sulci, “as it was not well appreciated in the photographs provided.” Id. She noted that she
consulted with a pediatric neuropathologist to confirm her findings as is standard in autopsy
practice. Id. Dr. Vargas found the “measured weight of the brain was well in line with [Z.S.’s]
height and other organ weights, and this normal weight further supports the absence of any excess
brain fluid.” Id.

        In response to Dr. Ophoven, Dr. Vargas noted that “the findings observed in the brain are
fully in keeping with postmortem change[.]” Id. at 6. In sum, Dr. Vargas found “no antemortem
signs or symptoms of brain swelling or other brain disease, no grossly evident features of
antemortem brain swelling or other brain disease, and no microscopic features supporting
antemortem brain swelling or other brain disease.” Id.

        Dr. Vargas opined it “seems incomplete to confine one’s assessment of the anatomic
feature only to the brain/neuropathology, and to opine about the cause of death without a full
examination of all available histologic material.” Id. at 7. Dr. Ophoven’s reliance on the temporal
relationship between vaccination and Z.S.’s death and the lack of an alternative explanation is
misplaced, according to Dr. Vargas. Id. Dr. Vargas also questioned why Dr. Ophoven discounted
positional asphyxia as an alternative cause, noting “positional asphyxia can cause death at any
age.” Id. at 8.

        Both Drs. Vargas and Ophoven agreed that Z.S. was beyond the cutoff age for SIDS;
however, Dr. Vargas asserted that “[t]his concept of undiagnosed disease has been extended to
children dying over the age of 12 months.” Id. She noted that she has been “involved in reviewing
cases for Dr. Hannah Kinney’s ongoing study on “sudden unexpected death in childhood.” Id. At
the hearing, Dr. Vargas explained that even after infancy, young children can still suffer from
sudden unexpected death, known as “SUDC.” Tr. 202:13–16. The term SUDC refers to SIDS-like
cases in a child over one year old, where “sudden death occur[s] in a sleep environment.” Tr.
208:17–18. Dr. Vargas testified that “you could use the word ‘SIDS-like’ even though you can[not]

24
   A petechia is “a pinpoint, non[-]raised, perfectly round, purplish red spot caused by intradermal or
submucous hemorrhage.” Dorland’s at 1422. Thymic pertains to the thymus. Id. at 1924–25.
25
   An epicardial petechia refers to petechiae on the inner layer of the pericardium that is in contact with the
surface of the heart. Dorland’s at 630, 1422.
                                                      12
call it SIDS technically because if the child is even a day over the range, the arbitrarily defined
SIDS range, you can[not] use the term.” Tr. 206:5–9. The “somewhat arbitrary division is age-
based,” and the unexpected death of a child over one year old would be characterized as SUDC
instead of sudden unexpected death in infants (“SUDI”). Tr. 202:23–24. SUDI, according to Dr.
Vargas, “is a less strict category than SIDS[]” and can be used in cases that are unexpected but not
entirely undetermined, like where there is an incidence of co-sleeping. Tr. 203:14–21.
Undetermined cases do not have the “strong level of certainty” implication that a determined death
designation would have. Tr. 204:21–22. Dr. Vargas explained that these deaths could have
numerous causes like asphyxia or arrhythmia. Tr. 206:18–20. She then clarified that “if you define
SIDS as not having a cause and then once you find a cause, you can[not] call it SIDS anymore.”
Tr. 207:4–6. Cases that have a suspected cause of death that cannot be conclusively proven could
still be labeled undetermined. Tr. 207:23–25. Dr. Vargas noted that there is evidence of several
potential causes of death in this case, even if they cannot be proven. Tr. 211:5–9.

        To help determine which factors listed in the autopsy report are relevant to cause of death,
Dr. Vargas explained that “we start by looking at the child’s length or height.” Tr. 214:21–22.
Next, “we line up the observed weight and the expected weight and then look them over and see
if anything seems unusual or out of line with the others.” Tr. 215:6–9. Looking at Z.S.’s growth,
“she [wa]s still in a greater percentage for height than weight.” Tr. 219:23–24. Dr. Vargas also
noted that “the pediatrician raised the concern for poor growth – or poor weight gain.” Tr. 220:1–
3. Dr. Vargas used a child growth chart to determine that Z.S. would have been in the 75th
percentile for height, using the numbers from her November 18, 2014 doctor’s appointment, or the
95th percentile, using the numbers from the autopsy. Tr. 224:21. Based on her autopsy height (83.8
centimeters), Z.S.’s brain weight was consistent with a child ranging from 20 to 24 months of age.
Tr. 221:24–25, 222:1–6. Dr. Vargas acknowledged that during autopsy a child would be still, and
“that could be a factor that leads you to think that the medical examiner’s measurement is closer[]”
to Z.S.’s actual height. Tr. 229:7–9. Dr. Vargas then clarified that with “[e]ither measurement
anyway, the brain is still well within expected values.” Tr. 229:13–14.

        Dr. Vargas addressed the autopsy weights of Z.S.’s organs. Dr. Vargas opined that “the
lungs stood out as a bit heavy, particularly the right lung. And the spleen was a bit large.” Tr.
222:24–25. The right lung, “is kind of 50 percent more than the expected average for this – for a
child this height.” Tr. 225:22–23. She explained that this “fit very well with the lung disease that
[is seen] under the microscope.” Tr. 225:24–25. As support, Dr. Vargas described the
“lymphocytes particularly surrounding airways and aggregating there in forming lymphoid
aggregates with germinal centers, which is the characteristic feature for follicular bronchitis and
follicular bronchiolitis.” Tr. 225:25, 226:1–4. She continued that there was accumulation of
macrophages in Z.S.’s lungs, “also supporting some physiologic significance to airway disease.”
Tr. 226:12–13. These findings, along with the positive finding for rhinovirus/enterovirus, “fit[]
very well with a viral infection that infected the respiratory tract, including all the way down into
the lungs.” Tr. 227:13–15. Dr. Vargas did not believe that anything else “stood out to [her] as
something that you would want to try to correlate with a potential disease.” Tr. 223:1–2. When
asked about infection as a possible cause of death for Z.S., Dr. Vargas explained

       Everything falls together that she had a viral infection, that clinical – with the
       cough, the lung weights, the airway lymphoid hyperplasia and the lung

                                                 13
       macrophages . . . combined with the positive test, that all fits . . . . Some kinds of
       viral infection that affect airways can overlap with asphyxial [sic] death,
       suffocation with not getting enough air.

Tr. 235:20–25, 236:1–4.

        In addition to viral disease, Dr. Vargas also identified evidence suggestive of asphyxiation.
She noted the body’s fixed, anterior surface lividity as an indication that Z.S. was lying face down
postmortem for some time. Tr. 230:2–4. She opined that Z.S. was in the prone position “probably
closer to the beginning of her sleep time than – probably closer to after when she was put down
than closer to when she was found.” Tr. 230:5–8. Dr. Vargas also noted a stain found near Z.S.’s
mouth and nose, Tardieu spots, and epicardial petechiae. Tr. 230:22–24, 231:19–20, 232:2–3. She
explained that Tardieu spots “are classically in the literature associated with asphyxia, but they are
not very – they are not specific for asphyxia seen in infant causes of death.” Tr. 231:16–18. The
epicardial petechiae “are most common in SIDS and SIDS-like deaths and asphyxia.” Tr. 232:9–
10. Dr. Vargas disagreed with Dr. Ophoven and opined that positional asphyxia can occur in
children over twelve months and even in adults. Tr. 233:1–2. Dr. Vargas generally discussed
several other mechanisms that have been associated with sudden death in young children,
including genetic and metabolic disorders and cardiac channelopathies. See Tr. 241.

        On cross-examination, Dr. Vargas sought clarification of several terms and questions prior
to rendering an opinion. She acknowledged that there was no evidence of the cause of death in this
case, except for the death itself. She was unable to answer questions about the process of making
factual findings, or the certainty of medical practices. Tr. 253:19–20, 254:4–5. Dr. Vargas testified
that “there[ is] always a lot of variability in how terms are used and there[ are] not always clear
definitions. And that[ is] one of the challenges of pathology.” Tr. 257:23–25. Dr. Vargas continued
that moderate edema, for example, “has been used to describe physiologic postmortem brain
swelling.” Tr. 259:5–7. In this case, Dr. Vargas asserted that the lividity preceded the edema, and
she would not have included that finding in her autopsy report. Tr. 260:23–24. She would have
“put sudden unexpected death in childhood” with a note explaining potential causes. Tr. 261:8–
10. Dr. Vargas stated that she “definitely believe[s] that it[ is] more likely than not that [Z.S.] died
of the other causes and mechanisms [] referenced than a vaccination.” Tr. 266:2–5. When asked
what was the most likely cause of Z.S.’s death, Dr. Vargas testified that she did not know. Tr.
309:20–21.

           c. Respondent’s Expert, Sandra Alexandrescu, M.D.

        Dr. Alexandrescu received her medical degree from the University of Medicine and
Pharmacy, “Victor Babes,” in Timisoara, Romania in 2004. Resp’t’s Ex. G at 1, ECF No. 38-9.
Dr. Alexandrescu completed a residency in anatomic pathology at the same institution in 2006. Id.
She completed a second residency in pathology at the University of Texas Health Science Center
in Houston, TX in 2012. Id. From 2012–2013, Dr. Alexandrescu completed a fellowship in
pediatric pathology at Boston Children’s Hospital and Harvard Medical School. Id. Dr.
Alexandrescu completed a two-year fellowship in neuropathology at the University of California
– San Francisco in 2015. Id. Dr. Alexandrescu has been a clinical instructor of pathology at
Harvard Medical School since 2015. Id. She has served as a staff pathologist at Boston Children’s

                                                  14
Hospital since 2015. Id. at 2. As of 2016, Dr. Alexandrescu has also served as a staff pathologist
at the Beth-Israel Deaconess Medical Center, the Dana Farber Cancer Institute, and Brigham and
Women’s Hospital. Id. She holds several editorial roles and has memberships in professional and
scientific societies and committees. Id. at 2–3. Her curriculum vitae lists extensive publications,
including articles, reviews, case reports, abstracts, and presentations or lectures, of which she is a
listed author. See id. at 6–9.

        During the hearing, Dr. Alexandrescu noted that her pathology training included forensic
pathology. Tr. 311:8–10. While “in Houston, [she] had to rotate for one month to the [medical
examiner]’s office[,] which is quite a busy one.” Tr. 311:10–12. Her neuropathology fellowship
“also required [her] to go to the San Francisco [medical examiner]’s office . . . where [she] was
exposed to all aspects of brain examination[.]” Tr. 311:12–15. As part of her responsibilities at
Boston Children’s Hospital, she reviews “specimens that are taken at surgery from children . . .
under the microscope and render[s] a report.” Tr. 312:6–12. Her teaching responsibilities include
lecturing on brain findings in sudden infant death. Tr. 314:1–6. Dr. Alexandrescu testified that she
is board certified in anatomic, clinical, and pediatric pathology, and neuropathology. Tr. 311:17–
20. Respondent offered Dr. Alexandrescu as an expert in pediatric pathology and pediatric
neuropathology without objection, and I recognized her as such. Tr. 316:1–15.

        Dr. Alexandrescu’s expert report includes her detailed assessment of the autopsy slides and
coroner’s report. Resp’t’s Ex. F, ECF No. 38-8. Dr. Alexandrescu testified that she was asked “to
examine the brain specifically and all medical records.” Tr. 316:21–23. She noted that external
photographs of Z.S. showed a “pattern of established lividity [that] is remarkably similar to Figure
14.8 in Byard’s chapter on SIDS, 26 indicating that the child had been lying prone for a significant
time after death.” Resp’t’s Ex. F at 4 (citing Resp’t’s Ex. F, Tab 1 at 11, ECF No. 39-1). Dr.
Alexandrescu was unable to assess the presence or absence of herniation, but available autopsy
images “demonstrate [a] brain with a normal pattern of gyri and sulci.” Resp’t’s Ex. F at 4. She
determined that “the mild expansion of gyri and narrowing of the sulci described in the forensic
report is of the degree that is seen as postmortem expected edema/expansion of the brain,
particularly in the absence of herniation and/or a brain of increased weight.” Id. at 5. This is further
supported, in her opinion, by the coroner’s statement indicating that an “[e]xamination of the
formalin-fixed brain reveal[ed] normal gross architecture, and no obvious abnormalities.” Id.

        She defined encephalopathy as a clinical term that “refers to the fact that the brain does not
function well.” Tr. 320:20. She noted that “not all cases of brain swelling mean encephalopathy.”
Tr. 320:24–25. Dr. Alexandrescu provided an example, “edema in the setting of
hyponatremia[,]”27 and noted that “in those cases, you are not really encephalopathic.” Tr. 321:2–
3. She provided another example when there is a hypoxic ischemic change, 28 stating “you will see
edema – that[ is] a diffuse type of change.” Tr. 321:12–14. Another type of encephalopathy can

26
   Roger W. Byard, Sudden Death in the Young, Ch. 14 (Cambridge University Press eds., 3rd ed. 2010).
27
   Hyponatremia is “the deficiency of sodium in the blood.” Dorland’s at 903.
28
   A hypoxic ischemic change refers to hypoxic ischemic encephalopathy. It is defined as “encephalopathy
resulting from asphyxia. In infants presumed to have suffered prenatal or perinatal asphyxia, common
symptoms are lethargy, feeding difficulties, and convulsions; serious cases may involve necrosis of neurons
in the brain with psychomotor retardation and spastic motor deficits such as cerebral palsy. In adults,
syndromes range from cortical blindness to irreversible coma.” Dorland’s at 908.
                                                    15
involve a focal change, such as “a tumor and if you have mass effect or if you have a hemorrhage
that increased the intracranial pressure more or less acutely.” Tr. 321:16–19. Dr. Alexandrescu
noted that encephalopathy can also involve brain atrophy29 and does not necessarily involve
swelling. Tr. 322:3–6. She then defined edema “as excessive fluid in a tissue.” Tr. 322:23–24.

        Dr. Alexandrescu explained that edema can occur postmortem. In support of her position,
Respondent submitted an article from the European Journal of Radiology30 that notes
“[d]iagnosing brain edema after death can be difficult.” Resp’t’s Ex. F, Tab 6 at 8, ECF No. 39-6.
This is partly due to the tendency of radiologists “to use the same criteria for both living and
deceased patients in assessing brain edema.” Id. at 3. The purpose of this article was “to compare
postmortem computed tomography with forensic autopsy regarding their diagnostic reliability to
differentiate between pre-existing cerebral edema and physiological postmortem brain swelling.”
Id. During a forensic autopsy, this includes “the subjective assessment of flattened gyri and filled
sulci, as well as [a] swollen hippocampus, herniated cerebellar tonsils[,] and a midline shift in
cases in which the edema is unilateral.” Id. The article explains that standard measurements “could
not be applied as a reliable method for the differentiation between typical postmortem brain
changes and antemortem or agonal brain edema.” Id. Using tomography, the authors offer “two
diagnostic criteria for identifying antemortem brain edema (as opposed to postmortem changes of
an otherwise normal brain): (1) the lack the delineation of the temporal horn and (2) tonsillar
herniation, especially in the presence of symmetric bilateral herniation.” Id. Finally, the limitations
of the study included an acknowledgement that “the determination of brain edema is also partially
based on the pathologist’s judgement and experience (an elevated brain weight does not
necessarily indicate brain edema).” Id. at 9.

        Dr. Alexandrescu clarified that brain swelling “does not translate into – increased weight
of the brain,” herniation, or other changes. Tr. 324:4–7. Modifications to the gyri and sulci can
appear because “the cellular metabolism in the brain stops” after death. Tr. 324:11–12. This leads
to “more electrolyte[s] in the cell, and that draws more water into the cell.” Tr. 324:15–16. Z.S.’s
“autopsy report does not comment at all if [the edema] happened premortem or postmortem,” and
Dr. Alexandrescu does not believe it to be the former. Tr. 328:20–21.

        In this case, “it[ is] a mild change that is common in postmortem intervals that are above
24 hours[.]” Tr. 328:25. She continued, “in the absence of increased brain weight, in the absence
of herniation or a fullness of the temporal lobes, [there is no] support to think that this is a
premortem edema, but the changes are most consistent with postmortem physiological swelling.”
Tr. 329:1–6. Dr. Alexandrescu explained that she prefers to use the term swelling because “it[ is]
difficult to distinguish between postmortem and premortem edema.” Tr. 329:11–13. Citing the
Berger 31 article, Dr. Alexandrescu asserted that “the best way to say if an edema was mild and
moderate[ and] was premortem or postmortem is to assess the presence of bilateral tonsillar
herniation and fullness of the temporal lobe.” Tr. 335:12–15 (citing Resp’t’s Ex. F, Tab 6). She
warned that “you cannot use just a mild or moderate assessment of the gyri and sulci.” Tr. 336:8–

29
   Atrophy is “a wasting away; a diminution in the size of a cell, tissue, organ, or part.” Dorland’s at 175.
30
   N. Berger, et al., Racking the Brain: Detection of Cerebral Edema on Postmortem Computer Tomography
Compared with Forensic Autopsy, 84(4) EUR. J. RADIOL. 643–51 (2015).
31
   See id.
                                                     16
9. Rather, she continued, “[y]ou have to put it in the context with the brain weight, with the
presence or absence of herniation, particularly bilateral tonsillar herniation and fullness of the
temporal lobe[,] and to put that then in the clinical context.” Tr. 336:10–15.

         Responding to Dr. Ophoven’s assertion that there was evidence of spongiosis in this case,
Dr. Alexandrescu asserted that “spongiform encephalopathy [] is a completely different type of
disease that is not applicable [here].” Tr. 338:2–4. This case involves “nothing more than [a]
coincidental, a temporal coincidence.” Tr. 341:12. At Z.S.’s age, “from birth to one year and a
half, is the time when the children get vaccinated the most.” Tr. 341:5–7. That means, if there is a
tragic event that occurs during that time, “there will be a vaccination close to the event.” Tr.
341:10. Dr. Alexandrescu was unable to specify what caused Z.S.’s death. Tr. 344:4. She stated
that the entire premise of vaccination-causation was based on edema in the brain, but “that[ is] an
overinterpretation of a normal brain with postmortem changes.” Tr. 342:15–17. Dr. Alexandrescu
agreed that interpreting “the expansion of the gyri and the narrowing of the sulci is subjective and
should not be interpreted as one – as a per se sign of anything but needs to be placed [i]n a context
that includes weight, includes herniation, includes clinical history.” Tr. 350:24–25, 351:1–4. The
fact that the autopsy report notes there is no unequivocal link between Z.S.’s vaccinations and
death, is in Dr. Alexandrescu’s opinion, less telling than the inverse. Tr. 351:12–20. She opined
that the report does not state “the association is equivocal,” and she “would have been more
worried if [the coroner] said that [it was].” Tr. 352:4–7.

           d. Respondent’s Expert, Max Wiznitzer, M.D.

        Dr. Wiznitzer received his medical degree from Northwestern University in 1977. Resp’t’s
Ex. E at 1, ECF No. 38-7. Dr. Wiznitzer completed a residency in pediatrics at the Children’s
Hospital Medical Center in Cincinnati, OH in 1980. Id. He also completed fellowships in
developmental disorders at the Cincinnati Center for Developmental Disorders in 1981, pediatric
neurology at the Children’s Hospital of Philadelphia in 1984, and higher cortical functions through
the NIH’s National Research Service Award in 1986. Id. He has served as an associate pediatrician
and associate neurologist at the University Hospitals of Cleveland since 1986. Id. at 2. Dr.
Wiznitzer has been an associate professor at Case Western Reserve University in the topics of
international health since 1994, and of pediatrics and neurology since 2013. Id. at 1–2. He has
received numerous grants for his research. Id. at 3–4. He holds several editorial roles, serves on
many advisory boards, and has memberships in professional and scientific societies and
committees. Id. at 5–9. Dr. Wiznitzer’s curriculum vitae lists hundreds of publications, including
lectures, articles, book chapters, and abstracts of which he is a listed author. See id. at 10–62.

        During the hearing, Dr. Wiznitzer explained that as part of his role as a neurologist at
Children’s Hospital in Cincinnati he “sees patients . . . [with] a variety of different neurological
conditions[,]” including epilepsy, neurodevelopmental disabilities, and autism. Tr. 358:3–25,
359:1–5. Dr. Wiznitzer noted that he has been involved in “developing [the] diagnostic criteria for
different neurological injuries . . . to be used in vaccine safety studies.” Tr. 360:10–25, 361:1. He
indicated that he is board certified in pediatrics, neurology with special qualifications in child
neurology, and the neurodevelopment of disabilities. Tr. 359:14–22. Dr. Wiznitzer has testified in
prior Table encephalopathy cases in the Program. Tr. 362:9–12. Respondent offered Dr. Wiznitzer

                                                 17
as an expert in pediatric neurology without objection, and I recognized him as such. Tr. 361:22–
25, 362:1–8.

         Dr. Wiznitzer’s expert report was concise. See Resp’t’s Ex. D, ECF No. 38-6. He noted
that Z.S.’s autopsy “demonstrated cerebral edema on macroscopic and microscopic examinations
of the brain with no reported evidence of herniation.” Id. at 3. He noted that “[i]n the absence of
herniation and its effects on brainstem function, including respiration and cardiovascular control,
it is unlikely that the cerebral edema on autopsy is the cause of death.” Id. If Z.S. died as a result
of the edema, Dr. Wiznitzer argued that “there would be evidence of cerebral herniation.” Tr.
374:16–18. He noted there were “no structural abnormalities indicative of cerebral edema, no
evidence of infection, no evidence of [a] diffuse or focal tumor, and no evidence of metabolic
disturbance.” Tr. 375:13–19. Dr. Wiznitzer further noted no evidence of a Table encephalopathy
based on “no abnormally decreased level of consciousness . . . or clinical evidence of increased
intracranial pressure.” Resp’t’s Ex. D at 3. He concluded that Z.S.’s “irritability was a
manifestation of the discomfort from her immunization[s] and not a symptom of an acute
encephalopathy.” Id.

        Dr. Wiznitzer testified about the distinction between the general definition of
encephalopathy and the use of the term in the context of the Vaccine Injury Compensation Act. In
clinical practice, Dr. Wiznitzer agreed that encephalopathy refers to “a disorder of the brain that
affects brain function or structure.” Tr. 363:7–8. To satisfy the requirement for a Table
encephalopathy however, Petitioner must show an altered mental state or impairment in
consciousness. Tr. 363:16–24. Dr. Wiznitzer continued that this can manifest through the lack of
awareness of people around you or poor eye contact, and “it should be a change in consciousness
that results in[,] or should result in[,] admission to a hospital.” Tr. 364:17–19. There is “a clinical
consequence, that the brain is[ not] right and it[ is] causing you not to function correctly.” Tr.
365:17–19.

         He noted that Z.S., according to family reports, “was acting okay[]” post vaccination. Tr.
367:4. Dr. Wiznitzer opined that tiredness and fever are not sufficient indicators of encephalopathy
and are common responses to vaccination. Tr. 368:5–10. Dr. Wiznitzer noted that Z.S.’s father did
not “notice any change or impairment in her consciousness.” Tr. 367:15–16. Instead, “[s]he just
did[ not] feel good.” Tr. 368:17–18. If Z.S. was experiencing a Table encephalopathy, she would
have been in a stupor or coma and impossible to wake. Tr. 369:5–7. She “would not have been
able to localize pain,” or recognize her parents. Tr. 369:12–13. Dr. Wiznitzer also identified several
“clinical signs and symptoms that people have within [sic] increased intracranial pressure:
[c]omplaints of headache or acting as if your head hurts, vomiting, [or a] progressive worsening
level of consciousness.” Tr. 371:25, 372:1–3. Dr. Wiznitzer clarified that “sleep, by definition, is
a change in consciousness.” Therefore, there must be a way “to differentiate between the sleep
state and an impairment in consciousness[,] which would be stupor or coma.” Tr. 389:14–18.

       He opined that because “a child dies within 24 hours of a vaccination, it does not mean that
they definitely had an encephalopathy.” Tr. 380:14–16.

   V.      Legal Arguments

                                                  18
       a. Petitioners’ Briefings

        Petitioners initially asserted that Z.S.’s death was caused-in-fact by the vaccinations she
received on November 18, 2014. Pet. at 1. In pre-hearing submissions, Petitioners then noted that
“[t]he facts of this case also meet the definition of ‘encephalopathy’ as that term is defined under
the [QAIs] of the Vaccine Table.” Pet’r’s Pre-Hrg. Br. at 7. Petitioners’ expert testified that Z.S.
suffered from an acute encephalopathy as defined by the Vaccine Injury Table. Dr. Ophoven relied
on Z.S.’s moderate cerebral edema, “opining the brain was swollen based on the appearance and
texture of the brain, the weight of the brain based on the child’s anticipated growth and
development, and microscopic images of the brain.” Pet’r’s Post-Hrg. Br. at 13.

        Relying on their expert’s testimony, Petitioners argue that Z.S. suffered an encephalopathy
consistent with the NIH definition: “diffuse disease of the brain that alters brain function or
structure.” Id. at 12. As further support, Petitioners relied on Dr. Ophoven’s explanation that the
cerebral edema noted in Z.S.’s autopsy is evidence of a brain that is abnormal and swollen. Id.
Petitioners testified that the change in Z.S.’s behavior is additional evidence of altered brain
function. Id. at 18–19. Petitioners further testified that Z.S. showed signs of decreased
consciousness during lunchtime and nap time. See id. In post-hearing briefings, Petitioners argue
that “in dying, [Z.S.] suffered the most profound and permanent change in level of consciousness.”
Pet’r’s Reply at 5.

        Petitioners’ post-hearing briefings also argue that Respondent’s experts did not provide
reliable evidence to rebut a Table encephalopathy claim. Dr. Vargas, Petitioners assert, “did not
testify regarding encephalopathy and did not provide an opinion as to whether or not [Z.S.]
suffered an encephalopathy.” Id. at 11. Dr. Alexandrescu does not diagnose encephalopathy as a
part of her practice. Id. at 14. More importantly, she agreed that edema usually does not accompany
SIDS and can occur without herniation. Id. at 14–15. Dr. Wiznitzer has testified in at least 90
vaccine injury cases on behalf of Respondent. Id. at 15. Furthermore, Dr. Wiznitzer agreed that
“loss of consciousness sustained from [a] point on until either the time of death or 24 hours would
meet the criteria for Table encephalopathy.” Tr. 388. This, asserts Petitioners, is what happened in
this case.

       b. Respondent’s Briefings

        In his post-hearing brief, Respondent notes that “Petitioners no longer appear to be
asserting a causation-in-fact claim.” Resp’t’s Resp. at 8. Table encephalopathy claims require
preponderant evidence of the “definition of encephalopathy under the Vaccine Table[, which] is a
more narrow interpretation than what is commonly accepted in the medical community.” Id. (citing
Paz v. Sec’y of Health & Hum. Servs., No. 14-290V, 2015 WL 4557119, at *5 (Fed. Cl. Spec.
Mstr. June 23, 2015)). Respondent asserts that Z.S. did not suffer from a Table encephalopathy
because Z.S. did not demonstrate a significantly decreased level of consciousness. In accordance
with the QAIs, he argues Z.S. did not demonstrate a decreased or absent response to her
environment, decreased or absent eye contact, or inconsistent or absent responses to external
stimuli. Furthermore, the QAIs specifically address all of Z.S.’s symptoms. Respondent asserts,
“[a]s Dr. Wiznitzer testified, [P]etitioners’ description of [Z.S.’s] behaviors indicate that she

                                                19
simply ‘did[ not] feel good’ due to the known, usual effects of being vaccinated.” Resp’t’s Resp.
at 14 (citing Tr. 367–68).

           Respondent also disputes Petitioners’ assertion that there is evidence that Z.S. had
increased intracranial pressure. He addresses, in turn, the four factors that Dr. Ophoven relied on
to reach that conclusion: “(1) her training and experience, (2) [Z.S.’s] brain weight, (3) brain
swelling observed by the [medical examiner], and (4) the presence of water in the brain cells.”
Resp’t’s Resp. at 14. Dr. Ophoven opined that water in the brain cells was the cause of the swelling
in Z.S.’s brain. Tr. 175. Despite Dr. Ophoven’s reliance on the NIH’s definition of encephalopathy
to use the terms “swelling” and “edema” interchangeably, Respondent notes that the definition
“does not mention swelling.” Resp’t’s Resp. at 14. More importantly, Dr. Alexandrescu opined
that Z.S.’s cerebral edema occurred postmortem. The parties also disagree on whether Z.S.’s brain
weight was actually normal. Respondent relies on Z.S.’s body measurements during autopsy to
assert that her brain was not heavy. Lastly, Respondent reiterates that “Dr. Ophoven is not board
certified in pathology, 32 has not done a fellowship in neuropathology, last worked in a hospital in
1996, and last worked as a practicing forensic pathologist in 2010.” Id. at 12, 14. In contrast, Dr.
Alexandrescu is “a fellowship trained, board-certified neuropathologist.” Id. at 18.

        Z.S.’s death is “the only requirement of a Table encephalopathy that has been met here.”
Id. at 19. Respondent asserts that this is not enough. Id. He argues that Petitioners have not offered
preponderant evidence that Z.S. “suffered the clinical manifestations of an acute encephalopathy
that resulted in her death.” Id.

        Although Respondent and Petitioners agree that this claim is no longer based on causation-
in-fact, Respondent notes that “Dr. Ophoven confirmed that she had no medical theory or
biological mechanism of vaccine causation for [Z.S.’s] death.” Id. (citing Tr. 167–69). Respondent
also notes that Dr. Ophoven “attributed [Z.S.’s] death to [her] vaccination[s] based on timing and
[the] lack of alternative causes.” Resp’t’s Resp. at 20 (citing Tr. 176–77). He cites the Federal
Circuit’s holding that “neither a mere showing of a proximate temporal relationship between
vaccine and injury, nor a simplistic elimination of other potential causes of injury” is sufficient to
establish causation.” Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1323 (Fed. Cir.
2010). That is true “even if the off-Table injury occurs within a time period set forth in the Table.”
Id. He concludes that Petitioners have not established a Table encephalopathy or provided
evidence of causation-in-fact; therefore, he does not have a burden to present any rebuttal evidence.
Resp’t’s Resp. at 21–22.

     VI.    Analysis 33

32
   Dr. Ophoven testified that she is “board certified in forensic pathology and anatomic pathology. Pediatric
pathology boards did not exist.” Tr. 91:5–7.
33
   Dr. Vargas submitted a coherent and informative written report. However, during her testimony, Dr.
Vargas was equivocal and nonresponsive. She did not agree that certain words have specific meanings in
the medical field and questioned the general meaning of several non-medical words. Tr. 253:19–20, 254:4–
5, 257:23–24, 258:21–22, 260:2. On one occasion, I was forced to intervene in the cross-examination of
Dr. Vargas to get a direct answer to a question. Tr. 298:13–25, 299:1–23. She also reversed herself on more
than one occasion. Tr. 276:10, But see Tr. 278:4–5, 284:3–7. As a result, her testimony was less helpful,
and I did not rely on her opinion in this Decision.
                                                     20
        To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:
(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently
developing a listed injury within the time frame prescribed by the Vaccine Injury Table set forth
at 42 U.S.C. § 300aa-14, as amended by 42 C.F.R. § 100.3; or (2) that the petitioner suffered an
“off-Table injury,” one not listed on the Table, as a result of his receiving a covered vaccine. See
42 U.S.C. §§ 300aa-11(c)(1)(C); Moberly, 592 F.3d at 1321; Capizzano v. Sec’y of Health & Hum.
Servs., 440 F.3d 1317, 1319–20 (Fed. Cir. 2006). Off-Table claims require a petitioner to prove
that the alleged injury was caused-in-fact by a Table vaccine.

        In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs., the Federal
Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal
link between a vaccine and the claimed injury. See 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). The
Althen test requires petitioners to set forth: “(1) a medical theory causally connecting the
vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination
was the reason for the injury; and (3) a showing of a proximate temporal relationship between
vaccination and injury.” Id. at 1278. To establish entitlement to compensation under the Program,
a petitioner is required to establish each of the three prongs of Althen by a preponderance of the
evidence. See id.

        Petitioners in this case have abandoned any argument that Z.S.’s death was an off-Table
injury, caused-in-fact by her vaccinations. They did not offer evidence of a biological mechanism,
pursuant to Althen prong one; nor did they offer evidence of a clear and logical pathogenesis of
the injury that ultimately led to Z.S.’s death, pursuant to Althen prong two. They argue only that
following her DTaP vaccination, Z.S. suffered an encephalopathy that ultimately resulted in her
death, and that “[t]his is a Table injury case.” Pet’r’s Post-Hrg. Br. at 7.

        The statute’s definition of encephalopathy in December of 2015 was the “significant
acquired abnormality of, or injury to, or impairment of function of the brain. Among the frequent
manifestations of encephalopathy are focal and diffuse neurological signs, increased intracranial
pressure, or changes lasting at least 6 hours in level of consciousness with or without convulsions.”
42 U.S.C. § 300aa-14(b)(3)(A). The QAIs further defined Table encephalopathy in the Code of
Federal Regulations: “[f]or children less than 18 months of age who present without an associated
seizure event, an acute encephalopathy is indicated by a significantly decreased level of
consciousness lasting for at least 24 hours.” 42 C.F.R. § 100.3(b)(2)(i)(A). An increase in
intracranial pressure “may be a clinical feature of acute encephalopathy in any age group.” 42
C.F.R. § 100.3(b)(2)(i)(C). Petitioners must also show that acute encephalopathy is followed by
the persistence of chronic encephalopathy for more than six months beyond the date of vaccination.

         A significantly decreased level of consciousness is indicated by the presence of at least one
or more of the following clinical signs: “(i) decreased or absent response to environment (responds,
if at all, only to loud voice or painful stimuli); (ii) decreased or absent eye contact (does not fix
gaze upon family members or other individuals); or (iii) inconsistent or absent responses to
external stimuli (does not recognize familiar people or things).” 42 C.F.R. § 100.3(b)(2)(i)(D).
“The following clinical features alone or in combination, do not demonstrate an acute
encephalopathy or a significant change in either mental status or level of consciousness as

                                                 21
described above: [s]leepiness, irritability (fussiness), high-pitched and unusual screaming,
persistent inconsolable crying and bulging fontanelle.” 42 C.F.R. §100.3(b)(2)(i)(E). 34

         The QAIs further define a significantly decreased level of consciousness as one that
“implies a state of diminished alertness that is much more than mere sleepiness or inattentiveness
. . . [it] requires markedly impaired or strikingly absent-responsiveness to environmental or
external stimuli for a sustained period of at least 24[]hours.” Wright v. Sec’y of Health & Hum.
Servs., No. 12-423, 2015 WL 6665600, at *6 (Fed. Cl. Spec. Mstr. Sept. 21, 2015) (quoting
Waddell v. Sec’y of Health & Hum. Servs., No. 10-316, 2012 WL 4829291, at *7 (Fed. Cl. Spec.
Mstr. Sept. 19, 2012)).

         In order to establish a Table claim for entitlement resulting from a DTaP vaccination, a
petitioner must show that the encephalopathy manifested within seventy-two hours of vaccine
administration. 42 C.F.R. §100.3 (effective July 23, 2015 to March 20, 2017). There is no dispute
between the parties that Z.S.’s death occurred within seventy-two hours of her vaccination. Z.S.’s
death was a superseding factor that nullifies a showing of a chronic encephalopathy. Petitioners
assert that Z.S.’s encephalopathy was the intervening injury, and therefore, this timeframe is within
the window for a Table encephalopathy. See id.

       The material question in this case is whether Petitioners have presented preponderant
evidence of a Table encephalopathy. Petitioners note, and the medical record supports, that Z.S.
was healthy prior to vaccination, and her sudden death would qualify any preceding
encephalopathy as acute. There is nothing in the record to dispute this presumption. At issue here
is whether the medical records, death investigation, autopsy findings, and Petitioners’ account of
the hours between Z.S.’s vaccination and death provide sufficient evidence of an encephalopathy.
That question is further complicated by a dispute over what, if any, distinction there is between
the medical definition of encephalopathy and a Table encephalopathy. For Petitioners to prevail,
they must provide preponderant evidence that Z.S. suffered from an encephalopathy and that said
encephalopathy meets the definition articulated in the QAIs for a Table injury.

        Dr. Ophoven defined encephalopathy as diffuse disease in the brain. During the hearing,
there was substantial discussion of how to define various medical terms, but what constitutes
disease was not covered. Dorland’s Illustrated Medical Dictionary 35 defines “disease” as “any
deviation from or interruption of the normal structure or function of a part, organ, or system of the
body as manifested by characteristic symptoms and signs; the etiology, pathology, and prognosis
may be known or unknown.” See Dorland’s at 527. The key provision of this definition is the
explanation that the manifestation of symptoms and signs help determine whether a deviation or
interruption is present. Fever, irritability, and lethargy can certainly be signs that a child is unwell.
However, without more, those symptoms are too common to identify a deviation or interruption
of a specific part, organ, or bodily system, such as the brain. See Lankford v. Sec’y of Health &

34
   The Vaccine Injury Table statute has similar but slightly different language: “Signs and symptoms such
as high pitched and unusual screaming, persistent inconsolable crying, and bulging fontanel are compatible
with an encephalopathy, but in and of themselves are not conclusive evidence of encephalopathy.” 42
U.S.C. § 300aa-14(b)(3)(A). This difference has no bearing on my Decision as the language is consistent.
35
   Dorland’s defines encephalopathy as a degenerative disease of the brain, which is a more profound and
specific deviation of the function of the brain. See Dorland’s at 614.
                                                   22
Hum. Servs., 37 Fed. Cl. 723, 725–26 (1996) (affirming the special master’s reliance on the
medical expert’s assertion that symptoms including fever, diminished appetite, drowsiness,
localized swelling at the injection site, and difficult arousal are no more pronounced in severity
than the adverse systemic reactions typically encountered in the administration of that vaccine).
Dr. Wiznitzer 36 fine-tuned this point by explaining that these symptoms are not sufficient
indicators of encephalopathy but are common responses to vaccination. For comparison, Dr.
Wiznitzer identified several applicable signs and symptoms of encephalopathy, such as coma,
stupor, headache, vomiting, and other evidence of decreased consciousness.

        Notably, the Federal Circuit has cautioned against discounting death as evidence of
encephalopathy. Jay v. Sec’y of Health & Hum. Servs., 998 F.2d 979, 984 (Fed. Cir. 1993) (finding
that the petitioners were entitled to judgment as a matter of law where the “undisputed facts of
record . . . include that an otherwise healthy child received a [diphtheria-pertussis-tetanus (“DPT”)]
shot; the DPT shot caused fever[ and limpness;] the child missed his normal nightly feeding; the
child died within 18 hours of the shot; the autopsy was inconclusive; and a medical expert testified,
uncontradicted, that the DPT shot caused the death, the medical theory being that an
encephalopathy occurred.”). In Jay, the special master, in the absence of rebuttal evidence, refused
to consider the child’s death as evidence of the encephalopathy on a motion for summary judgment.
See id. at 983. The Federal Circuit, however, noted that “[n]otwithstanding two hearings and
numerous written submissions, [the Department of Health and Human Services] ha[d] not
contradicted [the petitioners’] evidence.” Id.

        In the present case, Respondent has disputed Petitioners’ evidence by way of expert
testimony and medical literature. This case is not one wherein an expert presented testimony that
“reflects a reasoned evaluation of undisputed facts and stands uncontradicted by any opposing
medical opinion.” See Lankford, 37 Fed. Cl. at 726. Indeed, the death of Z.S. has been discussed
at length by experts from both sides. It is, as Petitioners assert, the most “profound and permanent
change in level of consciousness” that can occur. See Pet’r’s Reply at 5. However, as noted in
Lankford, “death is recognized to be a compensable Table injury when medically identified as an
acute complication or sequela of an encephalopathy.” See 37 Fed. Cl. at 726. The Federal Claims
Court, in distinguishing Jay, noted that Petitioners cannot assert that “because a death occurred, it
would be more logical to assume the adverse clinical signs that preceded that event bespoke an
encephalopathic process rather than simple drowsiness.” Id. Rejecting that argument, Lankford
held that the statute demands that “a medically justified determination of encephalopathy must
precede the occurrence of death.” Id.

       Petitioners’ expert Dr. Ophoven asserted that cerebral edema is inherently encephalopathic.
She asserted that encephalopathy reflects abnormal brain tissue that is typically associated with
brain swelling. Tr. 114:14–15. She did not provide any authority for this assumption or address
Dr. Alexandrescu’s rebuttal. By comparison, Dr. Alexandrescu explained that not all brain
swelling is encephalopathy (for example, when caused by hyponatremia), and not all
encephalopathy is characterized by edema (in the case of atrophy). She also disagreed with Dr.
Ophoven’s contention that encephalopathy is always diffuse and gave a counter example of a focal
brain tumor. Dr. Alexandrescu’s examples were extremely helpful, and her testimony was

36
   While Dr. Wiznitzer provided helpful testimony as it relates to identifying an encephalopathy, his
argumentative nature and tone was at times, counterproductive.
                                                 23
persuasive. Therefore, I do not find that Petitioners have presented preponderant evidence that
cerebral edema is always encephalopathic.

        The QAIs note that for a child Z.S.’s age who presents without seizure, the presence of one
or more decreased consciousness factors indicate an acute encephalopathy. Petitioners were asked
if Z.S. exhibited any signs of decreased consciousness. Ms. Adal noted that Z.S. could recognize
her mother’s voice and other sounds around her. She recognized her family members, and she did
not lose consciousness. Ms. Adal noted the lack of other symptoms and signs of disease,
specifically vomiting, or headache. Ms. Adal testified that she did not notice Z.S. acting differently
and that Z.S. just seemed tired. Ms. Adal and Mr. Shiel both used the word “lethargic” to describe
Z.S. and described her as hot, fussy, and tired. Mr. Shiel testified that Z.S. was not her “bouncy”
self. He agreed that Z.S. was perfectly conscious. He reiterated that she did not have any decreased
consciousness until she died in her sleep. Mr. Shiel also testified that he would have responded to
any unusual noise he heard from her during the night.

        The QAIs specifically note that sleepiness and fussiness, even when taken together, are
insufficient, without more, to establish a Table encephalopathy. In prior cases, special masters
have also determined that diminished alertness requires little to no responsiveness to
environmental or external stimuli. Wright, 2015 WL 6665600, at *6. There is no evidence that Z.S.
did not recognize or respond to her parents or did not maintain eye contact. There is no evidence
that she only responded to loud or painful stimuli. There is no evidence that she was in a coma or
stupor-like state. Her mother’s account that she was more difficult to wake from her nap seems
more consistent with the sleepiness type of behavior that should be distinguished from an actual
“state of diminished alertness” exemplified in those more severe examples. There is no evidence
of seizure, tremor, headache, paralysis, or loss of or decreased consciousness. Z.S.’s behavior, in
the hours between vaccination and bedtime, does not support a finding of decreased consciousness
as required for a Table encephalopathy. In this case, Petitioners did not present preponderant
evidence to rebut their admitted initial belief, that Z.S.’s tiredness and fussiness were caused by
discomfort from her vaccinations.

        Although Dr. Ophoven asserted that cerebral edema is de facto encephalopathic, she also
relied on autopsy findings to support her contention that Z.S. suffered from an acute
encephalopathy. Petitioners did present evidence, and Respondent’s experts did not dispute, that
edema can be evidence of encephalopathy. Dr. Ophoven testified that a fatal edema typically is
evident because of intercranial pressure or “interference with vital signs through the process of
herniation.” Tr. 161:19–20. Interference with vital signs is consistent with the Dorland’s definition
for encephalopathy, a deviation, or interruption of function. See Dorland’s at 614. It is also
consistent with the Table definition of diminished consciousness. Petitioners assert that the
widening of gyri and narrowing of sulci is evidence of intracranial pressure. Dr. Alexandrescu’s
explanation of the relationship between brain swelling, intercranial pressure, and injury is more
nuanced. She testified that unlike a mild cerebral edema, significant brain swelling will increase
the intercranial pressure and lead to fullness of the temporal lobe and tonsillar herniation that
presses on the brainstem. These symptoms would be in addition to the less significant widening
and narrowing that often occurs after death.

                                                 24
        Drs. Ophoven and Alexandrescu both discussed the subjective nature of pathology. Dr.
Alexandrescu specifically noted that “there[ is] literature saying that the expansion of the gyri and
narrowing of the sulci is subjective and should not be interpreted as one – as per se a sign of
anything.” Tr. 350:24–25, 351:1–2. The Berger37 article supports Dr. Alexandrescu’s assertion
that the mild to moderate cerebral edema noted at autopsy occurred postmortem. Resp’t’s Ex. F,
Tab 6. The authors identified increased brain weight as one criterion for antemortem edema, but
they noted “the subjective assessment of flattened gyri and filled sulci,” and included additional
indicators such as “a swollen hippocampus, herniated cerebellar tonsils[,] and a midline shift in
cases in which the edema is unilateral.” Id. at 3. Both experts agree that fatal edema can lead to
complications such as herniation and diminished consciousness. There is no evidence in the record
of herniation or a midline shift, and the autopsy report does not address intercranial pressure. Given
the medical literature in support of Dr. Alexandrescu’s opinion of post-mortem edema, Dr.
Ophoven’s reliance on the autopsy note that edema is present is not preponderant evidence of
encephalopathy.

        Petitioners also rely on Z.S.’s November 18, 2014 wellness-exam for her baseline weight
and height and argue that her brain was heavy and swollen at autopsy. However, Dr. Ophoven
conceded that she underestimated the anticipated brain weight for a child with the height and
weight recorded the last day of Z.S.’s life. Using the wellness-exam measurements proffered by
Petitioners, along with their submitted medical literature, 38 Z.S.’s brain should have weighed 1,042
to 1,050 grams. The autopsy measurements proffered by Respondent would be consistent with a
normal brain weight of 1,059 to 1,064 grams. Z.S.’s brain weight of 1,060 is within one standard
deviation of either set of numbers, rendering the dispute moot. The autopsy itself provides the best
evidence of whether the coroner believed there was a significant acquired abnormality of, injury
to, or impairment of function of Z.S.’s brain. The comments from the general examination of the
Z.S.’s head note “moderate cerebral edema” and “normal gross architecture and no obvious
abnormalities.” Pet’r’s Ex. 8 at 7. A microscopic examination of the brain revealed “mild cerebral
edema” with “development consistent with the child’s age and no diagnostic microscopic
pathologic changes.” Id. at 9. These notations of mild and moderate edema are subjective, as
evidenced by the coroner’s use of different descriptors, and do not explicitly state or implicitly
suggest swelling sufficient to cause abnormality, injury, or impairment that led to Z.S.’s death.
The coroner’s note that the brain is normal with no abnormalities further makes the point. The
evidence in the record of Z.S.’s cerebral edema noted at autopsy is not preponderant evidence of
a Table encephalopathy.

        Without preponderant evidence of a Table encephalopathy, Respondent is under no burden
to identify the cause of Z.S.’s injury. Dr. Ophoven noted in her written reports that the timing of
Z.S.’s death in relation to her vaccinations, and the lack of alternate causes, is largely the basis for
her opinion in this case. While those factors warrant further consideration of the applicability of a
Table injury, neither is sufficient to establish a Table encephalopathy in this case. Furthermore,
the medical history, behavioral changes, and autopsy report did not provide preponderant evidence
that Z.S. suffered any of the following: significant acquired abnormality of, injury to, or
impairment of function of the brain; increased intracranial pressure; or a significantly decreased
level of consciousness to establish a Table encephalopathy.
37
     See Berger, et al., supra note 30.
38
     See supra note 21.
                                                  25
   VII.    Conclusion

        Petitioners’ claim is solely one of a Table encephalopathy. There is no other theory,
biological mechanism, or logical sequence of cause and effect for me to consider. There is not
preponderant evidence that edema is per se encephalopathic. Despite the temporal relationship
between Z.S.’s vaccinations and her death, there is not preponderant evidence that Z.S. suffered
from encephalopathy during that time. Finally, there is not preponderant evidence that Z.S.
suffered from a Table encephalopathy pursuant to the QAI factors. The QAIs provide guidance for
identifying injuries in cases where there is little to no evidence or understanding. There must be
some applicability of one or more of the defining factors for injury, lest we hold that any death
occurring within 24 hours of vaccination is de facto vaccine caused. Given the childhood
vaccination schedule, that position is untenable.

        The death of a child is an unimaginable loss, and the lack of information available to
medical professionals to provide answers when such a tragedy occurs can exacerbate the loss. To
understand what happened in this case and why, the medical record, expert reports, medical
literature, and hearing testimony were all thoroughly reviewed and considered, even if not
explicitly referenced herein. Considering the totality of the record in this case, there is not
preponderant evidence of a Table encephalopathy resulting from Z.S.’s November 18, 2014
vaccinations.

       Accordingly, I have no choice but to DENY Petitioners’ claim and DISMISS this
petition.

       IT IS SO ORDERED.

                                     s/Herbrina D. Sanders
                                     Herbrina D. Sanders
                                     Special Master

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