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JOURNAL OF MEDICAL
CASE REPORTS
Editor-in-Chief: Michael Kidd
Case report of the year 2010
Statin-associated weakness in myasthenia gravis: a case report
Michael J Keogh , John M Findlay , Simon Leach and John Bowen
Most accessed article of the year
Atrial fibrillation in healthy adolescents after highly caffeinated beverage
consumption: two case reports
Jennifer R Di Rocco, Adelaide During, Peter J Morelli, Marybeth Heyden and Thomas A Biancaniello
Visual recovery in a patient with total hyphema, neovascular glaucoma, long-standing
retinal detachment and no light perception vision: a case report
Olusola Olawoye, Christopher C Teng, Uri Shabto, Jeffrey M Liebmann, Francis A L’Esperance and Robert Ritch
Car sunshade-induced craniofacial injury: a case report
Mahdi Sharif-Alhoseini, Hadi Khatibi, Mojtaba Chardoli and Vafa Rahimi-Movaghar
Using an Ishikawa diagram as a tool to assist memory and retrieval of relevant medical
cases from the medical literature
Kam Cheong Wong
JOURNAL OF MEDICAL
CASE REPORTS
JOURNAL OF MEDICAL
CASE REPORTS
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Editor-in-Chief
Professor Michael Kidd AM
Flinders University, Australia
“In the era of evidence-based practice, we need practice-based evidence. The basis of
this evidence is the detailed information from the case reports of individual people
which informs both our clinical research and our daily clinical care. Each case report
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Professor Michael Kidd AM is the Executive Dean of the Faculty of Health Sciences
at Flinders University in Australia, past president of the Royal Australian College of
General Practitioners and president-elect of the World Organization of Family Doctors
(WONCA). He is the founder and Editor-in-Chief of the Journal of Medical Case Reports, the world’s
first journal devoted to case reports from all medical disciplines.
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Dr Elie Dib Professor Christian Koch Dr Richard Rison Dr Jean Karl Soler Dr Geoff Wong Sanford School of Medicine, USA
University of Mississippi Medical Center, USA
Neurology Consultants Medical Group, USA
The Family Practice, Malta
University College London, UK
JOURNAL OF MEDICAL
Case Report of the Year 2010
CASE REPORTS
CASE REPORT
Open Access
Statin-associated weakness in myasthenia gravis:
a case report
Michael J Keogh*, John M Findlay, Simon Leach, John Bowen
Abstract
Introduction: Myasthenia gravis is a commonly undiagnosed condition in the elderly. Statin medications can
cause weakness and are linked to the development and deterioration of several autoimmune conditions, including
myasthenia gravis.
Case presentation: We report the case of a 60-year-old Caucasian man who presented with acute onset of
dysarthria and dysphagia initially attributed to a brain stem stroke. Oculobulbar and limb weakness progressed
until myasthenia gravis was diagnosed and treated, and until statin therapy was finally withdrawn.
Conclusion: Myasthenia gravis may be underappreciated as a cause of acute bulbar weakness among the elderly.
Statin therapy appeared to have contributed to the weakness in our patient who was diagnosed with myasthenia
gravis.
Introduction
Myasthenia gravis (MG) is characterised by fatigable
muscle weakness and has an incidence of only 1 in 5 to
10,000 people [1]. Autoimmune myasthenia gravis, often
in association with thymus hyperplasia or thymoma, can
affect young adults. However, it is now recognized that
myasthenia gravis is actually more prevalent in middleaged and older groups than younger age groups [2]. In
elderly patients, bulbar presentation is common [3] and
often mislabeled as a stroke [4] leading to poorer rates
of survival [5].
Statins (inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA
reductase) lower the incidence of cerebrovascular disease and coronary heart disease. Statin use has increased
dramatically over the last decade, with a four-fold
increase from 1996 to 1998 [6].
Although generally well-tolerated, statins may have
primary care discontinuation rates of up to 30% [7] due
to their side effects such as headache, myalgia, paraesthesia, and abdominal discomfort.
Here, we report a case of acute myasthenia gravis presenting in a 60-year-old Caucasian man whose condition
deteriorated until immunosuppressive therapy was commenced and statin therapy was withdrawn.
* Correspondence: [email protected]
Department of Stroke Medicine, United Lincolnshire Hospitals Trust, Lincoln
County Hospital, Lincoln, LN2 5QY, UK
Case presentation
A 60-year-old Caucasian man of British origin was
admitted to our hospital in September 2007 following
acute onset of dysarthria and dysphagia. He was diagnosed with diabetes mellitus and hyperlipidaemia three
months prior to presentation.
He had no visual disturbance or sensorimotor symptoms in his limbs or torso on presentation. He was commenced on gliclazide, ramipril and aspirin when he was
diagnosed with diabetes and hyperlipidemia 3 months
earlier. He was also started on simvastatin at that time,
but this was stopped following the development of proximal muscle weakness, myalgia, and an elevated creatine
kinase (CK) of 2599 (normal: <200), which all resolved
upon the termination of this medication. Gliclazide,
ramipril and aspirin, however, were continued.
Aside from the finding of mild dysarthria, examination
revealed that our patient had no remarkable conditions.
Results of routine haematology, biochemistry, thyroid
function tests, and creatine kinase were also unremarkable. His serum cholesterol was 6.1 mmol/L and his random blood glucose was 11.2 mmol/L.
An initial diagnosis of a brain stem stroke was considered, so dipyridamole and atorvastatin were added to his
medication four days after his admission to our hospital.
Meanwhile, a computed tomography (CT) brain scan
showed that he had no obvious infarct.
© 2010 Keogh et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
Keogh et al. Journal of Medical Case Reports 2010, 4:61
http://www.jmedicalcasereports.com/content/4/1/61
Our patient remained stable over the next few days
with a mild dysarthria and dysphagia (tolerating soft
food), but no other symptoms or signs were noted.
One week after his admission to our hospital, his dysarthria and dysphagia worsened. Bilateral fatigable ptosis, diplopia, fatigable weakness of his neck flexion, and
shoulder abduction were noted for the first time. A previously planned cranial magnetic resonance brain scan
was thus cancelled.
Edrophonium testing demonstrated a dramatic transient improvement in his dysarthria, and a diagnosis of
myasthenia gravis with high titre anti-acetylcholine
receptor antibodies was confirmed. A serum immunoglobulin assay revealed an IgA level of <0.05 g/L. He
was noted to have normal IgG and IgM, and no paraprotein band.
Our patient was then commenced on treatment with
pyridostigmine. He was also started on incrementally
increasing prednisolone every other day. Regular monitoring of his respiratory function was also initiated.
His respiratory function worsened over the next 3
days. His spirometry also deteriorated. He developed a
new fatigable diplopia and an inability to stand from a
low squat position, together with increasing neck and
proximal limb weakness.
In view of his deteriorating state, intravenous immunoglobulin therapy (IVIg) was commenced. Following
immunological advice regarding his low IgA titre, it was
decided to use Vigam Immunoglobulin (2 g/kg over the
next 4 days), which did not result in any adverse effect.
No objective gains were noted over the subsequent
week, and a repeat CK yielded a result of 842 mmol/L.
His atorvastatin medication was then stopped two weeks
after it had been introduced. Following this, our patient
showed significant improvement in ptosis, a resolution
of diplopia, and improved neck, shoulder, and elbow
power. His ability to stand from a low squat position
returned, and significant spirometric improvements
were also seen.
His CK readings fell over this period and returned to
normal levels one week after the cessation of his statin
medication (Figure 1).
Our patient remained stable until two weeks later
when, just prior to a planned discharge, a further deterioration and unresponsiveness to a second course of
IVIg necessitated respiratory and nutritional support,
intensive care, and plasma exchange.
Following prolonged treatment, his muscle strength
improved and he returned to independent living at
home four months after his admission to our hospital.
His gastrostomy feeding tube and tracheostomy were
removed 10 months after he was discharged from our
hospital.
Discussion
Myasthenia gravis has an incidence of only 1 in every 5
to 10,000 people and is potentially fatal. A recent study
suggests that 2.2% of patients admitted with myasthenia
gravis overall died during admission [8], and that the
risk could be reduced by 69% if the patient is under the
care of a neurologist. It is thus important not to readily
dismiss the condition and that appropriate referrals are
made.
The actual incidence of statin-exacerbated myasthenia
is unknown, and only a handful of reports of statinassociated myasthenia gravis have ever been described
[9-11].
Out of 6 published case reports, only 5 patients were
noted to have some degree of recovery and only one
patient had a complete recovery upon termination of
statin therapy [11].
How statins could appear to exacerbate MG is
unclear. It is possible that the mechanism actually
reflects a “double hit” phenomenon of defective neuromuscular transmission secondary to antibody-mediated
post-synaptic acetylcholine receptor dysfunction in combination with a statin-induced myopathy.
The clear development of a statin myopathy with simvastatin treatment prior to the onset of myasthenia in
our patient is consistent with the possibility of a second
(atorvastatin- induced) myopathy coalescing with the
onset of myasthenia gravis. The symptomatic improvement that followed his withdrawal from atorvastatin
treatment resulted from the resolution of this statin
myopathy.
We also considered other potential causes of deterioration such as sepsis, steroid-induced worsening of
MG, steroid myopathy, and cholinergic crisis, but we
considered their development less likely based on clinical grounds.
We cannot rule out completely the possibility that the
worsening of our patient’s MG simply reflected a progression of his MG. However, the clinical course of his
condition, as well as the statin-induced proximal limb
pain and weakness (without bulbar features) he experienced prior to his presentation, raises at the very least
the possibility that a component of his initial deterioration was statin-related.
Similarly, we note that his improvement could have
reflected the immunosuppressive effects of therapy for
his MG rather than the withdrawal of his atorvastatin
treatment. It seems probable, however, that both factors
played a significant role in the improvement of his clinical state.
The development of other autoimmune disorders such
as dermatomyositis [12], polymyalgia rheumatica, vasculitis [13], and Lupus-like syndrome [14] upon initiation
Keogh et al. Journal of Medical Case Reports 2010, 4:61
http://www.jmedicalcasereports.com/content/4/1/61
Figure 1 This image of a graph shows creatinine kinase readings during admission, and a correlation to clinical progress.
of statin therapy [13] raises the possibility that in predisposed individuals, statins may precipitate an immunological trigger that is analogous to penicillamine-induced
MG [15] although clearly different in temporal respect.
However, given the paucity of reports and the widespread use of statins, the possibility of chance association cannot be excluded still.
Conclusion
Myasthenia gravis is a potentially fatal condition that
should be considered in elderly patients with bulbar
symptoms. Statin medication should be introduced cautiously and considered as a potential cause or precipitant of worsening muscle strength in patients with
myasthenia gravis.
Consent
Written informed consent was obtained from the
patient for publication of this case report and any
accompanying images. A copy of the written consent is
available for review by the Editor-in-Chief of this
journal.
Abbreviations
CK: creatinine kinase; CT: computed tomography; IVIg: intravenous
immunoglobulins; MG: myasthenia gravis.
Acknowledgements
None
Authors’ contributions
MJK reviewed the patient’s clinical data, performed the literature search, and
wrote the initial draft of the manuscript. JMF, SL and JB reviewed the initial
draft and finalized the manuscript. All authors read and approved the final
manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 29 January 2008
Accepted: 20 February 2010 Published: 20 February 2010
References
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3. Vincent A, Clover L, Buckley V, Evans JG, Rothwell PM: Evidence of
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9. Prvin A, Kawasaki A, Smith K, Kestler A: Statin-associated myasthenia
gravis: report of 4 cases and review of the literature. Medicine (Baltimore)
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10. Cartwright M, Jeffery D, Nuss G, Donofrio P: Statin-associated exacerbation
of myasthenia gravis. Neurology 2004, 63:2188.
11. Parmar B, Francis P, Ragge N: Statins, fibrates and ocular myasthenia.
Lancet 2002, 360:717.
12. Khattak FH, Morris IM, Branford WA: Simvastatin-associated
dermatomyositis. Br J Rheumatology 1994, 33:199.
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literature. Medicine 1998, 77:378-383.
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doi:10.1186/1752-1947-4-61
Cite this article as: Keogh et al.: Statin-associated weakness in
myasthenia gravis: a case report. Journal of Medical Case Reports 2010
4:61.
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Most accessed article of the year
CASE REPORT
JOURNAL OF MEDICAL
CASE REPORTS
Open Access
Atrial fibrillation in healthy adolescents after
highly caffeinated beverage consumption:
two case reports
Jennifer R Di Rocco1, Adelaide During2, Peter J Morelli3*, Marybeth Heyden3, Thomas A Biancaniello3
Abstract
Introduction: Energy drinks and highly caffeinated drinks comprise some of the fastest growing products of the
beverage industry, often targeting teenagers and young adults. Cardiac arrhythmias in children related to high
caffeine consumption have not been well described in the literature. This case series describes the possible
association between the consumption of highly caffeinated drinks and the subsequent development of atrial
fibrillation in the adolescent population.
Case presentations: We report the cases of two Caucasian adolescent boys of 14 and 16 years of age at the time
of presentation, each without a significant cardiac history, who presented with palpitations or vague chest
discomfort or both after a recent history of excessive caffeine consumption. Both were found to have atrial
fibrillation on electrocardiogram; one patient required digoxin to restore a normal sinus rhythm, and the other
self-converted after intravenous fluid administration.
Conclusion: With the increasing popularity of energy drinks in the pediatric and adolescent population, physicians
should be aware of the arrhythmogenic potential associated with highly caffeinated beverage consumption. It is
important for pediatricians to understand the lack of regulation in the caffeine content and other ingredients of
these high-energy beverages and their complications so that parents and children can be educated about the risk
of cardiac arrhythmias with excessive energy drink consumption.
Introduction
Atrial fibrillation is extremely rare in the pediatric population, almost always occurring in association with structural heart disease, such as rheumatic mitral valve
disease, congenital heart disease with dilated atria, and
rarely, as a complication of intra-atrial surgery [1].
Patients may present with palpitations, dyspnea, fatigue,
light-headedness, or syncope. The electrocardiogram is
characterized by disorganized atrial activity without discrete P waves. The ventricular response is often irregularly irregular. Without a prior cardiac or family history,
other inciting causes such as thyrotoxicosis, infectious
pericarditis, and pulmonary emboli should be considered
in the previously healthy child presenting with newonset atrial fibrillation [2].
* Correspondence: [email protected]
3
Stony Brook University Department of Pediatric Cardiology, HSC T-11, 040,
Stony Brook, NY, 11794-8111, USA
Full list of author information is available at the end of the article
Exogenous causes of atrial fibrillation through a substrate such as caffeine have not been widely reported in
the literature, especially in the pediatric population.
A large-scale Danish study evaluating adult human caffeine consumption and arrhythmias did not find a
higher risk of atrial fibrillation or flutter with variable
oral consumption of caffeine from everyday sources [3].
A controlled trial of escalating doses of caffeine in dogs
surprisingly found that serum caffeine actually decreased
the propensity for atrial fibrillation [4]; another canine
trial demonstrated an increase in cardiac arrhythmias
with high doses of caffeine administered [5]. A recent
case report outlined a correlation between prolonged
inhaled salbutamol and concurrent chocolate abuse,
leading to an atrial arrhythmia in an adult, postulating
that the caffeine in the chocolate coupled with the
short-acting beta agonist triggered the arrhythmia [6].
Another case report described a 58-year-old man with
atrial fibrillation and a dilated cardiomyopathy, which
© 2011 Di Rocco et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Di Rocco et al. Journal of Medical Case Reports 2011, 5:18
http://www.jmedicalcasereports.com/content/5/1/18
resolved when he discontinued his excessive caffeine
consumption [7].
Caffeine is a natural stimulant found in tea leaves, coffee beans, and cacao, and is one of the most popular
psychoactive substances used today. Caffeine causes central and peripheral nervous system stimulation through
antagonism of adenosine receptors and also has dopaminergic properties, which lend to its addictive potential
[8]. The half-life of caffeine in a normal healthy adult is
estimated to be from 2.5 to 10 hours, depending on the
individual. Long-term consumption of caffeine or consumption of large amounts of caffeine will prolong its
half-life [9,10]. The US Food and Drug Administration
deems, “caffeine is generally recognized as safe when
used in cola-type beverages up to a level of 0.02 percent” [11]. The population as a whole has variable sensitivity to the stimulant effects of caffeine; one’s tolerance
and dependence on caffeine seem to be somewhat heritable and may be linked to genetic polymorphisms [8].
The physiologic and psychological effects of caffeine
have been studied in adults but have not been systematically analyzed in children [8].
Energy drinks and highly caffeinated drinks comprise
some of the fastest-growing products of the beverage
industry, often targeting teenagers and young adults
[8,12]. This case series describes the possible association
between the consumption of highly caffeinated drinks
and the development of cardiac arrhythmias, specifically
atrial fibrillation, in the adolescent population. We
report two cases of atrial fibrillation in healthy adolescent boys after the consumption of energy drinks.
Case presentation
Case 1
A 14-year-old Caucasian boy with no significant past
medical history presented with persistent “heart fluttering” two hours after a running race. He denied recent
illness and denied drug ingestion, but reported drinking
an unknown quantity of a highly caffeinated drink the
day before. He also reported drinking a Red Bull™
energy drink five days before admission and feeling the
same fluttering sensation. His physical examination
revealed an irregularly irregular heart rate at approximately 130 beats per minute with a 1/6 vibratory systolic ejection murmur at the left lower sternal border.
Thyroid-function tests and serum calcium were normal.
His electrocardiogram (ECG) showed narrow-complex
tachycardia with atrial fibrillation and occasional atrial
flutter (Figure 1). Cardiac ECG revealed a structurally
normal heart without thrombus. He was treated with
one dose of digoxin as a partial load at 7.5 μg/kg and
quickly converted to normal sinus rhythm with a heart
rate of 70 to 80 beats per minute (Figure 2). On followup examination in cardiology clinic one month later, the
patient had a normal cardiac examination, a normal
ECG, and no further symptoms of arrhythmia.
Figure 1 Electrocardiogram showing narrow-complex tachycardia with atrial fibrillation and occasional atrial flutter with irregularly
irregular ventricular response. Heart rate, 122 beats per minute; QRS, 88 ms; QTc, 433 ms.
Di Rocco et al. Journal of Medical Case Reports 2011, 5:18
http://www.jmedicalcasereports.com/content/5/1/18
Figure 2 ECG showing normal sinus rhythm restored to 65 beats per minute after a dose of digoxin. PR interval, 129 ms; QRS, 100 ms;
QTc, 398 ms.
Case 2
A 16-year-old Caucasian boy with a history of attention-deficit hyperactivity disorder, asthma, and allergies
presented to the emergency department with intoxication and vomiting after falling and sustaining minor
head trauma. He had ingested an unknown quantity of
Red Bull™ mixed with vodka at a party. He denied
chest pain, syncope, palpitations, shortness of breath,
and fever. His home medications included amphetamine and dextroamphetamine (Adderall XL), 30 mg
daily; montelucast (Singulair), 10 mg daily; loratadine
(Claritin), 10 mg daily; and doxycycline, 100 mg daily
for acne. Physical examination revealed an irregularly
irregular heartbeat at 160 beats per minute with no
murmurs. ECG showed chaotic atrial tachycardia/atrial
fibrillation with rapid ventricular response (Figure 3).
Blood ethanol level was 155 mg/dl. Cardiac enzymes
were unremarkable, and serum electrolytes, thyroidfunction tests, and a lipid profile were normal. A cardiac ECG revealed a structurally normal heart without
thrombus. Computed tomography of his brain was
normal. The patient was given a bolus of 2 L of normal saline, and his heart rate responded by decreasing
from 160 beats per minute to 90 to 110 beats per minute. He remained hemodynamically stable and was
placed on a cardiac monitor overnight with continued
intravenous fluid support. Approximately 12 hours
after presentation, he spontaneously reverted to a
normal sinus rhythm (Figure 4). He remained asymptomatic with a normal sinus rhythm during subsequent
cardiology follow-up the next week.
Of note, the Division of Pediatric Cardiology at the
Stony Brook University Medical Center has cared for
two other cases of atrial fibrillation in healthy adolescents after excessive caffeine consumption in the past
five years. These cases were not included in this series,
as the patients were unable to be located to provide
their consent.
Discussion
Soft drinks containing caffeine are the major source of
caffeine intake in children and adolescents, and their
caffeine consumption has risen exponentially in the last
30 years [8]. The fastest-growing trend is toward highly
caffeinated beverages known as “energy drinks,” which
differ from “sports drinks” such as Gatorade™. The general public is unlikely to be educated about the amount
of caffeine in energy drinks and the possible ill effects
that these drinks may cause in children and adolescents
who consume them [13]. Energy drinks contain three to
four times the caffeine as a typical soda and promise to
boost performance and to enhance metabolism. Energy
drinks like Full Throttle™, Red Bull™, SoBe No Fear™,
and Monster™ typically contain a combination of caffeine, carbohydrates, B vitamins, amino acids, and other
ingredients. One 8.2-ounce can of Red Bull™ contains
Di Rocco et al. Journal of Medical Case Reports 2011, 5:18
http://www.jmedicalcasereports.com/content/5/1/18
Figure 3 ECG showing chaotic atrial tachycardia/atrial fibrillation with rapid ventricular response at a rate of 166 beats per minute.
QRS, 97 ms; QTc, 492 ms.
80 mg of caffeine (0.03%), twice as much as a 12-ounce
soda; and one 16-ounce can of SoBe No Fear™ contains
141 mg of caffeine, four times as much as a soda.
Mountain Dew™, which is marketed along with other
sodas, contains more caffeine than other typical sodas at
55 mg per 12 ounces (Figure 5) [14,15]. Little regulation
occurs with the production and marketing of energy
drinks in the United States of America, with caffeine
content between energy drinks ranging from 50 mg to
505 mg per bottle [16]. With the lack of regulation and
strong marketing campaign toward young male athletes,
energy drinks are becoming a serious threat to adolescents and are postulated to have caused grave consequences in an Australian athlete [17].
Figure 4 ECG showing restoration of normal sinus rhythm to 85 beats per minute after intravenous fluids. PR interval, 117 ms; QRS, 96
ms; QTc, 416 ms.
Di Rocco et al. Journal of Medical Case Reports 2011, 5:18
http://www.jmedicalcasereports.com/content/5/1/18
Figure 5 Caffeine content of common commercial beverages
as compared with FDA-approved safe content of up to 0.02%
(6 mg/ounce).
In our case series, both patients had essentially normal
ECGs, ruling out endogenous cardiac causes for their
arrhythmia, and both had admitted to consuming highly
caffeinated drinks before atrial fibrillation developed.
The patient in Case 1 admitted to consumption of a
highly caffeinated beverage the day before his presentation, which was likely metabolized by the time he
received medical care; one could argue that he may have
had a prolonged caffeine half-life because of his chronic
caffeine use. He did complain of the same palpitations
after energy-drink consumption earlier that week; perhaps his high caffeine intake led to intermittent atrial
fibrillation, which was exacerbated by his vigorous athletic activity on the day of presentation.
The patient in Case 2 had concurrent ingestion of
alcohol with energy drinks and was also taking a baseline stimulant medication at the time of his presentation
in atrial fibrillation. It is unclear how these other factors
contributed to his arrhythmia; he certainly could have
induced atrial fibrillation by alcohol intoxication, especially as his arrhythmia resolved with fluid resuscitation
alone. As he did receive medical care within the
expected half-life of caffeine, the timeline would fit for
atrial fibrillation influenced by caffeine intoxication; the
combination of alcohol and caffeine intoxication could
have certainly led to his arrhythmia.
Conclusion
With the increasing popularity of energy drinks in the
pediatric and adolescent population, physicians should
be aware of the arrhythmogenic potential associated
with their consumption. It is important for pediatricians
to understand the lack of regulation in the caffeine content and other ingredients of these high-energy beverages and their complications, so that parents and
children can be educated at well visits and sports physicals. We must inform the public on the potential health
hazards related to excessive intake of caffeine-containing
beverages by children and adolescents; the caffeine content of energy drinks should be better regulated and
reported on food labels; and the purchase of energy
drinks by the young consumer should be more closely
monitored.
Given the possibility of cardiac arrhythmias and other
untoward effects developing from caffeine use and
abuse, further clinical trials reviewing the physiological
effects and addictive potential for children and adolescents should be pursued, given the paucity of caffeine
literature in this age group. Perhaps future studies could
evaluate serum caffeine levels in pediatric patients who
present with arrhythmias and concurrent caffeine consumption; this may be a useful measure to quantify into
a risk model, should this correlation continue to be
observed.
Patient’s Perspective
“One night...I felt dizzy and lightheaded. I realized that
my heart was beating abnormally fast. My chest felt
alien to me because my heart was beating with no set
rhythm and was shifting around inside my rib cage.
I thought I had somehow knocked my heart loose from
its rightful place and now it was swinging about inside
my body, beating erratically. I was admitted to the
intensive care unit...I was amazed at the professional
intensity with which the doctors and nurses performed
their duties. The cardiologist told us it could be a fluke
occurrence maybe caused by sugar or caffeine intake.
I was put on a drug through my IV. The next morning...
(my heart rate) had dropped to normal...I was instantly
in a more affable mood...Some may say this was the
spark that ignited a fire inside me to pursue a career in
the medical field.”
Consent
Written informed consent has been obtained from the
patient and parent of a patient who was a minor at the
time for publication of this case report and accompanying images. Copies of the written consents are available
for review by the Editor-in-Chief of this journal.
Author details
The Medical College of Wisconsin, Pediatric Hospital Medicine, Suite C560,
CCC, P.O. Box 1997, Milwaukee, WI, 53201-1997, USA. 2Beth Israel Medical
Center, 1st Ave at 16th Street, New York, NY, 10003, USA. 3Stony Brook
University Department of Pediatric Cardiology, HSC T-11, 040, Stony Brook,
NY, 11794-8111, USA.
1
Authors’ contributions
JRDR compiled, edited, and wrote the cases and also wrote the abstract,
introduction, and discussion, and performed an updated review of the
literature. AD initially summarized two cases, performed a literature review,
Di Rocco et al. Journal of Medical Case Reports 2011, 5:18
http://www.jmedicalcasereports.com/content/5/1/18
and contributed to the introduction and discussion. PM was heavily involved
in caring for the patients, selecting them for the case report and editing the
manuscript; MBH and TAB were both directly involved in the care of the
patients, helped select them for this case report series, and remained
supportive of the manuscript and its editing. All authors read and approved
the final manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 17 November 2009 Accepted: 19 January 2011
Published: 19 January 2011
References
1. Nanthakumar K, Lau YR, Plumb VJ: Electrophysiological findings in
adolescents with atrial fibrillation who have structurally normal hearts.
Circulation 2004, 110:117-123.
2. Dubin A: Cardiac Arrhythmias: Nelson’s Textbook of Pediatrics.Edited by:
Kliegman et al. Philadelphia: Saunders Elsevier; , 18 2007:1942-1947.
3. Frost L, Vestergaard P: Caffeine and risk of atrial fibrillation or flutter: the
Danish diet, cancer, and health study. Am J Clin Nutr 2005, 81:578-582.
4. Rashid A, Hines M, Scherlag BJ, Yamanashi WS, Lovallo W: The effects of
caffeine on the inducibility of atrial fibrillation. J Electrocardiol 2006,
39:421-425.
5. Mehta A, Jain AC, Mehta MC, Billie M: Caffeine and cardiac arrhythmias:
an experimental study in dogs with review of literature. Acta Cardiol
1997, 52:273-283.
6. Patanè S, Marte F, La Rosa FC, Rocca RL: Atrial fibrillation associated
with chocolate intake abuse and chronic salbutamol inhalation abuse.
Int J Cardiol 2009, E pub.
7. Peake STC, Mehta PA, Dubrey SW: Atrial fibrillation-related
cardiomyopathy: a case report. J Med Case Rep 2007, 1:111.
8. Temple JL: Caffeine use in children: what we know, what we have left to
learn, and why we should worry. Neurosci Biobehav Rev 2009, 33:793-806.
9. Magkos F, Kavouras S: Caffeine use in sports, pharmacokinetics in man,
and cellular mechanisms of action. Crit Rev Food Sci Nutri 2005,
45:535-562.
10. Kaplan GB, Greenblatt DJ, Ehrenberg BL, Goddard JE, Cotreau MM,
Harmatz JS, Shader RI: Dose-dependent pharmacokinetics and
psychomotor effects of caffeine in humans. J Clin Pharm 1997,
37:693-703.
11. FDA Basics: “Why isn’t the amount of caffeine a product contains
required on a food label?”. U.S. Food and Drug and Administration;
[http://www.fda.gov].
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A survey of energy drink consumption patterns among college students.
J Nutr 2007, 6:35.
13. O’Dea J: Consumption of nutritional supplements among adolescents:
usage and perceived benefits. Health Ed Res 2003, 18:98-107.
14. McCusker RR, Goldberger BA, Cone EJ: Caffeine content of energy drinks,
carbonated sodas, and other beverages. J Analyt Toxicol 2006, 30:112-114.
15. The Caffeine Database. [http://www.energyfiend.com/the-caffeinedatabase].
16. Reissig CJ, Strain EC, Griffiths RR: Caffeinated energy drinks: a growing
problem. Drug Alcohol Dep 2009, 99:1-10.
17. Berger AJ, Alford K: Cardiac arrest in a young man following excess
consumption of caffeinated “energy drinks”. Med J Aust 2009, 190:41-43.
doi:10.1186/1752-1947-5-18
Cite this article as: Di Rocco et al.: Atrial fibrillation in healthy
adolescents after highly caffeinated beverage consumption: two case
reports. Journal of Medical Case Reports 2011 5:18.
Submit your next manuscript to BioMed Central
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JOURNAL OF MEDICAL
CASE REPORTS
CASE REPORT
Open Access
Visual recovery in a patient with total hyphema,
neovascular glaucoma, long-standing retinal
detachment and no light perception vision:
a case report
Olusola Olawoye1, Christopher C Teng1,2*, Uri Shabto1, Jeffrey M Liebmann1,3, Francis A L’Esperance4 and
Robert Ritch1,2
Abstract
Introduction: We report the case of a patient with total hyphema, neovascular glaucoma, long-standing retinal
detachment and no light perception vision, who regained counting fingers vision with complete regression of
neovascularization following anterior chamber washout, intravitreal bevacizumab, pars plana vitrectomy, and
silicone oil placement. This represents a rare case in which a patient with no light perception vision was able to
regain functional vision.
Case presentation: A 63-year-old Caucasian man with a 55-year history of long-standing retinal detachment after
trauma presented to our facility with pain and redness, a total hyphema, no light perception vision and an
intraocular pressure of 60 mmHg (right eye). He had a history of diabetes mellitus and coronary artery disease.
Following anterior chamber washout, he was found to have neovascular glaucoma, for which intravitreal
bevacizumab was administered. After washout and intraocular pressure control, his visual acuity improved to light
perception. He subsequently underwent vitrectomy, membrane peeling, endolaser and silicone oil placement to
reattach his retina, and then a second retinal reattachment procedure. Following these procedures, he had visual
recovery to counting fingers vision in his right eye at five metres, complete regression of neovascularization, and
intraocular pressure of 10 to 12 mmHg on one antiglaucoma medication.
Conclusion: Functional vision can be regained despite long-standing retinal detachment.
Introduction
Long-standing retinal detachments (over one year) with
poor visual acuity are typically associated with cystic
degeneration of the macula and retina, loss of pigment
from the underlying retinal pigment epithelium, proliferative vitreoretinopathy, and poor visual outcome after
retinal reattachment surgery [1].
Chronic retinal detachment is a cause of rubeosis iridis and neovascularization of the anterior chamber
angle with subsequent neovascular glaucoma (NVG).
NVG represents one of the most severe forms of secondary glaucoma, caused by a number of ocular and
* Correspondence: [email protected]
1
Einhorn Clinical Research Center, The New York Eye and Ear Infirmary, New
York, NY, USA
Full list of author information is available at the end of the article
systemic conditions. Retinal ischemia and hypoxia initiate the release of angiogenesis factors, with consequent
development of new vessels.
We report the case of a patient with total hyphema,
NVG, long-standing retinal detachment and no light
perception (NLP) vision, who regained counting fingers
(CF) vision with complete regression of the neovascularization following anterior chamber (AC) washout, intravitreal bevacizumab, and two retinal reattachment
surgeries.
Case presentation
A 63-year-old Caucasian man presented to our facility
with a four-week history of pain and redness in his right
eye. He had had a traumatic retinal detachment of the
right eye (55 years ago) after being struck in the eye
© 2011 Olawoye et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Olawoye et al. Journal of Medical Case Reports 2011, 5:221
http://www.jmedicalcasereports.com/content/5/1/221
with a stone. He subsequently developed a cataract in
his right eye, for which he underwent cosmetic lensectomy at age 25. His best corrected visual acuity post lensectomy was light perception (LP), with a persistent
retinal detachment. He was left aphakic in his right eye.
At age 39, he had laser retinopexy in his left eye for lattice degeneration. He had a history of diabetes mellitus,
quadruple cardiac bypass surgery, and defribillator
implantation.
On examination, his visual acuity was NLP (right eye)
and 20/20 (left eye). External examination showed ptosis
and exotropia in his right eye. Slit lamp examination
revealed right eye nasal and temporal band keratopathy,
mild corneal edema, total hyphema and no posterior
view given the hyphema (Figure 1). He had an unremarkable examination of his left eye, with early nuclear
sclerosis. Intraocular pressure (IOP) by Goldmann
applanation tonometry was 60 mmHg (right eye) and 10
mmHg (left eye). Dilated fundus examination of his left
eye revealed two areas of laser retinopexy surrounding
lattice degeneration at 1:00 and 3:00 o’clock. Ultrasound
of the right eye revealed low-lying retinal detachment
with vitreous hemorrhage (Figure 2).
Immediate AC paracentesis to relieve pain and pressure reduced the IOP to 38 mmHg. Over the following
two weeks, his IOP fluctuated between 36 to 50 mmHg
(right eye), with no resolution of the hyphema or pain.
AC washout was performed, and during surgery he was
noted to have NVG with 360° rubeosis iridis, and vitreous
hemorrhage with ghost cells. Over the next three weeks,
he had two doses of 1.25 mg/0.05 ml intravitreal bevacizumab two weeks apart to treat his neovascularization.
Over eight weeks, his IOP gradually decreased to 15
mmHg (right eye) on four antiglaucoma medications,
and his visual acuity improved from NLP to LP. His
Figure 1 Total hyphema (right eye).
Figure 2 Ultrasonography (right eye) at presentation,
indicating low retinal detachment and vitreous hemorrhage.
retina was noted to be normal in color and not necrotic
or cystic. Given the good appearance of the retina and
because he had recovered LP vision, we decided to see if
vision would improve further by repairing the detachment. At two months after AC washout and three
months after presentation, pars plana vitrectomy, membrane peel, retinotomy with aspiration of subretinal
blood, endolaser retinopexy, inferior iridotomy, air/fluid
exchange and retinal reattachment with silicone oil were
performed.
Following surgery, his vision improved to counting fingers vision in the right eye at five metres, with IOP of 12
to 17 mmHg (right eye) on two antiglaucoma medications.
There was complete regression of the rubeosis. His IOP
remained stable over the next year on the same medication regimen. Fundus photography performed during a
follow-up visit revealed a flat retina in both eyes, though
there was residual fibrosis in the right eye (Figure 3). However, one year after retinal reattachment, he was noted to
have an inferior tractional retinal detachment in the right
eye with areas of subretinal fibrosis.
He subsequently had a second membrane peeling,
removal of subretinal membranes, drainage of subretinal
fluid, controlled retinectomy, and endolaser retinopexy.
Postoperatively, his best corrected visual acuity remained
Olawoye et al. Journal of Medical Case Reports 2011, 5:221
http://www.jmedicalcasereports.com/content/5/1/221
Figure 3 The right eye following first retinal detachment repair (A) and second retinal detachment repair (B).
CF in the right eye at five metres and his IOP remained
stable at 10 to 12 mmHg on timolol 0.25% once daily.
The optic nerve and macula had retinal pigment epithelial hypertrophy and subretinal fibrosis (Figure 3). Our
patient is currently being monitored with visual acuity of
CF at five metres in the right eye and IOP 19 mmHg on
timolol 0.25% once daily at last follow-up.
Discussion
With modern surgical techniques, a greater than 90%
primary anatomic success rate can be expected following
retinal detachment repair [1]. Despite this high level of
anatomic success, visual results may remain compromised because of permanent functional damage due to
macular detachment. The most important predictor of
visual recovery after retinal detachment repair is preoperative visual acuity, which is directly related to the
height of macular detachment [2]. A shorter duration of
detachment and younger age are also important in
visual recovery. Visual recovery following macula-off retinal detachment declines in an exponential fashion in
relation to increasing duration of the detachment [3].
Chronic retinal detachments can also lead to complications such as proliferative vitreoretinopathy and
rubeosis iridis. Iris neovascularization (INV) and NVG
are highly correlated with retinal ischemia, which stimulates production of vascular endothelial growth factor
(VEGF), a key molecule mediating neovascularization
[4]. Intravitreal injection of VEGF has been shown to
produce INV and NVG in non-human primates, and
inhibition of endogenous VEGF is effective for suppressing the retinal ischemia induced INV [5].
Bevacizumab (Genentech, San Francisco, CA, USA) is
a full-length humanized monoclonal antibody that binds
all isoforms of VEGF. Recent reports using intravitreal
bevacizumab injections have reported rapid and marked
regression of neovascular vessels in INV and NVG [6].
Complete resolution of iris and angle neovascularization
has also occurred after intravitreal bevacizumab.
Our patient presented with a total hyphema, NVG,
elevated IOP, and long-standing traumatic retinal
detachment with NLP vision. Trauma accounts for
approximately one in 10 retinal detachments; the visual
prognosis for eyes with NLP vision after trauma is dismal [7]. Of 52 eyes with a presenting vision of NLP, two
improved to hand motion and two improved to LP
vision following surgery [7]. Eyes with an initial acuity
of hand motions or better correlated with significantly
better visual outcome, but when the initial vision was
LP or NLP, poor visual outcomes (57% to 100%) were
more likely.
Brinton et al. [8] reported a series of 106 eyes with
trauma involving the posterior segment; 55 eyes (52%)
achieved final visual acuity of 20/100 or better following
surgery. The eyes that underwent vitrectomy within 14
days of the injury had a better final visual outcome than
those that underwent later vitrectomy. In 1982, Burton
[3] reported that of patients with macula-off retinal
detachments, 53% of patients who underwent surgery by
nine days achieved visual acuity 20/20 to 20/50, with
poor outcomes for long-standing detachments.
Despite our patient’s 55-year duration of long-standing
retinal detachment, following AC hyphema washout, the
retina had good color. Given this finding, the decision
was made to repair the detachment and he was able to
regain CF vision after two retinal surgeries. Suzuki and
Hirose [9] reported a case of visual recovery from NLP
in total retinal detachment of three months duration.
Olawoye et al. Journal of Medical Case Reports 2011, 5:221
http://www.jmedicalcasereports.com/content/5/1/221
Their patient was able to regain CF vision after two surgeries and postulated that some retinal receptors were
able to escape deterioration.
We believe that our patient was able to regain vision
because of the low height of the long-standing retinal
detachment. Previous studies have shown a positive relationship between the extent of the macular elevation
and final visual acuity [3]. In experimental detachments
in owl monkeys, Machemer [10] found that photoreceptor cell degeneration increased as the distance between
the pigment epithelial layer and the photoreceptors
increased. Our patient likely had areas of neurosensory
retina intact, which allowed him to have some visual
recovery after the retinal procedures.
Additionally, IOP control likely contributed to the
improvement of vision. Wittstrom et al. [11] reported
that a significant lowering of IOP seemed to improve
the function of the central retina, as demonstrated by
increased amplitudes and reduced implicit times
assessed with multi-focal electroretinography.
To the best of our knowledge, there has been no previous similar report of visual recovery in a patient with
long-standing traumatic retinal detachment. We hope
that with future advances, stem cells and retinal progenitor cells may be transplanted into diseased retinas
to integrate and develop synaptic connections with host
cells, and further improve visual function.
Conclusion
Functional visual recovery is possible despite long-standing retinal detachment with NLP vision.
Consent
Written informed consent was obtained from the patient
for publication of this case report and any accompanying images. A copy of the written consent is available
for review by the Editor-in-Chief of this journal.
Competing interests
The authors declare that they have no competing interests.
Received: 29 November 2009 Accepted: 17 June 2011
Published: 17 June 2011
References
1. Ross WH: Visual recovery after macula-off retinal detachment. Eye 2002,
16:440-446.
2. Davidorf FH, Havener WH, Lang JR: Macular vision following retinal
detachment surgery. Ophthalmic Surg 1975, 6:74-81.
3. Burton TC: Recovery of visual acuity after retinal detachment involving
the macula. Trans Am Ophthalmol Soc 1982, 80:475-497.
4. Tripathi RC, Li J, Tripathi BJ, Chalam KV, Adamis AP: Increased level of
vascular endothelial growth factor in aqueous humor of patients with
neovascular glaucoma. Ophthalmology 1998, 105:232-237.
5. Adamis AP, Shima DT, Tolentino MJ, Gragoudas ES, Ferrara N, Folkman J,
D’Amore PA, Miller JW: Inhibition of vascular endothelial growth factor
prevents retinal ischemia-associated iris neovascularization in a
nonhuman primate. Arch Ophthalmol 1996, 114:66-71.
6. Avery RL: Regression of retinal and iris neovascularization after
intravitreal bevacizumab (Avastin) treatment. Retina 2006, 26:352-354.
7. Matthews GP, Das A, Brown S: Visual outcome and ocular survival in
patients with retinal detachments secondary to open- or closed-globe
injuries. Ophthalmic Surg Lasers 1998, 29:48-54.
8. Brinton GS, Aaberg TM, Reeser FH, Topping TM, Abrams GW: Surgical
results in ocular trauma involving the posterior segment. Am J
Ophthalmol 1982, 93:271-278.
9. Suzuki R, Hirose T: Visual recovery from no light perception in total
retinal detachment with massive subretinal haemorrhage. Br J
Ophthalmol 1997, 81:705.
10. Machemer R: Experimental retinal detachment in the owl monkey. II.
Histology of retina and pigment epithelium. Am J Ophthalmol 1968,
66:396-410.
11. Wittström E, Schatz P, Lövestam-Adrian M, Ponjavic V, Bergström A,
Andréasson S: Improved retinal function after trabeculectomy in
glaucoma patients. Graefes Arch Clin Exp Ophthalmol 2010, 248:485-495.
doi:10.1186/1752-1947-5-221
Cite this article as: Olawoye et al.: Visual recovery in a patient with total
hyphema, neovascular glaucoma, long-standing retinal detachment and
no light perception vision: a case report. Journal of Medical Case Reports
2011 5:221.
Acknowledgements
This study was supported by the Arthur and Phyllis Bargonetti fund of the
New York Glaucoma Research Institute, New York, NY. OO was an
International Council of Ophthalmology Fellow.
Author details
1
Einhorn Clinical Research Center, The New York Eye and Ear Infirmary, New
York, NY, USA. 2Departments of Ophthalmology, New York Medical College,
Valhalla, NY, USA. 3New York University Medical Center, New York, NY, USA.
4
Columbia University College of Physicians and Surgeons, New York, NY,
USA.
Authors’ contributions
OO and CCT were involved in acquiring data, conception, design and
writing the manuscript; US and FAL were involved in patient care and
manuscript preparation; RR and JML were involved in patient care,
conception, design, drafting and revising the manuscript. All authors have
read and approved the final manuscript.
Submit your next manuscript to BioMed Central
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Submit your manuscript at
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JOURNAL OF MEDICAL
CASE REPORTS
CASE REPORT
Open Access
Car sunshade-induced craniofacial injury:
a case report
Mahdi Sharif-Alhoseini1, Hadi Khatibi2, Mojtaba Chardoli3 and Vafa Rahimi-Movaghar1,4*
Abstract
Introduction: We report the case of a man who sustained a craniofacial injury after spontaneous lateral airbag
deployment resulting in his face being struck by a car sunshade. This highlights the potential damage that can be
caused by any object placed between a lateral airbag and a car occupant.
Case presentation: We report the case of a 33-year-old Caucasian man who was the driver in a frontal collision.
He had opened the car sunshade and turned it 90° towards the left. As he was driving, he struck a bus, causing
the driver’s lateral airbag to spontaneously deploy. The airbag pushed the sunshade against his face and injured
him.
Conclusions: Car sunshades can cause significant craniofacial injury. We suggest that sunshade design must be
improved to reduce the risk of potential injuries to car occupants. We recommend a new, safer sunshade design.
Introduction
Although there are reports of injuries caused by airbags
[1-5], we are unaware of any literature describing injuries
from car sunshades. We report a case of severe craniofacial injury after spontaneous lateral airbag deployment
that caused the sunshade to strike the driver’s head. We
also discuss the mechanism of sunshade induced injuries.
skull base and nose. He also suffered superficial right
forearm burns due to the rupture of the steering wheel
airbag. His left hand was caught in the steering wheel,
resulting in left distal radial and ulnar fractures. He
underwent operative fixation of his nose and wrist factures and was referred to an ophthalmologist for evaluation of his retinal injury.
Case presentation
A 33-year-old Caucasian man was referred to ShahidRasi Hospital in Shahindezh (West Azarbaijan province,
Northwestern Iran) after a motor vehicle crash. He was
driving on a two-way mountain road in a south-north
direction before sunset. Because of sunlight, he opened
the car sunshade and turned it 90° towards the left. As
he was driving at 60 km/hour on a sharp curve in the
road, his car suddenly hit a bus coming from the opposite direction. The driver’s lateral and steering wheel airbags spontaneously deployed. The lateral airbag pushed
the sunshade against his face so hard that the sunshade
was completely deformed and caused injury to the left
side of the face (Figure 1). He suffered abrasions on the
left side of the face, retinal damage, and fractures of the
Discussion
Airbag-associated injury occurs in 43% of airbag deployments [6]. Typically, airbag-related injuries are minor,
but severe or fatal injuries are also reported [7]. Minor
injuries such as abrasions, contusions and lacerations
are usually detected on the face, neck, chest, and upper
extremities [8,9]. Airbag deployment also releases hightemperature gases, including nitrogen and carbon dioxide, and produces sodium hydroxide, a very irritating
alkaline material, which can cause superficial and even
full thickness burns [10,11]. As demonstrated by this
case, an opened and turned sunshade can also be a
potentially dangerous object between a lateral airbag
and a driver or passenger.
* Correspondence: [email protected]
1
Sina Trauma and Surgery Research Center, Sina Hospital, Tehran University
of Medical Sciences, Tehran, Iran
Full list of author information is available at the end of the article
Conclusions
When the lateral airbag deploys, it pushes the sunshade
onto the occupant’s face and head. Consequently, it seems
that vehicles with side airbags should not have moveable
© 2011 Sharif-Alhoseini et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Sharif-Alhoseini et al. Journal of Medical Case Reports 2011, 5:175
http://www.jmedicalcasereports.com/content/5/1/175
References
1. Nguyen CS, Chase DM, Wing DA: Severe fetal skull fracture and death
subsequent to a motor vehicle crash with frontal airbag deployment.
J Trauma 2009, 67:E220-E221.
2. Bard MR, Shaikh S, Pestaner J, Newell MA, Rotondo MF: Direct fetal injury
due to airbag deployment and three-point restraint. J Trauma 2009, 67:
E98-E101.
3. Huber CD, Lee JB, Yang KH, King AI: Head injuries in airbag-equipped
motor vehicles with special emphasis on AIS 1 and 2 facial and loss of
consciousness injuries. Traffic Inj Prev 2005, 6:170-174.
4. Yoganandan N, Pintar FA, Zhang J, Gennarelli TA: Lateral impact injuries
with side airbag deployments - a descriptive study. Accid Anal Prev 2007,
39:22-27.
5. Monkhouse SJ, Kelly MD: Airbag-related chest wall burn as a marker of
underlying injury: a case report. J Med Case Rep 2008, 2:91.
6. Serra C, Delattre O, Despeignes RL, Cousin A: Upper limb traumatic lesions
related to airbag deployment: a case report and review of literature.
J Trauma 2008, 65:704-707.
7. Usumoto Y, Hikiji W, Kudo K, Tsuji A, Ikeda N: An unusual case of fatal
airbag injury. Fukuoka Igaku Zasshi 2008, 99:225-229.
8. Subash M, Manzouri B, Wilkins M: Airbag-induced chemical eye injury.
Eur J Emerg Med 2010, 17:22-23.
9. Sato Y, Ohshima T, Kondo T: Air bag injuries- a literature review in
consideration of demands in forensic autopsies. Forensic Sci Int 2002,
128:162-167.
10. Heimbach D: Full-thickness burn to the hand from an automobile airbag.
J Burn Care Rehabil 2000, 21:288-289.
11. Corazza M, Trincone S, Zampino MR, Virgili A: Air bags and the skin.
Skinmed 2004, 3:256-258.
Figure 1 Lateral airbag deployment pushed the sunshade
against driver’s face. The sunshade was completely deformed and
caused injury to the left side of the temporal skull, orbit, face, and
nose. This figure is a model, and the model has provided informed
written consent to his image being used.
doi:10.1186/1752-1947-5-175
Cite this article as: Sharif-Alhoseini et al.: Car sunshade-induced
craniofacial injury: a case report. Journal of Medical Case Reports 2011
5:175.
sunshades that can be placed in the lateral position. We
suggest the design and use of sunshades that do not project into the vehicle or the use of sunglasses.
Consent
Written informed consent was obtained from the patient
for publication of this case report and any accompanying images. A copy of the written consent is available
for review by the Editor-in-Chief of this journal.
Author details
1
Sina Trauma and Surgery Research Center, Sina Hospital, Tehran University
of Medical Sciences, Tehran, Iran. 2Donya-e-Khodro Weekly, Tehran, Iran.
3
Emergency Department of Hazrat-e-Rasool Hospital, Tehran University of
Medical Sciences, Tehran, Iran. 4Research Centre for Neural Repair, University
of Tehran, Tehran, Iran.
Authors’ contributions
MS wrote the case report and performed the literature search. HK wrote the
Farsi version of the draft and organized the photographs. MC and VRM
designed the methodology, discussed, and edited the draft. All authors read
and approved the final manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 7 June 2010 Accepted: 10 May 2011 Published: 10 May 2011
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• Thorough peer review
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• Immediate publication on acceptance
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Submit your manuscript at
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JOURNAL OF MEDICAL
CASE REPORTS
EDITORIAL
Open Access
Using an Ishikawa diagram as a tool to assist
memory and retrieval of relevant medical cases
from the medical literature
Kam Cheong Wong1,2,3,4
Abstract
Studying medical cases is an effective way to enhance clinical reasoning skills and reinforce clinical knowledge. An
Ishikawa diagram, also known as a cause-and-effect diagram or fishbone diagram, is often used in quality
management in manufacturing industries.
In this report, an Ishikawa diagram is used to demonstrate how to relate potential causes of a major presenting
problem in a clinical setting. This tool can be used by teams in problem-based learning or in self-directed learning
settings.
An Ishikawa diagram annotated with references to relevant medical cases and literature can be continually
updated and can assist memory and retrieval of relevant medical cases and literature. It could also be used to
cultivate a lifelong learning habit in medical professionals.
Introduction
Doctors are accustomed to learning from their more
experienced peers as well as from their own experiences
in treating their patients [1]. Because of this, it is important that they develop learning techniques that are
proactive and encourage a lifelong learning orientation.
Case reports can provide valuable sources of information for others to learn from. Studying medical cases is
an effective way to enhance clinical reasoning skills and
reinforce clinical knowledge [2]. A case report provides
important and detailed information about a patient that
is often lost in larger studies [3]. Reading case reports is
also intellectually stimulating. When clinicians or medical students analyze a clinical problem, they usually start
with potential common causes. For example, if a patient
presents with secondary amenorrhea, a clinician will
consider common causes such as pregnancy and use of
contraceptive medications before exploring other less
common but critical causes such as hyperprolactinemia,
ovarian cancer and so on.
When clinicians are faced with a puzzling clinical problem, they may search journals that publish clinical
Correspondence: [email protected]
1
University of Sydney, Sydney Medical School, NSW, Australia
Full list of author information is available at the end of the article
cases for information about the condition [4]. There are
various sources for medical cases such as the Journal of
Medical Case Reports, BMJ Case Reports and the New
England Journal of Medicine. However, because of the
diversity of the case reports, it may be difficult to recall
and organize the located material in a systematic manner in order to explain a clinical problem. Ishikawa diagrams are an efficient way of organizing case reports in
a clinical setting.
Methods
The Ishikawa diagram was invented by Kaoru Ishikawa,
who pioneered quality management techniques in Japan
in the 1960 s. The diagram is considered one of the
seven basic tools of quality control [5]. It is also known
as a fishbone diagram because of its shape. The ‘fish
head’ represents the main problem. The potential causes
of the problem, usually derived from brainstorming sessions or research, are indicated in the ‘fish bones’ of the
diagram.
As an example for illustration, ‘secondary amenorrhea/
oligomenorrhea’ has been chosen as the main presenting
problem. ‘Secondary amenorrhea/oligomenorrhea’
is indicated in the head of the Ishikawa diagram (Figure 1).
When searching for the potential causes of the main presenting problem, one can either work in a team with others
© 2011 Wong; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
Wong Journal of Medical Case Reports 2011, 5:120
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Woman
reproductive
system
Pregnant [6]
Other systems in
the body
Hypothyroidism [13]
Polycystic ovary
syndrome [6]
Cushing syndrome [16]
Ovarian tumor [15]
Hyperprolactinaemia [14]
Ovarian failure
Eating disorder (e.g.
Anorexia nervosa) [7]
Secondary
Amenorrhea/
Oligomenorrhea
Chemo & radiotherapy [8]
Excessive stress [11]
Excessive physical
exercise [9, 10]
Prolonged use of
drugs e.g.
antipsychotic [7, 12]
Post oral contraceptive/ depot
medroxyprogesterone [7]
Psycho-social
Miscellaneous
Figure 1 Ishikawa diagram. ‘Woman’s reproductive system’ includes causes such as pregnancy, polycystic ovary syndrome, ovarian tumor, and
ovarian failure. ‘Other systems in the body’ includes causes such as hypothyroidism, Cushing syndrome, hyperprolactinemia, and eating
disorders. ‘Psychosocial’ includes causes such as excessive stress and excessive physical exercise. ‘Miscellaneous’ includes causes such as
prolonged use of drugs, for example anti-psychotics, and after oral contraceptive/depot medroxyprogesterone treatment.
or in a self-directed learning setting. Clinicians would
conduct brainstorming sessions and search the relevant
journals to find potential causes for secondary amenorrhea/oligomenorrhea, listing them on a whiteboard or
flipchart. The list would then be reviewed to extract relevant causes in the context of the main presenting problem. These causes would then be organized in the ‘fish
bones’ of an Ishikawa diagram (Figure 1). There is no
limit to the number of ‘fish bones’ in the diagram. Each
‘fish bone’ can be subdivided into smaller ‘bones’ if necessary to show the relationship of all potential causes to the
presenting problem. For example, ‘chemotherapy and
radiotherapy’ are indicated in the branch of the ‘fishbone’
that shows the cause of ovarian failure, a potential cause
for secondary amenorrhea/oligomenorrhea (Figure 1).
The cited references for the relevant case reports and literatures are also indicated in the Ishikawa diagram so
that readers can retrieve the case reports and relevant literatures easily.
The potential causes for secondary amenorrhea/oligomenorrhea have been identified and categorized in four
groups related to ‘women’s reproductive systems’, ‘other
systems in the body’, ‘psychosocial’, and ‘miscellaneous,
for example drugs’. The causes include pregnancy [6],
polycystic ovarian syndrome [6], amenorrhea after oral
contraceptive/depot medroxyprogesterone treatment [7],
eating disorder (for example, anorexia nervosa) [7],
premature ovarian failure [8], excessive physical exercise
[9,10], excessive stress [11], prolonged use of
anti-psychotic [7,12], hypothyroidism [13], hyperprolactinemia [14], ovarian cancer [15], and Cushing syndrome [16]. Thus the Ishikawa diagram illustrates and
summarizes the potential causes for secondary amenorrhea/oligomenorrhea (Figure 1).
Conclusions
Rare but critical cases should be studied and included in
an Ishikawa diagram to remind clinicians of relevant
information during their clinical reasoning processes.
For example, the Journal of Medical Case Reports has
published the case of a 22-year-old lactating woman
who presented with four months of amenorrhea associated with signs of virilization. The patient was diagnosed as having an androgen secreting steroid cell
Wong Journal of Medical Case Reports 2011, 5:120
http://www.jmedicalcasereports.com/content/5/1/120
tumor of the ovary [15]. In addition, BMJ Case Reports
has published a case demonstrating the relationship
between hypothyroidism and secondary amenorrhea.
Important learning points are highlighted: serum thyroid
stimulating hormone (TSH) should be measured in
every adolescent with menstrual irregularities, multicystic ovaries as a presenting manifestation of juvenile
hypothyroidism is a rare occurrence and represents
advanced disease, and appropriate diagnosis and
levothyroxine replacement therapy is effective and it can
prevent inadvertent surgery [13].
Furthermore, the reader should appraise the published
case to assess the credibility of the information and
should look for updated information in the future. For
example, if the readers are not fully convinced of the
explanation for the pathophysiology of ‘specificity spill
over’ phenomenon that may contribute to multicystic
ovaries [13,17], he or she should search for more information about it and look out for future publications on
this topic. Information gathered from other sources can
be included in the diagram as well, such as the paper
published in the British Journal of Obstetrics and Gynaecology, which has substantiated information about ovarian cancers and amenorrhea [8]. In this way, continually
organizing and updating information on an Ishikawa
diagram can cultivate lifelong learning habits in medical
professionals.
Medical educators can also apply Ishikawa diagrams to
facilitate problem-based learning when teaching medical
students and junior doctors. Starting with a clinical
vignette, facilitators can help medical students and
junior doctors to identify the main presenting problem
of a patient, conduct brainstorming sessions and search
in the literature to find the potential causes, then categorize these causes in an Ishikawa diagram. The Ishikawa diagram can then be kept by individual learners
for continual updating when they acquire new or relevant information. In short, an Ishikawa diagram can
assist memory and the retrieval of relevant medical case
reports and literatures.
Acknowledgements
I would like to thank the Journal of Medical Case Reports and BMJ Case
Reports for providing access to the case reports, and the peer reviewers and
Dr Myra Dunn (Education Officer at Beyond Medical Education, Australia) for
their comments and suggestions. The author’s Academic Registrar position
was funded by General Practice Education & Training (GPET), Canberra,
Australia.
Author details
1
University of Sydney, Sydney Medical School, NSW, Australia. 2University of
Western Sydney, School of Medicine, NSW, Australia. 3Beyond Medical
Education, NSW/VIC, Australia. 4George Street Medical Practice, Bathurst,
NSW, Australia.
Received: 16 November 2010 Accepted: 29 March 2011
Published: 29 March 2011
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doi:10.1186/1752-1947-5-120
Cite this article as: Wong: Using an Ishikawa diagram as a tool to assist
memory and retrieval of relevant medical cases from the medical
literature. Journal of Medical Case Reports 2011 5:120.
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