1 

WR 59,201-03

EX PARTE RICHARD VASQUEZ

* * *

IN THE DISTRICT COURT

148

TH DISTRICT

NUECES COUNTY, TEXAS

Returnable to

THE TEXAS COURT OF CRIMINAL APPEALS

AUSTIN, TEXAS

* * *

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

COURT OF CRIMINAL APPEALS

AUSTIN, TEXAS

Transmitted 4/20/2015 12:00:00 AM

Accepted 4/20/2015 8:11:52 AM

ABEL ACOSTA

CLERK

 RECEIVED COURT OF CRIMINAL APPEALS 4/20/2015 ABEL ACOSTA, CLERK 
2

WR-59,201-03

 

EX PARTE § IN THE DISTRICT COURT

§

 § 148

TH 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)
16

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 

T HE STATE OF TEXA S 

COUNT Y OF NUECE S 

BEFORE ME , 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 April 17, 2015,1 reviewed the attached photographs of a stool that 

had been admitted into evidence as SX#9 in the murder trial of Richard 

Vasquez, Cause No. 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 tall 

Further affiant saith naught. 

Subscribed and sworn to before me by the said John Mitchell this 17th day of 

April, 2015, to certify which witness my name and seal of office. 
2
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 

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Senior Editor 

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Editor 

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Account Manager 

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Director, Advertising 

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Coordinator 

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International Advertising 

Representative 

American Journal of Forensic Medicine and Pathology (ISSN: 0195-7910) is published quarterly by Lippincott Williams & 

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Indexed in Index Medicus/MEDllNE, Current Contents/Clinical Medicine, SCISEARCH, Excerpta Medica/EMBASE, and Biomedical 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 injury in infants and children, including the potential 

lethality of a short-distance fall, a lucid interval in an ultimately fatal head injury, and the specificity of retinal 

hemorrhage for inflicted trauma. There is scant objective 

evidence to resolve these questions, and more information is needed. The objective of this study was to determine whether there are witnessed or investigated fatal 

short-distance falls that were concluded to be accidental. 

The author reviewed the January l, 1988 through June 

30, 1999 United States Consumer Product Safety Commission database for head injury associated with the use 

of playground equipment. The author obtained and reviewed the primary source data (hospital and emergency 

medical services' records, law enforcement reports, and 

coroner or medical examiner records) for all fatalities involving a fall. 

The results revealed 18 fall-related head injury fatalities in the database. The youngest child was 12 months 

old, the oldest 13 years. The falls were from 0.6 to 3 meters (2-10 feet). A noncaretaker witnessed 12 of the 18, 

and 12 had a lucid interval. Four of the six children in 

whom funduscopic examination '"'as documented in the 

n1edical record had bilateral retinal hemorrhage. The author concludes that an infant or ciiild may suffer a fatal 

bead injury from a fall of less than 3 meters (10 feet). 

The injury may be associated with a lucid interval and 

bilateral retinal hemorrhage. 

Key Words: Child abuse-Head injury-Lucid intervalRetinal hemorrhage-Subdural hematoma. 

1\1anuscript received April 10, 2000; revised September 15, 

2000; accepted September 24, 2000. 

From the DepartmentS of Pathology and Medical Education, 

Regina Medical Center, 1175 Nininger Road, Hastings MN 

55033, U.S.A.; Email: plunkettj@reginarnedical.com. 

I 

Many physicians believe that a simple fall cannot cause serious injury or death (1-9), that a 

lucid interval does not exist in an ultimately fatal 

pediatric head injury (7-13), and that retinal hemorrhage is highly suggestive if not diagnostic for 

inflicted trauma (7,12,14-21). However, several 

have questioned these conclusions or urged caution when interpreting head injury in a child 

(15,22-28). This controversy exists because most 

infant injuries occur in the home (29,30), and if 

there is history of a fall, it is usually not witnessed 

or is seen only by the caretaker. Objective data are 

needed to resolve this dispute. It would be helpful 

if there were a database of fatal falls that were 

witnessed or wherein medical and law enforcement investigation unequivocally concluded that 

the death was an accident. 

The United States Consumer Product Safety 

Commission (CPSC) National Injury Information 

Clearinghouse uses four computerized data sources 

(31). The National Electronic Injury Surveillance 

System (NEISS) file collects current injury data associated with 15,000 categories of consumer products from 101 U.S. hospital emergency departments, 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 provided 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 Examiner 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 summaries of investigations performed by CPSC staff 

based on reports received from the NEISS, DC, or 

IR files (34). The AI files provide details about 

the incident from victim and witness interviews, 

accident reconstruction, and review of law enforce-
2 J. PLUNKETT 

ment, health care facility, and coroner or medical 

examiner records (if a death occurred). 

METHODS 

I reviewed the CPSC, DC, IR, and AI files for all 

head and neck injuries involving playground equipment recorded by the CPSC from January 1, 1988 

through June 30, 1999. There are 323 entries in the 

playground equipment IR file, 262 in the AI file, 47 

in the DC file, and more than 75,000 in the NEISS 

file. All deaths in the NEISS file generated an IR or 

AI file. If the file indicated that a death had occurred from a fall, I obtained and reviewed each 

original source record from law enforcement, hospitals, emergency medical services (EMS), and 

coroner or medical examiner offices except for one 

autopsy report. However, I discussed the autopsy 

findings with the pathologist in this case. 

RESULTS 

There are 114 deaths in the Clearinghouse database, 18 of which were due to head injury from a 

fall. The following deaths were excluded from this 

study: those that iuvolved equipment that broke or 

collapsed, striking a person on the head or neck 

(41); those in which a person became entangled in 

the equipment and suffocated or was strangled ( 45), 

those that involved equipment or incidents other 

than playground (6 [including a 13.7-meter fall 

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 

by neck (carotid vessel, airway, or cervical spinal 

cord) injury ( 4 ). 

The falls were from horizontal ladders (4), 

swings (7), stationary platforms (3), a ladder attached to a slide, a "see-saw'', a slide, and a retaining wall. Thirteen occurred on a school or public 

playground, and five occurred at home. The database is uot limited to infants and children, but a 

13-year-old was the oldest fatality (range: 12 

months-13 years; mean, 5.2 years; median, 4.5 

years). The distance of the fall, defined as the distance of the closest body part from the ground at 

the beginning of the fall, could be determined from 

CPSC or law enforcement reconstruction and actual 

measurement in 10 cases and was 0.6 to 3.0 meters 

(mean, 1.3 ± 0.77; median, 0.9). The distance 

could not be accurately determined in the seven fatalities involving swings and one of the falls from a 

horizontal ladder, and may have been from as little 

as 0.6 meters to as much as 2.4 meters. The maximum height for a fall from a swing was assumed to 

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

be the highest point of the arc. Twelve of the 18 

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 funduscopic examination was performed had bilateral 

retinal hemorrhage (Table 1). 

CASES 

Case 1 

This 12-month-old was seated on a porch swing 

between her mother and father when the chain on 

her mother's side broke and all three fell sideways 

and backwards 1.5 to 1.8 meters (5-6 feet) onto 

decorative rocks in front of the porch. The mother 

fell first, then the child, then her father. It is not 

known if her father landed on top of her or if she 

struck only the ground. She was unconscious immediately. EMS was called; she was taken to a 

local hospital; and was ictal and had decerebrate 

posturing in the emergency room. She was intubated, hyperventilated, and treated with mannitol. 

A computed tomography (CT) scan indicated a 

subgaleal hematoma at the vertex of the skull, a 

comrninuted fracture of the vault, parafalcine subdural hemorrhage, and right parietal subarachnoid 

hemorrhage. There was also acute cerebral edema 

with effacement of the right frontal horn and compression of the basal cisterns. She had a cardiopulmonary arrest while the CT scan was being done 

and could not be resuscitated. 

Case2 

A 14-month-old was on a backyard "see-saw" 

and was being held in place by his grandmother. 

The grandmother said that she was distracted for a 

moment and he fell backward, striking the grasscovered ground 0.6 meters (22.5 inches) below the 

plastic seat. He was conscious but crying, and she 

carried him into the house. Within 10 to 15 minutes 

he became lethargic and limp, vomited, and was 

taken to the local hospital by EMS personnel. He 

was unconscious but purposefully moving all extremities when evaluated, and results of funduscopic examination were normal. A CT scan indicated an occipital subgaleal hematoma, left-sided 

cerebral edema with complete obliteration of the 

left frontal horn, and small punctate hemorrhages 

in the left frontal lobe. There was no fracture or 

subdural hematoma. He was treated with mannitol; 

his level of consciousness rapidly improved; and he 

was extubated. However, approximately 7 hours 

after admission he began to have difficulty breathing, both pupils suddenly dilated, and he was reinI 

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 

herniation 

5' DC 9312060661 23 mos F Platform 0.70/2.3 Yes 10 minutes Bilateral, NOS Yes Yes 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 <.., 

" herniation No 

8 Al 910515HCC2182 3 yrs F Ladder 0.6/2.0 yes 15 minutes N/R Yes Yes Complex calvarial fracture, Yes ~ t;J ' (autopsy only) contusions, cerebral 

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 2.1/7.0 No No N/R Yes No Acute subdural hematoma Yes ~ ladder with acute cerebral 

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 ;,,, 

';-I ladder with herniation ti ,. 13 Al 881229HCC3070 6 yrs F Horizontal 0.9/3.0 Yes 1 +hour N/R Yes +IHF Yes Subdural and subarachnoid Yes 

, [;i ladder hemorrhage, cerebral 

~ '-. 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 " f;l , ladder to carotid/vertebral artery ,. < thrombosis ;,;, ~ 15 Al 970409HCC1096 8 yrs F Retaining 0.9/3.0 Yes 12+ hours N/R Yes Yes Acute subdura! hematoma Yes .. .wall (autopsy only) 

~ "' 16 Al 890621 HCC3195 10 yrs M Swing 0.9-1.5/3.0-5.0 Yes 10 minutes Bilateral Yes Yes Acute subdural hematoma 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 

,.. hemorrhage1 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 progression of the left hemispheric edema despite medical 

management, and he was removed from life support 22 hours after admission. 

Case3 

This 17-month-old had been placed in a baby 

carrier-type swing. attached to an overhead tree 

limb at a daycare provider's home. A restraining 

bar held in place by a snap was across her waist. 

She was being pushed by the daycare provider to 

an estimated height of 1.5 to 1.8 meters (5-6 feet) 

when the snap came loose. The child fell from the 

swing on its downstroke, striking her back and 

head on the grassy surface. She was immediately 

unconscious and apneic but then started to breathe 

spontaneously. EMS took her to a pediatric hospital. A CT scan indicated a large left-sided subdural hematoma with extension to the interhemispheric fissure anteriorly and throughout the length 

of the falx. The hematoma was surgically evacuated, but she developed malignant cerebral edema 

and died the following day. A postmortem examination indicated symmetrical contusions on the 

buttock and midline posterior thorax, consistent 

with impact against a fiat surface; a small residual 

left-sided subdural hematoma; cerebral edema 

with anoxic encephalopathy; and uncal and cerebellar tonsillar herniation. There were no cortical 

contusions. 

Case4 

A 20-month-old was with other family members 

for a reunion at a public park. She was on the platform portion of a jungle gym when she fell from 

the side and struck her head on one of the support 

posts. The platform was 1.7 meters (67 inches) 

above the ground and I.I meters (42 inches) above 

the top of the support post that she struck. Only her 

father saw the actual fall, although there were a 

number of other people in the immediate area. She 

was initially conscious and talking, but within•5 to 

10 minutes became comatose. She was taken to a 

nearby hospital, then transferred to a tertiary-care 

facility. A CT scan indicated a right occipital skull 

fracture with approximately 4-mm of depression 

and subarachnoid and subdural hemorrhage along 

the tentorium ·and posterior falx. Funduscopic examination indicated extensive bilateral retinal and 

preretinal hemorrhage. She died 2 days later because of uncontrollable increased intracranial pressure. A limited postmortem examination indicated 

an impact subgaleal hematoma overlying the fracture in the mid occiput. 

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

Cases 

A 23-month-old was playing on a plastic gym set 

in the garage at her home with her older brother. 

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. 

She lost her balance and fell headfirst onto a I-cm 

(%-inch) thick piece of plush carpet remnant covering the concrete floor. She struck the carpet first 

with her outstretched hands, then with the right 

front side of her forehead, followed by her right 

shoulder. Her grandmother had been watching the 

children play and videotaped the fall. She cried 

after the fall but was alert and talking. Her grandmother walked/carried her into the kitchen, where 

her mother gave her a baby analgesic with some 

water, which she drank. However, approximately 5 

minutes later she vomited and became stuporous. 

EMS personnel airlifted her to a tertiary-care university hospital. A CT scan indicated a large rightsided subdural hematoma with effacement of the 

right lateral ventricle and minimal subfalcine herniation. (The soft tissue windows for the scan could 

not be located and were unavailable for review.) 

The hematoma was immediately evacuated. She remained comatose postoperatively, developed cerebral edema with herniation, and was removed from 

life support 36 hours after the fall. Bilateral retinal 

hemorrhage, not further described, was documented in a funduscopic examination performed 24 

hours after admission. A postmortem examination 

confirmed the right frontal scalp impact injury. 

There was a small residual right subdural hematoma, a right parietal lobe contusion (secondary to 

the surgical intervention), and cerebral edema with 

cerebellar tonsillar herniation. 

Case6 

A 26-month-old was on a playground swing 

being pushed by a 13-year-old cousin when he fell 

backward 0.9 to 1.8 meters (3--6 feet), striking his 

head on hard-packed soil. The 13-year-old and several other children saw the fall. He was immediately unconscious and was taken to a local emergency room, then transferred to a pediatric hospital. 

A CT scan ' indicated acute cerebral edema and a 

small subdural hematoma adjacent to the anterior 

interhemispheric falx. A funduscopic examination 

performed 4 hours after admission indicated extensive bilat~ral retiqal hemorrhage, vitreous hemorrhage in the left eye, and papilledema. He had a 

subsequent cardiopulmonary arrest and could not 

be resuscitated. A postmortem examination confirmed the retinal hemorrhage and indicated a right 

parietal scalp impact injury but no calvarial frac-
FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 5 

ture, a "film" of bilateral subdural hemorrhage, 

cerebral edema with herniation, and· focal hemorrhage in the right posterior midbrain and pons. 

. Case7 

This 3-year-old with a history of TAR (thrombocytopenia-absent radius) syndrome was playing 

with other children on playground equipment at his 

school when he stepped through an opening in a 

platform. He fell 0.9 meters (3 feet) to the hardpacked ground, striking his face. A teacher witnessed the incident. He was initially conscious and 

able to walk. However, approximately 10 minutes 

later he had projectile vomiting and became comatose, was taken to a local hospital, and subsequently transferred to a pediatric hospital. A CT 

scan indicated a small subdural hematoma and diffuse cerebral edema with uncal herniation, according to the admission history and physical examination. (The original CT report and scan could not be 

located and were unavailable for review.) His 

platelet count was 24,000/mm3

, and he was treated 

empirically with platelet transfusions, although he 

had no evidence for an expanding extra-axial mass. 

Resuscitation was discontinued in the emergency 

room. 

Case8 

This 3-year-old was at a city park with an adult 

neighbor and four other children, ages 6 to 10. She 

was standing on the third step of a slide ladder 0.6 

meters (22 inches) above the ground when she fell 

forward onto compact dirt, striking her head. The 

other children but not the adult saw the fall. She 

was crying but did not appear to be seriously injured, and the neighbor picked her up and brought 

her to her parents' home. Approximately 15 minutes later she began to vomit, and her mother called 

EMS. She was taken to a local emergency room, 

then transferred to a pediatric hospital. She was initially lethargic but responded to hyperventilation 

and mannitol; she began to open her eyes with 

stimulation and to spontaneously move all extre;nities and was extubated. However, she developed 

malignant cerebral edema on the second hospital 

day and was reintubated and hyperventilated but 

died the following day. A postmortem examination 

indicated a subgaleal hematoma at the vertex of the 

skull associated with a complex fracture involving 

the left frontal bone and bihiteral temporal bones. 

There were small epidural and subduraJ bematomas 

(not identifiable on the CT scan), bilateral "contracoup" contusions of the inferior surfaces of the 

frontal and temporal lobes, and marked cerebral 

eden1a with uncal herniation. 

Case9 

A 4-year-old fell approximately 2.1 meters (7 

feet) from a playground slide at a state park, land' 

ing on the dirt ground on his buttock, then falling to 

his left side, striking his head. T:ljere was no loss of 

consciousness, but his family took him to a local 

emergency facility, where an'. evaluation was normal. However, be began vomiting and complained 

of left neck and bead pain approximately 3 hours 

later. He was taken to a second hospital, where a 

CT scan indicated a large left parietal epidural 

hematoma with a midline shift. He was transferred 

to a pediatric hospital and the hematoma was evacuated, but he developed malignant cerebral edema 

with right occipital and left parietal infarcts and 

was removed from the respirator 10 days later. A 

postmortem examination indicated a small residual 

epidural hematoma, marked cerebral edema, bilateral cerebellar tonsillar and uncal herniation, and 

hypoxic encephalopathy. There was no identifiable 

skull fracture. 

Case 10 

A 5-year-old was apparently walking across the 

horizontal ladder of a "monkey bar," part of an interconnecting system of homemade playground 

equipment in his front yard, when his mother 

looked out one of the windows and saw him laying 

face down on the ground and not moving. The horizontal ladder was 2.1 meters (7 feet) above compacted dirt. EMS were called, be was taken to a 

local hospital, and then transferred to a pediatric 

hospital. A CT scan indicated a right posterior temporal linear fracture with a small underlying 

epidural hematoma, a 5-mm thick acute subdural 

hematoma along the right temporal and parietal 

lobes, and marked right-sided edema with a 10-mm 

midline shift. He was hyperventilated and treated 

with mannitol, but the hematoma continued to enlarge and was surgically evacuated. However, he 

developed uncontrollable cerebral edema and was 

removed from life support 10 days after the fall. 

Case 11 

A 6-year-old was on a playground swing at a private lodge with his 14-year-old sister. His sister 

heard a "thump,'' turned around, and saw him on 

the grass-covered packed earth beneath the swing. 

The actual fall was not witnessed. The seat of the 

swing was 0.6 meters (2 feet) above the ground, 

and the fall distance could have been from as high 

as 2.4 meters (8 feet). He was initially conscious 

and talking but within 10 minutes became comatose and was taken to a local emergency room, 

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 

hematoma with extension into the anterior interhemispheric fissure and a significant midline shift 

with obliteration of the left lateral ventricle. There 

were no retinal hemorrhages. He was treated ag· 

gressively with dexamethasone and hyperventilation, but there was no surgical intervention. He died 

the following day. 

Case 12 

This 6-year-old was at school and was sitting on 

the top crossbar of a "monkey bar" approximately 3 

meters (10 feet) above compacted clay soil when an 

unrelated noncaretaker adult saw him fall from the 

crossbar to the ground. He landed flat on his back 

and initially appeared to have the wind knocked out 

of him but was conscious and alert. He was taken to 

the school nurse who applied an ice pack to a contusion on the back of bis bead. He rested for approximately 30 minutes in the nurse's office and 

was being escorted back to class when be suddenly 

collapsed. EMS was called, and be was transported 

to a pediatric hospital. He was comatose on admission, the fundi could not be visualized, and a bead 

CT scan was interpreted as normal. However, a CT 

scan performed the following morning approximately 20 hours after the fall indicated diffuse cerebral edema with effacement of the basilar cisterns 

and fourth ventricle. There was no identifiable subdural hemorrhage or cal varial fracture. He developed transtentorial herniation and died 48 hours 

after the fall. 

Case 13 

This 6-year-old was playing on a school playground with a 5th grade student/friend. She was 

hand-over-hand traversing the crossbar of a "monkey bar" 2.4 meters (7 feet 10 inches) above the 

ground with her feet approximately 1 meter ( 40 

inches) above the surface. She attempted to slide 

down the pole when she reached the end of the 

crossbar but lost her grip and slid quickly to the 

ground, striking the compacted dirt first with her 

feet, then her buttock and back, and finally 'her 

head. The friend inforn1ed the school principal of 

the incident, but the child seemed fine and there 

was no intervention. She went to a relative's home 

for after-school care approximately 30 minutes 

after the fall, watched TV for a while, then complained of a l\eadache and laid down for a nap. 

When her parents arrived at the home later that 

evening, 6 hours after the incident, they discovered 

that she was incoherent and "drooling." EMS transported her to a tertiary-care medical center. A CT 

scan indicated a right parieto-occipital skull fracAm J Forensic Med Pathol, Vol. 22, No. J, March 2001 

ture, subdural and subarachnoid hemorrhage, and a 

right cerebral hemisphere infarct. The infarct included the posterior cerebral territory and was 

thought most consistent with thrombosis or dissection of a right carotid artery that bad a persistent 

fetal origin of the posterior c'erebral artery. She 

remained con1atose and was removed from the 

respirator 6 days after admission. A postmortem 

examination indicated superficial abrasions and 

contusions over the scapula, a prominent right parietotemporal subgaleal bematoma, and a right pari-

, eta! skull fracture. She bad a 50-ml subdural 

bematoma and cerebral edema with global hypoxic 

or iscbemic injury ("respirator brain"), but the 

carotid vessels were normal. 

Case 14 

A 7-year-old was on the playground during 

school hours playing on the horizontal ladder of a 

"monkey bar" when he slipped and fell 1.2 to 2.4 

meters (4-8 feet). According to one witness, be 

struck his forehead on the bars of the vertical ladder; according to another eyewitness he struck the 

rubber pad covering of the asphalt ground. There 

are conflicting stories as to whether he had an initial loss of consciousness. However, he walked 

back to the school, and EMS was called because of 

the history of the fall. He was taken to a local hospital, where evaluation indicated a Glasgow coma 

score of 15 and a normal CT scan except for an occipital subgaleal bematoma. He was kept overnight 

for observation because of the possible loss of consciousness but was released the following day. He 

was doing homework at home 2 days after the fall 

when his grandmother noticed that he was stumbling and had slurred speech, and she took him 

back to the hospital. A second CT scan indicated a 

left carotid artery occlusion and left temporal and 

parietal lobe infarcts. The infarcts and subsequent 

edema progressed; he had brainstem herniation; 

and be was removed from life support 3 days later 

(5 days after the initial fall). A postmortem exanlination indicated ischemic infarcts of the left parietal, temporal, and occipital lobes, acute cerebral 

edema with herniation, and thrombosis of the left 

vertebral artery. Occlusioli. of the carotid artery, 

suspected premortem, could not be confirmed. 

Case 15 

This 8-year-old was at a public playground near 

her home· with se;,,eral friends her age. She was 

hanging by her hands from the horizontal ladder of 

a "monkey bar" with her feet approximately 1.1 

meters (3.5 feet) above the ground when she attempted to swing from the bars to a nearby 0.9-
FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 7 

meter (34-inch) retaining wall. She landed on the 

top of the wall but then lost her balance and fell to 

the ground, either to a hard-packed surface (one 

witness) or to a 5.1-cm (2-inGh) thick.resilient rubber mat (a second witness), striking her back and 

head. She initially cried and complained of a 

headache but continued playing, then later went 

home. Her mother said that she seemed normal and 

went to bed at her usual time. However, when her 

mother tried to awaken her at approximately 8:30 

the following morning (12 hours after the fall) she 

complained of a headache and went back to sleep. 

She awoke at 11 a.m. and complained of a severe 

headache then became unresponsive and had a 

seizure. EMS took her to a nearby hospital, but she 

died in the emergency room. A postmortem examination indicated a right temporoparietal subdural 

hematoma, extending to the base of the brain in the 

middle and posterior fossae, with flattening of the 

gyri and narrowing of the sulci. (The presence or 

absence of herniation is not described in the autopsy report.) There was no calvarial fracture, and 

there was no identifiable injury in the scalp or 

galea. 

Case 16 

A 10-year-old was swinging on a swing at his 

school's playground during recess when the seat detached from the chain and he fell 0.9 to 1.5 meters 

(3-5 feet) to the asphalt surface, striking the back of 

his head. The other students but not the three adult 

playground supervisors saw him fall. He remained 

conscious although groggy and was carried to the 

school nurse's office, where an ice pack was placed 

on an occipital contusion. He suddenly lost consciousness approximately 10 minutes later. and 

EMS took him to a local hospital. He had decerebrate posturing when initially evaluated. Funduscopic examination indicated extensive bilateral confluent and stellate, posterior and peripheral 

preretinal and subhyaloid hemorrhage. A CT scan 

showed a large acute right frontoparietal subdural 

hematoma with transtentorial herniation. i Trhe 

hematoma was surgically removed, but he developed malignant cerebral edema and died 6 days later. 

A postmortem examination indicated a right parietal 

subarachnoid AV malformation, contiguous with a 

small amount of residual subdural hemorrhage, and 

cerebral edema with anoxic encephalopathy and herniation. There was no calvarial fracture. 

Case 17 

A 12-year-old was at a public playground with a 

sister and another friend and was standing on the 

seat of a swing when the swing began to twist. She 

lost her balance and fell 0.9 tol.8 )lleters (3-6 feet) 

to the asphalt surface, striking her posterior thorax 

and occipital scalp. She was inunediately unconscious and was taken to a tertiary-care hospital 

emergency room, where she was, pronounced dead. 

A postmortem examination ii;idic'ated an occipital 

impact injury associated with an extensive comminuted occipital fracture extending into both middle cranial fossa and "contra-coup" contusions of 

both inferior frontal and temporal lobes. 

Case 18 

This 13-year-old was at a public playground with 

a friend. She was standing on the seat of a swing 

with her friend seated between her legs when she 

lost her grip and fell backwards 0.6 to 1.8 meters 

(2-6 feet), striking either a concrete retaining wall 

adjacent to the playground or a resilient 5.1-cm (2 

inch) thick rubber mat covering the ground. She 

was immediately unconscious and was given emergency first aid by a physician who was nearby 

when the fall occurred. She was taken to a nearby 

hospital and was purposefully moving all extremities and had reactive pupils when initially evaluated. A CT scan indicated interhemispheric subdural hemorrhage and generalized cerebral edema, 

which progressed rapidly to brain death. A postmortem examination indicated a linear nondepressed midline occipital skull fracture, subdural 

hemorrhage extending to the occiput, contusion of 

the left cerebellar hemisphere, bifrontal "contracoup" contusions, and cerebral edema. 

DISCUSSION 

General 

Traumatic brain injury (TBI) is caused by a force 

resulting in either strain (deformation/unit length) 

or stress (force/original cross-sectional area) of the 

scalp, skull, and brain (35-37). The extent of injury 

depends not only on the level and duration of force 

but also on the specific mechanical and geometric 

properties of the cranial system under loading 

(38-40). Different parts of the skull and brain have 

distinct biophysical characteristics, and calculating 

deformation and stress is complex. However, an applied force causes the skull and brain to move, and 

acceleration, the time required to reach peak acceleration, and the duration of acceleration may be 

measured at specific locations (36,41). These kine1natic parameters do not cause the . actual brain 

damage but are useful for analyzing TBI because 

they are easy to quantify. Research in TBI using 

physical models and animal experiments has shown 

that a force resulting in angular acceleration proAm J Forensic Med Pathol, Vol. 22, No. I, March 2001 
8 J PLUNKETT 

duces primarily diffuse brain damage, whereas a 

force causing exclusively translational acceleration 

produces only focal brain damage (36). A fall from 

a countertop or table is often considered to be exclusively translational and therefore assumed incapable of producing serious injury (3, 7-9). However, 

sudden impact deceleration must have an angular 

vector unless the force is applied only through the 

center of mass (COM), and deformation of the 

skull during impact must be accompanied by a volume change (cavitation) in the subdural "space" 

tangential to the applied force (41). The angular ' 

and deforn1ation factors produce tensile strains on 

the surface veins and mechanical distortions of the 

brain during impact and may cause a subdural 

hematoma without deep white matter injury or even 

unconsciousness (42-44). 

Many authors state that a fall from less than 3 

meters (10 feet) is rarely if ever fatal, especially if 

the distance is Jess than 1.5 m~ters (5 feet) 

(1-6,8,9). The few studies concluding that a shortdistance fall may be fatal (22-24,26,27) have been 

criticized because the fall was not witnessed or was 

seen only by the caretaker. However, isolated reports of observed fatal falls and biomechanical 

analysis using experimental animals, adult human 

volunteers, and models indicate the potential for serious head injury or death from as little as a 0.6-

meter (2-foot) fall (48-52). There are limited 

experimental studies on infants (cadaver skull fracture) (53,54) and none on living subadult nonhuman primates, but the adult data have been extrapolated to youngsters and used to develop the 

Hybrid II/III and Child Restraint-Air Bag Interaction (CRAB!) models (55) and to propose standards 

for playground equipment (56,63). We simply do 

not know either kinematic or nonkinematic limits 

in the pediatric population (57,58). 

Each of the falls in this study exceeded established adult kinematic thresholds for traumatic 

brain injury (41,48-52). Casual analysis of the falls 

suggests that most were primarily translational. 

However, deformation and internal angular acceleration of the skull and brain caused by the itnpact 

produce the injury. What happens during the impact, not during the fall, determines the outcome. 

Snbdural Hemorrhage 

A "high strain" impact (short pulse duration and 

high rate for deceleration onset) typical for a fall is 

more likely to cause subdural hemon-hage than a 

"low strain" in1pact (long pulse duration and low 

rate for deceleration onset) that is typical of a 

motor vehicle accident (42,61). The duration of deceleration for a head-impact fall against a nonyieldAm J Forensic Med Pathol, Vol. 22, No. 1, March 2001 

ing surface is usually less than 5 milliseconds 

(39,59-61). Experimentally, impact duration longer 

than 5 milliseconds will not cause a subdural 

hematoma unless the level of angular acceleration 

is above 1.75 X 105 rad/s2 (61). A body in motion 

with an angular acceleration of 1.75 X 105 rad/s2 

has a tangential acceleration of 17 ,500 rn/s2 at 0.1 

meters (the distance from the midneck axis of rotation to the midbrain COM in the Duhaime model). 

A human cannot produce this level of acceleration 

by impulse ("shake") loading (62). 

An injury resulting in a subdural hematoma in an 

infant may be caused by an accidental fall 

(43,44,64). A recent report documented the findings 

in seven children seen in a pediatric hospital emergency room after an accidental fall of 0.6 to 1.5 

meters who had subdural hemon-hage, no Joss of 

consciousness, and no symptoms (44). The characteristics of the hemon-hage, especially extension 

into the posterior interhemispheric fissure, have 

been used to suggest if not confirm that the injury 

was nonaccidental (9,62,65-68). The hemon-hage 

extended into the posterior interhemispheric fissure 

in 5 of the 10 children in this study (in whom the 

blood was identifiable on CT or magnetic resonance scans and the scans were available for review) and along the anterior falx or anterior interhemispheric fissure in an additional 2 of the 10. 

Lucid Interval 

Disruption of the diencephalic and midbrain portions of the reticular activating system (RAS) 

causes unconsciousness (36,69,70). "Shearing" or 

"diffuse axonal" injury (DAI) is thought to be the 

primary biophysical mechanism for immediate 

traumatic unconsciousness (36,71). Axonal injury 

has been confirmed at autopsy in persons who had 

a brief loss of consciousness after a head injury and 

who later died from other causes, such as coronary 

artery disease (72). However, if unconsciousness is 

momentary or brief ("concussion") subsequent ~eterioration must be due to a mechanism other than 

DAI. Apnea and catecholamine release have been 

suggested as significant factors in the outcome following head injury (73,74). In addition, the centripetal theory of traumatic unconsciousness states 

that primary disruption of the RAS will not occur 

in isolation and that structural brainstem damage 

from inertial (impulse) or impact (contact) loading 

must be accompanied by evidence for cortical and 

subcortical damage (36). This theory has been validated by magnetic resonance imaging and CT scans 

in adults and children (75,76). Only one of the children in this study (case 6) had evidence for any 

component of DAI. This child had focal hemor-
z 

0 

-0 

g 

> " m 

FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 9 

rhage in the posterior midbrain and pons, thought 

by the pathologist to be primary, although there 

was no skull fracture, only "a film" of subdural 

hemorrhage, no tears in thr:~corpus, _<;:allosum, and 

no lacerations of the cerebral white matter (grossly 

or microscopically). 

The usual cause for delayed deterioration in infants and children is cerebral edema, whereas in 

adults it is an expanding extra-axial hematoma 

(77). If the mechanism for delayed deterioration 

(except for an expanding extra-axial mass) is venospasm, cerebral edema may be the only morphologic marker. The "talk and die or deteriorate 

(TADD)" syndrome is well characterized in adults 

(78). Two reports in the pediatric literature discuss 

TADD, documenting 4 fatalities among 105 children who had a lucid interval after head injury and 

subsequently deteriorated (77,79). Many physicians 

believe that a lucid interval in an ultimately fatal 

pediatric head injury is extremely unlikely or does 

not occur unless there is an epidural hematoma 

(7,8,11). Twelve children in this study had a lucid 

interval. A noncaretaker witnessed 9 of these 12 

falls. One child had an epidural hematoma. 

Retinal Hemorrhage 

The majority of published studies conclude that 

retinal hemorrhage, especially if bilateral and posterior or associated with retinoschisis, is highly 

suggestive of, if not diagnostic for, nonaccidental 

injury (9,14-21). Rarely, retinal hemorrhage has 

been associated with an accidental head injury, but 

in these cases the bleeding was unilateral (80). It is 

also stated that traumatic retinal hemorrhage may 

be the direct mechanical effect of violent shaking 

(15). However, retinal hemorrhage may be caused 

experimentally either by ligating the central retinal 

vein or its tributaries or by suddenly increasing intracranial pressure (81,82); retinoschisis is the result of breakthrough bleeding and venous stasis not 

"violent shaking" (15,83). Any sudden increase in 

intracranial pressure may cause retinal hemorrhage 

(84-87). Deformation of the skull coincident t& an 

impact nonselectively increases intracranial pressure. Venospasm secondary to traumatic brain injury selectively increases venous pressure. Either 

mechanism may cause retinal hemorrhage irrespective of whether the trauma was accidental or inflicted. Further, retinal and optic nerve sheath hemorrhages associated with a ruptured vascular 

malformation are due to an increase in venous pressure not extension of blood along extravascular 

spaces (81-83,88). Dilated eye examination with an 

indirect ophthalmoscope is thought to be more sensitive for detecting retinal bleeding than routine examination and has been recommended as part of 

the evaluation of any pediatric patient with head 

trauma (89). None of the children in this study had 

a formal retinal evaluation, and only six had funduscopic examination .documented in the medical 

record. Four of the six had bilateral retinal hemorrhage. ' 

Pre-existing Conditions 

One of these children (case 16) had a subarachnoid AV malformation that contributed to development of the subdural hematoma, causing his death. 

One (case 7) had-TAR syndrome (90), but his death 

was thought to be caused by malignant cerebral 

edema not an expanding extra-axial mass. 

Cerebrovascnlar Thrombosis 

Thrombosis or dissection of carotid or vertebral 

arteries as a cause of delayed deterioration after 

head or neck injuries is documented in both adults 

and children (91,92). Case 14 is the first report of a 

death due to traumatic cerebrovascular thrombosis 

in an infant or child. Internal carotid artery thrombosis was suggested radiographically in an additional death (case 13) but could not be confirmed at 

autopsy. However, this child died 6 days after admission to the hospital, and fibrinolysis may have 

removed any evidence for thrombosis at the time 

the autopsy was performed. 

Limitations 

1. Six of the 18 falls were not witnessed or were 

seen only by the adult caretaker, and it is possible that another person caused the nonobserved injuries. 

2. The exact height of the fall could be determined in only 10 cases. The others (7 swing 

and 1 stationary platform) could have been 

from as little as 0.6 meters (2 feet) to as much 

as 2.4 meters (8 feet). 

3. A minimum impact velocity sufficient to 

cause fatal brain injury cannot be inferred 

from this study. Likewise, the probability that 

an individual fall will have a fatal outcome 

cannot be stated because the database depends 

on voluntary reporting and contractual agreements with selected U.S. state agencies. The 

NEISS summaries for the study years estimated that there were more than 250 deaths 

due to head and neck injuries associated with 

playground equipment, but there are only 114 

in the files. Further, this study does not include other nonplayground equipment-related 

fatal falls, witnessed or not witnessed, in the 

CPSC database (32). 

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

CONCLUSIONS 

E . fall is a complex event. There must be a 1. very . . 'd . biOme"chanical analysis for any inc1 ent 1n 

hich the severity of the injnry appears to be w . . lncOnsistent with the history. The question 1s 

not "Can an infant or child be seriously injured or killed from a short-distance fall?''. but 

rather "If a child falls (x) meters and strikes 

his other head on a nonyielding surface, what 

will happeu ?" 

2. Retinal hemorrhage may occur whenever intracranial pressure exceeds venous pressure or 

whenever there is venous obstruction. The 

characteristic of the bleeding cannot be used 

to determine the ultimate cause. 

3. Axonal damage is unlikely to be the mechanism for lethal injnry in a low-velocity impact 

such as from a fall. 

4. Cerebrovascular thrombosis or dissection 

must be considered in any injury with apparent delayed deterioration, and especially in 

one with a cerebral infarct or an unusual distribution for cerebral edema. 

5. A fall from less than 3 meters (10 feet) in an infant or child may cause fatal head injury and 

may not cause irrunediate syinptoms. The injnry may be associated with bilateral retinal 

hemorrhage, and an associated subdural 

hematoma may extend into the interhemispberic fissure. A history by the caretaker that 

the child may have fallen cannot be dismissed. 

Acknowledgements: The author thanks the law enforcement, emergency medical services, and medical 

professionals who willingly helped him obtain the original source records and investigations; Ida Harper-Brown 

(Technical Information Specialist) and Jean Kennedy 

(Senior Compliance Officer) from the U.S. CPSC, whose 

enthusiastic assistance made this study possible; Ayub K. 

Ommaya. M.D., and Werner Goldsmith. Ph.D .• for critically reviewing the manuscript; Jan E. Leestrna, M.D., 

and Faris A. Bandak, Ph.D., for helpful conunents; Mark 

E. Myers, M.D., and Michael B. Plunkett, M.D., for review of the medical imaging studies; Jeanne Reuter and 

Kathy Goranowski, for patience, humor, and completing 

the manuscript; and all the families who shared ~e stories of their sons and daughters and for whom this work 

is dedicated. 

APPENDIX 

Newtonian mechanics involving constant acceleration may be used to determine the impact velocity 

in a gravitational fall. However, c6nstant acceleration formulas cannot be used to calculate the relations among velocity, acceleration, and distance 

traveled during an impact because the deceleration 

Am J Forensic Med Pathol, Vol. 22, No. 1, March 2001 

is not uniform (45). This analysis requires awareness 

of the shape of the deceleration curve, knowledge of 

the mechanical properties and geometry of the cranial system, and comprehension of the stress and 

strain characteristics for the specific part of the skull 

and brain that strikes the ground. A purely translational fall requires that the body is rigid and that the 

external forces acting on the body pass only through 

the COM, i.e., there is no rotational component. A ! -

meter-tall 3-year-old hanging by her knees from a 

horizontal ladder with the vertex of her skull 0.5 meters above hard-packed earth approximates this 

model. If she looses her grip and falls, striking the 

occipital scalp, her impact velocity is 3.1 m/second. 

An exclusively angular fall also requires that the 

body is rigid. In addition, the rotation must be about 

a fixed axis or a given point internal or external to 

the body, and the applied moment and the inertial 

moment must be at the identical point or axis. If this 

same child has a 0.5-meter COM and has a "matchstick" fall while standing on the ground, again striking her occiput, her angular velocity is 5.42 rad/second and tangential velocity 5.42 m/second at impact. 

The impact velocity is higher than predicted for an 

exclusively translational or external-axis angular fall 

when the applied moment and the inertial moment 

are at a different fixed point (slip and fall) or when 

the initial velocity is not zero (walking or running, 

then trip and fall), and the vectors are additive. However, the head, neck, limbs, and torso do not move 

uniformly during a fall because relative motion occurs with different velocities and accelerations for 

each component. Calculation of the impact velocity 

for an actual fall requires solutions of differential 

equations for each simultaneous translational and 

rotational motion ( 45). Fnrther, inertial or impulse 

loading (whiplash) may cause head acceleration 

more than twice that of the midbody input force and 

may be important in a fall where the initial impact is 

to the feet, buttock, back, or shoulder, and the final 

impact is to the head (46,47). 

The translational motion of a rigid body at constant gravitational acceleration (9.8 m/s2

) is calculated from: 

F =ma v2 = 2as v =at 

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

(newton), m = mass (kg), a = acceleration (rnls2), 

v =velocity (mis), s =distance (m), and t =time (s). 

The angular motion.of a rigid body about a fixed 

axis at a given point of the body under constant 

gravitational acceleration (9.8 m/s2

) is calculated 

from: 

M =Ia 

or 

loc 

cc 

(n 

(rr 

ge 

L 

gL 

tic 

2 

3 

4 

s 

]( 

1: 

l 

[. 

1 
!SS 

of 

~and 

111 

lahe 

gh 

la 

eLis 

ie 

d. 

1e 

ut 

to 

al 

is 

ilko-

:t. 

Lil 

11 

1t 

m 

1-

·e 

,_ 

y 

!.I 

d 

e 

n 

d 

s 

Ll 

y 

i 

t 

i 

FATAL HEAD INJURIES WITH SHORT-DISTANCE FALLS 11 

where M = the applied moment about the COM 

or about the fixed point where the axis of rotation is 

located, I = the inertial moment about this same 

COM or fixed point, a = angular acceleration 

(rad/s2), w = angular velocity. (radfs·), r = radius 

(m), v' = tangential velocity (mis), and a' = tangential acceleration (rn/s2

). 

The angular velocity w for a rigid body of length 

L rotating about a fi>~d point is calculated from: 

lfI0w2 = maL/2 I0 = (1/3) rnL2 

where I 0 = the initial inertial moment, w = angular velocity (rad/s), m = mass (kg), a = gravitational acceleration (9.8 rn/s2

), and L = length. 

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85. Weedn VW, Mansour AM, Nichols .MJvf. Retinal hemorrhage in an infant after cardiopulmonary resuscitation. Am 

J Forensic Med Pathol 1990;11:79-82. 

86. David DB, Mears T, Quinlan NIP. Ocular complications associated with bungee jumping. Br J Ophthalmol 1994;78: 

234-5. 

87. Jain BK, Talbot EM. Bungee jumping and intraoc.ular hemorrhage. Br J Ophthalm·ot 1994;78:236-7, 

88, Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of 

subarachnoid hemorrhage. N Engl J Med 2000;342:29-36. 

89. Becker H, Gupta BK. Recognizing abusive head trauma in 

children. JAMA 1999;282:1421. 

90. Hall JG, Levin J, Kuhn JP, et al. Thrombocytopenia with 

absent radius (TAR). Medicine (Baltitnore) 1969;48: 411-

39. 

9L Pozzati E, Giuliani G, Poppi M, FaenzaA. Blunt traumatic 

carotid dissection with delayed symptoms. Stroke 1989;20: 

4l2--6. 

92. Martin PJ, Enevoldson TP, Humphrey PRD. Causes of ischaemic stroke in the young. PostgradMedJ 1997;73:8-16. 
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 

Abstract: Several controversies exist regarding ultimately lethal 

head injuries in small children. Death from short falls, timing of 

head injury, lucid intervals, presence of diffuse axonal inJUt)' (DAI), 

and subdural hernatoma (SDH) as marker of DAI are the n1ost recent 

controversial topics of debate in this evolving field of study. In this 

area of debate, \Ve present a case of delayed death from a witnessed 

fall backwards off a bed in a 9-month-old black male child who 

struck his head on a concrete floor and was independently witnessed 

as "healthy" postfall for 72 hours until he was discovered dead in 

bed. Grandn1other, babysitter, and mother all independently corroborated under police investigation that the child "acted and behaved 

normally" after the fall until death. Autopsy showed a linear nondisplaced parietal skull fracture, diastasis of adjacent occipital suture, subgaleal hemorrhage 'Nith evidence of aging, small posterior 

clotting SDH, marked cerebral eden1a, and a sinall tear of the 

midsuperior body of the corpus calloswn consistent with focal 

axonal injury (F Al). No DAI was seen, and there \Vere no retinal 

hemorrhages. All other causes of death were excluded upon thorough police and medical examiner investigation. Although this 

seems to be a rare phenomenon, a delayed,, seemingly symptom-free 

interval can occur between a clinically apparent mild head injury 

and accidental death in a young child. 

(Am J Forensic Med Pathol 2003;24: 371-376) 

CASE REPORT 

I\ 9-rnonth-old black male child weighing 22 pounds (10 

/'"'\kg) and measuring 28 inches (71 crn), 80th percentile and 

501

h percentile for age, respectively, with a history of asth1na 

Manuscript received March 19, 2003; accepted May 29, 2003. 

From the Cook County Office of the Medical Examiner, and Deparlmt'nt of 

Pathok1gy, Rush College of Medicine, Chicago, Illinois (J.S.D.), and 

Knox County Office of the Medical Examiner. and Department of 

Pathology, Graduate School of Medicine, Univt:rsity of Tt:nnessee, 

Knoxville, Tennessee (D.M.). 

Reprints: Darinka Mih.msnic, MD, PhD, Regional Forensic Center, University of Tennessee Memorial Hospital, 1924 Alcoa Highway, Knoxville, 

1N 37920. E-mail: dmileusn@mc.utmck.edu 

Copyright© 2003 by Lippincott Williams & Wilkins 

0195-7910/03/2404-037 l 

DOI: I 0.1097/0 ! .paf.0000097851.18478.16 

treated with nebulizer, was witnessed by his grandmother to 

fall backwards off the edge of a queen-sized bed, 30 inches 

off the floor. The child was sitting on the edge of the bed as 

the grandmother dressed her 2-year-uld daughter. The child 

fell back vvards and rotated fron1 the sitting position, striking 

the 1nidback of his head on a vinyl-covered concrete floor at 

8:00 AM. He i1n111ediately began crying, and the grandmother 

placed ice on a knot on the back of his head. He stopped 

crying and was consolable within a few minutes. The child 

was taken to the babysitter's residence, where the babysitter 

was told of the fall and to watch for any behavioral changes. 

The tnother \Vas at work the tnorning when the fall occurred. 

When the mother picked the child up at the babysitter's in the 

afternoon. he appeared 'Nell. The babysitter reported no 

problems and that he acted, ate, and behaved as usual. For the 

next 2 days, the grandmother, mother, and babysitter did not 

notice any abnormalities in either behavior or appearance of 

the child. 

Approximately 72 hours after the fall off the bed, the 

child was found at the foot of the mother's bed, where he 

usually slept, prone, cold, and unresponsive. Paramedics were 

called, and in spite of resuscitative.: efforts, he was pronounced dead upon arrival at the hospital. He \·vas last seen 

alive 8 hours prior when he was fed by his mother and given 

his usual albuterol breathing treahnent. No abnormalities on 

the child were seen in the emergency department. There was 

no evidence of overlying or asphyxia. 

Medical and family history revealed that the child was 

born full-term weighing 7 pounds 4 ounces. He was diagnosed with asthma after complaints of \Vheezing episodes and 

was prescribed an a!buterol nebulizer twice daily. The child's 

father, who does not reside in the hon1e, bas asthma. The 

n1other and grandn1other reside together in a public housing 

develop1nen1. Depart1nent of Child and Family Services 

records revealed no prior incidents concerning the deceased, 

but the mother had I report of being a victitn of prior abuse. 

The grand1nother has a remote history of cocaine abuse. Her 

2-year-old daughter is well and lives with her. 

Autopsy revealed a well-developed and well-nourished 

black 111alc child appearing the stated age and without exterThe American journal of Forensic Medicine and Pathology • Volume 24, Number 4, December 2003 3 71 
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 fractme, 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 1. View of the linear skull fracture Involving the posterior right parietal bone1 after removal of the overlying subgaleal hemorrhage. 

372 

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. Comprehensive 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 neutrophilic inflammation. Decalcified sections of the parietal 

fracture showed an acute fracture with early periosteal reaction at the fracture margin. Lung sections showed mild focal 

peribronchial lymphocytic aggregates consistent with bronchitis without asthma changes. There were neither eosinophils nor 1nucus plugs. Sections of remaining organs were 

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

FIGURE 3. Coronal section of the corpus callosum showing 

wedge-shaped laceration (right upper corner) surrounded by a 

rim of hemorrhage, FAI and activated microglia (1 OOX, hematoxylin-eosin). 

without pathologic changes. The eyes were examined by an 

ophthalmic pathologist consultant and were normal. A forensic radiologist consultant also reviewed postmortem radiographs and repo1ted no additional findings. 

Follow-up Investigation 

Prior to the autopsy, Chicago police detectives \Vere 

notified of the skull fracture and attended the examination. 

After autopsy, police re1nanded the grandmother and mother 

to the police station, where they were interviewed separately 

about the injuries. Upon extensive questioning about any 

possibility of inflicted trauma and abuse that the baby could have 

sustained, they both spontaneously gave the similar story of the 

fall 3 days prior. The babysitter was questioned and confinned 

the accounts and timing of the reported events. Police detectives 

and evidence technicians accompanied the mother and grandmother back to their residence and verified the scene and 

reenactment of the fall. A week later, the prosector pathologist (JSD) and a specialist child death scene investigator of 

the Medical Exa1niner's Office went to the residence and 

again inspected the residence, interviewed the grandmother 

and 1notber. and reenactcJ. the fi.lll. As with the police detectives, all felt the grandmother and mother to be truthful and 

grieving appropriately for the circumstances. After consideration of the autopsy, toxicologic, histologic, consultative, and 

investigative findings, the death was certified as craniocerebral injuries due to a fall fron1 the bed backwards onto a 

concrete floor. The manner was determined accidental. 

DISCUSSION 

Ce1tain issues in pediatric head trauma, such as lethality of short falls, timing of head injury, and presence of DAI 

© 2003 Lippincott Williams & Wilkins 

Copyright Lippincott 

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 im1nediately 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 undetectable 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, 

in living children would be a rarity rather than a com1non 

place.2 

In this present case, we discuss the death of a 9-monthold 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 

tonsillary herniation, and a small tear in the body of the 

corpus callosu1n, which appeared histologically as F AL Analysis of the fall revealed a rotational component of the body 

and head movement, 1.vhich could account for the described 

injuries. The location and appearance of the prin1at)' injury 

was consistent viith flipping backward and striking the back 

of the head. There was no diffuse axonal da1nage or retinal 

hemorrhage. Thorough workup, including scene investigation 

and independent police questioning of all individuals involved in the care of the infant, prior to, during, and after the 

accident, were unanin1ous. There were no inconsistencies, 

and the stories have never varied from the beginning to the 

conclusion of the investigation. There were no other instances 

of trau1na to the head observed by the caretakers. Based on 

several independent accounts, the infant's behavior following 

the head trauma up to his sudden death was ordinary and did 

not require medical attention, qualifying as a lucid or symptom-free interval. 

Deciding whether head injury in a very young child is 

accidental or nonaccidental has always been proble1natic for 

clinicians and forensic pathologists alike. 3

·

4 We realize that a 

number of child abuse experts would have a problem with the 

accidental detenninlltion of the manner of death in the present 

case. We do not argue the widely noted observation that 

simple falls from low heights rarely result in significant 

prin1ary brain injury. 5 However, every fall is different, as well 

as the individual reaction to the pri tnary insult. Son1e experts 

in head trauma consider the term minor head injury an 

oxymoron. 6 We believe that a series of secondary injuries, 

known to occur after a primary insult, resulted in the extreme 

swelling of the brain and death of the child. What is widely 

understated and so1ncti1nes forgotten about is secondary brain 

373 
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 determining the outco1ne after a see1ningly trivial head injury.7

- 12 

Another frequently forgotten factor is the influence of age and 

sex on the presentation and the outco1ne of head injury. The 

grouping together of different pathologies such as subdural 

hemorrhages, cerebral contusions, FAI, and DAI, as well as 

lumping together of infants, toddlers, and preschool children, 

needs to be addressed. It has been shown that infants and 

young toddlers lose consciousness less frequently, and a 

smaller proportion of their head injuries lead to immediate 

coma in comparison to other children with the same grades of 

traumatic energy. 13 Pohl et a1 9 demonstrated that evolution of 

posttraumatic brain da1nage after head trauma in developing 

rodents is a highly dynamic process exhibiting age-dependent 

excitotoxic and distant apoptotic cell death. 

Reviewing the literature on childhood head trauma, one 

can clearly see that a gradual sideway drift or evolution of 

findings and conclusions of the original reports, research, and 

data had taken place. One of them, also frequently encountered in cou1t, is that ve1y young children, especially infants, 

are auton1atically assu1ned to be the victi1ns of "shaken baby 

syndrome." 14- 16 However, fro1n the literature and from personal experience, findings of direct impact to the head prevail. The problem is not only se1nantic in nature but has 1najor 

and far-reaching consequences since the character, location, 

and clinical presentation of the injuries arc different from the 

rare purely shaken babies. 17·

18 

Another encountered fallacy is that the children who 

die of head trau1na, especially abusive head trau1na, sustain 

DAL Going back to some of the original research, it is clear 

that the authors explicitly stated that the 2 worst types of head 

injury are SDH and DAI. These 2 have different mechanisms 

of causation: SDH occurs much more commonly in nonvehicular injuries, such as falls and abusive head trauma, while 

DAI is caused almost exclusively by vehicular mechanisms.19-22 Although both injuries frequently share a common mechanical cause such as angular acceleration, they 

differ in degree. SDH usually occurs with a rotational injury 

of short duration and a high rate of acceleration. Conversely, 

motor vehicle accidents tend to cause longer-duration, loweracceleration-rate injuries leading to DAI rather than SDH.8

·

21 

SDHs occur in a greater number in children with inflicted 

versus noninflicted traumatic brain inju1y, whereas shear 

injuries are commonly visualized in the noninflicted inju1y 

group.22 Therefore, current supposition that the presence of 

SDH is a marker of DAI is likely inaccurate. 

A frequently asked question is whether delayed 1nental 

status deterioration can occur following head injury in children. This is critically important in unwitnessed circu1nstances such as child abuse. A widely held dogma is that if a 

child becomes unresponsive while in the care of an individual 

who is reporting the onset of unconsciousness, that same 

individual must be the perpetrator. Currently, some special374 

ists involved in the care of abused children accept as true that 

all children who eventually die, regardless of the type of the 

head injury, must be severely disabled, usually comatose 

from the ve1y moment the injury occurred.23 From personal 

experience and based on the literature review, this tenet is not 

necessarily true.24'

25 Although there are clearly scenarios in 

which this principle could be applicable, there is undoubtedly 

a subpopulation of infants and especially toddlers with a 

completely different constellation of injuries and a dissitnilar 

presentation. Occasionally, these children have nonspecific 

symptoms for several hours to a day prior to the onset of 

either coma or seizure followed by coma. Common observations include reduced physical activity, lethargy, drowsiness, 

irritability, temperature irregularities, poor feeding, and gastrointestinal symptoms. 232627 Careful analysis of the history 

and the events leading to the critical symptoms indicate that 

there was a certain progression of symptomatology. 

Occult intracranial injury in infants younger than 12 

months of age is not uncommon.28 Clinical symptoms and 

signs are insensitive indicators of intracranial inju1y in infants.29 Radiologic observations can so1netimes be of litnited 

value as well. 30 Also, slow deterioration following mild head 

injuries in children have been reported. 31 Furthermore) l of 

the most frequently cited articles on restricting the time of 

injury in fatal inflicted head injuries draws its pediatric 

population mainly from motor vehicle accidents, with the 

average age of the study group patients being 8.5 years, with 

a SD of 4.0 yearsn 

Although many studies have offered guidelines for 

determining the age of cerebral injuries, various factors limit 

the reliability of these 1nethods; for example, reduced cerebral blood flow n1ay impede the ceilular response. Not infrequently, injured children survive in the hospital for additional 

2 to 3 days or even longer, sometimes undergoing craniotomy, rendering timing of the injuries based on the autopsy 

findings, including histologic examination of the cerebral 

injuries, extre1nely difficult. 8

-

23 -33-35 

DAI is most likely a rarity in nonaccidental head 

trauma, and the term is misleading. 17•

18'

36 Coma may be more 

of a reflection of the severity of axonal damage in particular 

regions of the brain, most notably the brainstem, rather than 

the total su1n of axonal injury distributed throughout the 

brain. Furthermore, the plane of head rotational acceleration 

plays an important role in determining both the distribution of 

axonal damage and the production of coma.36 The localized 

axonal damage demonstrated in corticospinal tracts in the 

lower brainstem and rostral cervical cord, presumably caused 

by stretch to the neuroaxis produced by cervical hyperextension, may be more significant This finding also provides an 

explanation for the frequent occurrence of apnea at presentation. Tn many of the cases reported by Geddes et al, 18 the 

axonal damage at the craniocervical junction was survivable; 

what was life-threatening was the subsequent hypoxic injury 

© 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 

are peculiar to the brains of young infants, represent localized 

"shearing" between gray and white inatter after an impact and 

should not automatically imply DAL 17 

Cerebral hypoperfusion, followed by hypoxia/ische1nia 

and diffuse brain swelling, characteristic in injured children 

younger than 24 months of age, are key pathophysiological 

findings associated with poor outcome following severe traumatic brain injury. s,37- 39 Primary brain damage occurs at 

impact and appears irrunediately or shortly after injury. Secondary brain injury may be more important, particularly in 

delayed fatalities, and occurs distant to the ilnpact. Secondary 

events may not becon1e apparent until several hours after 

injury. The largest controlled neuropathological study of 

nonaccidental infant head injury showed that axonal damage 

occurred in the brain of both head-injured subjects and in 

controls in the same distribution. This is not DAI but rather 

diffuse vascular or hypoxic-ischc1nic injury due to brain 

swelling and raised intracranial pressure. The study demonstrated that the diffuse brain damage responsible for loss of 

consciousness is a hypoxic secondary reaction and argues 

against DAI. One of the inain conclusions of the study was 

that focal, localized axonal injury and secondary vascularhypoxic changes characterize the mechanism of brain 

death. 18 

In conclusion, we present a case of a seetningly minor 

brain injury in an infant with a symptom-free interval, which 

resulted in delayed, sudden death. The importance of the 

mechanism of injury, location of injury, age of the child, 

and secondary brain injury with special reference to nonaccidental head trauma of childhood, as well as need for 

further research, are discussed. Although this is a rare 

presentation of a traumatic brain injury, based on recent 

advances in traumatic neuropathology, it is conceivable, as 

in this case, that a delayed asymptomatic deterioration to 

death can occur. 

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29. Greenes DS, Schutzman SA. Clinical indicators of intracranial injury in 

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© 2003 Lippincott Williams & Wilkins 
Diagnosis of Traumatic 

Diffuse Axonal Injury 

To the Editor: 

In the December 2003 issue of the 

American Journal of Forensic i\!fedicine 

and Pathology, there was a case report 

written by Drs. Scott Denton and 

Darinka Mileusnic titled "Delayed Sudden Death in an Infant Following an 

Accidental Fall: A Case Report With 

Review of the Literature." This article 

presented a case of delayed. death in a 

9-month-old infant a'i a result of severe 

craniocerebral injuries, which were sustained from an accidental fall in the 

domestic environment. The authors had 

affirmed that there was no evidentiary 

finding of diffuse axonal injury (DAI). 

The scientific validity of this assertion 

remains in doubt since the authors neither mentioned nor perfonned any tissue 

/3-amyloid precursor protein (/3-APP) 

immunohistochemical analyses, given 

our current level of knowledge in the 

diagnosis of severe traumatic brain injury, including DAL 1

- 6 Since the 1980s, 

tissue innnunohistochemistry for /3-APP 

has emerged as the most sensitive methodology and gold standard for the detection, confirmation, and diagnosis of diffuse and focal axonal injuty. With the 

absence of any /3-APP in1n1unohistochemical confirmation of DAI, what the 

authors had referred to as a "laceration" 

of the splenium of the corpus ca1Iosun1 

may actually represent Adan1 's grade Tl 

DAJ7

•

8 since DAI is accentuated in the 

splenium of the corpus callosum.9 In 

Adam's grade I DAI, there is no gross 

evidence of axonal injury; however, 

there is diffuse /3-APP inununopositi vity for axonal injury. In Adam's grade ll 

DAI, there are gross lesions (parenchymal heinorrhages) of the corpus callosun1, in addition to /3-APP tissue immunopositivity. In Adam's grade lII DAI, 

there are gross lesions (parenchymal 

hemorrhages) of the corpus callosum 

and dorsolateral 1nidbrain/pons, in addition to diffuse /3-APP tissue immunopositivity .7•8 

LETTERS TO THE EDITOR 

/3-APP is a single me1nbranespanning protein, which is present in 

membranous structures of the cell such 

as the endoplasmic reticulum, Golgi 

compartment, and the cell 1nembrane, 

encoded by the APP gene localized to 

chroinosome 21. and is ubiquitously expressed in 1nany cell and tissue types, 

including endotheha, glia, and neurons 

of the brain. /3-APP is a resotrrce-rich 

molecule that is involved in diverse normal cell functions, being the center of 

many converging metabolic and regulatory patlnvays, including cell adhesion, 

intercellular signaling, membrane-to-nucleus signaling, cholesterol metabolism, 

gene transcription, axonal transport, and 

neurotrophic and ncttroproliferative activity.1 

In the neuron, /3-APP is synthesized in the perikaryon and transported 

anterogradely and retrogra<le!y in the 

axon by fast/rapid axonal transport ( 100 

to 400 mm/day). In normal, structurally 

intact axons, /3RAPP does not accumulate to a level that allows its detection in 

tissue sections. However, once structural a.xonal injury and damage occur 

and the fast axonal transport is irnpaired, 

J3-APP accun1ulates in the proximal and 

distal axonal seg1nent to a level that 

allows its dctectiun by tissue immunohistochen1istry within l.75 to 3 hours 

following injury. /3-APP has been reported to retnain detectable by tissue 

immunohistochemistry for up to 99 days 

following axonal injury. 1

•

6 

For this specified case report by 

Scott Denton and Darinka Mileusnic, 

/3-APP tissue in1rnunohistochemistry 

that is performed according to the recommended medicolegal protocoJ 10 n1ay 

reveal grades l or II DAL This finding 

tnay additionally and 1nore interestingly 

reaffinn that children who sustain low 

grades of DAI may 1nanifest a delayed, 

symptomatic, or fatal presentation. 

Bennet I. Omalu, MD 

Division of Forensic Neuropathology 

Allegheny County Coroner's Office 

Pittsburgh, Pennsylvania 

REFERENCES 

1. Tun1er PR, O'Connor K, Tate WP, et al. Roles 

ofamyloid pr~cursor protein and its fragments 

in reguloi1ing neurnl activity, plasticity and 

memory. Frog Neurn!Jiol. 2003;10:1-32. 

2. Smith C, Graham DI, Geddes JF, et al. The 

interpretation of Beta-APP immunoreactivity: 

a respons~ to C. Neiss et al., Acta Neuroparhof 

(2002) 104:79. Acla Neuropathol. 2003;106: 

97-98. 

3. Smith DH, Meaney OF, Shull WH. Diffuse 

axonal injury in head trauma. J Head Trauma 

Rehabi!. 2003;18:307-316. 

4. Medana JM, Esiri MM. Axonal damage: a lrny 

predictor of outcome in human CNS diseases. 

Brain. 2003;126:515-530. 

5. Blumbergs PC, Scott G, Manavis J, et al. 

Topography of axona! lnJUry as defined by 

amyloid precursor protein and the s~L:!or scoring method in mild and severe closed head 

injury. J Neurotrauma. 1995;!2:565-572. 

6. McKenzie KJ, McLellan DR, Gentleman SM, 

et al. ls J3-APP a marker \.ifaxonal dan1age in 

short-surviving head injury'! Acta Neuropatho!. !996;92:608-613. 

7. Adams JH, Doyle D, Ford I, et al. Diffuse 

axonal injury in head injury: definition, diagnosis and grading. Ilistopatholo'b'V· l 989; 15: 

49-59. 

8. Ellison D, Love S, Chimelli L, et al. 

Neuropathology: A Reference Text of CNS 

Pathology. Philadt:lphia, PA: Harcourt Publishers Limitcti: 2000. 

9. Lec!erc4 PD, McKenzie JE. Graham DI, et al. 

Axonal injury is accentuated in the caudal 

corpus callosum of head-injured patients. 

J Neurotrauma. 2001;!8:1-9. 

JO. Geddes JF, Whitwell HL, Graham DI. 

Traumatic axona! injury: practical issues for 

diagnosis Ill medicolegal cases. Neuropathof 

Appl Neurobiol. 2000;26: [05-116. 

Response to letter 

From Dr. Omalu 

We thank Dr. Omalu for his comments regarding our recent case report. 1 

Dr. Omalu certainly seems knowledgeable in his review of f3 amyloid precursor protein (/3-APP) and is apparently a 

strong advocate for {3-APP itnmunohistochemistry in cases of head injw-y. Dr. 

Omalu stated that there was no scientific 

validity that diffuse axonal iajmy (DAI) 

\Nas not there in our case. Dr. Omalu 

also asserted that the tear in the corpus 

callosum \Vas an advanced stage of DAL 

We would have expected to see microscopic evidence of DAI on the numer270 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, 

given the tilne interval from the witnessed fall to the child's death. The tear 

of the corpus eallosum was frotn the 

impact fro1n the fall as the corpus callosun1 struck the falx cerebri. We would 

argue the assertion that 13-APP is accepted as the most sensitive methodology and gold standard for detection of 

DAI and the 1nedicolegal protocol referenced in Dr. 01nalu's letter above is not 

accepted as such in our practices. We do 

not perform routine /3-APP testing in 

our offices. 

We respect Dr. 01nalu's advocacy 

for {3-APP testing, although we do not 

feel {3-APP would have changed our 

conclusions or shown hidden DAI. We 

do note that we have received advertisen1ents fro1n Dr. 01nalu and his Forensic 

NeLffopathology Consultation Service 

for performing {3-APP testing. As of 

note, in his advertisen1ent Dr. On1alu 

states that in ht>ad injury deaths it "has 

been established and highly ITcommended that /3-APP immunostaining be 

perfonned in multiple topographically 

targeted regions of the brain" and that 

applications include "tin1ing of injury 

sustenance and determination of tin1e of 

death." We are unaware of this timing of 

injury and death data that would surely 

solve the major critical proble1ns in pediatric head injury deaths. We sincerely 

\vish Dr. Omlllu well in advancing his 

/3-APP research and enterprise. 

Sincerely, 

Scott Denton, MD 

Deputy Medical Examiner 

Cook County Medical Examiners Office 

Assistant Professor of Pathology 

Rush University Medical Center 

Chicago, IL 

Darinka Miluesnic, MD, PhD 

Assistant Chief Medical Examiner 

Knox County Me<lica[ Exan1iners Office 

University ofTenne~see Mec.lical Center 

Knox ville, Tennessee 

REFERENCES 

1. Denton S. Mileusnic D. Delayed sudden death 

in an infant following an ac:cidental fall: a case 

repl1rt with review of the litwature. Am J Forensic J.fed Pathol. 2003;24.371-376. 

The American journal of Forensic Medicine and Pathology • Volume 251 Number 31 September 2004 271 

CopyriQht © Lippincott Williams & Wilkins. Unauthoriz0d rnproduclion of this article is prohibite<L