Spring 2016

JBJS Journal of Orthopaedics
for Physician Assistants
Journal Mission
The JBJS Journal of Orthopaedics for Physician
Assistants (JOPA) is an academic resource created to
deliver ongoing orthopedic education for physician
assistants. The journal is a unique forum to share
our knowledge and experiences with colleagues in
the profession. JOPA strives to publish timely and
practical articles covering all subspecialties. Each
article is peer reviewed to ensure accuracy, clinical
relevance, and readability.
Contents
4
5
10
13
Certification Review for the Ortho
PA
Fat Embolism Syndrome in Long
Bone Fractures
Bone Up: Bone Health Column
Monthly Image Quiz Follow-up
16
19
Discoid Lateral Meniscus
Bennett fracture
Charcot Arthropathy
22
Reactive Arthritis: A Case Study
Dagan Cloutier, PA-C
Editor
269 Pasture Drive
Manchester, NH 03102
dcloutier@jbjs.org
BOARD OF
ASSOCIATE EDITORS
Hand
Bruce Gallio
Natanya McDonough
John J. Shaff
Sports Medicine
Larry Collins
Brian Downie
Sean Hazzard
General Orthopaedics
Charles Dowell
Charles D. Frost
Jill Knight
Brad Salzmann
Arthroplasty
Chris Davis
Randall Pape
JOPA is proud to partner with the Clinical Advisor
to provide an orthopedic focused educational
resource for all Physician Assistants and Nurse
Practitioners.
Spine
Jay DaCruz
Travis Palmer
Mike Houle
Trauma
Caitlin Eagen
Jonathan Hull
Keith Paul
John Riehl, MD
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ISSN 2470-1122
2
JOPA
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Certification Review for the Ortho PA
It’s not all bones on the boards
David Beck MPAS, PA-C
A 20-year-old Asian American man with a
medical history of pneumonia because of acute
influenza as well as secondary pneumonia 2
weeks ago presents with complaints of “extreme
fatigue” in his legs and arms over the past 10
days. He notes that he has greatest difficulty with
standing up from a seated position and lifting his
backpack. He also states that today he noticed
difficulty moving his facial muscles when talking
and that he can walk only short distances before
he has to stop and rest. He reports no vision
changes but has noticed a “tingling” sensation in
his thighs. On physical examination, you note that
his thigh muscles (both anterior and posterior)
are atrophied and that he has weakness of all
extremity and facial muscle motions. Which of the
following is the most likely diagnosis?
A.
B.
C.
D.
Amyotrophic lateral sclerosis
Guillain-Barré syndrome
Myasthenia gravis
Spinal muscular atrophy
EXPLANATION: This is a classic presentation of
Guillain-Barré syndrome, an acute, autoimmune,
fulminant polyradiculoneuropathy. Most cases
occur in adults, with a slight male preponderance,
and occur within 3 weeks after an acute infection,
especially of the respiratory or gastrointestinal
tract1,2. The usual pattern of involvement is
“ascending paralysis,” often first noticed as
weakness or instability that evolves over hours
to days and begins in the legs1,2. This patient
also demonstrated the tingling dysesthesias
that often accompany the motor symptoms1,2.
Amyotrophic lateral sclerosis is typically first
evident asymmetrically in the distal portion of an
extremity3. Myasthenia gravis characteristically
presents with weakness of the cranial muscles,
often first affecting eye alignment and lid position,
before progressing to generalized weakness4.
Spinal muscular atrophy is a rare genetic disease
most commonly diagnosed as severe weakness
in the first 6 months of life. Type IV can present
in adults as mild-to-moderate proximal muscle
weakness but is not associated with paresthesias
4
JOPA
or a recent infection5.
The correct answer is B.
References
1. Hauser SL, Amato AA. Guillain-Barré syndrome and other
immune-mediated neuropathies. In: Kasper D, Fauci A, Longo
D, Jameson J, Loscalzo J, editors. Harrison’s Principles of
Internal Medicine. 19th ed. New York: McGraw-Hill; 2015. p
2694-99.
2. Ropper AH, Samuels MA, Klein JP. Diseases of the
Peripheral Nerves. In: Ropper AH, Samuels MA, Klein JP,
editors. Adams & Victor’s Principles of Neurology. 10th ed.
New York: McGraw-Hill; 2014. p 1310-91.
3. Brown RH Jr. Amyotrophic lateral sclerosis and other
motor neuron diseases. In: Kasper D, Fauci A, Longo D,
Jameson J, Loscalzo J, editors. Harrison’s Principles of
Internal Medicine. 19th ed. New York: McGraw-Hill; 2015. p
2631-35.
4. Ropper AH, Samuels MA, Klein JP. Myasthenia gravis
and related disorders of the neuromuscular junction. In:
Ropper AH, Samuels MA, Klein JP, editors. Adams & Victor’s
Principles of Neurology. 10th ed. New York: McGraw-Hill;
2014. p 1472-90.
5. Genetics Home Reference. Spinal muscular atrophy. 2016
Apr 20. https://ghr.nlm.nih.gov/condition/spinal-muscularatrophy. Accessed 2016 Apr 22.
David Beck MPAS, PA-C is the Academic Coordinator
for the University of Pittsburgh Physician Assistant
Studies Program. Mr. Beck has been involved in
physician assistant education for over 10 years, and
has authored questions for the Physician Assistant
Education Association’s (PAEA) End of RotationTM
Exams. His clinical background is focused in
emergency and internal medicine.
Fat Embolism Syndrome in Long Bone Fractures
Robin Hughes, PA-C
Assistant Professor at High Point University’s PA Program
High Point, NC
Abstract
Fat embolism was first diagnosed in
humans in 1861. More than a century later,
Gurd described fat embolism syndrome (FES)
using a triad of findings: hypoxia, confusion,
and petechia. Long bone fractures, such as
femoral shaft fractures, produce fat emboli but
infrequently cause FES. It has been suggested
that early fracture fixation and reaming of the
intramedullary canal prior to fixation decrease
the prevalence of FES. The diagnosis of FES
remains a dilemma for clinicians. Hopefully,
with improvement of imaging studies or further
evaluation of interleukin-6 levels, the prevalence
of undiagnosed FES will decrease.
Introduction
Fat embolism syndrome (FES), a clinical
entity most likely to occur after a long bone
fracture, frequently goes undiagnosed. The most
commonly seen features of FES are hypoxia,
confusion, and petechia, which occur as a
result of fat being released into the circulation.1
However, the complete triad does not appear
in every patient with FES. As a result, FES has
remained a diagnostic challenge for clinicians.
This paper is an overview of the history,
pathophysiology, and diagnostic criteria of FES;
imaging studies used for diagnosis; and treatment
of both the fracture and the syndrome.
History
Fat embolism in canines was first
described over 3 centuries ago.2,3 In 1861, Zenker
was the first to document a case of fat embolism
in humans, after he observed fat globules in the
pulmonary system of a man who had sustained
a deadly crush injury to his torso.2,3,4 Later that
decade, Wagner associated the escape of bone
marrow at the site of a fracture to the fat globules
found in lungs. In 1873, Von Bergman described
FES in a patient with a femoral fracture. Two years
later, neurological symptoms of fat emboli were
observed by Czerny.2
Guass speculated that 3 conditions must
be present in order for fat embolism to occur: fat
tissue damage, vascular trauma near the injury
site, and bodily trauma that allows the passage of
fat globules into the vessels. This became known
as the mechanical theory. Three years later,
Lehman and Moore submitted the biochemical
theory of fat embolism, stating that inflammatory
chemical mediators from the blood could cause
the formation of fat globules from fat mobilized
from body fat storage.2,3,4 Finally, Gurd defined
FES by the clinical characteristics of hypoxia,
neurological changes, and petechia.5
Pathophysiology
Although the pathophysiologic process
of FES is not fully understood, mechanical and
biochemical theories are the 2 most respected
postulates. It is hypothesized that most cases
of FES are a combination of both of these two
theories.
Mechanical Theory
The mechanical theory suggests that fat
escapes the bone marrow after trauma, such
as in a long bone fracture, and then accesses
the venous circulation. These fats cells exhibit
inflammatory and thrombotic properties that can
produce platelet aggregation and fibrin formation
as they travel through the veins. They can then
enter the respiratory system and wedge in the
pulmonary capillary beds of the lung, causing
respiratory distress from interstitial bleeding and
swelling, alveolar collapse, and vasoconstriction
secondary to an oxygen deficiency. The nonpulmonary symptoms, petechia and neurological
changes such as confusion, are thought to arise
from the fat cells entering the arterial system via
a patent foramen ovale or pulmonary capillary
bed.6
Biochemical Theory
The biochemical theory suggests that the
escaped fat from the bone marrow of a long bone
fracture goes through lipolysis, forming glycerol
and toxic free fatty acids, which can cause
pulmonary edema and hemorrhage. This release
of glycerol and toxic free fatty acids can also
JOPA 5
impair the lung lining, causing an inflammatory
cytokine cascade, which could lead to acute
respiratory distress syndrome.6
Epidemiology
The risk of developing FES is very low.
Trauma patients with multiple fractures that
include a femoral shaft fracture have the highest
risk (2.35% compared with 0.4% for patients
with an isolated femoral shaft fracture). The
prevalence of FES is 7.6 times higher with a
femoral shaft fracture than with a femoral neck
fracture. Also, the prevalence of FES is much
greater with long bone fractures of the lower
extremity than with long bone fractures of the
upper extremity.8 In a study by Gupta et al. in
2011, men were shown to develop FES 3 times
more frequently than women.7 It is speculated
that this may be the result of a higher prevalence
of trauma in men.8 Lastly, children are at a very
low risk to develop FES because their bone
marrow has less of the fat olein, which appears to
be the fat most associated with FES.8
Clinical Presentation
FES generally does not occur within the
first 12 hours after trauma, but rather 12 to 72
hours after the initial injury.2 It is most commonly
associated with long bone fractures of the lower
extremity, with closed femoral shaft fractures
being the fractures most frequently associated
with FES.9
Patients with FES may initially experience
dyspnea, hypoxia, tachypnea, or respiratory
failure.1 This is thought to result from fat escaping
the fracture site during manipulation of the
fracture while the patient is being transferred
from the stretcher to the bed or during surgery.
This manipulation of the fracture can cause a
fat globule to enter the circulation, resulting in
a fat embolus. The patient’s respiratory status
may decline rapidly, requiring supplemental
oxygen through a nasal cannula. In an extreme
case of respiratory distress, such as is seen with
acute respiratory distress syndrome (ARDS),
mechanical ventilation may be necessary.4
A change in mental status may be the first
clinical sign of FES recognized by a clinician.7 This
can be secondary to an unrecognized cerebral
fat embolus. Although this is the most common
neurological sign, hemiplegia, aphasia, apraxia,
anisocoria, and visual field disturbances have also
been mentioned in the literature.2 In patients who
survive FES, these findings almost always resolve
6
JOPA
completely.3
A petechial rash, which may develop 48
to 72 hours after the onset of FES, is thought to
be the finding most pathognomonic for FES.10 The
rash, which is a result of capillary embolization
causing extravasation of red blood cells, occurs
in 30% to 60% of patients who develop FES and
is most frequently seen on the oral mucosa and
conjunctiva. It may also be seen on some other
nondependent areas of the body anteriorly, but is
unlikely to be observed on the posterior aspect of
the body.10
Diagnostic Criteria
In 1970, Gurd described the syndrome
of fat embolism using 3 physical signs: hypoxia,
neurological symptoms, and petechia.5 The
diagnostic criteria were updated in 1974 in
conjunction with Wilson. Gurd and Wilson devised
a table of major and minor criteria and wrote that,
in order to be diagnosed with FES, a patient had to
exhibit 2 major symptoms, or 1 major and 4 minor
symptoms (Table 1).11
Later, in 1983, Schonfeld et al. proposed a
scoring system whereby 7 criteria were variably
rated. A total score of >5 was indicative of FES
Table 1: Gurd and Wilson Criteria – 2 Major or 1
Major and 4 Minor
Major criteria:
1) Respiratory symptoms plus positive
radiographic changes – bilateral fluffy infiltrates
2) Central nervous system changes beyond
what is expected from hypoxia – confusion,
drowsiness, coma
3) Petechial rash – conjunctiva, buccal mucosa,
axilla, neck
Minor criteria:
1) Tachycardia > 110 bpm
2) Pyrexia > 38.5°C
3) Fat globules in blood
4) Sudden thrombocytopenia – drop > 50% of
admission value
5) Retinal fat or petechia
6) Sudden drop in hemoglobin > 20% of
admission value
7) High sedimentation rate > 71 mm/h
8) Jaundice
9) Renal changes – anuria or oliguria
Table 2: Schonfeld et al. Criteria – Score of >5
Points
Criteria
Points
1) Diffuse petechia
2) Alveolar infiltrates on chest
radiograph
3) Hypoxemia – PaO2 < 70 mm Hg
4) Confusion
5) Fever > 38°C
6) Heart rate > 120 bpm
7) Respiratory rate > 30/min
5
4
3
1
1
1
1
Table 3: Lindeque et al. Criteria – Requires
Only 1 for FES diagnosis
Criteria:
1) PaO2 < 60 mm Hg on room air
2) PaCO2 > 55 mm Hg or pH < 7.3
3) Respiratory rate > 35 bpm even after
sedation
4) Clinical signs of difficulty breathing and
tachycardia
(Table 2).12
In 1987, Lindeque et al. stated that,
because Gurd and Wilson did not include an
arterial blood gas level in their criteria and
hypoxia is frequently the first symptom seen
in FES, their system was not sensitive enough.
Therefore, Lindeque et al. based the diagnosis
of FES on abnormal arterial blood gas levels
(hypoxia) and tachypnea (Table 3).13
Diagnostic Studies
There is no gold standard diagnostic
study for FES. The diagnosis is based on a
combination of the trauma description (as FES
is typically seen with a long bone fracture),
physical signs and symptoms (petechia,
respiratory distress, and neurological changes
such as confusion), timing of the onset of
symptoms (>12 hours and <72 hours after injury),
and positive results on imaging studies, which
will be discussed below.1
Chest radiographs may be completely
normal in FES or could show bilateral patchy
infiltrates consistent with ARDS.9 Chest
computerized tomography may show infiltrates
earlier than a chest radiograph, but it does not
provide any substantial information that may lead
to the diagnosis of FES.14
Both brain magnetic resonance imaging
(MRI) and transcranial Doppler sonography are
used to help diagnose cerebral FES (CFES). It was
initially reported that CFES and diffuse axonal
injury (DAI), a brain injury in which damage in
the form of extensive lesions in the white-matter
tracts occur (the most common and devastating
type of traumatic brain injury), appeared similar
on a brain MRI.15 However, in a retrospective
study, Bodanapally et al. noted findings that
differentiated between CFES and DAI on MRI. The
study revealed that micro-hemorrhages were
more numerous and substantially smaller in
CFES. These micro-hemorrhages extended into
the white matter, which is more susceptible to
edema, but also involved the gray matter, making
it a more extensive finding in CFES.15 Kou et al
suggested 5 different MRI patterns (in 3 stages) in
CFES. In the acute stage of CFES, diffuse cytotoxic
edema is seen. In the subacute phase, the edema
is coalescent. In the late stage, demyelination and
cerebral degeneration are noted. In all 3 stages,
coalesced petechial hemorrhages are observed.16
Transcranial Doppler sonography can
identify both particulate and gaseous emboli in
real time, making it a useful tool for diagnosing
FES. Forteza et al., utilizing transcranial Doppler
sonography of bilateral cerebral arteries in
patients with a femoral shaft fracture before
any sign of FES, noted numerous micro-embolic
signals in patients’ brains. As a result, noting
cerebral emboli on transcranial Doppler
sonography in a patient without classic signs of
FES can make it easier to anticipate neurological
changes in the patient, who may be developing
FES.17
Another diagnostic study, transesophageal
echocardiography (TEE), can be used
intraoperatively to monitor blood flow through
the heart. It is very efficient at identifying fat
emboli in the right atrium. It can also be used
to diagnose right-to-left shunts. If a right-to-left
shunt is present, and the patient is noted to have
a fat embolus in the right atrium, then a clot
to the brain is more likely to occur, leading to
neurological changes.18
Treatment of Long Bone Fractures
Since FES most commonly occurs after a
fracture of a long bone, particularly the femur,
research has been performed to determine if the
JOPA 7
timing of the fixation of the fracture, and reaming
versus not reaming the intramedullary canal,
lessen the likelihood that FES will occur.
Scalea stated that he encountered fewer
complications such as FES with early fixation,
within 24 hours after injury.19 However, if fracture
fixation is delayed for some reason, and FES
develops before the fracture can be repaired, then
fracture fixation needs to be delayed until the
patient improves from the FES.20
Femoral shaft fractures are frequently
treated with intramedullary rods. There has
been discussion as to whether reaming the
intramedullary canal increases the chances
of developing FES. In a 2010 study by Högel
et al., 24 Swiss mountain sheep had femoral
shaft osteotomies performed, followed by
intramedullary nailing. The study revealed a
statistically significant difference between the
occurrence of FES following reaming versus that
without reaming the intramedullary canal. In the
group of sheep that had intramedullary nailing
without reaming, 16% showed fat emboli in the
lungs. In the other group, in whom the canal
had been reamed before nail insertion, 6% to
7% of the sheep’s lungs revealed fat emboli. It
was hypothesized that the lower prevalence of
fat emboli in the reamed group was secondary
to the large femoral shaft diameter allowing
translocation of the medullary contents. It was
also noted that the fat emboli in the lungs were
smaller in the reamed group.21
Issack et al. reported that reaming, which
they performed with an awl and rasp connected
to a vacuum, lessened the intramedullary
pressure and thus reduced the prevalence of fat
emboli.22 In 2010, Green showed that removal
of intramedullary contents via vacuum suction
could lessen the prevalence of fat emboli.23 Zhao
et al., in a 2015 study, found that irrigation of the
medullary canal of the tibia and femur in total
knee replacements reduced the size and quantity
of fat emboli.24 From this, it can be speculated
that performing the same procedure for femoral
shaft fractures could also reduce the size and
quantity of fat emboli.
Treatment of FES
There is no clearly defined medical care
for FES. Early recognition, supportive treatment,
and prevention are of utmost importance.2 Since
hypoxia is the most common presenting symptom
of FES, early recognition may occur by closely
monitoring all patients with long bone fractures
8
JOPA
with pulse oximetry so that subtle falls in
oxygenation are recognized early.25 Although there
is no specific treatment of FES, it is very important
to provide supportive care including oxygenation
via a nasal cannula, a facemask, or mechanical
ventilation; use of intravenous fluids to maintain
vascular volume; blood product transfusions as
necessary; maintenance of proper nutrition; and
deep vein thrombosis prophylaxis. When FES is
diagnosed early and supportive care is initiated
quickly, mortality rates are usually <10%.7
Corticosteroid administration has been
suggested as a means of preventing FES. Gupta et
al. stated that the benefit of using corticosteroids
for the prevention of FES was disputable, with
only a small number of studies showing a
decrease in the prevalence of FES7. In a metaanalysis by Bederman et al. in 2008, the use of
corticosteroids was assessed to determine if they
would reduce the prevalence of FES in patients
with long bone fractures. The findings suggested
that corticosteroid use in patients with long bone
fractures may prevent FES and hypoxia from
occurring but would not prevent mortality. Steroid
use could inhibit both bone and wound healing.26
Other treatments, such as heparin, have been
studied for patients with FES, but no randomized
controlled trials or retrospective studies support
its use.1 The concern with heparin use is that it
increases free fatty acids, thereby aggravating the
inflammatory process of FES.3
A prognosticator of FES is a significantly
increased interleukin-6 level 12 hours after injury.
Interleukin-6 is an inflammatory marker. In a 2013
study, Prakash et al. noted a significant rise in the
serum interleukin-6 level at 12 hours post-injury
in patients who developed FES compared with a
moderate rise in those that did not develop FES.
Although they reported some limitations in their
study, including a small sample size and use of
only Gurd’s criteria, Prakash et al. thought that
additional studies need to be performed at the
molecular level of FES regarding interleukin-6
to explore possible treatment of FES with
interleukin-6 receptor antibodies or antagonists.27
Conclusion
Fat embolism syndrome, usually resulting
from substantial trauma such as a long bone
fracture, is a clinical conundrum to diagnose
and therefore may not be diagnosed as often as
it occurs.7 As a result of fat being released into
the circulation, clinical findings such as hypoxia,
neurological changes, and petechia may occur,
leading a clinician to consider this syndrome.5
However, more times than not, the clinical signs
may be vague and therefore dismissed as a
sequela of surgery, anesthesia, or narcotic use.
Since hypoxia is the most common symptom, and
usually the first to appear, any trauma patient,
especially one with a long bone fracture, should
be monitored for difficulty breathing or signs
of hypoxia throughout the duration of their
hospitalization for early detection of FES.27
References
1. Kosova E, Bergmark B, Piazza G. Fat embolism
syndrome. Circulation. 2015 Jan 20;131(3):317-20.
2. Tzioupis CC, Giannoudis PV. Fat embolism
syndrome: What have we learned over the years?
Trauma. 2011;13(4):259-81.
3. Talbot M, Schemitsch EH. Fat embolism syndrome:
history, definition, epidemiology. Injury. 2006
Oct;37(Suppl 4):S3-7.
4. Kwiatt ME, Seamon MJ. Fat embolism syndrome. Int
J Crit Illn Inj Sci. 2013 Jan;3(1):64-8.
5. Gurd AR. Fat embolism: an aid to diagnosis. J Bone
Joint Surg Br. 1970 Nov;52(4):732-7.
6. Husebye EE, Lyberg T, Røise O. Bone marrow fat in
the circulation: clinical entities and pathophysiological
mechanisms. Injury. 2006 Oct;37(Suppl 4):S8-18.
7. Gupta B, D’souza N, Sawhney C, Farooque K, Kumar
A, Agrawal P, Misra MC. Analyzing fat embolism
syndrome in trauma patients at AIIMS Apex Trauma
Center, New Delhi, India. J Emerg Trauma Shock. 2011
Jul;4(3):337-41.
8. Stein PD, Yaekoub AY, Matta F, Kleerekoper
M. Fat embolism syndrome. Am J Med Sci. 2008
Dec;336(6):472-7.
9. Akhtar S. Fat embolism. Anesthesiol Clin. 2009
Sep;27(3):533-50.
10. Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat
embolism syndrome. A 10-year review. Arch Surg. 1997
Apr;132(4):435-9.
11. Gurd AR, Wilson RI. The fat embolism syndrome. J
Bone Joint Surg Br. 1974 Aug;56B(3):408-16.
12. Schonfeld SA, Ploysongsang Y, DiLisio R, Crissman
JD, Miller E, Hammerschmidt DE, Jacob HS. Fat
embolism prophylaxis with corticosteroids. A
prospective study in high-risk patients. Ann Intern
Med. 1983 Oct;99(4):438-43.
13. Lindeque BG, Schoeman HS, Dommisse GF, Boeyens
MC, Vlok AL. Fat embolism and the fat embolism
syndrome. A double-blind therapeutic study. J Bone
Joint Surg Br. 1987 Jan;69(1):128-31.
14. Filomena LT, Carelli CR, Figuerdo da Silva NC,
Pessoa de Barros Filho DE, Amatuzzi MM. Fat
embolism: A review for current orthopaedic practice.
Acta Ortop Bras. 2005;13:196-208.
15. Bodanapally UK, Shanmuganathan K,
Saksobhavivat N, Sliker CW, Miller LA, Choi AY,
Mirvis SE, Zhuo J, Alexander M. MR imaging and
differentiation of cerebral fat embolism syndrome from
diffuse axonal injury: application of diffusion tensor
imaging. Neuroradiology. 2013 Jun;55(6):771-8. Epub
2013 Mar 21.
16. Kuo KH, Pan YJ, Lai YJ, Cheung WK, Chang FC,
Jarosz J. Dynamic MR imaging patterns of cerebral fat
embolism: a systematic review with illustrative cases.
AJNR Am J Neuroradiol. 2014 Jun;35(6):1052-7. Epub
2013 May 02.
17. Forteza AM, Koch S, Campo-Bustillo I, Gutierrez
J, Haussen DC, Rabinstein AA, Romano J, Zych GA,
Duncan R. Transcranial Doppler detection of cerebral
fat emboli and relation to paradoxical embolism: a pilot
study. Circulation. 2011 May 10;123(18):1947-52. Epub
2011 Apr 25.
18. Shine TS, Feinglass NG, Leone BJ, Murray PM.
Transesophageal echocardiography for detection of
propagating, massive emboli during prosthetic hip
fracture surgery. Iowa Orthop J. 2010;30:211-4.
19. Scalea TM. Optimal timing of fracture fixation: have
we learned anything in the past 20 years? J Trauma.
2008 Aug;65(2):253-60.
20. Sharma RM, Setlur R, Upadhyay KK, Sharma AK
Mahajan S. Fat embolism syndrome: A diagnostic
dilemma. MJAFI. 2007;63:394-6.
21. Högel F, Gerlach UV, Südkamp NP, Müller CA.
Pulmonary fat embolism after reamed and unreamed
nailing of femoral fractures. Injury. 2010;41:1317-22.
22. Issack PS, Lauerman MH, Helfet DL, Sculco TP, Lane
JM. Fat embolism and respiratory distress associated
with cemented femoral arthroplasty. Am J Orthop
(Belle Mead NJ). 2009 Feb;38(2):72-6.
23. Green J. History and development of suctionirrigation-reaming. Injury. 2010 Nov;41(Suppl 2):S24-31.
24. Zhao J, Zhang J, Ji X, Li X, Qian Q, Xu Q. Does
intramedullary canal irrigation reduce fat emboli?
A randomized clinical trial with transesophageal
echocardiography. J Arthroplasty. 2015 Mar;30(3):451-5.
Epub 2014 Oct 14.
25. Powers KA, Talbot LA. Fat embolism syndrome after
femur fracture with intramedullary nailing: case report.
Am J Crit Care. 2011 May;20(3):267: 264-6.
26. Bederman SS, Bhandari M, McKee MD, Schemitsch
EH. Do corticosteroids reduce the risk of fat embolism
syndrome in patients with long-bone fractures? A metaanalysis. Can J Surg. 2009 Oct;52(5):386-93.
27. Prakash S, Sen RK, Tripathy SK, Sen IM, Sharma RR,
Sharma S. Role of interleukin-6 as an early marker of fat
embolism syndrome: a clinical study. Clin Orthop Relat
Res. 2013 Jul;471(7):2340-6. Epub 2013 Feb 20.
JOPA 9
Bone Up
Bone Health Column
Karen Cummings, PA-C
A fracture liaison service (FLS),
embedded within the orthopaedic clinic, has
gained substantial momentum and popularity
as efforts to enhance disease management in
an efficient and quality-based manner are under
way. The need for an FLS is directly correlated
to the growing number of fragility fractures seen
annually, the historical inadequacy of diagnosis
and treatment of poor bone quality following
fractures, and the high cost with regard to both
patient quality of life and our national economy.
From the systems perspective in public health,
the FLS, although not an “upstream solution,” is at
least a “midstream” one. Our previous complacent
response, which was to treat the fracture and
send the patient off with the hope that someone
else would take responsibility for him or her, has
put us in a position of giving incomplete care,
often with poor future outcomes.
There is a plethora of studies confirming
what we know: “fracture begets fracture.” A
fracture at any site is associated with a doubling
of future fracture risk, and 50% of patients
presenting with a hip fracture have incurred a
previous fracture. Many of us have witnessed
this in our own practices with “repeat-customer”
visits, with the patient seen initially for a distal
radial fracture, then for a vertebral wedge
fracture, and finally for the most ominous of
all—a hip fracture. We must be cognizant of the
mortality and morbidity associated with hip
fracture, which can cause such pain and suffering
for both patients and their families. Given that
treatment has been shown to reduce the risk of
future fracture by up to 50%, why turn our backs
when we can so easily help?
Meeting the challenge of quickly responding
to the first fracture in a way that prevents the
second is where we start, along with persisting
with public health messages that promote a
healthy bone lifestyle.
While a dedicated FLS is ideal, even
nominal efforts, including bone health discussion,
ordering basic laboratory tests and dual x-ray
absorptiometry (DXA) scans, along with sending
a templated letter to the patient’s primary
care physician (PCP), can be steps in the right
direction.
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JOPA
If you are as lucky as I was to have practice
administration buy in to a dedicated program,
run with it. Build your program to include a
fracture clinic where you can assess, treat, and
educate. Build your referral system to include fall
prevention, mobility enhancement, and exercise
programs. Know what community smoking
cessation and alcohol moderation/cessation
programs are available to you. Build your
relationships with rheumatology, endocrinology,
and geriatrics practitioners for oversight and
future referral. Send short templated letters to
your patients’ PCPs so that they know you are
working with them, not against them.
Consider erecting community education
programs for your elderly patients, a local
support group, or better yet an educational forum
at your local community college where you might
even have a direct “upstream” effect.
Our captive audience—the fracture
patient, still feeling the pain of this sentinel
event—deserves our swift response and quality
care.
Going forward, each quarterly issue of
JOPA will feature an article on osteoporosis
education, including a case study and other
fragility fracture information that you might find
helpful. These articles will raise osteoporosis
awareness and provide all PAs and NPs with a
better understanding of diagnosis and treatment.
We hope this might increase your knowledge
base, and encourage some of you to take a step
toward creating your own FLS.
CASE STUDY
A 63-year-old man presented to the
emergency department (ED) with a femoral neck
fracture that he sustained from a fall while biking.
He incurred a fracture of the contralateral hip 5
years previously, also from a fall while biking.
His medical history was significant for mild
hypertension and gastroesophageal reflux disease
(GERD). His medications included lisinopril and
Nexium (esomeprazole). He had no known drug
allergies.
He was married and worked as an
accountant. He had a remote smoking history,
having quit at age 30. He reported drinking 1
glass of red wine daily. He was a strict vegan, with
minimal or no calcium intake, and did not take
any supplements.
His family history was significant in that
his mother had sustained a hip fracture.
While in the ED, the patient reported pain and
tenderness over the lateral aspect of the hip.
His sensation was intact. Radiographs showed a
comminuted and displaced fracture of the femoral
neck. His blood pressure was 145/92, pulse was 92
bpm, respiration rate was 20 breaths/min, weight
was 197 lb (89.3 kg), and height was 75 in (190.5
cm).
Laboratory values included a calcium level
of 8.5 mg/dL, albumin level of 3.4 g/dL, vitamin
D 25-hydroxy level of 16 ng/mL, parathyroid
hormone (PTH) level of 54 pg/mL, and a normal
complete blood-cell count (CBC).
The patient underwent surgical fixation
and fared well without complications. He
was prescribed pain medication as well as
ergocalciferol (50,000 IU weekly for 6 weeks)
and was discharged to a local extended-care
facility for rehabilitation. He returned 2 weeks
postoperatively for a wound check and staple
removal. On examination, he had a negative
review of symptoms. His examination showed
a healing surgical wound. DXA scheduled prior
to the visit showed a lumbar T-score of −1.9. His
FRAX (Fracture Risk Assessment Tool) score
indicated a 25% risk of a major bone fracture and
a 3.4% risk of a hip fracture in the next 10 years.
I discussed my role specific to the
fracture with the patient, stating that I wanted to
determine why the fracture occurred, to assist
in the healing of his fracture, and to prevent
another fracture. I discussed his DXA scan
showing low bone mineral density (BMD) in
his spine and how I calculated his FRAX score,
which was elevated. He was informed that the
World Health Organization (WHO) recommends
treating patients with FRAX scores of >20% (for
the risk of a major fracture) and >3% (for the risk
of a hip fracture), as they are at increased risk of
another fracture. We additionally discussed how
his limited dietary calcium, low vitamin-D and
albumin levels, and family history of hip fracture
contributed to his osteoporosis.
Recommendations included (1) 600
mg of calcium citrate twice daily (citrate is
recommended for patients concurrently taking
proton pump inhibitors, as carbonate requires
acid to break it down), (2) completion of his
6-week course of ergocalciferol to be followed
by 2,000 IU vitamin D-3 daily, (3) limitation of
alcohol intake to <3 servings daily, and (4) crosstraining to include at least 4 hours of weightbearing exercise a week after being released from
restrictions. Orders were placed for a further
work-up, including an 8 A.M. measurement of the
testosterone level, and a 24-hour urine calcium
test to screen for primary hypercalciuria. We
further discussed medication management and
the risks versus benefits of treatment. Finally he
was given a referral to a nutritionist.
The 8 A.M. testosterone level came back
low at 2.10 ng/mL, whereas the 24-hour urine
calcium level was normal. The patient was
informed of these results at a 6-week followup appointment. We discussed that his low
testosterone level may be a contributor to his
low BMD. We also discussed that he would be
best served by seeing his internist regarding
treatment, as there is some controversy relative
to the effect of testosterone replacement therapy
(TRT) both on the risk of cardiovascular disease
and on prostate-specific antigen (PSA) levels.
He asked whether optimization of calcium and
vitamin D alone would be enough. I told him that,
although this was necessary for bone remodeling,
it would not have the needed effect alone on
microarchitecture.
Given his young age, and history
of bilateral hip fracture, I chose Forteo
(teriparatide) injection for this patient; although
I did not know his hip BMD, his bone quality was
certainly suspect. In my clinic, I tend to be more
aggressive with the treatment of younger patients
who have already sustained a fracture, especially
one of the hip. An anabolic drug has more utility
by improving bone quality or microarchitecture.
The patient had no contraindications to taking
this drug (history of skeletal malignancy, external
beam radiation, hypercalcemia, or kidney stones).
He was given injection-pen training, demonstrated
proficiency, and began treatment immediately.
A templated letter was sent to his PCP regarding
the findings and treatment, and encouraging
future efforts in managing his osteoporosis.
DISCUSSION
Fragility fractures are generally described
as fractures that occur from a low-energy
incident, such as a fall from a standing height.
This is a particularly interesting case given that
the patient was an otherwise healthy, active man
JOPA 11
with what could be considered a high-velocity
fracture sustained from a bike crash. Given that
this was his second hip fracture, he was astutely
referred to the Fragility Clinic for evaluation.
Osteoporosis has typically been thought of as
a disease affecting women; however, it is well
known that 1 in 4 men over age 50 will incur an
osteoporosis-related fracture in their lifetime. Of
all fractures, a hip fracture in a man carries the
greatest mortality and morbidity, with 1 in 3 male
patients dying within the first year and another 1
in 3 incurring another fracture in their lifetime.
Osteoporosis in men can be classified
as either primary or secondary. Primary
osteoporosis is age-related and/or idiopathic.
Age-related osteoporosis usually occurs over the
age of 70, while idiopathic osteoporosis is defined
as >1 fractures in a patient with low BMD between
the ages of 65 and 70 years. There may be a
genetic predisposition or familial tendency.
When not related to aging, secondary
osteoporosis is likely related to chronic
disease such as chronic obstructive pulmonary
disease, coronary artery disease, autoimmune
disease, or hypogonadism. Lifestyle behaviors
including alcohol or tobacco abuse, poor
nutrition, or chronically low levels of vitamin
D could be contributors. Medications such as
glucocorticoids, anticonvulsants, or androgen
deprivation are well known offenders to bone.
The National Osteoporosis Foundation
(NOF), the Endocrine Society, and the
International Society of Clinical Densitometry
(ISCD) recommend screening of all men age 70
or older and younger men with prior fractures or
other risk factors. Had we known to follow these
guidelines when this patient incurred his initial
hip fracture, perhaps the second hip fracture
could have been prevented.
The literature on master male cyclists
shows an increased occurrence of low BMD in
the spine and low hip T-scores. This, combined
with a high risk for falls associated with
competitive cycling, can be the perfect setup for
fracture. Promotion of weight-bearing exercise is
paramount in this population.
Overall, male osteoporosis is an
underdiagnosed condition and a major public
health concern. Establishing guidelines in your
clinic to evaluate all men age 50 and over with risk
factors and a fracture is imperative to reducing
morbidity and mortality in this population.
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JOPA
Articles reviewed in this case study:
1. Willson T, Nelson SD, Newbold J, Nelson RE,
LaFleur J. The clinical epidemiology of male
osteoporosis: a review of the recent literature.
Clin Epidemiol. 2015;7:65-76. Epub 2015 Jan 09.
2. Mathis SL, Farley RS, Fuller DK, Jetton AE,
Caputo JL. The relationship between cortisol
and bone mineral density in competitive male
cyclists. Journal of Sports Medicine. 2013.
3. Nagle KB, Brooks MA. A systematic review
of bone health in cyclists. Sports Health. 2011
May;3(3):235-43.
4. Friel J. Bones and cyclists. 2011 Mar 8. www.
joefrielsblog.com. Accessed 2016 Apr 28.
5. Snyder PJ, Ellenberg SS, Cunningham GR,
Matsumoto AM, Bhasin S, Barrett-Connor E,
Gill TM, Farrar JT, Cella D, Rosen RC, Resnick
SM, Swerdloff RS, Cauley JA, Cifelli D, Fluharty
L, Pahor M, Ensrud KE, Lewis CE, Molitch ME,
Crandall JP, Wang C, Budoff MJ, Wenger NK,
Mohler ER 3rd, Bild DE, Cook NL, Keaveny TM,
Kopperdahl DL, Lee D, Schwartz AV, Storer
TW, Ershler WB, Roy CN, Raffel LJ, Romashkan
S, Hadley E; The Testosterone Trials. The
Testosterone Trials: Seven coordinated trials of
testosterone treatment in elderly men [Epub].
Clin Trials. 2014 Mar 31;11(3):362-75. Epub 2014
Mar 31.
March Image Quiz: Discoid Lateral Meniscus
Figure 1. Standing bilateral anteroposterior
(AP) radiograph
A 13-year-old girl presents to your office
with a 4-month history of anterior-lateral right
knee pain. She believes the pain started when
she fell while skiing. She has since played
through her basketball season and is now
playing lacrosse. She had occasional swelling
after games and episodic “popping” with knee
extension, especially with sports and going down
stairs. She reports no locking or giving way of
the knee. Radiographs made in the office show
no abnormalities or fracture. Sagittal MRI of
the right knee shows a discoid lateral meniscus
with extensive horizontal tearing. Arthroscopic
findings of a normal medial meniscus and discoid
lateral meniscus are shown above.
Sagittal magnetic resonance imaging (MRI)
showing a discoid lateral meniscus with
extensive horizontal tearing.
Figure 3. Discoid lateral meniscus
seen during arthroscopy.
What is the recommended treatment for this
patient’s discoid lateral meniscus tear?
A. Total lateral meniscectomy
B. Arthroscopic saucerization
C. Lateral meniscus repair
D. Observation
A meniscus is a C-shaped cartilaginous
pad that acts as a shock absorber to protect
articular cartilage in the knee. A discoid meniscus
is an anatomical variant in which the meniscus
is wider and thicker than normal. The discoid
Figure 4. Normal medial meniscus
seen during arthroscopy.
JOPA 13
March Image Quiz: Discoid Lateral Meniscus
meniscus covers more of the tibial plateau than
normal and is therefore more prone to get stuck
with knee extension, undergo degeneration, and
tear. This anatomical variant is found in 3% to
5% of the United States population and is more
prevalent in the lateral meniscus. Discoid menisci
occur bilaterally in up to 20% of cases and rarely
occur on the medial side.
Discoid menisci are classified based on
arthroscopic findings and include complete vs.
incomplete and stable vs. unstable. The Watanabe
classification system describes “complete,” or
type 1, as a lateral meniscus that covers the
entire lateral tibial plateau and “incomplete,” or
type 2, as a lateral meniscus that covers <80%
of the lateral tibial plateau. In a normal knee,
the lateral meniscus covers up to 70% of the
lateral tibial plateau. Both type 1 and type 2 have
normal peripheral attachments and are therefore
stable with arthroscopic probing. Watanabe
also described a third variant (type 3), or a
hypermobile Wrisberg type, that lacks posterior
meniscotibial attachment but otherwise has a
more normal shape. This lack of stability at the
posterior horn can cause hypermobility of the
meniscus with the knee in extension, resulting
in symptomatic “locking” or “popping.” These
symptoms are often referred to as “snapping knee
syndrome.” A Wrisberg-type discoid meniscus
appears normal on MRI, and arthroscopic
evaluation is necessary to confirm the diagnosis.
Discoid menisci are often asymptomatic and
found incidentally on MRI or during arthroscopy.
Due to their increased width and thickness,
they are, however, more prone to symptomatic
tears than are normal menisci. Patients most
often become symptomatic during adolescence;
symptoms may include pain, clicking, and
mechanical locking as the knee moves from
flexion to extension.
Diagnostic work-up includes radiographs
and MRI. AP radiographs may show widening
of the lateral joint space, squaring of the lateral
femoral condyle, and cupping of the lateral tibial
plateau. A normal lateral meniscus averages 4 to 5
mm in thickness whereas a discoid meniscus can
be 8 to 10 mm thick. A discoid lateral meniscus
14
JOPA
Figure 5. Arthroscopic saucerization
may result in varus knee alignment, which
increases the risk of progressive degenerative
arthrosis of the medial compartment. MRI is the
study of choice to determine if a discoid meniscus
is present, if the meniscus is torn, and if other
pathology is present. MRI findings include an
increased transverse diameter on coronal views
and continuity between the anterior and posterior
horns of the meniscus (“bow-tie sign”) seen on
contiguous sagittal views. A Wrisberg variant
(type 3) most likely appears normal on MRI, and
diagnostic arthroscopy may be necessary in
symptomatic patients.
A stable asymptomatic discoid meniscus
found incidentally on MRI or during arthroscopy
does not require treatment, as many patients
never have symptoms. Patients who have a tear
on MRI or present with mechanical symptoms
of pain, locking, swelling, or giving way should
be treated with knee arthroscopy. In the past,
complete and incomplete discoid menisci were
treated with total meniscectomy. However, a
better understanding of the correlation between
a meniscus-deficient knee and early cartilage
degeneration has led surgeons to preserve as
much normal meniscal tissue as possible. The
current standard of treatment is arthroscopic
March Image Quiz: Discoid Lateral Meniscus
saucerization to trim the meniscal tissue to
a normal crescent shape. Associated discoid
meniscal tears are treated with arthroscopic
partial meniscectomy. Torn meniscal tissue
is removed until a stable peripheral rim is
reestablished. A hypermobile Wrisberg type is
repaired to stabilize and prevent hypermobility.
Answer B.
References
1. Yaniv M, Blumberg N. The discoid meniscus. J
Child Orthop. 2007 Jul;1(2):89-96. Epub 2007 Jun
26.
2. Kramer DE, Micheli LJ. Meniscal tears and
discoid meniscus in children: diagnosis and
treatment. J Am Acad Orthop Surg. 2009
Nov;17(11):698-707.
3. Kim SJ, Bae JH, Lim HC. Does torn discoid
meniscus have effects on limb alignment and
arthritic change in middle-aged patients? J Bone
Joint Surg Am. 2013 Nov 20;95(22):2008-14.
4. Jordan MR. Lateral meniscal variants:
evaluation and treatment. J Am Acad Orthop Surg.
1996 Jul;4(4):191-200.
JOPA 15
April Image Quiz: Bennett fracture
Figure 1
A 25-year-old man presents with right
thumb pain after an all-terrain-vehicle accident
2 days ago. He had immediate pain and swelling
after the injury, and he has been unable to use the
thumb since. Radiographs obtained at an outside
urgent-care facility are shown above.
What is the recommended treatment?
A. Thumb spica cast immobilization
B. Activities to tolerance
C. Closed reduction and cast immobilization
D. Closed reduction and percutaneous pinning
E. Open reduction and internal fixation
Answer D. The patient sustained a
displaced Bennett fracture, which is a single
vertical intra-articular fracture at the base of
the carpometacarpal (CMC) joint. The most
common mechanism of injury is a direct blow
to the thumb with a partially flexed metacarpal.
The strong volar oblique ligament, or palmar
beak ligament, is the primary stabilizer of the
trapeziometacarpal joint. The ligament holds the
volar bone fragment in place as the main fragment
of the metacarpal shaft displaces. The metacarpal
shaft usually displaces radially and dorsally
from the pulling forces of the abductor pollicis
longus and the adductor pollicis. Subluxation
of the CMC joint can be seen on the patient’s
16
JOPA
Figure 2
radiographs. A Rolando fracture also involves
the trapeziometacarpal joint but has a different
fracture pattern with similar deforming forces. A
Rolando fracture is Y-shaped with intra-articular
comminution whereas a Bennett fracture has a
single fracture fragment. Anteroposterior (AP),
lateral, and oblique radiographs of the thumb
are necessary to determine the type of fracture
pattern present. Radiographs of a Bennett fracture
will show an avulsion off the volar prominence of
the metacarpal base as illustrated in Figure 1.
Treatment of metacarpal base fractures
is determined by the CMC joint stability, fracture
pattern, and amount of displacement. Extraarticular fractures of the thumb metacarpal
with angulation of up to 20 to 30 degrees in the
lateral plane can be treated nonoperatively with
a thumb spica cast for 6 weeks without functional
deficit; however, the cosmetic appearance may
be bothersome. Nondisplaced intra-articular
fractures can also be treated conservatively but
should be followed closely for displacement.
Displaced intra-articular Bennett fractures treated
nonoperatively lead to persistent subluxation
and a likelihood of post-traumatic arthritis.
Closed reduction should be attempted with the
patient under anesthesia and use of fluoroscopic
guidance to achieve a congruent joint space.
The reduction maneuver includes longitudinal
April Image Quiz: Bennett fracture
Figure 3. Bennett fracture illustration.
traction with abduction and extension of the
thumb metacarpal. The amount of residual
displacement after reduction correlates with the
severity of arthritis, so an anatomic reduction
is crucial. If closed reduction is achieved with
<2 mm of displacement then percutaneous
pinning is performed to stabilize the joint.
The deforming forces at the CMC joint tend to
displace the reduction, so percutaneous pinning
of the metacarpal shaft to the trapezium is used
to hold the metacarpal reduced. A pin is also
placed through the fracture fragment and into
the 2nd metacarpal base for further stability.
Percutaneous pinning also provides sufficient
stability for accurate healing of the stabilizing
ligaments. The pins are removed approximately
6 weeks postoperatively. Open reduction and
internal fixation is indicated when the fragment
cannot be closed reduced with less than a 2-mm
step-off and if the displaced fragment is >20% of
the articular surface. Cast immobilization with the
interphalangeal joint free is typically used for 6
to 8 weeks postoperatively. Progressive range-ofmotion exercises are initiated after cast removal,
with the goal of forceful pinch loading beginning
at 3 months. Residual instability is a more
prevalent complication than joint stiffness, so
patients should be advised to adhere to a slowly
progressive rehabilitation protocol.
Figure 4. Postoperative lateral radiograph
Figure 5. Postoperative AP radiograph
JOPA 17
April Image Quiz: Bennett fracture
References
1. Soyer AD. Fractures of the base of the first
metacarpal: current treatment options. J Am Acad
Orthop Surg. 1999 Nov-Dec;7(6):403-12.
2. Henry MH. Fractures and dislocations of the
hand. Bennett fracture. In: Bucholz RW, Heckman
JD, Court-Brown C, editors. Rockwood and
Green’s fractures in adults. 6th ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2005. p 836-850.
3. Cullen JP, Parentis MA, Chinchilli VM, Pellegrini
VD Jr. Simulated Bennett fracture treated with
closed reduction and percutaneous pinning. A
biomechanical analysis of residual incongruity
of the joint. J Bone Joint Surg Am. 1997
Mar;79(3):413-20.
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May Image Quiz: Charcot Arthropathy
Figure 1
Figure 2
A 73-year-old insulin-dependent diabetic
woman presents with left foot pain 1 week after
“stepping wrong” while getting out of the shower.
She has had pain, swelling, and erythema in
the foot since the injury. She is also having
increased pain with weight-bearing on the foot.
On examination, you notice swelling, erythema,
and pain on palpation over the midfoot. Lighttouch sensation and distal pulses are intact.
Anteroposterior (AP) and lateral radiographs of
the foot are shown above.
What is the most appropriate treatment plan?
A. Non-weight-bearing cast for 3 weeks; then
repeat radiographs in 2 weeks
B. Weight-bearing boot with physical therapy
C. Weight-bearing cast for 3 weeks; then repeat
radiographs in 4 weeks
D. Nonsteroidal anti-inflammatory drugs (NSAIDs)
and activities as tolerated
Answer A. Charcot arthropathy should
be suspected in diabetic patients >50 years
of age with erythema and foot pain resulting
from minimal or no known trauma. Although
Charcot arthropathy is most common in diabetic
patients, the condition can occur with other
causes of peripheral neuropathy including
chronic alcohol abuse, syphilis, syringomyelia,
and myelomeningocele. It is important to note
that the condition can occur in both insulindependent and non-insulin-dependent diabetics,
and the amount of sensation loss in the foot may
vary. Initial signs include swelling, erythema,
and increased warmth of the foot as a result of
an uncontrolled inflammatory response. The
exact mechanism is unclear, but the condition is
thought to be caused by a hypovascular response
that reduces bone density and healing ability in
the foot. Repetitive microtrauma that exceeds the
rate of healing causes a high incidence of fracture
and progressive osseous destruction. Without
early intervention and with continued weightbearing, severe foot destruction can occur. The
most commonly affected site is the midfoot or the
subtalar, talonavicular, or calcaneocuboid joint.
However, Charcot arthropathy can also occur in
JOPA 19
May Image Quiz: Charcot Arthropathy
the hindfoot, ankle, heel, and forefoot.
The Eichenholtz classification system is
commonly used to describe the stages of Charcot
arthropathy. Stage 0, with which this patient
presented, includes swelling and erythema of
the foot with normal radiographic findings. Nonweight-bearing or protected weight-bearing with
frequent follow-up radiographs is necessary to
monitor for disease progression. Often, a return to
weight-bearing is not allowed until inflammation
and pain have subsided, which may take several
weeks to months. Total contact casts are often
used to help reduce total load on the foot.
Casts should be changed every 2 to 4 weeks for
frequent skin checks. Stage 1 is the fragmentation
or dissolution phase, when pain continues and
fractures, dislocations, and deformity of the
midfoot may be evident on radiographs. Patients
with Stage 1 are treated with non-weight-bearing
in a total contact cast. Stage 1 can last from 2 to
6 months. Stage 2 is the coalescence phase with
osseous absorption and fusion of osseous debris.
Erythema and warmth begin to diminish in stage
2. Treatment of stage 2 involves a molded anklefoot orthosis that allows for weight-bearing while
providing immobilization. Stage 3 is the chronic
phase, when fracture fragments consolidate and
remodel. Erythema and swelling have subsided,
and the foot deformity or collapse stabilizes.
Treatment of stage 3 involves progression to
an accommodative shoe and insole. Stages 2
and 3 combined can last from 18 to 24 months.
Nonsurgical treatment has a success rate of
75%. Osseous collapse of the midfoot can lead
to the development of a rocker-bottom-type
deformity with valgus at the midfoot. Progressive
pain, deformity severity, infection, and skin
ulceration may be indications for surgery. Surgical
treatments include exostectomy (removal of the
ulcer-inciting osseous prominence), arthrodesis,
and amputation.
The stage at presentation and disease
progression can vary widely among patients.
Some patients may present very early with
no radiographic changes while others may
present with a severely destabilized foot.
Disease progression is also unpredictable and
may occur despite early intervention. Patients
should be educated about the potential for
20
JOPA
Figure 3. Rocker bottom deformity
permanent impairment and the fact that bilateral
involvement is common.
References
1. Charcot arthropathy.www.aofas.org. Accessed
2016 Apr 14.
2. Van der Ven A, Chapman CB, Bowker JH.
Charcot neuroarthropathy of the foot and ankle. J
Am Acad Orthop Surg. 2009 Sep;17(9):562-71.
3. de Souza LJ. Charcot arthropathy and
immobilization in a weight-bearing total contact
cast. J Bone Joint Surg Am. 2008 Apr;90(4):754-9
SEIZE THE INITIATIVE
Earn a CAQ
in Orthopaedic
Surgery.
Two exam windows this year: August 1-5; September 12-16.
You are building your reputation as a clinician, and
you want to set yourself apart. You’ve honed your skills.
You’ve gained knowledge and expertise. You’ve done
everything to be an accomplished orthopaedic surgery PA.
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Reactive Arthritis:
A Case Study
Dagan Cloutier, PA-C
An 8-year-old boy presented to the office
with left knee pain following a hockey injury 3
days before. The injury occurred as he was sliding
across the ice to block an opponent’s shot and
was struck on top of the lateral aspect of the left
knee. He was able to continue playing the rest
of the game and in 3 other games over the next
2 days. The day after the tournament ended, his
knee became increasingly painful and he starting
having trouble bearing weight. He then presented
to our orthopaedic clinic for evaluation. Physical
examination in the office revealed an ecchymotic
area on the superolateral aspect of his left knee
with severe tenderness to palpation over the area.
He had a moderate joint effusion but was able to
perform straight leg raising against resistance.
The collateral and cruciate ligaments were intact.
Anteroposterior (AP) and lateral radiographs
obtained in the office showed no acute fractures
or abnormalities. Magnetic resonance imaging
(MRI) was ordered to rule out intra-articular
pathology as a cause of the pain.
Three days later, when the patient
returned to the office for follow-up and a review
of the MRI, he reported that the pain and swelling
in the knee had worsened. MRI findings included
a large joint effusion, osseous contusion over
the lateral femoral condyle, and adjacent edema
around the lateral soft tissues where the puck
had struck. On examination during this follow-up
visit, he was noted to have a large joint effusion
without erythema, warmth, or other clinical
signs of a septic joint. In general he had an
aseptic appearance. He reported no current or
recent symptoms of fever, sore throat, fatigue, or
other constitutional symptoms. He also did not
remember any prior knee pain and was otherwise
a very healthy active 8-year-old. He was not
taking prescription medications at the time of
injury and had no known drug allergies. He did
not have any rashes or pain in other joints. Other
pertinent history included no recent travel, no
exposures to animals , and no known exposures
to tuberculosis. There was no family history of
autoimmune disorders. The patient’s mother did
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JOPA
Figure 1. AP Radiograph
Figure 2. Lateral Radiograph
report that he had had a dental examination with
a cleaning 2 weeks before his injury.
The knee pain and effusion were presumed
to be from the traumatic injury, and a therapeutic
aspiration was offered. The aspirated fluid had
a very cloudy yellowish color so it was sent for
a cell count, Gram stain, aerobic and anaerobic
cultures, and a polymerase chain reaction assay
(PCR) for Lyme disease. Synovial fluid analysis
revealed a white blood cell count of 115,250 cells/
mm3 with a neutrophil predominance of 86%,
3% lymphocytes, and 7% monocytes. With the
substantially elevated white cell count in the
aspirate, the presumptive diagnosis was a septic
joint and the patient was taken to the operating
room for urgent irrigation and debridement. All
antibiotics were withheld until surgical culture
specimens were obtained. Surgical findings
included a large joint effusion described as
“blood-tinged and straw-colored, not purulent.”
Other surgical findings included intact intraarticular cartilage with no other pathology. The
operative fluid specimen was sent for repeat
analysis and had 65,000 white blood cells/mm3
with 92% neutrophils.
The patient was treated with cefazolin
postoperatively to cover Staphylococcus aureus,
this being the most common causative organism
found in his age group. Laboratory tests on
admission included a peripheral white blood
cell count of 7.9 × 1,000 cells/µL (normal for
his age) and elevated levels of inflammatory
markers (C-reactive protein [CRP] = 14 mg/L
and erythrocyte sedimentation rate [ESR] = 67
mm/hr ). He was afebrile on admission but had
temperature spikes of 101°F (38.3°C) during the
first few postoperative days. An infectious disease
consult was obtained on postoperative day 1.
The final results of the Gram stain and
culture of the aspirate initially obtained in the
office revealed no organisms. After 3 days, the
laboratory reported a final result of no growth on
all operative cultures. Blood cultures also showed
no growth after 48 hours. The final results of the
Lyme PCR and serum Lyme titers had yet to be
obtained when the infectious disease specialist
switched the patient from cefazolin to ceftriaxone,
with the most likely diagnosis at that point being
Lyme arthritis. Two days later, on postoperative
day 4, the Lyme PCR and serum titers both came
back negative and the diagnosis remained elusive.
The patient was still having pain and trouble
bearing weight and was transferred to a pediatric
tertiary care center for a rheumatology work-up.
Figure 3. Sagittal Knee MRI
The patient was followed by rheumatology and
orthopaedic surgery specialists at the tertiary
facility. All final cultures from outside hospitals
came back negative, and he progressed well
over the 2 days that he remained as an inpatient.
He was discharged home after 2 days with
instructions to take naproxen after discharge.
The working diagnosis at the time of discharge
was reactive arthritis.
Two days after discharge, the knee pain
and swelling returned and the patient was
readmitted to the tertiary care center for further
work-up. On admission, he was unable to bear
weight and had a low-grade fever. Laboratory
tests on admission showed a peripheral
white blood cell count of 8.82 × 1,000 cells/
µL , hemoglobin level of 9.6 g/dL, hematocrit
of 29%, CRP of 21 mg/L, and ESR of 109 mm/
hr . A peripheral blood smear was performed
because of the anemia and showed no evidence
of atypical cells. MRI and biopsy findings were
also not consistent with an oncologic process.
A repeat MRI showed a large joint effusion with
hypertrophic, enhancing synovitis. The bone
marrow edema on the lateral femoral condyle
had remained stable since the previous MRI,
JOPA 23
and there was no suspicion of osteomyelitis.
Enlarged popliteal lymph nodes were present.
The day after admission, the patient underwent
repeat irrigation and debridement with a partial
synovectomy. As he had been off antibiotics for
4 days prior to the surgery, standard cultures as
well as PCR for Kingella kingae were performed.
Postoperatively, the patient was started
on clindamycin to cover for potential communityacquired methicillin-resistant S. aureus (MRSA).
However, examination performed 2 days later
showed deterioration of his condition, with knee
swelling, pain, and an inability to bear weight.
Repeated tests of inflammatory marker levels
also showed a continued trend upward. All final
operative cultures were again negative, and the
synovial biopsy showed acute inflammation. A
repeat MRI showed a larger effusion with some
improvement in synovial enhancement. A third
irrigation and debridement procedure was then
performed. Fluid was sent for a K. kingae PCR,
cytology, and cultures using blood culture media.
Broad-range bacterial, fungal, and mycobacterial
PCRs were all negative, as was a human leukocyte
antigen (HLA)-B27 test. A urinalysis and antistreptolysin O (ASLO) titer were both negative as
well. The patient was switched from clindamycin
to cefazolin postoperatively to cover K. kingae.
Given the unusual course and negative
cultures, the rheumatologist thought the most
likely diagnosis to be reactive arthritis, and
the patient was started on prednisone, 20 mg
daily. The knee swelling and motion began to
improve, and the inflammatory marker levels
began to drop—the CRP to 3.41 mg/L and the
ESR to 98 mm/hr (from a peak of 116 mm/hr
). He was responding well on cefazolin so he
was switched to oral cephalexin at discharge
because of the convenience of using an oral agent
at home. Antibiotic treatment was continued
prophylactically for 3 weeks after his last surgical
intervention but was discontinued when all
cultures came back negative. The CRP level
and ESR, measured weekly, continued to trend
downward. Prednisone was continued for 4 weeks
after the last irrigation and debridement as his
clinical condition slowly improved. However, after
the 4 weeks, while he was being weaned off the
prednisone, the pain increased and methotrexate
was started. At the time of writing, the patient
was improving clinically as he continued with
treatment. The anemia did resolve after 4 weeks
of prednisone treatment and was thought to have
been related to the initial inflammatory response.
24
JOPA
The patient will be slowly weaned off prednisone
and methotrexate if he continues to improve
clinically, although at 3 months after presentation
he had yet to return to sports.
Discussion
This patient’s clinical presentation was
unusual for a septic joint, but the white blood cell
count on aspiration yielded >100,000 cells/mm3.
Certainly, the immediate concern was the septic
joint after the aspirate results were obtained,
and the patient was appropriately brought to
the operating room for urgent irrigation and
debridement. However, his postoperative course
was quite unpredictable as the bacterial pathogen
could not be identified and inflammatory marker
levels remained elevated despite antibiotic
treatment. The differential diagnosis remained
broad and included culture-negative septic
arthritis, reactive arthritis, juvenile idiopathic
arthritis, traumatic synovitis, poststreptococcal
reactive arthritis, leukemic arthritis, rheumatic
fever, and hemophilia. There was no evidence of
pigmented villonodular synovitis, osteomyelitis,
or malignancy on MRI, which excluded these
conditions from the likely diagnosis.
After the aspiration yielded 100,000
white blood cells, the initial focus was on a
septic-joint work-up and treatment, which
closely followed the clinical practice guideline
developed by Kocher et al.1 to improve efficiency
of care for children who present with suspected
septic arthritis. The guidelines define signs and
symptoms of septic arthritis as solitary joint
involvement, limited range of motion, limping
or inability to bear weight, and fever. Patients
with these symptoms without specific rashes
such as psoriasis and erythema migrans should
have further laboratory work-up. Recommended
laboratory tests include CRP, ESR, CBC (complete
blood-cell count) with differential, Lyme titer,
blood culture, throat culture/rapid strep test,
and ASLO. Standard AP and lateral radiographs
are also recommended. A joint aspiration is
recommended if laboratory tests reveal any
abnormalities. If the aspiration yields <50,000
white blood cells and there is no clinical
suspicion of infection then a rheumatology
consult is recommended. If the aspiration yields
≥50,000 white blood cells, or a positive Gram stain
is found, then the patient should be treated as
if he/she has a septic joint, with irrigation and
debridement. Intravenous (IV) cefazolin is the
first-line treatment for postoperative antibiotic
coverage, with IV clindamycin recommended
if a penicillin allergy is present. Ceftriaxone is
recommended for adolescents if gonococcal
arthritis is suspected. If the patient improves
clinically (is afebrile with decreased swelling,
decreased pain, and an increased range of
motion) after 72 hours of IV antibiotics and
meets certain criteria (diagnosis made within 4
days after the onset of symptoms, no concurrent
osteomyelitis, and an ability to tolerate
medications by mouth), then he/she can switch
to oral antibiotics, which should be taken for 4
weeks.1
A potential source of culture-negative
septic arthritis in this patient is the difficult-toculture bacteria K. kingae. This is a gram-negative
bacillus found in normal flora of the pharynx in
young children, usually those under the age of 4
who attend a day care center2. K. kingae rarely
grows on standard laboratory cultures, leading
to frequent false-negative results. Placing the
joint fluid in an aerobic culture and immediately
plating on blood and chocolate agar helps grow
the bacteria. A PCR technique also improves
detection, but neither laboratory that received
the initial aspiration fluid from the patient in
this case study had this technology. K. kingae
is susceptible to beta-lactam antibiotics so the
IV cefazolin and 4 weeks of oral cephalexin
would have been adequate coverage. It was
thought that if the true diagnosis was culturenegative septic arthritis, possibly from K. kingae,
the patient would have had better clinical
improvement while on antibiotic therapy3.
However, the prolonged inflammatory process
and persistent clinical symptoms experienced
by this patient are not unusual for a child with a
septic knee. The immune response to bacterial
endotoxins released in the knee can lead to a
delayed recovery and residual joint damage.
Administration of corticosteroids with antibiotics
in the treatment of septic arthritis in children
has gained popularity as it enhances the rate
of clinical recovery4, although the prednisone
treatment used in this patient was aimed at
reducing inflammation caused by reactive
arthritis, not septic arthritis.
The suspicion of leukemic arthritis was
low in this case but considered in the differential
diagnosis. Leukemic arthritis presents as a
warm, tender, swollen knee and may be the initial
presentation of acute lymphocytic leukemia. The
joint fluid specimen should be reviewed under
smear to look for lymphoblasts in the joint. The
presence of leukopenia and thrombocytopenia
helps differentiate leukemic arthritis from other
potential diagnoses. Preoperative laboratory
tests showed the hemogram to be within normal
limits with a white blood cell count of 6.2 × 1,000
cells/µL and a platelet count of 363.6/µL , further
excluding leukemic arthritis from the likely
diagnosis.
Also included in the differential diagnosis
was new-onset juvenile idiopathic arthritis (often
referred to as juvenile rheumatoid arthritis), which
typically presents with a limp and progressive
joint pain. Less often, it presents as an acute
onset of knee pain and swelling after a known
injury or precipitating event. Juvenile idiopathic
arthritis involving <5 joints is referred to as
oligoarticular. Patients presenting with an effusion
may have pus-like fluid on aspiration with a
white blood cell count as high as 100,000 cells/
mm3, as reported by Matan and Smith5. Juvenile
idiopathic arthritis is difficult to diagnosis
acutely, as there are no diagnostic laboratory
tests. A positive antinuclear antibody (ANA) test
is common but nonspecific. Inflammatory marker
levels are typically normal or mildly elevated;
however, the presence of anemia with an elevated
ESR and CRP level is associated with a risk of
disease progression and polyarticular disease.
The diagnosis is made with the presence of
arthritis in <5 joints during the first 6 months of
the disease when other causes have been ruled
out. First-line treatment includes nonsteroidal
anti-inflammatory drugs (NSAIDs) or an intraarticular steroid injection , or a combination
of the two. Methotrexate, a disease-modifying
antirheumatic drug (DMARD), is recommended
for patients with severe disease activity or with
moderate disease activity that is not responding
to other treatments6. The acuity of the patient’s
presentation seemed to make the diagnosis of
juvenile idiopathic arthritis unlikely.
Although bacterial arthritis could not be
entirely excluded, ultimately the presumptive
diagnosis was reactive arthritis, a diagnosis that
is rarely made even by rheumatologists. The
diagnosis was based on the patient’s history
and clinical features as there are no laboratory
tests that can confirm the diagnosis. Reactive
arthritis is defined as arthritis that develops 2
to 4 weeks after an extra-articular infection and
when pathogens cannot be grown on culture
of specimens from the involved joint. The
source is thought to be enteric or genitourinary
JOPA 25
infection, either recognized or clinically silent.
The most common pathogens are thought to
include bacteria from the bowel (Campylobacter,
Salmonella, Shigella, and Yersinia) and from
the genitals (Chlamydia trachomatis). Reactive
arthritis most commonly occurs between the
ages of 20 and 50 years. Some patients have
extra-articular manifestations, including uveitis,
urethritis, oral mucosal ulcers, and a rash. The
term reactive arthritis has also been used to
describe Reiter syndrome, or a clinical triad
of post-infectious arthritis, urethritis, and
conjunctivitis. Levels of acute inflammatory
markers such as CRP and ESR may be elevated.
Tests for HLA-B27, which is more prevalent in
patients with forms of spondylarthritis (including
reactive arthritis), are positive in an estimated
30% to 50% of patients. Joint aspirate usually
yields an elevated white blood cell count,
generally not exceeding 64,000 cells/mm3, with
a neutrophilic predominance. Radiographs and
MRI are nondiagnostic for reactive arthritis7,8.
Treatment of reactive arthritis is very similar
to treatment of juvenile idiopathic arthritis. In
general, antibiotic therapy is not indicated for
the treatment of the arthritis itself. First-line
medications include NSAIDs such as naproxen,
diclofenac, indomethacin, or Celebrex (celecoxib).
Intra-articular and systemic glucocorticoids are
commonly used in patients who do not respond
adequately to NSAIDs. If symptoms persist
beyond 4 weeks despite treatment with NSAIDs
and glucocorticoids, or if the patient requires
ongoing daily doses of >7.5 mg of prednisone for
3 to 6 months, then treatment with a DMARD is
often necessary. Sulfasalazine and methotrexate
are commonly used DMARDs, generally for
a duration of 3 to 4 months at the maximally
tolerated therapeutic doses. The prognosis of
reactive arthritis varies considerably, but most
patients are symptom-free by 3 to 5 months.
However, symptoms may persist beyond 12
months, with 15% to 20% of patients experiencing
chronic arthritis beyond a year7,8.
Conclusion
This case is certainly an unusual
one but a good example of why a broad
differential diagnosis should be considered
for pediatric patients who present with a
suspected septic joint. Despite strong clinical
suspicion, the diagnosis of a septic joint could
not be established, as multiple cultures of
26
JOPA
joint specimens came back negative. It was
also unclear whether the patient’s clinical
improvement when taking prednisone was related
to a reduction in inflammation caused by reactive
arthritis or culture-negative septic arthritis. While
the working diagnosis was reactive arthritis,
leukemic arthritis cannot be entirely excluded,
although it is very unlikely given that the blood
work, MRI, and synovial biopsy showed no
evidence of malignancy. The patient will be
followed clinically with rheumatology office visits
every month. Full recovery is expected with up to
6 months of treatment if the current diagnosis of
reactive arthritis proves correct.
References
1. Kocher MS, Mandiga R, Murphy JM, Goldmann
D, Harper M, Sundel R, Ecklund K, Kasser JR.
A clinical practice guideline for treatment of
septic arthritis in children: efficacy in improving
process of care and effect on outcome of septic
arthritis of the hip. J Bone Joint Surg Am. 2003
Jun;85-A(6):994-9.
2. Williams N, Cooper C, Cundy P. Kingella kingae
septic arthritis in children: recognising an elusive
pathogen. J Child Orthop. 2014 Feb;8(1):91-5.
Epub 2014 Jan 23.
3.Yagupsky P, Katz O, Peled N. Antibiotic
susceptibility of Kingella kingae isolates
from respiratory carriers and patients with
invasive infections. Journal of Antimicrobrial
Chemotherapy. 2001 Feb;47(2):191-3.
4. Fogel I, Amir J, Bar-On E, Harel L.
Dexamethasone Therapy for Septic Arthritis in
Children. Pediatrics. 2015 Oct;136(4):e776-82.
Epub 2015 Sep 07.
5. Matan AJ, Smith JT. Pediatric septic arthritis.
Orthopedics. 1997 Jul;20(7):630-5, quiz :636-7.
6. Weiss PF. Oligoarticular juvenile idiopathic
athrtitis. http://www.uptodate.com/contents/
oligoarticular-juvenile-idiopathic-arthritis. 2015
Dec 9. Accessed 2016 Feb 3.
7. Yu DT. Reactive Arthritis. 2015 May 15. http://
www.uptodate.com/contents/reactive-arthritis.
Accessed 2016 Ap 3.
8. American College of Rheumatology. Reactive
arthritis. 2015 May. http://www.rheumatology.org/
I-Am-A/Patient-Caregiver/Diseases-Conditions/
Reactive-Arthritis. Accessed 2016 Apr 3.