Vasquez, Richard

WR 59,201-03 COURT OF CRIMINAL APPEALS AUSTIN, TEXAS Transmitted 4/20/2015 12:00:00 AM Accepted 4/20/2015 8:11:52 AM ABEL ACOSTA WR 59,201-03 CLERK

RECEIVED COURT OF CRIMINAL APPEALS EX PARTE RICHARD VASQUEZ 4/20/2015 ABEL ACOSTA, CLERK

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IN THE DISTRICT COURT 148TH DISTRICT NUECES COUNTY, TEXAS

Returnable to

THE TEXAS COURT OF CRIMINAL APPEALS AUSTIN, TEXAS

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STATE’S MOTION TO DISMISS AS ABUSIVE SUBSEQUENT 11.071 APPLICATION FOR WRIT OF HABEAS CORPUS AND TO DENY MOTION TO STAY EXECUTION

Douglas K. Norman State Bar No. 15078900 Assistant District Attorney 105th Judicial District of Texas 901 Leopard, Room 206 Corpus Christi, Texas 78401 (361) 888-0410 (361) 888-0399 (fax) douglas.norman@co.nueces.tx.us

Attorney for the State

WR-59,201-03

EX PARTE § IN THE DISTRICT COURT § § 148TH JUDICIAL DISTRICT § RICHARD VASQUEZ § NUECES COUNTY, TEXAS

COMES NOW the State of Texas, by and through its Assistant District Attorney for the 105th Judicial District of Texas, and pursuant to Texas Code of Criminal Procedure arts. 11.071 and 11.073, files this motion to dismiss as abusive the present subsequent application for writ of habeas corpus and to deny the motion to stay execution.

EXPLANATION FOR UNTIMELY PLEADING

The State is cognizant of this Court’s “Miscellaneous Rule 11-003" pertaining to procedures in death penalty cases involving requests for stay of execution and related filings, and if it applies to responsive pleadings such as this motion to dismiss Applicant’s subsequent application for writ of habeas corpus, the State offers this explanation for filing its motion less than seven days before the date of Applicant’s execution:

Applicant’s execution is scheduled for Thursday, April 23, 2015. Applicant did not file his motion for stay of execution and his subsequent application for post-conviction writ of habeas corpus until late in the *3 afternoon of Wednesday, April 15, 2015, the last day permitted for such filings pursuant to this Court’s “Miscellaneous Rule 11-003.” Consequently, it was impossible for the State to read and file a response to the 92-page application and exhibits attached thereto prior to the expiration of the deadline for a timely filing in this case. The State has worked diligently to prepare such response and is filing this, its motion to dismiss Applicant’s subsequent application for writ of habeas corpus as quickly as it can.

The State prays that this Court deem such circumstances as good cause for the untimely filing of this motion, if in fact this motion is considered a “pleading requesting affirmative relief in an impending execution case” under Miscellaneous Rule 11-003, and if in fact that rule applies to responsive pleadings such as this motion to dismiss.

STATEMENT OF FACTS

The State relies on this Court’s own knowledge of the facts of the case as set forth in its opinion on the direct appeal. In addition, the State would point this court to the following testimony that it believes to be particularly relevant to the present claims being made.

Deputy Constable Eric Giannamore, the first person to arrive at the scene, asked Vasquez what had happened. Vasquez replied that Miranda was *4 brushing her teeth in a hall bathroom and fell off a wooden stool, hitting her head. Giannamore testified, however, that there was no wooden stool in the area. (R.R. XXXIV - 19-21, 74-77; XLI - State's Exh. 37).

Emergency medical technician Eugenio Rangel asked what had happened and Vasquez replied that Miranda had fallen off a stool in the bathroom while brushing her teeth. While Vasquez kind of pointed when he said this, Rangel never saw a stool in the area. (R.R. XXXV - 76-78, 83, 85, 101, 108). As the paramedics cut Miranda's clothes off and turned her in order to place her on a back board, noticeable bruising of various stages was apparent down her back, as well as on her legs and arms. Miranda also had a bump on the back of her head and bruising around her eyes. There was no sign of toothpaste in Miranda's mouth. (R.R. XXXIV - 21-22; XXXV - 78-82, 85-87, 93-98, 101-102, 108-112; XLI - State's Exh. 37-39).

Dr. Michael Burke, a pediatric neurosurgeon, testified that Miranda had multiple bruises on her body. (R.R. XXXV - 95; XXXVI - 69-89; XLII -State's Exh. 60-63; C.R. I - 38-39, 51-53, 56-61, 69-71, 156-158). Burke said that her subdural hematoma was caused by trauma to the head and that Miranda's brain injuries were the equivalent to those she would have sustained had she been ejected from a car traveling 65 m.p.h. Miranda's injuries were consistent with being struck multiple times in the head. Burke *5 said his final diagnosis was severe brain injury from child abuse. He described this as a massive injury and summarized Miranda's condition by saying, "This child got the living daylights beat out of her to the point that she quit breathing and there was nothing that could be done at that point." (R.R. XXXVI - 78-79, 87, 91-94). Dr. Burke used his car accident and Shaken Baby Syndrome comments only as analogies to attempt to explain the force of the direct impact injuries in the present case and the lack of external signs, and he never testified or implied that Miranda had been in a car accident or that she had Shaken Baby Syndrome. (R.R. XXXVI - 92-93).

Leann Box, a sexual assault nurse examiner (SANE) at the hospital, testified that Miranda had extensive bruising in various stages of healing all over her body--head, face, chest, pelvic region, genitalia area, ankle, thigh, shoulder, back, and arms--and described each of those bruises. (R.R. XXXV - 175-185, 208-211; XLI - State's Exh. 46-48; C.R. I - 23, 27, 75-83, 175). There were multiple abrasions and tears on her labia majora, fossa, labia minora, fourchette, perineum, and anal area. Many were oozing tears, which meant they were fresh enough that they had not begun to scab, which generally started to occur within a few hours of injury. One such injury would have probably bled a great deal. Because very little blood was present *6 in the area when the examination took place, Box assumed it had been cleaned up. (R.R. XXXV - 185-197, 205-208, 211-215; XLII - State's Exh. 49-57; C.R. I - 18-21, 42, 50, 54-55, 72). The bruising on Miranda's hips was very consistent with injuries that could be caused by being held from behind while being sexually assaulted. The injuries to Miranda's genital-anal area were not consistent with a straddle injury. Rather, they were extremely consistent with someone or something passing over the area below the anus, tearing the top of the skin, skidding over the anus, and ripping apart the skin at the perineum. In over 200 sexual assault examinations, this was the first time Box had seen a complete full thickness tear at the perineum. (R.R.

XXXV - 177, 197-200).

In his formal statement to the police, Vasquez said that he had repeatedly asked Miranda why she always acted scared of him. She kept saying she was not scared of him until Vasquez "got pissed off" and pushed her. When she still replied that she was not scared of him, Vasquez told her to stop lying and hit her in the head. She did not fall down because he was holding her with his other hand. He hit her several more times. She just looked at him and looked stunned. He told her to go out and play and she went downstairs and out of the house. About 30 minutes later, Vasquez called out to Miranda through the window and told her to come inside and *7 brush her teeth or she would not get to go to his sister's house. When she walked in, Miranda's head was down. She went to Vasquez's mother's room and got the stool she used when she brushed her teeth. As she started to carry it to the other bathroom, she fell down. Vasquez told her to get up and go brush her teeth. Miranda staggered into the bathroom and began to brush her teeth. Then Vasquez heard what sounded like the stool tipping over. He called Miranda but she did not answer. He went in the bathroom and saw her lying on her back on the floor. He hit Miranda because he had a lot of anger because he couldn't straighten his life out. He could have hit her more than three times. He just lost it. He was sorry for what he did to her. (R.R. XXXIV - 56-59; XLI - Sx8).

Dr. Lloyd White, the Nueces County medical examiner who performed an autopsy on Miranda's body, noted bruising all over her body and head of various ages. (R.R. XXXVI - 23-33, 40, 49-50; XLII - State's Exh. 58-59). The damage to Miranda's genital region was typical of blunt trauma--pressure exerted to the area that caused scrapes of the skin and membranes and caused tears of those membranes. They could have been the result of being poked with an object. A penis could cause bruising, laceration, and fairly severe injuries in small children. (R.R. XXXVI - 39-40, 53-54, 58). White said the cause of Miranda's death was blunt force *8 injuries of the head and brain with cocaine intoxication as a contributing factor. He ruled the manner of death to be homicide. White could not say how many blows Miranda received but there were at least 20-30 areas of contusion on her body, including evidence of perhaps dozens of impacts to all areas of her head--back, under the chin, front, either side, and top. The bruising around Miranda's eyes, ear, surrounding face, and scalp, which was edematous, was due to recent impact. He could also not say how hard she was struck except that it was hard enough to produce fatal injury. He said it was very unlikely that Miranda would die from falling off the stool. White was of the opinion that the bruises to Miranda's back and chest were not the result of resuscitation efforts. The bruises to Miranda's hips were consistent with her being restrained and sexually assaulted from behind. (R.R. XXXVI - 38-43, 55-57; XLI - State's Exh. 45; C.R. I - 31-36). Dr. White explained that most fatal falls require at least 10 to 15 feet in height, but conceded that “[f]alls from so-called ground level or falls from a very low level producing fatal injuries are very, very rare; although they do occur.” (R.R. XXXVI -41-42).

Dr. James Lukefahr, a pediatrician who devotes a large part of his practice to child abuse, testified that he had reviewed the medical records and photographs in the case, and was of the opinion that Miranda's injuries *9 were the result of a sexual assault. He discussed the various injuries to the genital-anal area, noting in particular the large penetrating injury into the perineal body. That injury was quite deep as evidenced by deeper tissues which were visible in the photographs and the fact that a doctor had had to repair it with sutures that were completely buried well beneath the surface of the skin. Lukefahr said that the injuries were not consistent with a straddle injury. The bruises on Miranda's hips were very unlikely to be accidental because they were localized in an area that would generally be well cushioned by clothing. Lukefahr opined that they were sustained during the sexual assault and were probably the result of being restrained during the time the really violent act of penetration was occurring in Miranda's anal area. The injuries were also unusually symmetrical. They were more consistent with Miranda being conscious and struggling when they occurred than being sustained when she was unconscious. There was a suggestion that Miranda's anus had been penetrated but Lukefahr could not say for sure. The fact that semen was not found did not change Lukefahr's opinion that a sexual assault had occurred. He felt that most of the injuries were most consistent with having been caused by contact with an object which was in motion, so that the skin basically was rubbed off in those areas. The really deep wound in the perineal body, on the other hand, was a penetrating injury, *10 caused by an object penetrating into the substance of the perineal body. It would have taken a very substantial amount of penetrating force to have caused that injury because that area of the body has a lot of resilience and padding. There was no way to know whether that injury was caused by a man's penis or some other foreign object.

Vasquez testified in his own defense that he was mad and hit Miranda in the head. While he acknowledged hitting her in the head, Vasquez denied hitting her in her face. She was not doing anything wrong that required discipline. He claimed to not know how many times he hit her. Although in his written statement, Vasquez said he held Miranda by the head when he hit her, he testified that he did not do so. (R.R. XXXVII - 92-94, 116-117, 121-122, 135). When Miranda appeared, she looked dazed and could not keep her head up. Vasquez knew something was wrong with her. He told her to get her stool from his parents' room and go brush her teeth. As she returned with the stool, she fell down. She still could not keep her head up. (R.R. XXXVII - 94-96, 112-113, 136). Vasquez later went into the bathroom and found her with her head down and toothpaste on her face, and still later went back to the bathroom and found her with her head in the sink. He thought she hit her head with the faucet although he could not recall what type of faucet it was. (R.R. XXXVII - 96-97, 119-121). Vasquez repeatedly tried to *11 make Miranda stand by herself but she kept falling down. He then shook her and asked her what was going on. As he did that, he took her into his parents' bedroom and either threw or laid her on their bed. (R.R. XXXVII - 97-99, 117, 140). Vasquez said he did not try to kill Miranda and he did not know what his intent was when he hit her. He did not remember whether he had hit her until she became unconscious. (R.R. XXXVII - 110, 134-135, 140-141, 147). Vasquez admitted that he was the only adult in the house that morning. (R.R. XXXVII - 113, 125-126).

STATE’S RESPONSE TO THE PRESENT CLAIMS

The crux of all of Vasquez’s claims in this subsequent writ is that new scientific evidence supposedly shows that the victim’s fall from a small stool might reasonably have caused her fatal injury, contradicting trial testimony from Dr. Burke and Dr. White implying that this was not a plausible theory. Specifically, in the “Introduction” to his application, Vasquez asserts that “[i]n light of modern scientific knowledge, it is now clear that the child had actually died after falling from a stool, and that the science underlying the State experts’ conclusions [that Vasquez beat her to death] was fundamentally flawed.” (Subsequent Application p. 6) In discussing his primary claim, Vasquez further explains his claim that “science has now clarified that short falls, such as the one taken by Miranda from the stool, *12 can and in fact do cause the type of catastrophic head injury observed upon Miranda’s arrival in the emergency room.” (Subsequent Application p. 16) Vasquez’s other claims of new evidence regarding Shaken Infant Syndrome, biomechanics, and Second Impact Syndrome are either dependent upon the validity of the fall theory or are clearly unsupported and insufficient to justify relief.

Certainly it might be possible to imagine a case where the defendant claimed at trial that the victim fell from a sufficient height to have caused a fatal injury, where that theory was discredited by expert testimony considered valid at the time, and where new scientific evidence would suggest that the theory in question was a valid explanation for the fatal injury based on data comparing substantially similar fatal and non-fatal falls. Such a case might justify relief under Article 11.073. This is not that case, for many reasons.

This was not a case of a single head injury that could equally have been explained by either an intentional blow or an accidental fall. It was multiple blows to the head, as admitted by Vasquez himself, causing severe and extensive injury to the brain. This was not a case of an otherwise loving parent who had no proclivity to hurt the child in question. Vasquez was clearly an abusive parental figure by anyone’s measure, who the evidence *13 suggests not only hit the victim but also lethally injected her with cocaine and sexually assaulted her. This was not a case of an accidental fall from two-to-ten feet in the air. It was a stepping stool depicted in SX # 16 and which the State has measured to be approximately 10&1/2 inches high. (See Appendices A & B). This is not a case where the fall in question had been seen by some disinterested witness or otherwise verified. Vasquez was the only adult home at the time, the emergency responders did not even see the stool in question, and no toothpaste was found in the victim’s mouth, in spite of the fact that she had supposedly been brushing her teeth when she fell and lost consciousness.

Supporting Affidavits.

Vasquez has attempted to support his “new science” allegations with attached affidavits from two pathologists, Dr. Thomas Young and Dr. Waney Squier. These affidavits fall far short.

Dr. Young’s Affidavit.

Dr. Young, in his affidavit, pointed to two journal articles that supposedly “falsified the notion that short falls do not cause death in children.” (Exhibit A, Young Affidavit p. 3) However the two medical articles cited by Dr. Young do not even involve fatal brain injuries from falls that could reasonably be compared with the present short fall from a *14 10&1/2-inch stool by four-year-old Miranda.

Fatal Pediatric Head Injuries Caused by Short-Distance Falls (See Appendix C) – The only children four years and older who died from falls fell from at least three feet or from an undetermined height at least two feet but possibly as much as six to eight feet, these being falls from a swing. The falls in the study were from playground equipment and not from falling off something like a stool in the home. It stands to reason that the dynamics and motions involved in falling from a swing or other movable playground equipment are different from those involving in falling from a stationary stool, as well as the nature of the surface or structure onto which the child fell.

Delayed Sudden Death in an Infant Following an Accidental Fall (See Appendix D) – The case study involved only one death of a ninemonth-old, who fell from a bed some 30 inches high, onto a concrete floor. The authors of the case study admit that “lethality of short falls … are still controversial. One widely held belief is that short falls are almost never fatal.” The authors further submit, “We do not argue the widely noted observation that simple falls from low heights rarely result in significant primary brain injury.” (p. 373)

Moreover, both of these articles are based strictly on data from cases *15 where the falls in question did cause death, and do not contain data or comparisons with cases of non-fatal falls. Accordingly, there is no attempt in either article to address the frequency with which short falls of this nature are fatal or to refute the proposition that in the vast majority of cases short falls are not fatal, as is consistent with Dr. Burke’s and Dr. White’s testimony at trial.

Although Dr. Young also disagreed with certain statements made by Dr. Burke at trial concerning Shaken Baby Syndrome and comparison with injuries suffered in a high speed car accident, and with Dr. White and Dr. James Lukefahr’s opinions concerning sexual assault , he offered nothing to support a “new science” claim on these grounds. (Exhibit A, Young Affidavit pp. 3-4)

Dr. Squier’s Affidavit.

Dr. Squier, in her affidavit, asserted that “Miranda’s primary cause of death was blunt force injuries to the head consistent with a fall from a stool,” and that “[t]he strikes to Miranda’s head by Mr. Vasquez, on their own, were probably insufficient to cause fatal injuries.” However, she bases this conclusion on an unverified assumption that Vasquez, the only adult present at the time, was telling the truth about the sequence of events at the time of the injury. (Exhibit B, Squire Affidavit p. 2)

Dr. Squier also disagreed with Dr. Burke’s Shaken Baby Syndrome and high speed accident analogies, but not based on any “new science.” On the contrary, Dr. Squier attempts to support her assertions based on a study published in 1987, well before Vasquez’s trial. (Exhibit B, Squire Affidavit p. 3, n.2)

The only assertions that Dr. Squier makes that are arguably supported by new science involve her Second-Impact Syndrome claim that Miranda died as a result of the combined impact of being initially hit by Vasquez and then falling from the stool. (Exhibit B, Squire Affidavit p. 4) However, as discussed below, under Texas’ law concerning concurrent causation, this would not have relieved Vasquez of responsibility for the death.

Concurrent Causation.

With regard to causation, the Penal Code provides that “[a] person is criminally responsible if the result would not have occurred but for his conduct, operating either alone or concurrently with another cause, unless the concurrent cause was clearly sufficient to produce the result and the conduct of the actor clearly insufficient.” Tex. Pen. Code Ann. § 6.04 (a). The Court of Criminal Appeals has interpreted this to mean that, “[i]f the additional cause, other than the defendant's conduct, is clearly sufficient, by itself, to produce the result and the defendant's conduct, by itself, is clearly *17 insufficient, then the defendant cannot be convicted.” Robbins v. State, 717 S.W.2d 348, 351 (Tex. Crim. App. 1986); see also Turner v. State, 435 S.W.3d 280, 283 (Tex. App.—Waco 2014, pet. ref’d).

In the present case, there is no showing that Vasquez’s repeated blows to Miranda’s head were clearly insufficient to cause her death, and it remains highly unlikely that her fall from a short stool would have been sufficient, by itself, to cause the death. Accordingly, even under the supposedly newlydeveloping science of Second-Impact Syndrome, Vasquez cannot escape responsibility for her murder.

In addition, Vasquez’s initial blows arguably themselves caused Miranda to be in such a dazed state that she fell from the stool in question, making the second impact as well a direct result of his own conduct.

The Prejudice Prong.

In order to prevail under 11.073, the Court not only has to find that there is new, admissible, previously unavailable scientific evidence, but also that “had the scientific evidence been presented at trial, on the preponderance of the evidence, the person would not have been convicted.” (Emphasis added).

In the present case, even if some or all of the “new science” arguments are found to have some validity, it is highly unlikely that this new *18 science would have changed the outcome, as the evidence of guilt was overwhelming.

PRAYER

WHEREFORE, the State prays that the Court will dismiss as abusive the present subsequent application for writ of habeas corpus and deny the motion to stay execution.

Respectfully submitted,

/s/ Douglas K. Norman ___________________ Douglas K. Norman State Bar No. 15078900 Assistant District Attorney 105th Judicial District of Texas 901 Leopard, Room 206 Corpus Christi, Texas 78401 (361) 888-0410 (361) 888-0399 (fax)

CERTIFICATE OF SERVICE

This is to certify that a copy of this document was e-served on April 18, 2015, on Applicant’s attorneys, Mr. Andrew M. Edison, Andrew.edison@emhllp.com, and Mr. James Chambers, james.chambers@emhllp.com.

/s/ Douglas K. Norman ___________________ Douglas K. Norman

APPENDIX A

APPENDIX B

AFFIDAVIT

THE STATE OF T E X A S C O U N T Y OF N U E C E S

B E F O R E M E , the undersigned authority, on this day personally appeared John Mitchell, who after being by me duly swom upon oath says:

M y name is John Mitchell and I am a Deputy District Clerk for Nueces County and the Records Management Supervisor for the office. I am over 18 years of age, I have never been convicted of a crime, and I am tliliy competent to make this affidavit. I have personal knowledge of the facts stated herein, and they are all true and correct.

On A p r i l 17, 2015,1 reviewed the attached photographs of a stool that had been admitted into evidence as SX#9 in the murder trial o f Richard Vasquez, Cause N o . 98-CR-0730-E, in the 14^^^ District Court of Nueces County, Texas, and that I am presently holding as custodian ofthe evidence.

The attached photographs, with tape measure next to them, accurately show the height of the stool, which was measured to be approximately 10 &1/2 inches t a l l

Further affiant saith naught.

Subscribed and sworn to before me by the said John Mitchell this 17th day o f A p r i l , 2015, to certify which witness my name and seal of office.

APPENDIX C

r I

I The American Journal of Forensic Medicine and Pathology Volume 22 Number I March 2001

1 Fatal Pediatric Head Injuries Caused by Short-Distance Falls John Plunkett

13 Case Report of Sudden Death After a Blow to the Baell' of the Neck Gregory G. Davis and Jay M. Glass

19 Sudden Cardiac Death and Right Ventricular Dysplasia E. N. Michalodirnitrakis, D. D.-A. Tsiftsis, A. M. Tsatsakis, and I. Stiakakis

23 Simultaneous Sudden Infant Death Syndrome: A Proposed Definition and Worldwide Review of Cases Steven A. Koehler, Shaun Ladham, Abdulrezzak Shakir, and Cyril H. Wecht

33 Simultaneous Sudden Infant Death Syndrome: A Case Report Shaun Ladham, Steven A. Koehler, Abdulrezzak Shakir, and Cyril H. Wecht

(Continued)

Publication Staff

Ruth Weinberg Susan Deitch Anthony F. Trioli Ray Thibodeau Senior Editor Assistant Managing Account Manager Director, Advertising Editor Sales Frances R. DeStefano Cynthia Payne The Point of Difference Publisher Ad Production International Advertising Coordinator Representative

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Indexed in Index Medicus/MEDllNE, Current Contents/Clinical Medicine, SCISEARCH, Excerpta Medica/EMBASE, and Bio- medical Database, and abstracted in Criniinology & Penology Abstracts and Police Science Abstracts.

The American Journal of Forensic Medicine and Pathology 22(1):1-12, 2001. ©2001 Lippincott Williams & Wilk.ins, Inc., Philadelphia Fatal Pediatric Head.Injuries Caused by Short-Distance Falls John Plunkett, M.D.

Physicians disagree on several issues regarding head in- Many physicians believe that a simple fall can- jury in infants and children, including the potential not cause serious injury or death (1-9), that a lethality of a short-distance fall, a lucid interval in an ul- lucid interval does not exist in an ultimately fatal timately fatal head injury, and the specificity of retinal hemorrhage for inflicted trauma. There is scant objective pediatric head injury (7-13), and that retinal hem- evidence to resolve these questions, and more informa- orrhage is highly suggestive if not diagnostic for tion is needed. The objective of this study was to deter- inflicted trauma (7,12,14-21). However, several mine whether there are witnessed or investigated fatal have questioned these conclusions or urged cau- short-distance falls that were concluded to be accidental. tion when interpreting head injury in a child The author reviewed the January l, 1988 through June 30, 1999 United States Consumer Product Safety Com- (15,22-28). This controversy exists because most mission database for head injury associated with the use infant injuries occur in the home (29,30), and if of playground equipment. The author obtained and re- there is history of a fall, it is usually not witnessed viewed the primary source data (hospital and emergency or is seen only by the caretaker. Objective data are medical services' records, law enforcement reports, and needed to resolve this dispute. It would be helpful coroner or medical examiner records) for all fatalities in- volving a fall. if there were a database of fatal falls that were The results revealed 18 fall-related head injury fatali- witnessed or wherein medical and law enforce- ties in the database. The youngest child was 12 months ment investigation unequivocally concluded that old, the oldest 13 years. The falls were from 0.6 to 3 me- the death was an accident. ters (2-10 feet). A noncaretaker witnessed 12 of the 18, The United States Consumer Product Safety and 12 had a lucid interval. Four of the six children in whom funduscopic examination '"'as documented in the Commission (CPSC) National Injury Information n1edical record had bilateral retinal hemorrhage. The au- Clearinghouse uses four computerized data sources thor concludes that an infant or ciiild may suffer a fatal (31). The National Electronic Injury Surveillance bead injury from a fall of less than 3 meters (10 feet). System (NEISS) file collects current injury data as- The injury may be associated with a lucid interval and sociated with 15,000 categories of consumer prod- bilateral retinal hemorrhage. Key Words: Child abuse-Head injury-Lucid interval- ucts from 101 U.S. hospital emergency depart- Retinal hemorrhage-Subdural hematoma. ments, including 9 pediatric hospitals. The file is a probability sample and is used to estimate the num~ ber and types of consumer product-related injuries each year (32). The Death Certificate (DC) file is a demographic summary created by information pro- vided to the CPSC by selected U.S. State Health Departments. Tbe Injury/Potential Injury Incident (IR) file contains sun1Illaries, indexed by consun1er product, of reports to the CPSC from consumers, medical examiners and coroners' (Medical Exam- iner and Coroner Alert Project [MECAP]), and newspaper accounts of product-related incidents discovered by local or regional CPSC staff (33). The In-Depth Investigations (AI) file contains sum- maries of investigations performed by CPSC staff 1\1anuscript received April 10, 2000; revised September 15, based on reports received from the NEISS, DC, or 2000; accepted September 24, 2000. IR files (34). The AI files provide details about From the DepartmentS of Pathology and Medical Education, Regina Medical Center, 1175 Nininger Road, Hastings MN the incident from victim and witness interviews, 55033, U.S.A.; Email: plunkettj@reginarnedical.com. accident reconstruction, and review of law enforce-

I 2 J. PLUNKETT

ment, health care facility, and coroner or medical be the highest point of the arc. Twelve of the 18 examiner records (if a death occurred). falls were witnessed by a noncaretaker or were videotaped; 12 of the children had a lucid interval (5 minutes-48 hours); and 4 of the 6 in whom fun- METHODS duscopic examination was performed had bilateral I reviewed the CPSC, DC, IR, and AI files for all retinal hemorrhage (Table 1). head and neck injuries involving playground equip- ment recorded by the CPSC from January 1, 1988 through June 30, 1999. There are 323 entries in the CASES playground equipment IR file, 262 in the AI file, 47 Case 1 in the DC file, and more than 75,000 in the NEISS This 12-month-old was seated on a porch swing file. All deaths in the NEISS file generated an IR or between her mother and father when the chain on AI file. If the file indicated that a death had oc- her mother's side broke and all three fell sideways curred from a fall, I obtained and reviewed each and backwards 1.5 to 1.8 meters (5-6 feet) onto original source record from law enforcement, hos- decorative rocks in front of the porch. The mother pitals, emergency medical services (EMS), and fell first, then the child, then her father. It is not coroner or medical examiner offices except for one known if her father landed on top of her or if she autopsy report. However, I discussed the autopsy struck only the ground. She was unconscious im- findings with the pathologist in this case. mediately. EMS was called; she was taken to a local hospital; and was ictal and had decerebrate RESULTS posturing in the emergency room. She was intu- bated, hyperventilated, and treated with mannitol. There are 114 deaths in the Clearinghouse data- A computed tomography (CT) scan indicated a base, 18 of which were due to head injury from a subgaleal hematoma at the vertex of the skull, a fall. The following deaths were excluded from this comrninuted fracture of the vault, parafalcine sub- study: those that iuvolved equipment that broke or dural hemorrhage, and right parietal subarachnoid collapsed, striking a person on the head or neck hemorrhage. There was also acute cerebral edema (41); those in which a person became entangled in with effacement of the right frontal horn and com- the equipment and suffocated or was strangled (45), pression of the basal cisterns. She had a cardiopul- those that involved equipment or incidents other monary arrest while the CT scan was being done than playground (6 [including a 13.7-meter fall and could not be resuscitated. from a homemade Ferris wheel and a 3-meter fall from a cyclone fence adjacent to a playground]); and falls in which the death was caused exclusively Case2 by neck (carotid vessel, airway, or cervical spinal A 14-month-old was on a backyard "see-saw" cord) injury (4 ). and was being held in place by his grandmother. The falls were from horizontal ladders (4), The grandmother said that she was distracted for a swings (7), stationary platforms (3), a ladder at- moment and he fell backward, striking the grass- tached to a slide, a "see-saw'', a slide, and a retain- covered ground 0.6 meters (22.5 inches) below the ing wall. Thirteen occurred on a school or public plastic seat. He was conscious but crying, and she playground, and five occurred at home. The data- carried him into the house. Within 10 to 15 minutes base is uot limited to infants and children, but a he became lethargic and limp, vomited, and was 13-year-old was the oldest fatality (range: 12 taken to the local hospital by EMS personnel. He months-13 years; mean, 5.2 years; median, 4.5 was unconscious but purposefully moving all ex- years). The distance of the fall, defined as the dis- tremities when evaluated, and results of fundus- tance of the closest body part from the ground at copic examination were normal. A CT scan indi- the beginning of the fall, could be determined from cated an occipital subgaleal hematoma, left-sided CPSC or law enforcement reconstruction and actual cerebral edema with complete obliteration of the measurement in 10 cases and was 0.6 to 3.0 meters left frontal horn, and small punctate hemorrhages (mean, 1.3 ± 0.77; median, 0.9). The distance in the left frontal lobe. There was no fracture or could not be accurately determined in the seven fa- subdural hematoma. He was treated with mannitol; talities involving swings and one of the falls from a his level of consciousness rapidly improved; and he horizontal ladder, and may have been from as little was extubated. However, approximately 7 hours I as 0.6 meters to as much as 2.4 meters. The maxi- after admission he began to have difficulty breath- mum height for a fall from a swing was assumed to ing, both pupils suddenly dilated, and he was rein-

A1n J Forensic Med Pathol, VoL 22. No. 1, March 2001 I j

TABLE 1. Summary of cases Lucid Retinal Subdural No. CPSC No. Age Sex Fall from Distance M/F Witnesse;d interval hemorrhage hemorrhage Autopsy Cause of death FP

DC 9108013330 12 mos F Swing 1.5--1.8/5.0-6.0 No No N/R Yes +IHF No Complex calvarial fracture No with edema and contusions 2 Al 890208HBC3088 14 mos M See~saw 0.6/2.0 No 10-15 No No No Malignant cerebral edema No minutes with herniation 3 IR F910368A 17 mos F Swing 1.5-1.8/5.0-6.0 No No N/R Yes +IHF Yes Acute subdural hematorna Yes wit~.secondary cerebral edema 4 Al 921001 HCC2263 20 mos F Platform 1.1/3.5 No 5-10 Bilateral Yes +IHF Limited Occipital fracture with Yes minutes multilayered subdural/subarachnoid ~ hemorrhage progreSsing S2 to cerebral edema and r 5' DC 9312060661 23 mos F Platform 0.70/2.3 Yes 10 minutes Bilateral, NOS Yes Yes herniation Acute subdural hematoma Yes ~ ;,,: 6 DC 9451016513 26 mos M Swing 0.9-1 c8/3.0-6.0 Yes No Bilateral Yes +IHF Yes Subdural hematoma··Yflth Yes ti multi!ayered associated cerebral edema ~ <.., 7' Al 891215HcC2094 3 yrs M Platform 0.9/3.0 Yes 10 minutes N/R Yes No Acute cerebral edema with " 8 Al 910515HCC2182 3 yrs F Ladder 0.6/2.0 yes 15 minutes N/R Yes Yes herniation Complex calvarial fracture, No Yes ~ ' (autopsy only) contusions, cerebral t;J ~ edema with herniation 9 DC 9253024577 4 yrs M Slide 2.1/7.0 Yes 3 hours N/R No Yes Epidural hematoma Yes 10 Al920710HIVE4014 5 yrs M Horizontal ladder 2.1/7.0 No No N/R Yes No Acute subdural hematoma with acute cerebral Yes ~ edema ~ 11 Al 960517HCC5175 6 yrs M Swing 0.6-2.4/2.0-8.0 No 10 minutes No Yes +IHF No Acute subdural hematoma Yes a ;,,, 12 Al 970324HCC3040 6 yrs M Horizontal 3.0/10.0 Yes 45 minutes N/R No No Malignant cerebral edema Yes ladder with herniation ';-I

,,. 13 Al 881229HCC3070 6 yrs F Horizontal ladder 0.9/3.0 Yes 1 +hour N/R Yes +IHF Yes Subdural and subarachnoid hemorrhage, cerebral Yes ti [;i

~ '-. infarct, and edema :ii 14 Al 930930HIVE5025 7 yrs M Horizontal 1.2-2.4/4.0-8.0 Yes 48 hours N/R No Yes Cerebral infarct secondary Yes , ",. < ladder to carotid/vertebral artery thrombosis f;l . ~ 15

16 Al 970409HCC1096

Al 890621 HCC3195 8 yrs

10 yrs M F Retaining .wall Swing 0.9/3.0

0.9-1.5/3.0-5.0 Yes

Yes 12+ hours

10 minutes N/R

Bilateral Yes (autopsy only) Yes Yes

Yes Acute subdura! hematoma

Acute subdural hematoma Yes

No ;,;, ~ "'"" 0 ~ mum layered contiguous with an AV malformatiorl /ii ~ 17 Al 920428HCC1671 12 yrs F Swing 0.9-1.8/3.0-6.0 Yes No N/R No Yes Occipital fracture With Yes ,.., N extensive contra-coup contusions

,..~ 18 Al 891016HCC1511 13 yrs F Swing 0.6-1.8/2.0-6.0 Yes No N/R Yes +IHF Yes Occipital fracture, subdural Yes hemorrhage 1 cerebral edema §: ,. Cl ~he original CT scan for case #7 and the soft tissue CT windows for case #5 could not be located and were unavailable for review. N CPSC, Consumer Products Safety Commission; Al, accident investigation; IR, incident report; DC, death certificate; M, male; F, female; Distance, the distance of the closest body part § from the ground at the start of the fall (see text); M/F, meters/feet; Witnessed, witnessed by a noncaretaker or videotaped; N/R, not recorded; IHF, including interhemispheric or fa!x; FP, forensic pathologist-directed death investigation system. "'

4 J. PLUNKETT

tubated. A second CT scan demonstrated progres- Cases sion of the left hemispheric edema despite medical A 23-month-old was playing on a plastic gym set management, and he was removed from life sup- in the garage at her home with her older brother. port 22 hours after admission. She had climbed the attached ladder to the top rail above the platform and was straddling the rail, with her feet 0.70 meters (28 inches) above the floor. Case3 She lost her balance and fell headfirst onto a I-cm This 17-month-old had been placed in a baby (%-inch) thick piece of plush carpet remnant cover- carrier-type swing. attached to an overhead tree ing the concrete floor. She struck the carpet first limb at a daycare provider's home. A restraining with her outstretched hands, then with the right bar held in place by a snap was across her waist. front side of her forehead, followed by her right She was being pushed by the daycare provider to shoulder. Her grandmother had been watching the an estimated height of 1.5 to 1.8 meters (5-6 feet) children play and videotaped the fall. She cried when the snap came loose. The child fell from the after the fall but was alert and talking. Her grand- swing on its downstroke, striking her back and mother walked/carried her into the kitchen, where head on the grassy surface. She was immediately her mother gave her a baby analgesic with some unconscious and apneic but then started to breathe water, which she drank. However, approximately 5 spontaneously. EMS took her to a pediatric hospi- minutes later she vomited and became stuporous. tal. A CT scan indicated a large left-sided sub- EMS personnel airlifted her to a tertiary-care uni- dural hematoma with extension to the interhemi- versity hospital. A CT scan indicated a large right- spheric fissure anteriorly and throughout the length sided subdural hematoma with effacement of the of the falx. The hematoma was surgically evacu- right lateral ventricle and minimal subfalcine herni- ated, but she developed malignant cerebral edema ation. (The soft tissue windows for the scan could and died the following day. A postmortem exami- not be located and were unavailable for review.) nation indicated symmetrical contusions on the The hematoma was immediately evacuated. She re- buttock and midline posterior thorax, consistent mained comatose postoperatively, developed cere- with impact against a fiat surface; a small residual bral edema with herniation, and was removed from left-sided subdural hematoma; cerebral edema life support 36 hours after the fall. Bilateral retinal with anoxic encephalopathy; and uncal and cere- hemorrhage, not further described, was docu- bellar tonsillar herniation. There were no cortical mented in a funduscopic examination performed 24 contusions. hours after admission. A postmortem examination confirmed the right frontal scalp impact injury. Case4 There was a small residual right subdural hema- A 20-month-old was with other family members toma, a right parietal lobe contusion (secondary to for a reunion at a public park. She was on the plat- the surgical intervention), and cerebral edema with form portion of a jungle gym when she fell from cerebellar tonsillar herniation. the side and struck her head on one of the support posts. The platform was 1.7 meters (67 inches) Case6 above the ground and I.I meters (42 inches) above A 26-month-old was on a playground swing the top of the support post that she struck. Only her being pushed by a 13-year-old cousin when he fell father saw the actual fall, although there were a backward 0.9 to 1.8 meters (3--6 feet), striking his number of other people in the immediate area. She head on hard-packed soil. The 13-year-old and sev- was initially conscious and talking, but within•5 to eral other children saw the fall. He was immedi- 10 minutes became comatose. She was taken to a ately unconscious and was taken to a local emer- nearby hospital, then transferred to a tertiary-care gency room, then transferred to a pediatric hospital. facility. A CT scan indicated a right occipital skull A CT scan indicated acute ' cerebral edema and a fracture with approximately 4-mm of depression small subdural hematoma adjacent to the anterior and subarachnoid and subdural hemorrhage along interhemispheric falx. A funduscopic examination the tentorium ·and posterior falx. Funduscopic ex- performed 4 hours after admission indicated exten- amination indicated extensive bilateral retinal and sive bilat~ral retiqal hemorrhage, vitreous hemor- preretinal hemorrhage. She died 2 days later be- rhage in the left eye, and papilledema. He had a cause of uncontrollable increased intracranial pres- subsequent cardiopulmonary arrest and could not sure. A limited postmortem examination indicated be resuscitated. A postmortem examination con- an impact subgaleal hematoma overlying the frac- firmed the retinal hemorrhage and indicated a right ture in the mid occiput. parietal scalp impact injury but no calvarial frac-

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FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 5

ture, a "film" of bilateral subdural hemorrhage, Case9 cerebral edema with herniation, and· focal hemor- A 4-year-old fell approximately 2.1 meters (7 rhage in the right posterior midbrain and pons. feet) from a playground slide at a state park, land' . ing on the dirt ground on his buttock, then falling to Case7 his left side, striking his head. T:ljere was no loss of This 3-year-old with a history of TAR (thrombo- consciousness, but his family took him to a local cytopenia-absent radius) syndrome was playing emergency facility, where an'. evaluation was nor- with other children on playground equipment at his mal. However, be began vomiting and complained school when he stepped through an opening in a of left neck and bead pain approximately 3 hours platform. He fell 0.9 meters (3 feet) to the hard- later. He was taken to a second hospital, where a packed ground, striking his face. A teacher wit- CT scan indicated a large left parietal epidural nessed the incident. He was initially conscious and hematoma with a midline shift. He was transferred able to walk. However, approximately 10 minutes to a pediatric hospital and the hematoma was evac- later he had projectile vomiting and became co- uated, but he developed malignant cerebral edema matose, was taken to a local hospital, and subse- with right occipital and left parietal infarcts and quently transferred to a pediatric hospital. A CT was removed from the respirator 10 days later. A scan indicated a small subdural hematoma and dif- postmortem examination indicated a small residual fuse cerebral edema with uncal herniation, accord- epidural hematoma, marked cerebral edema, bilat- ing to the admission history and physical examina- eral cerebellar tonsillar and uncal herniation, and tion. (The original CT report and scan could not be hypoxic encephalopathy. There was no identifiable located and were unavailable for review.) His skull fracture. platelet count was 24,000/mm3 , and he was treated empirically with platelet transfusions, although he Case 10 had no evidence for an expanding extra-axial mass. A 5-year-old was apparently walking across the Resuscitation was discontinued in the emergency horizontal ladder of a "monkey bar," part of an in- room. terconnecting system of homemade playground equipment in his front yard, when his mother Case8 looked out one of the windows and saw him laying This 3-year-old was at a city park with an adult face down on the ground and not moving. The hor- neighbor and four other children, ages 6 to 10. She izontal ladder was 2.1 meters (7 feet) above com- was standing on the third step of a slide ladder 0.6 pacted dirt. EMS were called, be was taken to a meters (22 inches) above the ground when she fell local hospital, and then transferred to a pediatric forward onto compact dirt, striking her head. The hospital. A CT scan indicated a right posterior tem- other children but not the adult saw the fall. She poral linear fracture with a small underlying was crying but did not appear to be seriously in- epidural hematoma, a 5-mm thick acute subdural jured, and the neighbor picked her up and brought hematoma along the right temporal and parietal her to her parents' home. Approximately 15 min- lobes, and marked right-sided edema with a 10-mm utes later she began to vomit, and her mother called midline shift. He was hyperventilated and treated EMS. She was taken to a local emergency room, with mannitol, but the hematoma continued to en- then transferred to a pediatric hospital. She was ini- large and was surgically evacuated. However, he tially lethargic but responded to hyperventilation developed uncontrollable cerebral edema and was and mannitol; she began to open her eyes with removed from life support 10 days after the fall. stimulation and to spontaneously move all extre;ni- ties and was extubated. However, she developed Case 11 malignant cerebral edema on the second hospital A 6-year-old was on a playground swing at a pri- day and was reintubated and hyperventilated but vate lodge with his 14-year-old sister. His sister died the following day. A postmortem examination heard a "thump,'' turned around, and saw him on indicated a subgaleal hematoma at the vertex of the the grass-covered packed earth beneath the swing. skull associated with a complex fracture involving The actual fall was not witnessed. The seat of the the left frontal bone and bihiteral temporal bones. swing was 0.6 meters (2 feet) above the ground, There were small epidural and subduraJ bematomas and the fall distance could have been from as high (not identifiable on the CT scan), bilateral "contra- as 2.4 meters (8 feet). He was initially conscious coup" contusions of the inferior surfaces of the and talking but within 10 minutes became co- frontal and temporal lobes, and marked cerebral matose and was taken to a local emergency room, eden1a with uncal herniation. then transferred to a tertiary-care hospital. A CT

Am J Forensic Nled Parhol, Vol. 22, No. 1, March 2001 6 J. PLUNKETT

scan indicated a large left frontoparietal subdural ture, subdural and subarachnoid hemorrhage, and a hematoma with extension into the anterior inter- right cerebral hemisphere infarct. The infarct in- hemispheric fissure and a significant midline shift cluded the posterior cerebral territory and was with obliteration of the left lateral ventricle. There thought most consistent with thrombosis or dissec- were no retinal hemorrhages. He was treated ag· tion of a right carotid artery that bad a persistent gressively with dexamethasone and hyperventila- fetal origin of the posterior c'erebral artery. She tion, but there was no surgical intervention. He died remained con1atose and was removed from the the following day. respirator 6 days after admission. A postmortem examination indicated superficial abrasions and Case 12 contusions over the scapula, a prominent right pari- This 6-year-old was at school and was sitting on etotemporal subgaleal bematoma, and a right pari- the top crossbar of a "monkey bar" approximately 3 , eta! skull fracture. She bad a 50-ml subdural meters (10 feet) above compacted clay soil when an bematoma and cerebral edema with global hypoxic unrelated noncaretaker adult saw him fall from the or iscbemic injury ("respirator brain"), but the crossbar to the ground. He landed flat on his back carotid vessels were normal. and initially appeared to have the wind knocked out of him but was conscious and alert. He was taken to Case 14 the school nurse who applied an ice pack to a con- A 7-year-old was on the playground during tusion on the back of bis bead. He rested for ap- school hours playing on the horizontal ladder of a proximately 30 minutes in the nurse's office and "monkey bar" when he slipped and fell 1.2 to 2.4 was being escorted back to class when be suddenly meters (4-8 feet). According to one witness, be collapsed. EMS was called, and be was transported struck his forehead on the bars of the vertical lad- to a pediatric hospital. He was comatose on admis- der; according to another eyewitness he struck the sion, the fundi could not be visualized, and a bead rubber pad covering of the asphalt ground. There CT scan was interpreted as normal. However, a CT are conflicting stories as to whether he had an ini- scan performed the following morning approxi- tial loss of consciousness. However, he walked mately 20 hours after the fall indicated diffuse cere- back to the school, and EMS was called because of bral edema with effacement of the basilar cisterns the history of the fall. He was taken to a local hos- and fourth ventricle. There was no identifiable sub- pital, where evaluation indicated a Glasgow coma dural hemorrhage or cal varial fracture. He devel- score of 15 and a normal CT scan except for an oc- oped transtentorial herniation and died 48 hours cipital subgaleal bematoma. He was kept overnight after the fall. for observation because of the possible loss of con- sciousness but was released the following day. He Case 13 was doing homework at home 2 days after the fall This 6-year-old was playing on a school play- when his grandmother noticed that he was stum- ground with a 5th grade student/friend. She was bling and had slurred speech, and she took him hand-over-hand traversing the crossbar of a "mon- back to the hospital. A second CT scan indicated a key bar" 2.4 meters (7 feet 10 inches) above the left carotid artery occlusion and left temporal and ground with her feet approximately 1 meter (40 parietal lobe infarcts. The infarcts and subsequent inches) above the surface. She attempted to slide edema progressed; he had brainstem herniation; down the pole when she reached the end of the and be was removed from life support 3 days later crossbar but lost her grip and slid quickly to the (5 days after the initial fall). A postmortem exanli- ground, striking the compacted dirt first with her nation indicated ischemic infarcts of the left pari- feet, then her buttock and back, and finally 'her etal, temporal, and occipital lobes, acute cerebral head. The friend inforn1ed the school principal of edema with herniation, and thrombosis of the left the incident, but the child seemed fine and there vertebral artery. Occlusioli. of the carotid artery, was no intervention. She went to a relative's home suspected premortem, could not be confirmed. for after-school care approximately 30 minutes after the fall, watched TV for a while, then com- Case 15 plained of a l\eadache and laid down for a nap. This 8-year-old was at a public playground near When her parents arrived at the home later that her home· with se;,,eral friends her age. She was evening, 6 hours after the incident, they discovered hanging by her hands from the horizontal ladder of that she was incoherent and "drooling." EMS trans- a "monkey bar" with her feet approximately 1.1 ported her to a tertiary-care medical center. A CT meters (3.5 feet) above the ground when she at- scan indicated a right parieto-occipital skull frac- tempted to swing from the bars to a nearby 0.9-

Am J Forensic Med Pathol, Vol. 22, No. J, March 2001

FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 7

meter (34-inch) retaining wall. She landed on the lost her balance and fell 0.9 tol.8 )lleters (3-6 feet) top of the wall but then lost her balance and fell to to the asphalt surface, striking her posterior thorax the ground, either to a hard-packed surface (one and occipital scalp. She was inunediately uncon- witness) or to a 5.1-cm (2-inGh) thick.resilient rub- scious and was taken to a tertiary-care hospital ber mat (a second witness), striking her back and emergency room, where she was, pronounced dead. head. She initially cried and complained of a A postmortem examination ii;idic'ated an occipital headache but continued playing, then later went impact injury associated with an extensive com- home. Her mother said that she seemed normal and minuted occipital fracture extending into both mid- went to bed at her usual time. However, when her dle cranial fossa and "contra-coup" contusions of mother tried to awaken her at approximately 8:30 both inferior frontal and temporal lobes. the following morning (12 hours after the fall) she complained of a headache and went back to sleep. Case 18 She awoke at 11 a.m. and complained of a severe This 13-year-old was at a public playground with headache then became unresponsive and had a a friend. She was standing on the seat of a swing seizure. EMS took her to a nearby hospital, but she with her friend seated between her legs when she died in the emergency room. A postmortem exami- lost her grip and fell backwards 0.6 to 1.8 meters nation indicated a right temporoparietal subdural (2-6 feet), striking either a concrete retaining wall hematoma, extending to the base of the brain in the adjacent to the playground or a resilient 5.1-cm (2 middle and posterior fossae, with flattening of the inch) thick rubber mat covering the ground. She gyri and narrowing of the sulci. (The presence or was immediately unconscious and was given emer- absence of herniation is not described in the au- gency first aid by a physician who was nearby topsy report.) There was no calvarial fracture, and when the fall occurred. She was taken to a nearby there was no identifiable injury in the scalp or hospital and was purposefully moving all extremi- galea. ties and had reactive pupils when initially evalu- ated. A CT scan indicated interhemispheric sub- Case 16 dural hemorrhage and generalized cerebral edema, A 10-year-old was swinging on a swing at his which progressed rapidly to brain death. A post- school's playground during recess when the seat de- mortem examination indicated a linear nonde- tached from the chain and he fell 0.9 to 1.5 meters pressed midline occipital skull fracture, subdural (3-5 feet) to the asphalt surface, striking the back of hemorrhage extending to the occiput, contusion of his head. The other students but not the three adult the left cerebellar hemisphere, bifrontal "contra- playground supervisors saw him fall. He remained coup" contusions, and cerebral edema. conscious although groggy and was carried to the school nurse's office, where an ice pack was placed DISCUSSION on an occipital contusion. He suddenly lost con- sciousness approximately 10 minutes later. and General EMS took him to a local hospital. He had decere- Traumatic brain injury (TBI) is caused by a force brate posturing when initially evaluated. Fundus- resulting in either strain (deformation/unit length) copic examination indicated extensive bilateral con- or stress (force/original cross-sectional area) of the fluent and stellate, posterior and peripheral scalp, skull, and brain (35-37). The extent of injury preretinal and subhyaloid hemorrhage. A CT scan depends not only on the level and duration of force showed a large acute right frontoparietal subdural but also on the specific mechanical and geometric hematoma with transtentorial herniation. i Trhe properties of the cranial system under loading hematoma was surgically removed, but he devel- (38-40). Different parts of the skull and brain have oped malignant cerebral edema and died 6 days later. distinct biophysical characteristics, and calculating A postmortem examination indicated a right parietal deformation and stress is complex. However, an ap- subarachnoid AV malformation, contiguous with a plied force causes the skull and brain to move, and small amount of residual subdural hemorrhage, and acceleration, the time required to reach peak accel- cerebral edema with anoxic encephalopathy and her- eration, and the duration of acceleration may be niation. There was no calvarial fracture. measured at specific locations (36,41). These kine- 1natic parameters do not cause the . actual brain Case 17 damage but are useful for analyzing TBI because A 12-year-old was at a public playground with a they are easy to quantify. Research in TBI using sister and another friend and was standing on the physical models and animal experiments has shown seat of a swing when the swing began to twist. She that a force resulting in angular acceleration pro-

Am J Forensic Med Pathol, Vol. 22, No. I, March 2001 8 J PLUNKETT

duces primarily diffuse brain damage, whereas a ing surface is usually less than 5 milliseconds force causing exclusively translational acceleration (39,59-61). Experimentally, impact duration longer produces only focal brain damage (36). A fall from than 5 milliseconds will not cause a subdural a countertop or table is often considered to be ex- hematoma unless the level of angular acceleration clusively translational and therefore assumed inca- is above 1.75 X 105 rad/s 2 (61). A body in motion pable of producing serious injury (3, 7-9). However, with an angular acceleration of 1.75 X 105 rad/s 2 sudden impact deceleration must have an angular has a tangential acceleration of 17 ,500 rn/s 2 at 0.1 vector unless the force is applied only through the meters (the distance from the midneck axis of rota- center of mass (COM), and deformation of the tion to the midbrain COM in the Duhaime model). skull during impact must be accompanied by a vol- A human cannot produce this level of acceleration ume change (cavitation) in the subdural "space" by impulse ("shake") loading (62). tangential to the applied force (41). The angular ' An injury resulting in a subdural hematoma in an and deforn1ation factors produce tensile strains on infant may be caused by an accidental fall the surface veins and mechanical distortions of the (43,44,64). A recent report documented the findings brain during impact and may cause a subdural in seven children seen in a pediatric hospital emer- hematoma without deep white matter injury or even gency room after an accidental fall of 0.6 to 1.5 unconsciousness (42-44). meters who had subdural hemon-hage, no Joss of Many authors state that a fall from less than 3 consciousness, and no symptoms (44). The charac- meters (10 feet) is rarely if ever fatal, especially if teristics of the hemon-hage, especially extension the distance is Jess than 1.5 m~ters (5 feet) into the posterior interhemispheric fissure, have (1-6,8,9). The few studies concluding that a short- been used to suggest if not confirm that the injury distance fall may be fatal (22-24,26,27) have been was nonaccidental (9,62,65-68). The hemon-hage criticized because the fall was not witnessed or was extended into the posterior interhemispheric fissure seen only by the caretaker. However, isolated re- in 5 of the 10 children in this study (in whom the ports of observed fatal falls and biomechanical blood was identifiable on CT or magnetic reso- analysis using experimental animals, adult human nance scans and the scans were available for re- volunteers, and models indicate the potential for se- view) and along the anterior falx or anterior inter- rious head injury or death from as little as a 0.6- hemispheric fissure in an additional 2 of the 10. meter (2-foot) fall (48-52). There are limited experimental studies on infants (cadaver skull frac- Lucid Interval ture) (53,54) and none on living subadult nonhu- Disruption of the diencephalic and midbrain por- man primates, but the adult data have been extrap- tions of the reticular activating system (RAS) olated to youngsters and used to develop the causes unconsciousness (36,69,70). "Shearing" or Hybrid II/III and Child Restraint-Air Bag Interac- "diffuse axonal" injury (DAI) is thought to be the tion (CRAB!) models (55) and to propose standards primary biophysical mechanism for immediate for playground equipment (56,63). We simply do traumatic unconsciousness (36,71). Axonal injury not know either kinematic or nonkinematic limits has been confirmed at autopsy in persons who had in the pediatric population (57,58). a brief loss of consciousness after a head injury and Each of the falls in this study exceeded estab- who later died from other causes, such as coronary lished adult kinematic thresholds for traumatic artery disease (72). However, if unconsciousness is brain injury (41,48-52). Casual analysis of the falls momentary or brief ("concussion") subsequent ~e­ suggests that most were primarily translational. terioration must be due to a mechanism other than However, deformation and internal angular acceler- DAI. Apnea and catecholamine release have been ation of the skull and brain caused by the itnpact suggested as significant factors in the outcome fol- produce the injury. What happens during the im- lowing head injury (73,74). In addition, the cen- pact, not during the fall, determines the outcome. tripetal theory of traumatic unconsciousness states that primary disruption of the RAS will not occur Snbdural Hemorrhage in isolation and that structural brainstem damage A "high strain" impact (short pulse duration and from inertial (impulse) or impact (contact) loading high rate for deceleration onset) typical for a fall is must be accompanied by evidence for cortical and more likely to cause subdural hemon-hage than a subcortical damage (36). This theory has been vali- "low strain" in1pact (long pulse duration and low dated by magnetic resonance imaging and CT scans rate for deceleration onset) that is typical of a in adults and children (75,76). Only one of the chil- motor vehicle accident (42,61). The duration of de- dren in this study (case 6) had evidence for any celeration for a head-impact fall against a nonyield- component of DAI. This child had focal hemor-

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FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 9

rhage in the posterior midbrain and pons, thought amination and has been recommended as part of by the pathologist to be primary, although there the evaluation of any pediatric patient with head was no skull fracture, only "a film" of subdural trauma (89). None of the children in this study had hemorrhage, no tears in thr:~corpus, _<;:allosum, and a formal retinal evaluation, and only six had fun- no lacerations of the cerebral white matter (grossly duscopic examination .documented in the medical or microscopically). record. Four of the six had bilateral retinal hemor- The usual cause for delayed deterioration in in- rhage. ' fants and children is cerebral edema, whereas in adults it is an expanding extra-axial hematoma Pre-existing Conditions (77). If the mechanism for delayed deterioration One of these children (case 16) had a subarach- (except for an expanding extra-axial mass) is ve- noid AV malformation that contributed to develop- nospasm, cerebral edema may be the only morpho- ment of the subdural hematoma, causing his death. logic marker. The "talk and die or deteriorate One (case 7) had-TAR syndrome (90), but his death (TADD)" syndrome is well characterized in adults was thought to be caused by malignant cerebral (78). Two reports in the pediatric literature discuss edema not an expanding extra-axial mass. TADD, documenting 4 fatalities among 105 chil- dren who had a lucid interval after head injury and Cerebrovascnlar Thrombosis subsequently deteriorated (77,79). Many physicians Thrombosis or dissection of carotid or vertebral believe that a lucid interval in an ultimately fatal arteries as a cause of delayed deterioration after pediatric head injury is extremely unlikely or does head or neck injuries is documented in both adults not occur unless there is an epidural hematoma and children (91,92). Case 14 is the first report of a (7,8,11). Twelve children in this study had a lucid death due to traumatic cerebrovascular thrombosis interval. A noncaretaker witnessed 9 of these 12 in an infant or child. Internal carotid artery throm- z 0 falls. One child had an epidural hematoma. bosis was suggested radiographically in an addi- -0 tional death (case 13) but could not be confirmed at g autopsy. However, this child died 6 days after ad- > Retinal Hemorrhage mission to the hospital, and fibrinolysis may have " m The majority of published studies conclude that retinal hemorrhage, especially if bilateral and pos- removed any evidence for thrombosis at the time terior or associated with retinoschisis, is highly the autopsy was performed. suggestive of, if not diagnostic for, nonaccidental Limitations injury (9,14-21). Rarely, retinal hemorrhage has been associated with an accidental head injury, but 1. Six of the 18 falls were not witnessed or were in these cases the bleeding was unilateral (80). It is seen only by the adult caretaker, and it is pos- also stated that traumatic retinal hemorrhage may sible that another person caused the nonob- be the direct mechanical effect of violent shaking served injuries. (15). However, retinal hemorrhage may be caused 2. The exact height of the fall could be deter- experimentally either by ligating the central retinal mined in only 10 cases. The others (7 swing vein or its tributaries or by suddenly increasing in- and 1 stationary platform) could have been tracranial pressure (81,82); retinoschisis is the re- from as little as 0.6 meters (2 feet) to as much sult of breakthrough bleeding and venous stasis not as 2.4 meters (8 feet). "violent shaking" (15,83). Any sudden increase in 3. A minimum impact velocity sufficient to intracranial pressure may cause retinal hemorrhage cause fatal brain injury cannot be inferred (84-87). Deformation of the skull coincident t& an from this study. Likewise, the probability that impact nonselectively increases intracranial pres- an individual fall will have a fatal outcome sure. Venospasm secondary to traumatic brain in- cannot be stated because the database depends jury selectively increases venous pressure. Either on voluntary reporting and contractual agree- mechanism may cause retinal hemorrhage irrespec- ments with selected U.S. state agencies. The tive of whether the trauma was accidental or in- NEISS summaries for the study years esti- flicted. Further, retinal and optic nerve sheath hem- mated that there were more than 250 deaths orrhages associated with a ruptured vascular due to head and neck injuries associated with malformation are due to an increase in venous pres- playground equipment, but there are only 114 sure not extension of blood along extravascular in the files. Further, this study does not in- spaces (81-83,88). Dilated eye examination with an clude other nonplayground equipment-related indirect ophthalmoscope is thought to be more sen- fatal falls, witnessed or not witnessed, in the sitive for detecting retinal bleeding than routine ex- CPSC database (32).

Am J Forensic Med Pathol, Vol. 22, No. J, March 2001 10 J. PLUNKETT

CONCLUSIONS is not uniform (45). This analysis requires awareness of the shape of the deceleration curve, knowledge of or . fall is a complex event. There must be a 1. E very . . 'd . the mechanical properties and geometry of the cra- loc biOme"chanical analysis for any inc1 ent 1n nial system, and comprehension of the stress and cc which the severity of the injnry appears .to be. strain characteristics for the specific part of the skull (n lncOnsistent with the history. The question 1s and brain that strikes the ground. A purely transla- (rr not "Can an infant or child be seriously in- tional fall requires that the body is rigid and that the ge jured or killed from a short-distance fall?''. but external forces acting on the body pass only through rather "If a child falls (x) meters and strikes the COM, i.e., there is no rotational component. A ! - L a his other head on nonyielding surface, what meter-tall 3-year-old hanging by her knees from a will happeu ?" horizontal ladder with the vertex of her skull 0.5 me- 2. Retinal hemorrhage may occur whenever in- ters above hard-packed earth approximates this tracranial pressure exceeds venous pressure or model. If she looses her grip and falls, striking the gL whenever there is venous obstruction. The occipital scalp, her impact velocity is 3.1 m/second. tic characteristic of the bleeding cannot be used An exclusively angular fall also requires that the to determine the ultimate cause. body is rigid. In addition, the rotation must be about 3. Axonal damage is unlikely to be the mecha- a fixed axis or a given point internal or external to nism for lethal injnry in a low-velocity impact the body, and the applied moment and the inertial such as from a fall. 2 moment must be at the identical point or axis. If this 4. Cerebrovascular thrombosis or dissection same child has a 0.5-meter COM and has a "match- must be considered in any injury with appar- stick" fall while standing on the ground, again strik- 3 ent delayed deterioration, and especially in ing her occiput, her angular velocity is 5.42 rad/sec- one with a cerebral infarct or an unusual dis- ond and tangential velocity 5.42 m/second at impact. tribution for cerebral edema. The impact velocity is higher than predicted for an 4 5. A fall from less than 3 meters (10 feet) in an in- exclusively translational or external-axis angular fall fant or child may cause fatal head injury and s when the applied moment and the inertial moment may not cause irrunediate syinptoms. The in- are at a different fixed point (slip and fall) or when jnry may be associated with bilateral retinal the initial velocity is not zero (walking or running, hemorrhage, and an associated subdural then trip and fall), and the vectors are additive. How- hematoma may extend into the interhemi- ever, the head, neck, limbs, and torso do not move spberic fissure. A history by the caretaker that uniformly during a fall because relative motion oc- the child may have fallen cannot be dismissed. curs with different velocities and accelerations for Acknowledgements: The author thanks the law en- each component. Calculation of the impact velocity forcement, emergency medical services, and medical for an actual fall requires solutions of differential professionals who willingly helped him obtain the origi- equations for each simultaneous translational and nal source records and investigations; Ida Harper-Brown rotational motion (45). Fnrther, inertial or impulse (Technical Information Specialist) and Jean Kennedy (Senior Compliance Officer) from the U.S. CPSC, whose loading (whiplash) may cause head acceleration enthusiastic assistance made this study possible; Ayub K. more than twice that of the midbody input force and Ommaya. M.D., and Werner Goldsmith. Ph.D.• for criti- may be important in a fall where the initial impact is ]( cally reviewing the manuscript; Jan E. Leestrna, M.D., to the feet, buttock, back, or shoulder, and the final and Faris A. Bandak, Ph.D., for helpful conunents; Mark impact is to the head (46,47). E. Myers, M.D., and Michael B. Plunkett, M.D., for re- view of the medical imaging studies; Jeanne Reuter and The translational motion of a rigid body at con- Kathy Goranowski, for patience, humor, and completing stant gravitational acceleration (9.8 m/s 2 ) is calcu- the manuscript; and all the families who shared ~e sto- lated from: 1: ries of their sons and daughters and for whom this work 2 is dedicated. F =ma v = 2as v =at

where F = the sum of all forces acting on the body l

APPENDIX (newton), m = mass (kg), a = acceleration (rnls 2 ), [. v =velocity (mis), s =distance (m), and t =time (s). Newtonian mechanics involving constant acceler- The angular motion.of a rigid body about a fixed 1 ation may be used to determine the impact velocity axis at a given point of the body under constant in a gravitational fall. However, c6nstant accelera- gravitational acceleration (9.8 m/s 2 ) is calculated tion formulas cannot be used to calculate the rela- from: tions among velocity, acceleration, and distance traveled during an impact because the deceleration M =Ia Am J Forensic Med Pathol, Vol. 22, No. 1, March 2001

FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 11

!SS where M = the applied moment about the COM sociated systemic findings in suspected child abuse; a necropsy study. Arch Opthalmol 1990;108:1094-101. of or about the fixed point where the axis of rotation is 18. Williams DF, Swengel RM, Scbarre DW. Posterior seg- ~a­ located, I = the inertial moment about this same ment manifestations of ocular trauma. Retina 1990;10 nd COM or fixed point, a = angular acceleration (suppl):535-44. 19. Rosenberg NM, Singer J, Bolte R, et al. Retinal hemor- 111 (rad/s2 ), w = angular velocity. (radfs·), r = radius rhage. Pediatr Emerg Care 1994;10i303-5. la- (m), v' = tangential velocity (mis), and a' = tan- 20. Swenson J, Levitt C. Shaken baby Syndrome: diagnosis he gential acceleration (rn/s 2 ). and prevention. Minn Med 1997;80:41-4. 21. Altman RL, Kutscher ML, Brand DA. The "shaken-baby gh The angular velocity w for a rigid body of length syndrome." N Engl J Med 1998;339:1329-30. l- L rotating about a fi>~d point is calculated from: 22. Hall JR, Reyes HM, Horvat M, et al. The mortality of a childhood falls. J Trauma 1989;29:1273--5. lfI0 w2 = maL/2 I 0 = (1/3) rnL 2 23. Rieber GD. Fatal falls in childhood: how far must children e- fall to sustain fatal head injury: report of cases and review Lis where I 0 = the initial inertial moment, w = an- of the literature. Am J Forensic Med Pathol 1993;14: ie gular velocity (rad/s), m = mass (kg), a = gravita- 201-7. 24. Root I. Head injuries from short distance falls. Am J Foren- d. tional acceleration (9.8 rn/s 2 ), and L = length. sic Med Pathol 1992;13:85-7. 1e 25. Nashelsky MB, Dix JD. The time interval between lethal ut infant shaldng and onset of symptoms: a review of the REFERENCES shaken baby syndrome literature. Am J Forensic Med to 1. Chadwick DL, Chin S, Salemo C, et al. Deaths from falls Pathol 1995;16:154-7. al in children: bow far is fatal? J Trauma 1991;31:1353-5. 26. Wilkins B. Head injury: abuse or accident? Arch Dis Child is 2. Williams RA. 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APPENDIX D

CASE REPORT

Delayed Sudden Death in an Infant Following an Accidental Fall A Case Report With Review of the Literature Scott Denton, MD, and Darinka Mileusnic, MD, PhD

treated with nebulizer, was witnessed by his grandmother to Abstract: Several controversies exist regarding ultimately lethal head injuries in small children. Death from short falls, timing of fall backwards off the edge of a queen-sized bed, 30 inches head injury, lucid intervals, presence of diffuse axonal inJUt)' (DAI), off the floor. The child was sitting on the edge of the bed as and subdural hernatoma (SDH) as marker of DAI are the n1ost recent the grandmother dressed her 2-year-uld daughter. The child controversial topics of debate in this evolving field of study. In this fell back vvards and rotated fron1 the sitting position, striking area of debate, \Ve present a case of delayed death from a witnessed the 1nidback of his head on a vinyl-covered concrete floor at fall backwards off a bed in a 9-month-old black male child who 8:00 AM. He i1n111ediately began crying, and the grandmother struck his head on a concrete floor and was independently witnessed placed ice on a knot on the back of his head. He stopped as "healthy" postfall for 72 hours until he was discovered dead in crying and was consolable within a few minutes. The child bed. Grandn1other, babysitter, and mother all independently corrob- was taken to the babysitter's residence, where the babysitter orated under police investigation that the child "acted and behaved normally" after the fall until death. Autopsy showed a linear non- was told of the fall and to watch for any behavioral changes. displaced parietal skull fracture, diastasis of adjacent occipital su- The tnother \Vas at work the tnorning when the fall occurred. ture, subgaleal hemorrhage 'Nith evidence of aging, small posterior When the mother picked the child up at the babysitter's in the clotting SDH, marked cerebral eden1a, and a sinall tear of the afternoon. he appeared 'Nell. The babysitter reported no midsuperior body of the corpus calloswn consistent with focal problems and that he acted, ate, and behaved as usual. For the axonal injury (F Al). No DAI was seen, and there \Vere no retinal next 2 days, the grandmother, mother, and babysitter did not hemorrhages. All other causes of death were excluded upon thor- notice any abnormalities in either behavior or appearance of ough police and medical examiner investigation. Although this the child. seems to be a rare phenomenon, a delayed,, seemingly symptom-free Approximately 72 hours after the fall off the bed, the interval can occur between a clinically apparent mild head injury child was found at the foot of the mother's bed, where he and accidental death in a young child. usually slept, prone, cold, and unresponsive. Paramedics were (Am J Forensic Med Pathol 2003;24: 371-376) called, and in spite of resuscitative.: efforts, he was pro- nounced dead upon arrival at the hospital. He \·vas last seen alive 8 hours prior when he was fed by his mother and given CASE REPORT his usual albuterol breathing treahnent. No abnormalities on I\ 9-rnonth-old black male child weighing 22 pounds (10 the child were seen in the emergency department. There was /'"'\kg) and measuring 28 inches (71 crn), 80th percentile and no evidence of overlying or asphyxia. 50 1h percentile for age, respectively, with a history of asth1na Medical and family history revealed that the child was born full-term weighing 7 pounds 4 ounces. He was diag- nosed with asthma after complaints of \Vheezing episodes and Manuscript received March 19, 2003; accepted May 29, 2003. was prescribed an a!buterol nebulizer twice daily. The child's From the Cook County Office of the Medical Examiner, and Deparlmt'nt of father, who does not reside in the hon1e, bas asthma. The Pathok1gy, Rush College of Medicine, Chicago, Illinois (J.S.D.), and n1other and grandn1other reside together in a public housing Knox County Office of the Medical Examiner. and Department of Pathology, Graduate School of Medicine, Univt:rsity of Tt:nnessee, develop1nen1. Depart1nent of Child and Family Services Knoxville, Tennessee (D.M.). records revealed no prior incidents concerning the deceased, Reprints: Darinka Mih.msnic, MD, PhD, Regional Forensic Center, Univer- but the mother had I report of being a victitn of prior abuse. sity of Tennessee Memorial Hospital, 1924 Alcoa Highway, Knoxville, The grand1nother has a remote history of cocaine abuse. Her 1N 37920. E-mail: dmileusn@mc.utmck.edu Copyright© 2003 by Lippincott Williams & Wilkins 2-year-old daughter is well and lives with her. 0195-7910/03/2404-037 l Autopsy revealed a well-developed and well-nourished DOI: I 0.1097/0 ! .paf.0000097851.18478.16 black 111alc child appearing the stated age and without exter-

The American journal of Forensic Medicine and Pathology • Volume 24, Number 4, December 2003 371 Denton and Mileusnic The American journal of Forensic Medicine and Pathology • Volume 24, Number 4, December 2003

nal abnormality. There was no swelling or contusion of the back of the head. Complete postmortem radiographs revealed a linear, nondisplaced, posterior right parietal skull fracture. Internal exa1nination confirmed the skull fracture, as well as a patch or right posterior subgaleal hemorrhage that was centrally red with yellow margins. The underlying right posterior linear skull fracture was 3.0 inches (9.0 cm) long and extended to the right parieto-occipital suture, causing mild diastasis of the suture, 2.5 inches (7.5 cm) Jong (Fig. 1). There was a thin adherent clotted SDH underlying the frac- tme, 2.0 X 2.0 X 0.1 cm. The brain weighed 1035 g (expected average weight for age, 750 g) and showed severe edema with flattening of the gyri, loss of sulci, and notching of both unci and cerebellar tonsils (Fig. 2). After formalin fixation, serial sectioning of the brain revealed diffusely dusky white matter and a focal tear of the midsuperior corpus

FIGURE 2. Severely edematous brain demonstrating flattening of the gyri and narrowing of the sulci.

callosum, 1 1nrn, with surrounding hemorrhage, 2 n1m. There were no other gross neuropathologic findings. The remaining internal organs were unremarkable, without other new or old fractures, petechiae, or gross asthma changes. Comprehen- sive toxicologic screening using gas chromatography and nlass spectrometry was negative. Microscopically, the corpus callosum tear showed hemo1Thage with intact red blood cells, PAI, and 1nicroglial activation without inflammation (Fig. 3). Extensive sections of the brain showed only edema without evidence of DAL Sections of the subgaleal hemorrhage showed hen1orrhage of coalescing red blood cells with neu- trophilic inflammation. Decalcified sections of the parietal fracture showed an acute fracture with early periosteal reac- tion at the fracture margin. Lung sections showed mild focal FIGURE 1. View of the linear skull fracture Involving the pos- peribronchial lymphocytic aggregates consistent with bron- terior right parietal bone1 after removal of the overlying sub- chitis without asthma changes. There were neither eosino- galeal hemorrhage. phils nor 1nucus plugs. Sections of remaining organs were

372 © 2003 Lippincott Williams & Wilkins The American journal of Forensic Medicine and Pathology 111 Volume 24, Number 4, December 2003 Delayed Sudden Death

in the majority of lethal events, are still controversial. One \videly held belief is that short falls are almost never fatal. Second, if a child is going to die follo\ving head trauma, either accidental or abusive, he or she is severely impaired and inost likely i1nmediately unconscious, without a lucid interval. Finally, in severe injuries where children are im1ne- diately comatose and die shortly after the incident from either shaking and/or direct impact, it is believed that DAI is the 111echanism. Certain reviews have gone so far to identify subdural hemorrhage, frequently present in certain forms of early childhood abusive head traun1a, as a "marker" of unde- tectable DAL 1 1f this were true, then reports describing radiologically presen1 old and/or new subdural hemorrhages, with or without focal shear hemorrhages in the white matter, FIGURE 3. Coronal section of the corpus callosum showing in living children would be a rarity rather than a com1non wedge-shaped laceration (right upper corner) surrounded by a place. 2 rim of hemorrhage, FAI and activated microglia (1 OOX, hema- In this present case, we discuss the death of a 9-month- toxylin-eosin). old child who died 3 days after a witnessed backward fall from a bed on a concrete floor. Main pathologic findings consisted of a linear nondisplaced skull fracture, minimal clotting subdural hemorrhage, severe brain swelling with without pathologic changes. The eyes were examined by an tonsillary herniation, and a small tear in the body of the ophthalmic pathologist consultant and were normal. A foren- corpus callosu1n, which appeared histologically as FAL Anal- sic radiologist consultant also reviewed postmortem radio- ysis of the fall revealed a rotational component of the body graphs and repo1ted no additional findings. and head movement, 1.vhich could account for the described injuries. The location and appearance of the prin1at)' injury Follow-up Investigation was consistent viith flipping backward and striking the back Prior to the autopsy, Chicago police detectives \Vere of the head. There was no diffuse axonal da1nage or retinal notified of the skull fracture and attended the examination. hemorrhage. Thorough workup, including scene investigation After autopsy, police re1nanded the grandmother and mother and independent police questioning of all individuals in- to the police station, where they were interviewed separately volved in the care of the infant, prior to, during, and after the about the injuries. Upon extensive questioning about any accident, were unanin1ous. There were no inconsistencies, possibility of inflicted trauma and abuse that the baby could have and the stories have never varied from the beginning to the sustained, they both spontaneously gave the similar story of the conclusion of the investigation. There were no other instances fall 3 days prior. The babysitter was questioned and confinned of trau1na to the head observed by the caretakers. Based on the accounts and timing of the reported events. Police detectives several independent accounts, the infant's behavior following and evidence technicians accompanied the mother and grand- the head trauma up to his sudden death was ordinary and did mother back to their residence and verified the scene and not require medical attention, qualifying as a lucid or symp- reenactment of the fall. A week later, the prosector patholo- tom-free interval. gist (JSD) and a specialist child death scene investigator of Deciding whether head injury in a very young child is the Medical Exa1niner's Office went to the residence and accidental or nonaccidental has always been proble1natic for again inspected the residence, interviewed the grandmother clinicians and forensic pathologists alike. 3 ·4 We realize that a and 1notber. and reenactcJ. the fi.lll. As with the police detec- number of child abuse experts would have a problem with the tives, all felt the grandmother and mother to be truthful and accidental detenninlltion of the manner of death in the present grieving appropriately for the circumstances. After consider- case. We do not argue the widely noted observation that ation of the autopsy, toxicologic, histologic, consultative, and simple falls from low heights rarely result in significant investigative findings, the death was certified as craniocere- prin1ary brain injury. 5 However, every fall is different, as well bral injuries due to a fall fron1 the bed backwards onto a as the individual reaction to the pri tnary insult. Son1e experts concrete floor. The manner was determined accidental. in head trauma consider the term minor head injury an oxymoron. 6 We believe that a series of secondary injuries, DISCUSSION known to occur after a primary insult, resulted in the extreme Ce1tain issues in pediatric head trauma, such as lethal- swelling of the brain and death of the child. What is widely ity of short falls, timing of head injury, and presence of DAI understated and so1ncti1nes forgotten about is secondary brain

© 2003 Lippincott Williams & Wilkins 373 Copyright Lippincott Denton and Mileusnic The American journal of Forensic Medicine and Pathology • Volume 24, Number 4, December 2003

injury, which occasionally may be the principal force deter- ists involved in the care of abused children accept as true that mining the outco1ne after a see1ningly trivial head injury. 7- 12 all children who eventually die, regardless of the type of the Another frequently forgotten factor is the influence of age and head injury, must be severely disabled, usually comatose sex on the presentation and the outco1ne of head injury. The from the ve1y moment the injury occurred. 23 From personal grouping together of different pathologies such as subdural experience and based on the literature review, this tenet is not hemorrhages, cerebral contusions, FAI, and DAI, as well as necessarily true. 24 '25 Although there are clearly scenarios in lumping together of infants, toddlers, and preschool children, which this principle could be applicable, there is undoubtedly needs to be addressed. It has been shown that infants and a subpopulation of infants and especially toddlers with a young toddlers lose consciousness less frequently, and a completely different constellation of injuries and a dissitnilar smaller proportion of their head injuries lead to immediate presentation. Occasionally, these children have nonspecific coma in comparison to other children with the same grades of symptoms for several hours to a day prior to the onset of traumatic energy. 13 Pohl et a1 9 demonstrated that evolution of either coma or seizure followed by coma. Common observa- posttraumatic brain da1nage after head trauma in developing tions include reduced physical activity, lethargy, drowsiness, rodents is a highly dynamic process exhibiting age-dependent irritability, temperature irregularities, poor feeding, and gas- excitotoxic and distant apoptotic cell death. trointestinal symptoms. 232627 Careful analysis of the history Reviewing the literature on childhood head trauma, one and the events leading to the critical symptoms indicate that can clearly see that a gradual sideway drift or evolution of there was a certain progression of symptomatology. findings and conclusions of the original reports, research, and Occult intracranial injury in infants younger than 12 data had taken place. One of them, also frequently encoun- months of age is not uncommon. 28 Clinical symptoms and tered in cou1t, is that ve1y young children, especially infants, signs are insensitive indicators of intracranial inju1y in in- are auton1atically assu1ned to be the victi1ns of "shaken baby fants.29 Radiologic observations can so1netimes be of litnited syndrome." 14 - 16 However, fro1n the literature and from per- value as well. 30 Also, slow deterioration following mild head sonal experience, findings of direct impact to the head pre- injuries in children have been reported. 31 Furthermore) l of vail. The problem is not only se1nantic in nature but has 1najor the most frequently cited articles on restricting the time of and far-reaching consequences since the character, location, injury in fatal inflicted head injuries draws its pediatric and clinical presentation of the injuries arc different from the population mainly from motor vehicle accidents, with the rare purely shaken babies. 17 ·18 average age of the study group patients being 8.5 years, with Another encountered fallacy is that the children who a SD of 4.0 yearsn die of head trau1na, especially abusive head trau1na, sustain Although many studies have offered guidelines for DAL Going back to some of the original research, it is clear determining the age of cerebral injuries, various factors limit that the authors explicitly stated that the 2 worst types of head the reliability of these 1nethods; for example, reduced cere- injury are SDH and DAI. These 2 have different mechanisms bral blood flow n1ay impede the ceilular response. Not infre- of causation: SDH occurs much more commonly in nonve- quently, injured children survive in the hospital for additional hicular injuries, such as falls and abusive head trauma, while 2 to 3 days or even longer, sometimes undergoing craniot- DAI is caused almost exclusively by vehicular mecha- omy, rendering timing of the injuries based on the autopsy nisms.19-22 Although both injuries frequently share a com- findings, including histologic examination of the cerebral mon mechanical cause such as angular acceleration, they injuries, extre1nely difficult. 8-23 -33- 35 differ in degree. SDH usually occurs with a rotational injury DAI is most likely a rarity in nonaccidental head of short duration and a high rate of acceleration. Conversely, trauma, and the term is misleading. 17 • 18 ' 36 Coma may be more motor vehicle accidents tend to cause longer-duration, lower- of a reflection of the severity of axonal damage in particular acceleration-rate injuries leading to DAI rather than SDH. 8·21 regions of the brain, most notably the brainstem, rather than SDHs occur in a greater number in children with inflicted the total su1n of axonal injury distributed throughout the versus noninflicted traumatic brain inju1y, whereas shear brain. Furthermore, the plane of head rotational acceleration injuries are commonly visualized in the noninflicted inju1y plays an important role in determining both the distribution of group. 22 Therefore, current supposition that the presence of axonal damage and the production of coma. 36 The localized SDH is a marker of DAI is likely inaccurate. axonal damage demonstrated in corticospinal tracts in the A frequently asked question is whether delayed 1nental lower brainstem and rostral cervical cord, presumably caused status deterioration can occur following head injury in chil- by stretch to the neuroaxis produced by cervical hyperexten- dren. This is critically important in unwitnessed circu1n- sion, may be more significant This finding also provides an stances such as child abuse. A widely held dogma is that if a explanation for the frequent occurrence of apnea at presen- child becomes unresponsive while in the care of an individual tation. Tn many of the cases reported by Geddes et al, 18 the who is reporting the onset of unconsciousness, that same axonal damage at the craniocervical junction was survivable; individual must be the perpetrator. Currently, some special- what was life-threatening was the subsequent hypoxic injury

374 © 2003 Lippincott Williams & Wilkins The American journal of Forensic Medicine and Pathology • Volume 24, Number 41 December 2003 Delayed Sudden Death

and brain swelling. In addition, true contusional tears, which 9. Pohl D, Bittigau P, Ishimaru MJ, et al. N-methyl-D-aspartate antagonists are peculiar to the brains of young infants, represent localized and apoptotic cell death by head trauma in developing rat brain. Proc Natl Acad Sci. USA. 1999;96:2508-2513. "shearing" between gray and white inatter after an impact and 10. Gilles EE, Nelson MD. Cerebral complications of nonaccidental head should not automatically imply DAL 17 injury in childhood. Pediatr Nertrol. 1998;19:119-128. Cerebral hypoperfusion, followed by hypoxia/ische1nia 11. Bergsneider M, Hovda D, Lee SM, et al. Dissociation of cerebral glucose metabolism and level of consciousness during the period of and diffuse brain swelling, characteristic in injured children inetabolic depression following human traumatic brain injury. J Neuro- younger than 24 months of age, are key pathophysiological trauma. 2000;17:389-401. findings associated with poor outcome following severe trau- 12. Ruppel RA. Clark RS, Bayir H, et al. Critical mechanisms of secondary damage afl:er inflicted head injury in infants and children. Neurosurg matic brain injury. s,37- 39 Primary brain damage occurs at Clin North Am. 2002;13:169-182. impact and appears irrunediately or shortly after injury. Sec- 13. Barney J, Froidevaux A-C, Favier J. Paediatric head trauma: influence of ondary brain injury may be more important, particularly in age and sex, II: biomechanical and anatomo-clinica! correlations. Child Nerv Syst. 1994;10:517-523. delayed fatalities, and occurs distant to the ilnpact. Secondary 14. Caffey J. On the theory and practice of shaking infants: its potential events may not becon1e apparent until several hours after residual effocts of permanent brain damage and mental retardation. Am J injury. The largest controlled neuropathological study of Dis Child. 1972;124:161-169. 15. Caffey J. The whiplash shaken infant syndrome: manual shaking by the nonaccidental infant head injury showed that axonal damage extremities with whiplash-induced intracranial and lntraocular bleed- occurred in the brain of both head-injured subjects and in ings, linked with residual permanent brain damage and mental retarda- controls in the same distribution. This is not DAI but rather tion. Pediatrics. I 97454:396-403. 16. Levin AV. Retinal haemorrhages and child abuse. Rec Adv Paediatr. diffuse vascular or hypoxic-ischc1nic injury due to brain 2000; 18: 151-219. swelling and raised intracranial pressure. The study demon- 17. Geddes JF, Hackshaw AK, Vowles GH, et al. Neuropathology of strated that the diffuse brain damage responsible for loss of inflicted head injury in children, I: patterns of brain damage. Brain. 2001; 124: 1290-1298. consciousness is a hypoxic secondary reaction and argues 18. Geddes JF, Vowles OH, Hackshaw AK, et al. Neuropathology of against DAI. One of the inain conclusions of the study was inflicted head injury in children, II: microscopic brain injury in infants. that focal, localized axonal injury and secondary vascular- Brain. 2001;124:1299-1306. 19. Gennarelli TA, Thibault LE. Biomechanics of acute subdural hematoma. hypoxic changes characterize the mechanism of brain J Trauma. 1982;22:680-686. death. 18 20. Gennarelli TA, Thibault LE, Adams JH, et al. Diffuse axonal injury and In conclusion, we present a case of a seetningly minor traumatic coma in the primate. An11 Neurol. 1982;12:564-574. 21. Gennarelli TA. Head i11jury in man and experimental animals: clinical brain injury in an infant with a symptom-free interval, which aspects. Acta Neurochir. 1983;32(suppl):l-13. resulted in delayed, sudden death. The importance of the 22. Ewing-Cobbs L, Kramer L, Prasad M, et al. Neuroimaging. physical, mechanism of injury, location of injury, age of the child, and developmental findings after inflicted and noninflicted traumatic brain injury in young children. Pediatrics. 199Kl02:300-307. and secondary brain injury with special reference to non- 23. Duhaime A-C, Christian CW, Balian Rorke L, Zimmerman RA. accidental head trauma of childhood, as well as need for Nonaccidental head injury in infants-the "shaken-baby syndrome." further research, are discussed. Although this is a rare N Engl J Med. 1998;338: 1822-1829. 24. Nashelsky MB, Dix JD. The time interval between lethal infant shaking presentation of a traumatic brain injury, based on recent and onset of symptoms: a review of the shaken baby syndrome literature. advances in traumatic neuropathology, it is conceivable, as Am J Forensic Med Pathol. 1995;16:154-157. in this case, that a delayed asymptomatic deterioration to 25. Huntington RW UL Symptoms following head injury. Am J Forensic Med Pathol. 2002;23:105. death can occur. 26. Ward JD. Pediatric issues in head trauma. New Horiz. l 995;3:539-545. 27. Haviland J, Ross Russell Rl. Outcome after severe non-accidental head injury. Arch Di:f Child. 1997;77:504-507. REFERENCES 28. Greenes DS, Schutzman SA. Occult intracranial injury in infants. Ann 1. Case ME, Graham MA, Corey Handy T, et al. Position paper on fatal Emerg Med. 1998:32:680-686. abusive head injuries in infants and young children. Am J Forensic Med 29. Greenes DS, Schutzman SA. Clinical indicators of intracranial injury in Pathol. 2001;22: 112-122. head-injured infants. Pediatrics. 1999;104:861-867. 2. Demaerel P, Casteels l, Wilms G. Cranial imaging in child abuse. Eur 30. Dias MS, Backstrom J, Falk M, Veetai L. Serial radiography in the Radial. 2002;12:849-857. infant shaken impact syndrome. Pediatr Neurvsurg. 1998;29:77-85. 3. Maxeiner H. Lethal subdural bleedings of babies: accident or abuse? 31. Snoek JW, Minderhoud JM, Wilmink IT. Delayed deterioration follow- Med Law. 2001;20:463-482. ing mild head injury in children. Brain. 1984;107:15-36. 4. Fung ELW, Sung RYT, Severn Nelson EA, Poon WS. Unexplained 32. Willman KY, Bank: DE, Senac M, Chadwick DL. Restricting the time of subdural hematoma in young children: is it always child abuse? Pediatr injury in fatal inflicted head injuries. Child Abuse Neg/. 1997;2 l :929- Internat. 2002;44:37-42. 940. 5. Duhaime AC, Alario AJ, Lewander WJ, et al. Head injury in very young 33. McD. Anderson R, Opeskin K. Timing of early changes in brain trauma. children: n1echanisms, injury types, and ophthalmologic findings in 100 Am J Forensic Med Pathol. 1998;19:1-9. hospitalized patients younger than 2 years of age. Pediatrics. 1992;90: 34. Wilkinson AE, Bridges LR, Sivaloganathan S. Correlation of survival 179-185. time with size of axonal swellings in diffuse axonal injury. Acta 6. Schutzman SA, Greenes DS. Pediatric minor head trawna. Ann Emerg Neuropathol. 1999;98: 197-202. Med. 2001;37:65-74. 35. Oehmichcn M, Thcuerkaufl, Meissner C. Is traumatic axonal injury (AI) 7. Bruce DA. Head injuries in the pediatric population. Curr Prob! Pediatr. associated with an early microglial activation? Application of a double- 1990;20;61-107. laboling technique for simultaneous detection ofmicroglial and Al. Acta 8. Pearl GS. Traumatic neuropathology. Clin Lab Med. 1998:18:39-64. Neuropathol. 1999;97:491-494.

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36. Smith DH, Nonaka M, Miller R, et al. Immediate coma following 38. Ewing~Cobbs L, Prasad M, Kramer L, Landry S. Inflicted traumatic inertial brain injury dependent on axonal damage in the brainstem. brain injury: relationship of developmental outcome to severity of injury. J Neurosurg. 2000;93:315-322. Pediatr Neurosurg. l 999;31 :251-258. 37. Adelson PD, Clyde B, Kochanek PM, et al. Cerebrovascular response in 39. Tabori U, Kornecki A, Sofor S, et al. Repeat computed tomographic scan infants and young children following seveno traumatic brain injury: a within 24-48 hours of admission in children with moderate and severe preliminary report. Pediatr Neurosurg. 1997:26:200-207. head trauma. Crit Care Med. 2000~28:840-844.

376 © 2003 Lippincott Williams & Wilkins

LETTERS TO THE EDITOR

Diagnosis of Traumatic /3-APP is a single me1nbrane- REFERENCES spanning protein, which is present in 1. Tun1er PR, O'Connor K, Tate WP, et al. Roles Diffuse Axonal Injury membranous structures of the cell such ofamyloid pr~cursor protein and its fragments in reguloi1ing neurnl activity, plasticity and as the endoplasmic reticulum, Golgi memory. Frog Neurn!Jiol. 2003;10:1-32. To the Editor: compartment, and the cell 1nembrane, 2. Smith C, Graham DI, Geddes JF, et al. The In the December 2003 issue of the encoded by the APP gene localized to interpretation of Beta-APP immunoreactivity: a respons~ to C. Neiss et al., Acta Neuroparhof American Journal of Forensic i\!fedicine chroinosome 21. and is ubiquitously ex- (2002) 104:79. Acla Neuropathol. 2003;106: and Pathology, there was a case report pressed in 1nany cell and tissue types, 97-98. written by Drs. Scott Denton and including endotheha, glia, and neurons 3. Smith DH, Meaney OF, Shull WH. Diffuse Darinka Mileusnic titled "Delayed Sud- axonal injury in head trauma. J Head Trauma of the brain. /3-APP is a resotrrce-rich Rehabi!. 2003;18:307-316. den Death in an Infant Following an molecule that is involved in diverse nor- 4. Medana JM, Esiri MM. Axonal damage: a lrny Accidental Fall: A Case Report With mal cell functions, being the center of predictor of outcome in human CNS diseases. Review of the Literature." This article Brain. 2003;126:515-530. many converging metabolic and regula- 5. Blumbergs PC, Scott G, Manavis J, et al. presented a case of delayed. death in a tory patlnvays, including cell adhesion, Topography of axona! lnJUry as defined by 9-month-old infant a'i a result of severe intercellular signaling, membrane-to-nu- amyloid precursor protein and the s~L:!or scor- craniocerebral injuries, which were sus- ing method in mild and severe closed head cleus signaling, cholesterol metabolism, tained from an accidental fall in the injury. J Neurotrauma. 1995;!2:565-572. gene transcription, axonal transport, and 6. McKenzie KJ, McLellan DR, Gentleman SM, domestic environment. The authors had neurotrophic and ncttroproliferative ac- et al. ls J3-APP a marker \.ifaxonal dan1age in affirmed that there was no evidentiary short-surviving head injury'! Acta Neuro- tivity.1 finding of diffuse axonal injury (DAI). patho!. !996;92:608-613. In the neuron, /3-APP is synthe- 7. Adams JH, Doyle D, Ford I, et al. Diffuse The scientific validity of this assertion sized in the perikaryon and transported axonal injury in head injury: definition, diag- remains in doubt since the authors nei- nosis and grading. Ilistopatholo'b'V· l 989; 15: anterogradely and retrogra<le!y in the ther mentioned nor perfonned any tissue 49-59. axon by fast/rapid axonal transport ( 100 8. Ellison D, Love S, Chimelli L, et al. /3-amyloid precursor protein (/3-APP) immunohistochemical analyses, given to 400 mm/day). In normal, structurally Neuropathology: A Reference Text of CNS intact axons, /3RAPP does not accumu- Pathology. Philadt:lphia, PA: Harcourt Pub- our current level of knowledge in the lishers Limitcti: 2000. diagnosis of severe traumatic brain in- late to a level that allows its detection in 9. Lec!erc4 PD, McKenzie JE. Graham DI, et al. jury, including DAL 1- 6 Since the 1980s, tissue sections. However, once struc- Axonal injury is accentuated in the caudal tural a.xonal injury and damage occur corpus callosum of head-injured patients. tissue innnunohistochemistry for /3-APP J Neurotrauma. 2001;!8:1-9. has emerged as the most sensitive meth- and the fast axonal transport is irnpaired, JO. Geddes JF, Whitwell HL, Graham DI. odology and gold standard for the detec- J3-APP accun1ulates in the proximal and Traumatic axona! injury: practical issues for tion, confirmation, and diagnosis of dif- distal axonal seg1nent to a level that diagnosis Ill medicolegal cases. Neuropathof Appl Neurobiol. 2000;26: [05-116. fuse and focal axonal injuty. With the allows its dctectiun by tissue immuno- absence of any /3-APP in1n1unohisto- histochen1istry within l.75 to 3 hours chemical confirmation of DAI, what the following injury. /3-APP has been re- Response to letter authors had referred to as a "laceration" ported to retnain detectable by tissue of the splenium of the corpus ca1Iosun1 immunohistochemistry for up to 99 days From Dr. Omalu may actually represent Adan1 's grade Tl following axonal injury. 1•6 DAJ 7 •8 since DAI is accentuated in the For this specified case report by We thank Dr. Omalu for his com- splenium of the corpus callosum.9 In Scott Denton and Darinka Mileusnic, ments regarding our recent case report. 1 Adam's grade I DAI, there is no gross /3-APP tissue in1rnunohistochemistry evidence of axonal injury; however, Dr. Omalu certainly seems knowledge- that is performed according to the rec- there is diffuse /3-APP inununopositi v- able in his review of f3 amyloid precur- ommended medicolegal protocoJ 10 n1ay ity for axonal injury. In Adam's grade ll sor protein (/3-APP) and is apparently a reveal grades l or II DAL This finding DAI, there are gross lesions (parenchy- strong advocate for {3-APP itnmunohis- tnay additionally and 1nore interestingly mal heinorrhages) of the corpus callo- tochemistry in cases of head injw-y. Dr. reaffinn that children who sustain low sun1, in addition to /3-APP tissue immu- Omalu stated that there was no scientific grades of DAI may 1nanifest a delayed, nopositivity. In Adam's grade lII DAI, validity that diffuse axonal iajmy (DAI) symptomatic, or fatal presentation. there are gross lesions (parenchymal \Nas not there in our case. Dr. Omalu hemorrhages) of the corpus callosum Bennet I. Omalu, MD also asserted that the tear in the corpus and dorsolateral 1nidbrain/pons, in addi- Division of Forensic Neuropathology callosum \Vas an advanced stage of DAL tion to diffuse /3-APP tissue immuno- Allegheny County Coroner's Office We would have expected to see micro- positivity .7•8 Pittsburgh, Pennsylvania scopic evidence of DAI on the numer-

270 The American journal of Forensic Medicine and Pathology • Volume 25, Number 3, September 2004 CopyriQht Lippincott \!Vililarns & Wilkins. Unauttlorized n-;production of this articif) is prohibited

ous hen1atoxylin and eosin sections, do note that we have received advertise- Sincerely, given the tilne interval from the wit- n1ents fro1n Dr. 01nalu and his Forensic nessed fall to the child's death. The tear NeLffopathology Consultation Service Scott Denton, MD of the corpus eallosum was frotn the for performing {3-APP testing. As of Deputy Medical Examiner Cook County Medical Examiners Office impact fro1n the fall as the corpus callo- note, in his advertisen1ent Dr. On1alu Assistant Professor of Pathology sun1 struck the falx cerebri. We would states that in ht>ad injury deaths it "has Rush University Medical Center argue the assertion that 13-APP is ac- been established and highly ITcom- Chicago, IL cepted as the most sensitive methodol- mended that /3-APP immunostaining be ogy and gold standard for detection of perfonned in multiple topographically Darinka Miluesnic, MD, PhD DAI and the 1nedicolegal protocol refer- targeted regions of the brain" and that Assistant Chief Medical Examiner enced in Dr. 01nalu's letter above is not applications include "tin1ing of injury Knox County Me<lica[ Exan1iners Office accepted as such in our practices. We do sustenance and determination of tin1e of University ofTenne~see Mec.lical Center not perform routine /3-APP testing in death." We are unaware of this timing of Knox ville, Tennessee our offices. injury and death data that would surely We respect Dr. 01nalu's advocacy solve the major critical proble1ns in pe- REFERENCES for {3-APP testing, although we do not diatric head injury deaths. We sincerely 1. Denton S. Mileusnic D. Delayed sudden death in an infant following an ac:cidental fall: a case feel {3-APP would have changed our \vish Dr. Omlllu well in advancing his repl1rt with review of the litwature. Am J Fo- conclusions or shown hidden DAI. We /3-APP research and enterprise. rensic J.fed Pathol. 2003;24.371-376.

The American journal of Forensic Medicine and Pathology • Volume 25 1 Number 31 September 2004 271 CopyriQht © Lippincott Williams & Wilkins. Unauthoriz0d rnproduclion of this article is prohibite<L