|
On retinal hemorrhages in general:
"The cause is most likely VENOUS CONGESTION. The fetal head is compressed two
to four times more forcefully than other fetal parts during the second stage
of labor. Retinal hemorrhage is more common in promiparus deliveries and
after forceps or vacuum extraction; it is rare after cesarean section. It may
occur in normal deliveries."



http://www.sciencedaily.com/releases/2006/02/
060226114611.htm
Researchers Say Criterion For Diagnosing Child Abuse Not Always Accurate
ScienceDaily (Feb. 26, 2006) — When it comes to looking for damage to the
eyes to prove child abuse, new research shows that things aren't always as they
seem, according to Patrick Lantz, M.D., a forensic pathologist from Wake Forest
University Baptist Medical Center.
"Contrary to what many doctors have been taught, we found that number and
location of hemorrhages of the eye's retina aren't always proof of child abuse,"
said Lantz, who reported the results today at the 58th annual meeting of the
American Academy of Forensic Sciences in Seattle. "Retinal hemorrhages occur
more often than most doctors think are associated with a wide variety of
conditions."
Lantz found that about 16 percent of the 700 individuals he examined during
autopsy had hemorrhages of the retina, which is light-sensitive nerve tissue at
the back of the eye. The bleeding occurs when tiny blood vessels on the retina's
surface rupture. Lantz found the hemorrhages in individuals who had died from
ruptured aneurysms, falls, car wrecks, gunshot wounds, meningitis and even drug
overdose.
"Our research shows that you see the hemorrhages in a lot of different
situations," Lantz said. "Retinal hemorrhages occur in child abuse, but they
don't always mean a child was abused. Unfortunately, many pathologists,
pediatricians and ophthalmologists have been taught that retinal hemorrhages are
diagnostic of child abuse unless the child was involved in a high-speed car
crash or fell more than two stories."
Currently, when child abuse is suspected, doctors conduct an eye exam to look
for retinal hemorrhages and other eye changes that are considered proof of child
abuse. Lantz got the idea to question this common assumption after he found that
another eye condition, a buckling of the retina, is not always diagnostic for
shaken baby syndrome. He reported those results in the British Medical Journal.
To test his theory that retinal hemorrhages also may not always be indicative of
child abuse, Lantz decided to look for the condition during autopsies to learn
more about when they occur.
Previously, the only way to look for the hemorrhages during an autopsy was to
remove the eyes. Lantz came up with an alternative -- performing eye exams
during autopsies using a surgical headlight and a handheld lens. This simple
technique is sometimes used by ophthalmologists when more sophisticated
equipment is not available, but no one had ever reported using it during
autopsies.
The 700 deaths were in people ranging in age from birth to 96. Causes of death
or conditions associated with retinal hemorrhages included suffocation, sudden
infant death syndrome, meningitis, blunt trauma to the head, ruptured cerebral
aneurysms, hemorrhagic strokes, cancer that had spread to the brain, high blood
pressure, bleeding disorders, diabetes and gunshot wounds to the head.
"Many doctors have been taught to look for the hemorrhages when they suspect
child abuse and often will diagnose child abuse without considering other
possibilities," Lantz said. "Our research shows that you see the hemorrhages in
a variety of different situations in infants, children and adults."
According to medical literature, retinal hemorrhages in infants are rare except
in cases of abuse. "We're finding just the opposite," said Lantz. "We've found
more retinal hemorrhages in non-abuse cases than in abuse cases, but most
doctors don't look in the eyes of children unless they suspect child abuse."
Retinal hemorrhages were found in 30 children under age 14, yet only 6 cases
were associated with child abuse.
As one of the first pathologists to routinely look at the back of the eye during
autopsies, Lantz has learned that the technique can help diagnose hypertension,
glaucoma, Marfan syndrome and even diabetes. He has taught residents and medical
students to conduct the examinations and published an article in the Journal of
Forensic Science (Nov. 2005) on the technique.
Lantz's co-researcher was Constance A. Stanton, M.D., neuropathologist, from
Wake Forest University Baptist Medical Center.
--------------------------------------------------------------------------------
Adapted from materials provided by Wake Forest University Baptist Medical
Center, via EurekAlert!, a service of AAAS.
Need to cite this story in your essay, paper, or report? Use one of the
following formats:
APA
MLA
Wake Forest University Baptist Medical Center (2006, February 26). Researchers
Say Criterion For Diagnosing Child Abuse Not Always Accurate. ScienceDaily.
Retrieved October 24, 2008, from http://www.sciencedaily.com
/releases/2006/02/060226114611.htm

Perimacular retinal folds from childhood
head trauma
BMJ 2004;328:754-756 (27 March),
doi:10.1136/bmj.328.7442.754
P E Lantz, associate professor1, S H
Sinal, professor2, C A Stanton, associate professor1, R G Weaver, Jr,
associate professor3
Department of Pathology, Wake Forest University School of Medicine,
Winston-Salem, NC 27157, USA, 2 Department of Paediatrics, Wake Forest
University School of Medicine, 3 Department of Ophthalmology, Wake Forest
University School of Medicine
No abstract available but in summary it is a
case report of a 14month old child with retinal changes often described as
pathognomonic for NAI, but where the cause was clearly documented to be
accidental (A television fell on the child's head). This publication comes
at a time when the expert medical evidence for child abuse is coming under
increasing scrutiny following the publicity around Roy Meadows cases in the
UK. The Editorial (below) is worth reading if ever you might find yourself in
the witness stand. MIKE
Editorial - The evidence base for
shaken baby syndrome
BMJ 2004;328:719-720 (27 March)
We need to question the diagnostic criteria
The phrase "shaken baby syndrome" evokes a powerful image of abuse, in which
a carer shakes a child sufficiently hard to produce whiplash forces that
result in subdural and retinal bleeding. The theory of shaken baby syndrome
rests on core assumptions: shaking is always intentional and violent; the
injury an infant receives from shaking is invariably severe; and subdural and
retinal bleeding is the result of criminal abuse, unless proved otherwise.1
These beliefs are reinforced by an interpretation of the literature by
medical experts, which may on occasion be instrumental in a carer being
convicted or children being removed from their parents. But what is the
evidence for the theory of shaken baby syndrome?
Retinal haemorrhage is one of the criteria used, and many doctors consider
retinal haemorrhage with specific characteristics pathognomonic of shaking.
However, in this issue Patrick Lantz et al examine that premise (p 754) and
conclude that it "cannot be supported by objective scientific evidence."2
Their study comes hard on the heels of a recently published review of the
literature on shaken baby syndrome from 1966 to 1998, in which Mark Donohoe
found the scientific evidence to support a diagnosis of shaken baby syndrome
to be much less reliable than generally thought.3
Shaken baby syndrome is usually diagnosed on the basis of subdural and
retinal haemorrhages in an infant or young child,1 although the diagnostic
criteria are not uniform, and it is not unusual for the diagnosis to be based
on subdural or retinal haemorrhages alone.w1 The website of the American
Academy of Ophthalmology states that if the retinal haemorrhages have
specific characteristics "shaking injury can be diagnosed with confidence
regardless of other circumstances."4 Having reviewed the evidence base for
the belief that perimacular folds with retinal haemorrhages are diagnostic of
shaking, Lantz et al were able to find only two flawed case-control studies,
much of the published work displaying "an absence of... precise and
reproducible case definition, and interpretations or conclusions that
overstep the data."2 Their conclusions are remarkably similar to those of
Donohoe, who found that "the evidence for shaken baby syndrome appears
analogous to an inverted pyramid, with a very small database (most of it poor
quality original research, retrospective in nature, and without appropriate
control groups) spreading to a broad body of somewhat divergent opinions."3
His work entailed searching the literature, using the term "shaken baby
syndrome" and then assessing the methods of the articles retrieved, using the
tools of evidence based inquiry. Reviewing the studies achieving the highest
quality of evidence rating scores, Donohoe found that "there was inadequate
scientific evidence to come to a firm conclusion on most aspects of
causation, diagnosis, treatment, or any other matters," and identified
"serious data gaps, flaws of logic, inconsistency of case definition."3
The conclusions of Lantz et al and of Donohoe make disturbing reading,
because they reveal major shortcomings in the literature relating to a field
in which the opportunity for scientific experimentation and controlled trials
does not exist, but in which much may rest on interpretation of the medical
evidence.5
If the concept of shaken baby syndrome is scientifically uncertain, we have a
duty to re-examine the validity of other beliefs in the field of infant
injury. The recent literature contains a number of publications that disprove
traditional expert opinion in the field. A study of independently witnessed
low level falls showed that such falls may prove fatal, causing both subdural
and retinal bleeding.6 w2 A biomechanical analysis validates that serious
injury or death from a low level fall is possible and casts doubt on the idea
that shaking can directly cause retinal or subdural haemorrhages.7 w3 An
important lucid interval may be present in an ultimately fatal head injury in
an infant.8 Neuropathological studies have shown that abused infants do not
generally have severe traumatic brain injury and that the structural damage
associated with death may be morphologically mild.9 10 What is the relevance
of the craniocervical injuries to corticospinal tracts, dorsal nerve roots,
and so on that have been described?10 11 We do not know. What is the force
necessary to injure an infant's brain? Again, we do not know.
While most abused children indisputably show the signs of violence, not all
do. No one would be surprised to learn that a fall from a two storey building
or involvement in a high speed road traffic crash can cause retinal and
subdural bleeding, but what is the minimum force required? "It is one thing
clearly to state that a certain quantum of force is necessary to produce a
subdural hematoma; it is quite another to use examples of obviously extreme
force... and then suggest that they constitute the minimum force
necessary."12
Research in the area of injury to infants is difficult. Quality evidence may
need to be based on finite element modelling from data on infants' skulls,
brains, and neck structures, rather than living animals. Any studies on
immature animal models, if performed, will need to be validated against the
known mechanical properties of the human infant. Pending completion of such
studies, the reviews by Lantz and Donohoe are a valuable contribution and
provide a salutary check for anyone wishing to cite the literature in support
of an opinion. Their criticisms of lack of case definition or proper controls
can be levelled at the whole literature on child abuse. If the issues are
much less certain than we have been taught to believe, then to admit
uncertainty sometimes would be appropriate for experts. Doing so may make
prosecution more difficult, but a natural desire to protect children should
not lead anyone to proffer opinions unsupported by good quality science. We
need to reconsider the diagnostic criteria, if not the existence, of shaken
baby syndrome.
J F Geddes, retired (formerly reader in clinical neuropathology, Queen Mary,
University of London)
London (j.f.geddes@doctors.org.uk)
J Plunkett, forensic pathologist

Central Retinal Vein Occlusion
Last Updated: June 26, 2001 |
|
| Synonyms and related keywords:
nonischemic central vein occlusion, partial, incomplete, imminent,
threatened, incipient, impending, perfused, venous statis
retinopathy, ischemic central vein occlusion, complete, hemorrhagic,
nonperfused |
| |
AUTHOR INFORMATION
|
Section 1 of
10
 |
|
| Author:
Lakshmana M Kooragayala, MD, Staff Physician,
Assistant Professor of Ophthalmology, Department of Ophthalmology,
Louisiana State University Health Sciences Center at Shreveport
|
| Lakshmana M Kooragayala, MD, is a member of the following medical
societies: Louisiana State Medical
Society
|
| Editor(s): Vytautas A Pakainis, MD, Chief of
Ophthalmology, Dorn Veterans Administration Medical Center, Professor
of Ophthalmology, Ophthalmology, University of South Carolina School
of Medicine; Donald S Fong, MD, MPH, Assistant
Clinical Professor of Ophthalmology, UCLA School of Medicine;
Consulting Physician, Department of Ophthalmology, Southern
California Permanente Medical Group; Steve Charles, MD,
Director of Charles Retina Institute; Clinical Professor, Department
of Ophthalmology, University of Tennessee College of Medicine;
Lance L Brown, OD, MD, Ophthalmologist, Regional Eye
Center, Affiliated With Freeman Hospital and St John's Hospital,
Joplin, Missouri; and Hampton Roy, Sr, MD, Clinical
Associate Professor, Department of Ophthalmology, University of
Arkansas for Medical Sciences |
| |
INTRODUCTION
|
Section 2 of
10
 |
|
Background:
Central retinal vein occlusion (CRVO) is a common retinal vascular
disorder. Clinically, CRVO presents with variable visual loss; the fundus
may show retinal hemorrhages, dilated tortuous retinal veins, cotton-wool
spots, macular edema, and optic disc edema. In view of the devastating
complications associated with the severe form of CRVO, a number of
classifications were described in the literature. All these
classifications take into account the area of retinal capillary
nonperfusion and development of neovascular complications.
Broadly, CRVO can be divided into 2 clinical types, ischemic and
nonischemic. In addition, a number of patients may have an intermediate
in presentation with variable clinical course. On initial presentation,
it may be difficult to classify a given patient into either category,
since CRVO may change with time.
A number of clinical and ancillary investigative factors are taken
into account for classifying CRVO, including vision at presentation,
presence or absence of relative afferent pupillary defect, extent of
retinal hemorrhages, cotton-wool spots, extent of retinal perfusion by
fluorescein angiography, and electroretinographic changes.
Nonischemic CRVO is the milder form of the disease. It may present
with good vision, few retinal hemorrhages and cotton-wool spots, no
relative afferent pupillary defect, and good perfusion to the retina.
Nonischemic CRVO may resolve fully with good visual outcome or may
progress to the ischemic type.
Ischemic CRVO is the severe form of the disease. CRVO may present
initially as the ischemic type, or it may progress from nonischemic.
Usually, ischemic CRVO presents with severe visual loss, extensive
retinal hemorrhages and cotton-wool spots, presence of relative afferent
pupillary defect, poor perfusion to retina, and presence of severe
electroretinographic changes. In addition, patients may end up with
neovascular glaucoma and a painful blind eye.
Pathophysiology: The exact pathogenesis of the
thrombotic occlusion of the central retinal vein is not known. Various
local and systemic factors play a role in the pathological closure of the
central retinal vein.
Central retinal artery and vein share a common adventitial sheath,
as they exit the optic nerve head and pass through narrow opening in the
lamina cribrosa. Because of this narrow entry in the lamina cribrosa,
vessels are in a tight compartment with limited space for displacement.
This anatomical position predisposes formation of thrombus in the central
retinal vein by various factors, including slowing of blood stream,
changes in the vessel wall, and changes in the blood.
Arteriosclerotic changes in the central retinal artery transforms
the artery into a rigid structure and impinges upon the pliable central
retinal vein, causing hemodynamic disturbances, endothelial damage, and
thrombus formation. This mechanism explains the fact that there will be
an associated arterial disease with CRVO. However, this association has
not been proven consistently, and various authors disagree on this fact.
Thrombotic occlusion of the central retinal vein can occur as a
result of various pathologic insults, including compression of the vein
(mechanical pressure due to structural changes in lamina cribrosa, eg,
glaucomatous cupping, inflammatory swelling in optic nerve, orbital
disorders); hemodynamic disturbances (associated with hyperdynamic or
sluggish circulation); vessel wall changes (eg, vasculitis); and changes
in blood (eg, deficiency of thrombolytic factors, increase in clotting
factors).
Whatever the mechanism of the occlusion of the central retinal
vein, it leads to backup of blood in the retinal venous system and
increased resistance to venous blood flow. This increased resistance
causes stagnation of blood and ischemia of inner retinal layers. It has
been postulated that ischemic damage to the retina produces angiogenesis
factors, which stimulates abnormal vascularization of the posterior and
anterior segment. In addition, increased blood pressure in the venous
system causes break down of inner retinal barrier at the retinal
capillary endothelium, leading to abnormal leakage of fluid in the
retinal layers causing macular edema.
Prognosis of CRVO depends upon reestablishment of patency of the
venous system by recanalization, dissolution of clot, or formation of
optociliary shunt vessels.
Frequency:
 | In the US: CRVO and branch retinal vein
occlusion constitute the second most common retinal vascular disorder.
The nonischemic type is more common than the ischemic type. |
 | Internationally: A large population-based study
in Israel reported a 4-year incidence of retinal vein occlusion of 2.14
cases per 1000 of general population older than 40 years and 5.36 cases
per 1000 of general population older than 64 years.
In Australia, prevalence of vein occlusion ranges from 0.7% in
patients aged 49-60 years to 4.6% in patients older than 80 years. |
Mortality/Morbidity: CRVO is not associated directly
with increased mortality.
 | Nonischemic CRVO may resolve completely without any complications
in about 10% of cases. In about 50% of patients, vision may be 20/200
or worse. One third of patients may progress to the ischemic type,
commonly in the first 6-12 months after presentation. |
 | In more than 90% of patients with ischemic CRVO, final visual
acuity may be 20/200 or worse. Anterior segment neovascularization with
associated neovascular glaucoma develops in more than 60% of cases.
This can happen within a few weeks and up to 1-2 years afterward. |
 | It has been reported that the fellow eye may develop retinal vein
occlusion in about 7% of cases within 2 years. In another report, the
4-year risk of developing second venous occlusion is 2.5% in the same
eye and 11.9% in the fellow eye. Neovascular glaucoma may result in a
painful blind eye. |
Race: CRVO does not have any particular racial
preference.
Sex: CRVO occurs slightly more frequently in males
than in females.
Age: More than 90% of CRVO occurs in patients older
than 50 years, but it has been reported in all age groups.
History: Direct review of
systems toward various systemic and local factors predisposing the CRVO.
 | Significant history includes the following: |
 | Hypertension |
|
 | Diabetes mellitus |
 | Cardiovascular disorders |
|