Childhood Head Injury
A Short Bibliography of Must Read Articles
What follows is a short bibliography of the articles that anyone interested in the field of childhood head trauma must read. There are literally hundreds of articles written on the subject, but these are some of the essentials.
History of the Theories on Shaken Baby Syndrome and Non-accidental Trauma: Accident vs. Abuse
Barnes Patrick D. Ethical Issues in Imaging Nonaccidental Injury: Child Abuse Topics in Magnetic Resonance Imaging 2002. 13(2): 85-94.
Well respected Pediatric Radiologist, Patrick Barnes, questions the effectiveness of dating and timing subdural hematomas by CT and MRIs. The author calls into question some of the historical assumptions surrounding the theory of Shaken Baby Syndrome and dispels some of the radiological myths. He concludes that subdural hematomas and retinal hemorrhages come from rotational decelerational injuries, both accidental and nonaccidental, and that current radiological findings alone cannot tell you the nature or mechanism of injury. The article mentions coagulopathies, metabolic disorders and vaccines as conditions that could contribute to or be misdiagnosed as Shaken Baby Syndrome. Barnes says that MRI (T1 and T2 SE) is the most effective way to identify and date injuries and that CTs are often inadequate to determine the nature or age of fluid collections on the brain, particularly in the presence of an anemia or coagulopathy. The author also spells out the job of an expert witness and the windows for dating subdural hematomas with an MRI.
Caffey J. On the Theory and Practice of Shaking Infants. American Journal of Diseases in Childhood 1972; 124:161-9.
This is the original article discussing what is now called Shaken Baby Syndrome. Caffey says the constellation of injuries found in “shaken-whiplash syndrome” is generally found in conjunction with fractures of the long bones and/or bilateral symmetrical fractures of the arms and legs. Caffey discusses fractures of the bones and joints from whiplash injuries. The article cites cases of whiplash injury from a father swinging an infant over his head. Caffey says injuries can be caused by coughing, overly vigorous burping, “riding the horse,” tossing the baby up in the air, rough roads and flipping a toddler head over heels to his or her feet. Caffey says that CPR can also lead to an increase in venous pressure that causes these types of injuries.
Caffey J. The parent-infant traumatic stress syndrome: (Caffey-Kempe Syndrome), (Battered Baby Syndrome). Amer J Radiol 1972; 114:218-29.
The article was published later the same year altering Caffey’s theory of SBS. This article looked at 12 cases of “SBS” from other articles. Caffey uses anecdotal data from a nurse who confessed to shaking several children in her care. Some of those children showed Caffey’s signs of Shaken Baby Syndrome; some did not. The author goes through the literature on SBS and reviews babies used in other studies to prove his point. This study defines SBS triad as: 1) Retinal hemorrhage 2) Subdural hemorrhage, and 3) Lack of external signs of abuse. Some of the cases Caffey discusses show lucid intervals. Caffey cites that 14% of newborns show signs of retinal hemorrhage.
Caffey J. The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediat 1974; 54:396-403.
In this article, Caffey comes up with yet another rendition of his theory. The author posits that it is the whiplashing of the head onto the thorax that causes traction-stretching stresses and causes SBS. Now Caffey believes Shaken Whiplash Syndrome is characterized by: 1) Bilateral SDH, 2) Bilateral RH and 3) external signs of trauma to the head and neck.
American Academy of Pediatrics. American Academy of Pediatrics: Shaken Baby Syndrome: Rotational Cranial Injuries – Technical Report. Pediatrics 2001; 108(1)
This is the prosecutor’s tutorial on “Shaken Baby Syndrome” (SBS). It gives a brief description of the current dogma surrounding childhood head injuries. The article also gives a list of symptoms/signs to look for in a purported case of “shaken baby syndrome” or nonaccidental head trauma. Also included are some legal citations and tips for prosecutors on how to try these cases.
Donohoe M. Shaken Baby Syndrome and Nonaccidental Injuries: A Review. 1999.
This is an excellent article reviewing the medical theories around the “Shaken Baby Syndrome.” The author takes a thorough look at the five axioms of controversy in SBS cases and the lack of literature and scientific data on the subject. This is a good tutorial on Shaken Baby Syndrome and the evolution of the theory over the years. It is a must read for defense attorneys.
Duhaime A.C, Gennarelli T, Tibualt L.E, Bruce D.A, Margulies S.S, and Wiser R. The Shaken Baby Syndrome: A clinical, pathological, and biomechanical study. Journal of Neurosurgery 1987; 66:409-15.
The authors used a biomechanical model with the parameters of an infant’s head and an accelerometer placed in the model to study shaking vs. impact injuries. The study determined that angular decelerations for shaking were less than that for impact by a factor of 50. The authors found that shaking alone, of an otherwise normal infant, could not cause the degree of injuries generally associated with shaken baby syndrome.
Duhaime AC, Christian CW, Rorke LB, Zimmerman RA. Nonaccidental head injury in infants: The “shaken-baby syndrome”. New Engl J Med 1998; 338:1822-9.
The authors discuss translational vs. rotational forces with regards to nonaccidental head trauma. They analyze the significance of retinal hemorrhages and subdural hematomas and the degree of force needed to inflict the injuries seen in SBS cases. The authors looked at the timing of head injuries through radiological studies and autopsies.
Usinski Ron. Shaken Baby Syndrome: Fundamental Questions. British Journal of Neurosurgery 2002;16(3): 217-219.
The author reviews a history of the “Shaken Baby Syndrome” and highlights the fact that the theory is greatly disputed by medical and biomechanical evidence. The author does a quick tutorial in Newtonian physics and shows that the G Forces required to cause a subdural hematoma cannot be caused by human shaking alone; impact is necessary. The author indicates that prior to 1972, retinal hemorrhages were used in diagnosing increased intracranial pressure or head injury; now, it is said to be diagnostic of SBS. The author says that there is little dispute that chronic subdurals rebleed in adults during membrane formation and argues that there is no data to suggest that children’s brains react any different than adult brains.
Goetting MG, Sowa B. Retinal hemorrhage after cardiopulmonary resuscitation in children: an etiologic reevaluation. Pediatrics 85:585-588, 1990.
Two of every twenty children given CPR showed retinal hemorrhages with no history of trauma or abuse. The cases and mechanism of hemorrhages is discussed.
Greenwald MJ, Weiss A, Oestlerle CS, Friendly DS. Traumatic retinoschisis in battered babies. Ophth 1986; 93:618-25.
Retinal hemorrhages are found in cases with a sudden increase in cranial pressure. This article cites cases of retinal hemorrhages from CPR, swinging the child by the feet and vaginal delivery. The authors say fundus hemorrhages are found in battered babies. Necrosis of the inner layer of blood is said to be responsible for “late” RH. The authors document one case of RH with no SDH but elevated ICP. They theorize that mechanical forces involved in the shaking (lens shifting in vitreous humor) cause retinal hemorrhages; the forces applied to the eyes in shaking make the lens move back and forth within the ocular fluids. Force translates through the lens, vitreous gel and retina to create tugging on the retina and tearing of the blood vessels in the subdural space of the retina, (referred to as vitreous traction of the retina). Editorial comment by Torch says it’s not retinoschisis; it is retinal hemorrhage secondary to increased venous pressure changes. Other processes related to increased ICP include: central retinal vein occlusion, high altitude retinopathy and subarachnoid hemorrhages secondary to aneurysm.
Gutman, F. Evaluation of a Patient with Central Vein Occlusion. American Academy of Ophthalmology 1983; 90(5) 481-3.
This article says central retinal vein occlusion can cause retinal hemorrhages. The author documents all the reasons for central retinal vein occlusion and says blood-clotting disorders, alterations in viscosity of blood and abnormalities in the vein wall can cause increased intracranial pressure which then results in retinal hemorrhages.
Kaur B, & Taylor D. Current Topic: Retinal Hemorrhages. Arch. Dis. Child 1990; 65:1369-72.
This article describes the different types of retinal hemorrhages and their causes. The authors say that neonatal retinal hemorrhages are generally “dot-blot” or flame shaped and located at the posterior or periphery. This article indicates that 1/3 of babies born with occipital presentation have retinal hemorrhages. This incidence is increased with prolonged labor or obstetric procedures, and decreased with c-sections and breech presentations. Retinal hemorrhages are also more common in mothers with toxemia. With subarachnoid bleeding, there may be an increase in intracranial pressure, optic nerve sheath hemorrhage and an increase in the pressure within the optic nerve sheath because of raised central retinal venous pressure. Retinal hemorrhages occur 20-32% of the time with SAH: they occur simultaneously or within a few days. Streak and pre-retinal hemorrhages occur mainly around the optic disc. Pre-retinal hemorrhages may leak into the vitreous (Terson’s Syndrome). Retinal and pre-retinal hemorrhages are consistently seen in infants with SDH. Superficial retinal hemorrhages can occur from sneezing, crying, or squeezing of the chest (valsalva’s hemorrhagic retinopathy). Hemorrhages into all layers of the retina may be more common in nonaccidental trauma. This article also cites vomiting, epileptic seizures, crying, chest compressions and coughing spells as causes of retinal hemorrhages.
Kirschner R H, and Stein R J. The Mistaken Diagnosis of Child Abuse. American Journal of Diseases in Childhood 1985; 139:873-5.
The article reports a case of retinal hemorrhages after vigorous chest compressions on a 3-month-old infant. The article looks at differentiating diagnosis of abuse from coagulopathies, CPR, TCP, SIDS, meningitis, etc. The authors say mistaken diagnosis often occurs when a child dies with no explanation for his/her injuries and those injuries are consequently cited as indicators of abuse. The authors list other disease processes that mimic abuse.
Lantz, P E; Sinal, S H; Stanton, C A; Weaver, R G Jr. Perimacular retinal folds from childhood head trauma. British Medical Journal 2004; 328(27)
This is an evidence-based case report. It gives an account of a child who presented with extensive head injuries caused by a television falling on his head. The child deteriorated and died within 18 hours. Because the child had retinal hemorrhaging and retinal folds, CPS removed the other child from the home. Lantz et al. explain that “An evidence based analysis of indexed medical publications on shaken baby syndrome from 1966-1998 uncovered a weak scientific evidence base.” Lantz et al. conclude in saying that “Until good evidence is available, we urge caution in interpreting eye findings out of context.”
Tongue Andrea. The Ophthalmologists’ Role in Diagnosing Child Abuse. Ophthalmology 1991; 98(7): 1009-10.
The author indicates that retinal hemorrhages predominantly occur in children with central nervous system injuries. She says that although it is possible that certain types of hemorrhages are signs of Shaken Baby Syndrome, there is no evidence to date that establishes that any type of retinal hemorrhage was pathognomonic for nonaccidental trauma. Tongue recognizes that retinal hemorrhages are found in scenarios that do not include child abuse. They are seen in newborns, in infants after cataract surgery, in infants undergoing extra corporeal membrane oxygenation therapy, in infants with subdural or subarachnoid hemorrhages secondary to accidental trauma, and with bleeding byforasias and hemoglobinopathies. The author says nonaccidental trauma associated with retinal hemorrhage is most often found in children under the age of two, but there is no research out there to back up the pathology. The author says there is no proof that retinal folds are indicative of vitreous traction mechanisms or child abuse.
Plunkett. Fatal pediatric head injuries caused by short distance falls. American Journal of Forensic Medicine and Pathology 2001; 22:1-12.
This study analyzed the Consumer Product Safety Commission’s database on playground equipment falls between January 1988 and June 1999. Thirteen children had subdural hematomas, and twelve had lucid intervals ranging from five minutes to forty-eight hours. Four of the six children that had funduscope examinations had retinal hemorrhages. The study proves that short falls can kill children and retinal hemorrhages are not diagnostic of abuse. The study also calls into question our ability to time injuries and contradicts the theory that decomposition begins immediately after the SDH is formed.
Plunkett J. Biomechanical analysis of a fatal pediatric head injury caused by a short-distance fall. National Association of Medical Examiners 2000.
Abstract presented to the National Association of Medical Examiners on the death of a twenty-three-month old infant after a fall from the standing height of twenty-eight inches. The case documents a lucid interval and a gradual decline with vomiting and stupor. The incident was captured on video and has been used as documentation of a short fall death on a previously healthy toddler. (Accompanying the article are emails and listserve correspondences regarding the article.)
Howard M, Bell B.A, and Uttley D. The pathophysiology of infant subdural hematomas. British Journal of Neurosurgery 1993; 7: 355-6.
The authors did a retrospective review of 28 babies with SDH over a 20-year period (>18 months; N=18 boys and 10 girls). The study sample included 17 white, 10 nonwhite babies and 1 mixed race baby. Non-Caucasians with a head injury were more likely to have SDH than whites (67% v. 21%). Short falls (including high chairs) were often the cause of injury. 11 infants went unconscious immediately following the traumatic head injury, and 10 infants were observed having breathing difficulties. Babies were observed to experience vomiting (50%) and irritability (25%). Seizures were more common in non-whites (90%) than whites (41%). This article discusses 3 infants with chronic SDH that were not thought to be abused. All three had minor impact more than a week prior to their hospital admission. One other case presented with a CSDH and questionable circumstances. There was an absence of impact site in 29% of Caucasians and 80% of non-whites. 11/20 of the infants that had funduscope examinations had retinal hemorrhages: 9 were normal, 6 (33%) of white infants had evidence of extra cranial injuries; none of the non-whites had those signs. This is a great article for cases involving babies of color.
Reiber G. Fatal falls in childhood. The American Journal of Forensic Medicine and Pathology 1993; 14(3):201-7.
This article documents 3 cases of deaths from corroborated/witnessed short falls (10-20 feet). The author states that all three children had SDH and fractures. 2 of 3 children had lucid intervals and all 3 children died after a delayed period following the fall. 2 of 3 children showed periorbital echymosis. One child suffered a SDH and severe brain swelling from a 6-foot fall onto a carpeted floor. 1 child fell 2-3 feet from a rocking chair.
Chronic SDH and Rebleeds
Parent A.D. Pediatric chronic subdural hematoma: a retrospective comparative analysis. Pediatric Neurosurgery 1992; 18:266-71.
The author reviewed the literature on chronic subdural hematomas. Study looked at 28 children less than 18 months old, over two decades. Most of the children in the data set were less than 4 months old. Males were overly represented in both the first (78%) and second (60%) decade of study. Kids in both samples tended to present with macrocephaly, lethargy, failure to feed, apnea and seizures. Some children in the more recent sample, presented with headaches only, or no symptoms at all. Fractures were rarely seen with subdural hematomas in either sample. Mortality rates in the 1970s study were around 50%, whereas in the 1980s they were closer to 10%; Seizures increased from 40% to 46%, but psychomotor retardation reduced from 33% to 28%. The authors attributed 40% of subdurals in infants to child abuse. Birth traumas and rebleeds comprised a small percentage of the subdural bleeds. Parent discusses the evolution of a SDH and the tendency of those with them to develop hydrocephalus over time. The author also discusses ischemia secondary to chronic subdural hematoma because of impaired cerebral blood flow. The study found that craniotomies were rare as a course of treatment in modern times but were very popular in the 1980s. He cites the increased tendency in infants to bleed or to develop new subdurals after a membranectomy or craniotomy. Modern courses of treatment generally involve subdural taps or subdural peritoneal shunts. The author indicates that the histopathology of CSDH in children is the same as that in adults in that they tend to wax and wane and rebleed. He says that capillary fragility was the major cause of repeated hemorrhage in CSDH.
Piatt J. A pitfall in the Diagnosis of Child Abuse: External Hydrocephalus, Subdural Hematoma & Retinal Hemorrhages. Neurosurgical Focus 1999; 7(4)(4):1-9.
The author describes a child who developed SDH and retinal hemorrhage from external hydrocephalus (previously referred to as benign subdural effusions of infancy). Author discusses how conditions such as external hydrocephalus, internal hydrocephalus, an arachnoid cyst or a chronic subdural hematoma, can cause subdural hematomas from minor head injuries. The author says that development of a subdural hematoma after minor head trauma in an infant with craniocerebral disproportion might be the occasion for unjustified accusations of abuse. The existence of retinal hemorrhages in this case adds to the literature supporting the argument that retinal hemorrhages are caused by a sudden increase in ICP rather than abuse. Great article for rebleeds, hydrocephalus, retinal hemorrhages, etc.
Sherwood D. Chronic subdural hematoma in infants. Am J Dis Child 1930; 39:980.
This is a remarkable article that clearly shows that infants do get chronic subdurals that do “rebleed”…quotes articles from 1890s and early 1900s about chronic subdural patients WITH retinal hemorrhages. The issue of abuse is raised.
Swift, Dale M. Chronic Subdural Hematomas in Children. Journal of Chronic Subdural Hematomas 2000; July 11(3).
The author reviews the data on intracranial fluid collections. He says there are three ways to generate subdural fluid collections. 1) recurrent bleeding of the chronic subdural hematoma in the subdural space; 2) an opening in the subarachnoid allows the CSF to enter the subdural space. (This can occur after shunt placement in hydrocephalic or macrocephalic babies. The CSF then mixes with blood and results in a thin xanthochromic fluid, sometimes called subdural hygromas), and 3) response to an infection or process. Subdural empyemas can result from sinitis or otitis media, into the epidural space, and then into the subdural space. Purulent subdural collections are sometimes seen after bacterial meningitis, especially those due to hemophilia influenza. Bacterial cultures may or may not show organisms because the patient is usually started on antibiotics before the tests are completed. Fluid can also accumulate around the brain after destructive disease processes such as hypoxia. These rarely cause symptoms. The most common cause of subdural hematomas is trauma, but underlying tissue may predispose a baby to subdural bleeding with minor trauma. The author says that frequently the symptoms go unnoticed and without medical attention. Causes can be accidental or nonaccidental, and nonaccidental is the most common cause for children less than two years of age. The author says coagulopathy can underlie subdural bleeding or abnormalities in intracranial structure. The author indicates that the degree of trauma needed to produce injury in children with fluid collections in their brain is less than the normal infant population, and that childbirth can cause chronic subdural hematomas. The author indicates that the age of the infants is correlated with the presentation of subdural hematomas. Infants can present acutely with apnea or seizures, or more protracted, with a history of lethargy, vomiting, and a failure to feed. Older children present usually within two weeks after trauma with symptoms of headaches and advanced intracranial pressure. Chronic subdural hematomas tend to occur unilaterally in older children and bilaterally in younger children. The author indicates treatment has moved away from craniotomies and membranectomies to subdural shunts and burr holes.
Lucid Intervals/Asymptomatic SDH
Dacey R.G, Alves W, Rimel R, Winn R, and Jane J. Neurosurgical complications after apparently minor head injury. Neurosurgery 1986; 65:203-10.
The authors studied 610 patients at a Washington trauma center. Of 66 patients with skull fractures, 5 had intracranial hematomas, 13 had some type of neurosurgical complications. Neurological complications and lucid intervals were more likely to be found in boys than girls, and were more likely to occur in a fall rather than by some other mechanism. The increased ICP is found after about 50% of severe head injuries. Skull fractures increase likelihood of neurosurgical procedures. This article documents the existence of lucid intervals. The authors found that 3% of minor head injury cases will deteriorate after experiencing a lucid interval.
Jenny C, Hymel KP, Ritzen A, Reinert SE, Hay T. Analysis of missed cases of abusive head trauma. Journal of the American Medical Association 1999; 281(7):621-626.
Interesting article that analyzes missed diagnosis of abusive head trauma, but in so doing, documents the fact that many head injuries go unnoticed only to result in further complications at a later date. This factor provides proof for the existence of a lucid interval and complicates prosecutors’ theories that the last person holding the baby was to blame. In this study 40% of the cases of head trauma resulted in complications from original injuries. The article sites the signs of pre-existing injuries. These conditions included seizure disorders, chronic vomiting and increasing head size because of increasing untreated subdural hematomas.”
Greenes D, Schultzman S.A. Occult intracranial injury in infants. Annals of Emergency Medicine 1998; 32(6):680-6.
The study looked at infants admitted to the emergency room of Children’s Hospital Harvard (over a 6.5 year period). Occult (asymptomatic) injuries (i.e. lucid intervals) were seen in fourteen of the 52 infants (27%) under the age of 6 months, 5 of 34 babies (15%) 6 months to a year and in none of the infants over one year old. 95% of the children had scalp contusions or hematomas, and 95% had fractures. None of the infants with occult injuries required medical assistance such as surgery, etc. to manage increased intracranial pressure.
Nahelsky M, and Dix J. The time interval between lethal infant shaking and onset of symptoms: A review of the Shaken Baby Syndrome Literature. The American Journal of Forensic Medicine and Pathology 1995; 16(2):154-157.
The authors agree with the Bruce-Zimmerman and Duhaime who say you must have impact to create damages like those seen in SBS. This article discusses three cases of “shaking” injury where children experienced lucid intervals of 3 hours, 3 days and 4 days. The last child had bilateral retinal hemorrhages. The article concludes that there is very little data available to suggest the actual time limits between fatal head injuries and death. This article shows that lucid intervals do exist and that perpetrators cannot be narrowed down to the last person holding the baby.