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TINJAUAN PUSTAKA

OSTEOARTHRITIS
Definisi : penyakit degeneratif yang mengenai rawan sendi, yang ditandai oleh kehilangan
rawan sendi progresif dan terbentuknya tulang baru pada trabekula subkondral dan tepi tulang
(osteofit)
Background
The progression of osteoarthritis is characteristically slow, occurring over several years or
decades.
Over this period, the patient can become less and less active and thus more susceptible to
morbidities related to decreasing physical activity (including potential weight gain).
Early in the disease process, the joints may appear normal. However, the patients gait may
be antalgic if weight-bearing joints are involved.
Osteoarthritis predominantly involves the weight-bearing joints, including the knees, hips,
cervical and lumbosacral spine, and feet. Other commonly affected joints include the distal
interphalangeal (DIP), proximal interphalangeal (PIP), and carpometacarpal (CMC) joints.
Historically, osteoarthritis has been divided into primary and secondary forms, though this
division is somewhat artificial.
Secondary osteoarthritis is conceptually easier to understand : It refers to disease of the
synovial joints that results from some predisposing condition that has adversely altered the
joint tissues (eg, trauma to articular cartilage or subchondral bone). Secondary osteoarthritis
can occur in relatively young individuals
Primary osteoarthritis is related to the aging process and typically occurs in older
individuals, an idiopathic phenomenon, occurring in previously intact joints.

No specific laboratory abnormalities are associated with osteoarthritis. Rather, it is typically

diagnosed on the basis of clinical findings, with or without radiographic studies
Nonpharmacologic interventions :

Patient education

Weight loss

Exercise

Physical therapy

Occupational therapy

Joint unloading, in certain joints (eg, knee and hip)

Pharmacologic
Intra-articular

pharmacologic

therapy

includes

corticosteroid

injection

and

viscosupplementation, which may provide pain relief and have an anti-inflammatory effect on
the affected joint.
Oral pharmacologic therapy begins with acetaminophen for mild or moderate pain without
apparent inflammation.
If the clinical response to acetaminophen is not satisfactory or the clinical presentation is
inflammatory, consider nonsteroidal anti-inflammatory drugs (NSAIDs).
If all other modalities are ineffective and osteotomy is not viable, or if a patient cannot
perform his or her daily activities despite maximal therapy, arthroplasty is indicated.

Klasifikasi radiografi osteoarthritis menurut kriteria Kellgren-Lawrence

Derajat

Klasifikasi

Gambaran Radiologis

Normal

Tidak ada gambaran radiologis yang abnormal

Meragukan

Tampak osteofit kecil

Minimal

Tampak osteofit, celah sendi normal

Sedang

Osteofit jelas, penyempitan celah sendi

Berat

Penyempitan celah sendi berat dan adanya sklerosis

Symptoms

Pain is usually the initial source of morbidity in osteoarthritis, with the diseases
primary symptom being deep, achy joint pain exacerbated by extensive use.

Reduced range of motion and crepitus

Stiffness during rest (gelling) with morning joint stiffness < 30 minutes.

Initially, pain can be relieved by rest and may respond to simple analgesics. However, joints
may become unstable as the osteoarthritis progresses; therefore, the pain may become more
prominent (even during rest) and may not respond to medications.
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Patophysiology
Primary and secondary osteoarthritis are not separable on a pathologic basis, though bilateral
symmetry is often seen in cases of primary osteoarthritis, particularly when the hands are
affected.
Traditionally, osteoarthritis was thought to affect primarily the articular cartilage of synovial
joints; however, pathophysiologic changes are also known to occur in the synovial fluid, as
well as in the underlying (subchondral) bone, the overlying joint capsule, and other joint
tissues
Although osteoarthritis has been classified as a noninflammatory arthritis, increasing
evidence has shown that inflammation occurs as cytokines and metalloproteinases are
released into the joint. These agents are involved in the excessive matrix degradation that
characterizes cartilage degeneration in osteoarthritis.
In early osteoarthritis, swelling of the cartilage usually occurs, because of the increased
synthesis of proteoglycans; this reflects an effort by the chondrocytes to repair cartilage
damage. This stage may last for years or decades and is characterized by hypertrophic repair
of the articular cartilage.
As osteoarthritis progresses, however, the level of proteoglycans eventually drops very low,
causing the cartilage to soften and lose elasticity and thereby further compromising joint
surface integrity. Over time, the loss of cartilage results in loss of joint space.
In major weight-bearing joints of persons with osteoarthritis, a greater loss of joint space
occurs at those areas experiencing the highest loads. In the osteoarthritic knee, for example,
the greatest loss of joint space is commonly seen in the medial femorotibial compartment,
though the lateral femorotibial compartment and patellofemoral compartment may also be
affected.
Erosion of the damaged cartilage in an osteoarthritic joint progresses until the underlying
bone is exposed. Bone denuded of its protective cartilage continues to articulate with the
opposing surface. Eventually, the increasing stresses exceed the biomechanical yield strength
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of the bone. The subchondral bone responds with vascular invasion and increased cellularity,
becoming thickened and dense (a process known as eburnation) at areas of pressure.
The traumatized subchondral bone may also undergo cystic degeneration, which is
attributable either to osseous necrosis secondary to chronic impaction or to the intrusion of
synovial fluid. Osteoarthritic cysts are also referred to as subchondral cysts, pseudocysts, or
geodes (the preferred European term) and may range from 2 to 20 mm in diameter.
Osteoarthritic cysts in the acetabulum (see the image below) are termed Egger cysts.

This radiograph demonstrates osteoarthritis of the right hip, including the finding of
sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a
bilateral finding, but it may occur unilaterally in an individual who has a previous history of
hip trauma that was confined to that one side.
At areas along the articular margin, vascularization of subchondral marrow, osseous
metaplasia of synovial connective tissue, and ossifying cartilaginous protrusions lead to
irregular outgrowth of new bone (osteophytes). Fragmentation of these osteophytes or of the
articular cartilage itself results in the presence of intra-articular loose bodies (joint mice).
Along with joint damage, osteoarthritis may also lead to pathophysiologic changes in
associated ligaments and the neuromuscular apparatus. For example, lateral collateral
ligament complex abnormalities are common in knee osteoarthritis.
Pain mechanisms in osteoarthritis
Pain, the main presenting symptom of osteoarthritis, is presumed to arise from a combination
of mechanisms, including the following:
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Osteophytic periosteal elevation

Vascular congestion of subchondral bone, leading to increased intraosseous pressure

Synovitis with activation of synovial membrane nociceptors

Fatigue in muscles that cross the joint

Overall joint contracture

Joint effusion and stretching of the joint capsule

Torn menisci

Inflammation of periarticular bursae

Periarticular muscle spasm

Psychological factors

Crepitus (a rough or crunchy sensation)

Central pain sensitization

When the spine is involved in osteoarthritis, especially the lumbar spine, the associated
changes are very commonly seen from L3 through L5.
Symptoms include pain, stiffness, and occasional radicular pain from spinal stenosis.
Foraminal narrowing is caused by facet arthritic changes that result in compression of the
nerve roots. Acquired spondylolisthesis is a common complication of arthritis of the lumbar
spine.

Etiology
The daily stresses applied to the joints, especially the weight-bearing joints (eg, ankle, knee,
and hip), play an important role in the development of osteoarthritis.
Risk factors for osteoarthritis include the following :

Age
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Obesity

Trauma

Genetics (significant family history)

Reduced levels of sex hormones

Muscle weakness

Repetitive use (ie, jobs requiring heavy labor and bending)

Infection

Crystal deposition

Acromegaly

Previous inflammatory arthritis (eg, burnt-out rheumatoid arthritis)

Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, and Wilson disease)

Hemoglobinopathies (eg, sickle cell disease and thalassemia)

Neuropathic disorders leading to a Charcot joint (eg, syringomyelia, tabes dorsalis,

and diabetes)

Underlying morphologic risk factors (eg, congenital hip dislocation and slipped
femoral capital epiphysis)

Disorders of bone (eg, Paget disease and avascular necrosis)

Previous surgical procedures (eg, meniscectomy)

Advancing age
With advancing age come reductions in cartilage volume, proteoglycan content, cartilage
vascularization, and cartilage perfusion.
These changes may result in certain characteristic radiologic features, including a narrowed
joint space and marginal osteophytes.
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Obesity
Obesity increases the mechanical stress in a weight-bearing joint. It has been strongly linked
to osteoarthritis of the knees and, to a lesser extent, of the hips.
Other causes
Trauma or surgery (including surgical repair of traumatic injury) involving the articular
cartilage, ligaments, or menisci can lead to abnormal biomechanics in the joints and
accelerate osteoarthritis.
Although repairs of ligament and meniscal injuries usually restore joint function,
osteoarthritis has been observed 5-15 years afterward in 50-60% of patients.
Genetics
A hereditary component, particularly in osteoarthritis presentations involving multiple joints,
has long been recognized.
Several genes have been directly associated with osteoarthritis, and many more have been
determined to be associated with contributing factors, such as excessive inflammation and
obesity.
Epidemiology
Age-related demographics
Primary osteoarthritis is a common disorder of the elderly, and patients are often
asymptomatic.
Approximately 80-90% of individuals > 65 years have evidence of radiographic primary
osteoarthritis.
Symptoms typically do not become noticeable until after the age of 50 years.
The prevalence of the disease increases dramatically among persons older than 50 years,
likely because of age-related alterations in collagen and proteoglycans that decrease the
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tensile strength of the joint cartilage and because of a diminished nutrient supply to the
cartilage.
Sex-related demographics
In individuals > 55 years, the prevalence of osteoarthritis is higher among women than
among men.
Women are especially susceptible to osteoarthritis in the DIP joints of the fingers. Women
also have osteoarthritis of the knee joints more frequently than men do, with a female-to-male
incidence ratio of 1.7:1. Women are also more prone to erosive osteoarthritis, with a femaleto-male ratio of about 12:1.
Differential Diagnosis
1. Rheumatoid arthritis
Rheumatoid arthritis predominantly affects the wrists, as well as the metacarpophalangeal
(MCP) and proximal interphalangeal (PIP) joints. It rarely, if ever, involves the distal
interphalangeal (DIP) joints or the lumbosacral spine.
Rheumatoid arthritis is associated with prominent, prolonged (> 1 hour) morning stiffness
and overtly swollen, warm joints.
Radiographic findings include bone erosion (eg, periarticular osteopenia or marginal erosions
of bone) rather than formation.
Laboratory findings that further differentiate rheumatoid arthritis from osteoarthritis include
the following:

Systemic inflammation (elevated erythrocyte sedimentation rate [ESR] or C-reactive

protein [CRP] level)

Positive serologies (rheumatoid factor [RF] or anticyclic citrullinated peptide [antiCCP] antibodies)

Inflammatory joint fluid with a predominance of polymorphonuclear leukocytes

(PMNs)
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Elevated white blood cell (WBC) count

2. Additional arthritides
Back pain may result from spondyloarthropathy or from osteoarthritis with sacroiliac and
lumbosacral spine involvement. Clinical history and characteristic radiographic findings can
be used to differentiate these disorders.
Secondary osteoarthritis must be considered in individuals with any of the following:

Chondrocalcinosis

History of joint trauma

Metabolic bone disorders

Hypermobility syndromes

Neuropathic diseases

Workup
1. Plain Radiography
Plain radiography is the imaging method of choice because it is more cost-effective
than other modalities and because radiographs can be obtained more readily and
quickly

This radiograph demonstrates osteoarthritis of the right hip, including the finding of
sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip
is a bilateral finding, but it may occur unilaterally in an individual who has a previous
history of hip trauma that was confined to that one side.
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The elbow is not commonly affected in osteoarthritis. However, elbow arthritis (see
the images below) can occur as a result of trauma.

Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history
of previous trauma.
2. Arthrocentesis
A diagnostic joint aspiration for synovial fluid analysis can help exclude
inflammatory arthritis, infection, or crystal arthropathy.
The presence of noninflammatory joint fluid helps distinguish osteoarthritis from
other causes of joint pain.
Other synovial fluid findings that aid in the differentiation of osteoarthritis from other
conditions are negative Gram stains and cultures, as well as the absence of crystals
when fluid is viewed under a polarized microscope.

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Treatment
Pharmacologic
American College of Rheumatology guidelines
The American College of Rheumatology (ACR) has issued guidelines for pharmacologic
treatment of osteoarthritis of the hand, hip, and knee.[57] For hand osteoarthritis, the ACR
conditionally recommends using 1 or more of the following:

Topical capsaicin
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Topical nonsteroidal anti-inflammatory drugs (NSAIDs), including trolamine

salicylate

Oral NSAIDs

Tramadol

The ACR conditionally recommends against using intra-articular therapies or opioid

analgesics for hand osteoarthritis. For patients 75 years and older, the ACR conditionally
recommends the use of topical rather than oral NSAIDs.
For knee osteoarthritis, the ACR conditionally recommends using 1 of the following:

Acetaminophen

Oral NSAIDs

Topical NSAIDs

Tramadol

Intra-articular corticosteroid injections

Non-Pharmacologic
Lifestyle modification, particularly exercise and weight reduction, is a core component in the
management of osteoarthritis.
Guidelines from Osteoarthritis Research Society International (OARSI) advise that
nonpharmacologic treatment of hip and knee osteoarthritis should initially focus on self-help
and patient-driven modalities rather than on modalities delivered by health professionals.
The ACR strongly recommends the following nonpharmacologic measures for patients with
knee or hip osteoarthritis :

Cardiovascular or resistance land-based exercise

Aquatic exercise

Weight loss, for overweight patients

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The ACR conditionally recommends the following measures for patients with knee or hip
osteoarthritis:

Self-management programs

Manual therapy in combination with supervised exercise

Psychosocial interventions

Thermal agents

Walking aids, as needed

Instruct the patient to avoid aggravating stress to the affected joint. Implement corrective
procedures if the patient has poor posture.
Weight reduction relieves stress on the affected knees or hips. The benefits of weight loss,
whether obtained through regular exercise and diet or through surgical intervention, may
extend not only to symptom relief but also to a slowing in cartilage loss in weight-bearing
joints (eg, knees).
In addition, weight loss lowers levels of the inflammatory cytokines and adipokines that may
play a role in cartilage degradation.
Some patients with osteoarthritis benefit from heat placed locally over the affected joint. A
minority of patients report relief with ice.
Physical activity
Although people with osteoarthritis tend to avoid activity, exercise is an effective treatment
for this condition, producing improvements in pain, physical function, and walking distance.
Long-term walking and resistance-training programs have been shown to slow the functional
decline seen in many patients with osteoarthritis, including older patients.

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Osteoarthritis of the knee may result in disuse atrophy of the quadriceps. Because these
muscles help protect the articular cartilage from further stress, quadriceps strengthening is
likely to benefit patients with knee osteoarthritis. Stretching exercises are also important in
the treatment of osteoarthritis because they increase range of motion.
In a study of patients with knee osteoarthritis, Jan et al found that in most respects, non
weight-bearing exercise was as therapeutically effective as weight-bearing exercise. After an
8-week exercise program, the 2 types of exercise resulted in equally significant
improvements in function, walking speed, and muscle torque.
Swimming, especially the aerobic aquatic programs developed by the Arthritis
Foundation, can be helpful.
Assistive devices
The use of assistive devices for ambulation and for activities of daily living (ADLs) may be
indicated for patients with osteoarthritis.
Braces and appropriate footwear may also be of some use. A cane can be used in the
contralateral hand for hip or knee osteoarthritis. The patient can be taught joint-protection and
energy-conservation techniques.
In a randomized study of 126 patients with painful knee osteoarthritis, wearing a slip-on knee
brace for a median of 7.35 hours a day for 6 weeks reduced pain and bone marrow lesions.
Occupational therapy and physical therapy
Occupational adjustments may be necessary for some patients with osteoarthritis. An
occupational therapist can assist with evaluating how well the patient performs ADLs, as well
as with retraining of the patient as necessary. Joint-protection techniques should be
emphasized. Physical therapy modalities, especially those aimed at deconditioned patients,
can be helpful, particularly in patients with hip or knee involvement.
Prognosis

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The prognosis in patients with osteoarthritis depends on the joints involved and on the
severity of the condition. No proven disease- or structure-modifying drugs for osteoarthritis
are currently known; consequently, pharmacologic treatment is directed at symptom relief.
A systematic review found the following clinical features to be associated with more rapid
progression of knee osteoarthritis :

Older age

Higher BMI

Varus deformity

Multiple involved joints

Patients with osteoarthritis who have undergone joint replacement have a good prognosis,
with success rates for hip and knee arthroplasty generally exceeding 90%. However, a joint
prosthesis may have to be revised 10-15 years after its placement, depending on the patients
activity level. Younger and more active patients are more likely to require revisions, whereas
the majority of older patients will not.
Education
Educate patients on the natural history of and management options for osteoarthritis,
emphasizing the benefits of exercise and weight loss.
Explain the differences between osteoarthritis and more rapidly progressive arthritides, such
as rheumatoid arthritis.
Through education, patients can learn and implement strategies for reducing pain and
improving joint function. Emphasize the need for physician follow-up visits.

RHEUMATOID ARTHRITIS
Background

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Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown cause. An

external trigger (eg, cigarette smoking, infection, or trauma) that triggers an autoimmune
reaction, leading to synovial hypertrophy and chronic joint inflammation along with the
potential for extra-articular manifestations, is theorized to occur in genetically susceptible
individuals.

Etiology
The cause of RA is unknown. Genetic, environmental, hormonal, immunologic, and
infectious factors may play significant roles. Socioeconomic, psychological, and lifestyle
factors (eg, tobacco use, the main environmental risk) may influence disease outcome
Signs and symptoms
Persistent symmetric polyarthritis (synovitis) that affects the hands and feet, although any
joint lined by a synovial membrane may be involved. The severity of RA may fluctuate over
time, but chronic RA most commonly results in the progressive development of various
degrees of joint destruction, deformity, and a significant decline in functional status. Extraarticular involvement of organs such as the skin, heart, lungs, and eyes can also be
significant.
Patients with RA may report difficulty performing activities of daily living (ADLs), such as
dressing, standing, walking, personal hygiene, or use of hands.
In most patients, RA has an insidious onset. It may begin with systemic features (eg, fever,
malaise, arthralgias, and weakness) before the appearance of overt joint inflammation and
swelling. A small percentage (approximately 10%) of patients with this disease have an
abrupt onset with the acute development of synovitis and extra-articular manifestations.
Spontaneous remission is uncommon, especially after the first 3-6 months.
In most patients with RA, onset is insidious, often beginning with fever, malaise, arthralgias,
and weakness before progressing to joint inflammation and swelling.
Physical examination :

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Upper extremities (metacarpophalangeal joints, wrists, elbows, shoulders)

Lower extremities (ankles, feet, knees, hips)

Cervical spine

During the physical examination, it is important to assess the following:

Stiffness

Tenderness

Pain on motion

Swelling

Deformity

Limitation of motion

Extra-articular manifestations

Rheumatoid nodules

Diagnosis
No test results are pathognomonic; instead, the diagnosis is made by using a combination of
clinical, laboratory, and imaging features. Potentially useful laboratory studies in suspected
RA include the following:

ESR

CRP

CBC

RF

Antinuclear antibody assay (ANA)

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Potentially useful imaging modalities include the following:

Radiography (first choice): Hands, wrists, knees, feet, elbows, shoulders, hips,
cervical spine, and other joints as indicated

Magnetic resonance imaging : Primarily cervical spine

Ultrasonography of joints : Joints, as well as tendon sheaths, changes and degree of

vascularization of the synovial membrane, and even erosions

Joint aspiration and analysis of synovial fluid may be considered, including the following:

Gram stain

Cell count

Culture

Assessment of overall appearance

Treatment
Pharmacologic
DMARDs
These agents can retard or prevent disease progression and, thus, joint destruction and
subsequent loss of function. Successful DMARD therapy may eliminate the need for other
anti-inflammatory or analgesic medications; however, until the full action of DMARDs takes
effect, anti-inflammatory or analgesic medications may be required as bridging therapy to
reduce pain and swelling.
Nonbiologic DMARDS include the following:

Hydroxychloroquine
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Azathioprine

Sulfasalazine

Methotrexate

Leflunomide

Cyclosporine

Gold salts

D-penicillamine

Minocycline

Biologic TNF-inhibiting DMARDs include the following:

Etanercept

Infliximab

Adalimumab

Certolizumab

Golimumab

Biologic non-TNF DMARDs include the following:

Rituximab

Anakinra

Abatacept

Tocilizumab

Tofacitinib

NSAIDs
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Interfere with prostaglandin synthesis through inhibition of the enzyme cyclooxygenase

(COX), thus reducing swelling and pain. However, they do not retard joint destruction and
therefore are not sufficient to treat RA when used alone. Like corticosteroids, NSAIDs can be
reduced in dose or discontinued with successful DMARD therapy. These agents decrease
intraglomerular pressure and decrease proteinuria.
The several dozen NSAIDs available can be classified into several different groups of
compounds. Commonly used NSAIDs include ibuprofen, naproxen, ketoprofen, celecoxib,
and diclofenac.
Corticosteroids
Potent anti-inflammatory drugs commonly used in patients with RA to bridge the time until
DMARDs become effective. Prednisone dosages as high as 10 mg/day are typically used, but
some patients may require even higher dosages. Adverse events associated with long-term
steroid use make dose reductions and cessation important in due course.
Analgesics

Non-Pharmacologic
Exercise, diet, massage, counseling, stress reduction, physical therapy, and surgery.
Prognosis
Outcome in RA is compromised when diagnosis and treatment are delayed. The clinical
course of RA is generally one of exacerbations and remissions. Approximately 40% of
patients with this disease become disabled after 10 years, but outcomes are highly variable.
Some patients experience a relatively self-limited disease, whereas others have a chronic
progressive illness.
Prognostic factors
It has been shown that intervention with DMARDs in very early RA (symptom duration < 12
weeks at the time of first treatment) gives the best opportunity for attempting to achieve
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disease remission. Better detection of early joint injury has provided a previously
unappreciated view of the ubiquity and importance of early joint damage. Nonetheless,
predicting the course of an individual case of RA at the outset remains difficult, though the
following all correlate with an unfavorable prognosis in terms of joint damage and disability:

HLA-DRB1*04/04 genotype

High serum titer of autoantibodies (eg, RF and ACPA)

Extra-articular manifestations

Large number of involved joints

Age younger than 30 years

Female sex

Systemic symptoms

Insidious onset

GOUT ARTHRITIS
Gout is caused by monosodium urate monohydrate crystals
Pathophysiology
Gout can be considered a disorder of metabolism that allows uric acid or urate to accumulate
in blood and tissues. When tissues become supersaturated, the urate salts precipitate, forming
crystals. In addition, the crystals also are less soluble under acid conditions and at low
temperatures, such as occur in cool, peripheral joints (eg, the metatarsophalangeal joint of the
big toe).

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Urate initially precipitates in the form of needlelike crystals. The light-retarding (phaseshifting) characteristics of urate crystals allow them to be recognized by polarizing
microscopy (see the image below).

Gout. Needles of urate crystals seen on polarizing microscopy

The presence of urate crystals in the soft tissues and synovial tissues is a prerequisite for a
gouty attack. However, these crystals can also be found in synovial fluid or on the cartilage
surface in the absence of joint inflammation.
Signs and symptoms

Podagra (initial joint manifestation in 50% of gout cases and eventually involved in
90%; also observed in patients with pseudogout and other conditions)

Arthritis in other sites In gout, the instep, ankle, wrist, finger joints, and knee; in
pseudogout, large joints (eg, the knee, wrist, elbow, or ankle)

Monoarticular involvement most commonly, though polyarticular acute flares are not
rare, and many different joints may be involved simultaneously or in rapid succession

In gout, attacks that begin abruptly and typically reach maximum intensity within 812 hours; in pseudogout, attacks resembling those of acute gout or a more insidious
onset that occurs over several days

Without treatment, symptom patterns that change over time; attacks can become more
polyarticular, involve more proximal and upper-extremity joints, occur more often,
and last longer

In some cases, eventual development of chronic polyarticular arthritis that can

resemble rheumatoid arthritis

Physical findings may include the following:

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Involvement of a single (most common) or multiple joints

Signs of inflammation Swelling, warmth, erythema (sometimes resembling

cellulitis), and tenderness

Fever (also consider infectious arthritis)

Migratory polyarthritis (rare)

Posterior interosseous nerve syndrome (rare)

Tophi in soft tissues (helix of the ear, fingers, toes, prepatellar bursa, olecranon)

Eye involvement Tophi, crystal-containing conjunctival nodules, band keratopathy,

blurred vision, anterior uveitis (rare), scleritis

Complications of gout include the following:

Severe degenerative arthritis

Secondary infections

Urate or uric acid nephropathy

Increased susceptibility to infection

Urate nephropathy

Renal stones

Nerve or spinal cord impingement

Fractures in joints with tophaceous gout

Diagnosis
Studies that may be helpful include the following:

Joint aspiration and synovial fluid analysis

Serum uric acid measurement (though hyperuricemia is not diagnostic of gout)

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24-hour urinary uric acid evaluation

Blood studies (including white blood cells [WBCs, triglyceride, high-density

lipoprotein, glucose, and renal and liver function tests)

Plain radiographs may show findings consistent with gout. Erosions with overhanging edges
are generally considered pathognomonic for gout (though also found in other diseases).
Characteristics of erosions typical of gout include the following:

Maintenance of the joint space

Absence of periarticular osteopenia

Location outside the joint capsule

Sclerotic (cookie-cutter, punched-out) borders

Asymmetric distribution among the joints, with a strong predilection for distal joints,
especially in the lower extremities

Ultrasonographic findings in established gout include the following:

A double-contour sign, consisting of a hyperechoic, irregular line of MSU crystals

on the surface of articular cartilage overlying an adjacent hyperechoic bony contour

Wet clumps of sugar, representing tophaceous material, described as hyperechoic

and hypoechoic heterogeneous material with an anechoic rim

Bony erosions adjacent to tophaceous deposits

Other imaging modalities that may be considered include the following:

Computed tomography (CT) Complementary to plain radiography for recognizing

erosions in gout

Magnetic resonance imaging (MRI) MRI with gadolinium is recommended when

tendon sheath involvement must be evaluated and when osteomyelitis is in the
differential diagnosis

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Management
Gout is managed in the following 3 stages:

Treating the acute attack

Providing prophylaxis to prevent acute flares

Lowering excess stores of urate to prevent flares of gouty arthritis and to prevent
tissue deposition of urate crystals

Acute treatment of proven crystal-induced arthritis is directed at relief of the pain and
inflammation. Agents used in this setting include the following:

Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin

Corticosteroids

Colchicine (now less commonly used for acute gout than it once was)

Adrenocorticotropic hormone (ACTH)

Combinations of drugs (colchicine plus NSAIDs, oral corticosteroids plus colchicine,

intra-articular steroids plus colchicine or NSAIDs)

Therapy to control the underlying hyperuricemia generally is contraindicated until the acute
attack is controlled (unless kidneys are at risk because of an unusually heavy uric acid load).
Long-term management of gout is focused on lowering uric acid levels. Agents used include
the following:

Allopurinol

Febuxostat

Probenecid

Because these agents change serum and tissue uric acid levels, they may precipitate acute
attacks of gout. This undesired effect may be reduced by prophylaxis with the following:

Colchicine or low-dose NSAIDs

Low-dose prednisone (if patients cannot take colchicine or NSAIDs)

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Other therapeutic agents that may be considered include the following:

Uricase and pegloticase

Vitamin C

Anakinra

Fenofibrate

Nonpharmacologic measures that may be warranted are as follows:

Avoidance or restricted consumption of high-purine foods

Avoidance of excess ingestion of alcoholic drinks, particularly beer

Avoidance of sodas and other beverages or foods sweetened with high-fructose corn
syrup

Limited use of naturally sweet fruit juices, table sugar, and sweetened beverages and
desserts, as well as table salt

Maintenance of a high level of hydration with water (8 glasses of liquids daily)

A low-cholesterol, low-fat diet, if such a diet is otherwise appropriate for the patient

Weight reduction in patients who are obese

Gout. Chronic tophaceous gout in untreated patient with end-stage renal disease.

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DRY EYES SYNDROME (KONJUNGTIVITIS DRY

EYES/KERATOKONJUNGTIVITIS SIKA)
Keratokonjungtivitis sika adalah suatu keadaan keringnya permukaan kornea dan konjungtiva
yang diakibatkan berkurangnya fungsi air mata
Kelainan-kelainan ini terjadi pada penyakit yang mengakibatkan :
1. Defisiensi komponen lemak air mata. Misal : blefaritis menahun, dan akibat
pembedahan kelopak mata
2. Defisiensi kelenjar air mata. Misal : sindrom Sjogren, obat-obat diuretik,
atropin, usia tua
3. Akibat penguapan yang berlebihan. Misal : hidup di gurun pasir
4. Karena jaringan parut pada kornea atau menghilangnya mikrovili kornea
Gejala Klinis

mata gatal, seperti berpasir, fotofobia, penglihatan kabur

mata tampak kering dan terdapat erosi kornea

konjungtiva bulbi edema, hiperemis, menebal dan kusam

sebaiknya dilakukan beberapa oemeriksaan seperti uji Scheimer dimana bila resapan air mata
pada kertas Scheimer kurang dari 5 menit dianggap abnormal.
Pengobatan
Artificial tears
Komplikasi

Ulkus kornea

Infeksi sekunder oleh bakteri

Parut kornea
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Neovaskularisasi kornea

GANGGUAN PENDENGARAN PADA GERIATRI

Tuli konduktif pada geriatri
Pada telinga luar dan telinga tengah proses degenerasi dapat menyebabkan perubahan atau
kelainan berupa:
1. Berkurangnya elastisitas dan bertambahnya ukuran pinna daun telinga
2. Atrofi dan bertambah kakunya liang telinga
3. Penumpukan serumen
4. Membrane timpani bertambah tebal dan kaku
5. Kekakuan sendi tulang- tulang pendengaran
Pada usila kelenjar seruman mengalami atrofi, produksi kelenjar serumen berkurang, dan
serumen lebih kering, mudah terjadi serumen prop yang mengakibatkan tuli konduktif.
Membrane timpani yang bertambah kaku dan tebal juga menyebabkan gangguan konduksi,
demikian pula halnya dengan kekakuan yang terjadi pada persendian tulang tulang
pendengaran.
Tuli saraf pada geriatri (Presbikusis)
Presbikusis adalah tuli sensorineural frekuensi tinggi, umumnya terjadi mulai usia 65 tahun,
simetris pada telinga kiri dan kanan. Presbikusis dapat mulai pada frekuensi 1000 Hz/ lebih.
Etiologi
Akibat proses degenerasi.
Diduga mempunyai hubungan dengan faktor herediter, pola makan, metabolism,
arteriosklerosis, infeksi, bising, gaya hidup atau bersifat multifactor.
Progesifitas dipengaruhi oleh usia dan jenis kelamin, laki- laki lebih cepat dari perempuan.
Patologi
Proses degenerasi menyebabkan perubahan struktur koklea dan N. VIII.
Pada koklea proses perubahan yang mencolok adalah atrofi dan degenerasi sel- sel rambut
penunjang pada organ corti. Proses atrofi disertai dnegan perubahan vascular juga terjadi
pada stria vaskularis. Terdapat pula perubahan berupa berkurangnya jumlah dan ukuran selsel ganglion dan saraf. Hal yang sama juga terjadi pada myelin akson saraf.
Klasifikasi

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Gejala klinik
Keluhan utama presbikusis berupa berkurangnya pendengaran secara perlahan- lahan dan
progresif, simetris pada kedua telinga.
Keluhan lainnya adalah telinga berdenging ( tinnitus nada tinggi). Pasien dapat mendengar
suara percakapan, tetapi sulit untuk memahaminya, terutama bila diucapkan dengan cepat di
tempat dengan latar belakang yang bising ( cocktail party deafness). Bila intensitas suara
ditinggikan akan timbul rasa nyeri di telinga, hal ini disebabkan oleh faktor kelelahan saraf
( recruitment).
Diagnosis
Dengan pemeriksaan otoskopik, tampak membrane timpani suram, mobilitas berkurang. Pada
tes penala didapatkan tuli sensorineural. Pemeriksaan audiometric nada murni menunjukkan
suatu tuli saraf nada tinggi, bilateral dan simetris.
Pada tahap awal terdapat penurunan yang tajam ( sloping) setelah frekuensi 2000Hz.
Garis ambang dengar pada metabolic dan mekanik lebnih mendatar kemudian pada tahap
berikutnya berangsur- angsur terjadi penurunan.
Pemeriksaan audiometric turut menunjukkan gangguan diskriminasi wicara. Keadaan ini jelas
terlihat pada presbikusis neural dan koklear.
Penatalaksanaan
Rehabilitasi sebagai upaya mengembalikan fungsi pendengaran dilakukan dengan
pemasangan alat bantu dengar ( hearing aid). Perlu dikombinasikan dengan latihan membaca,
ujaran dan mendengar bersama dengan ahli terapi wicara.

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PRESBYCUSIS
The term presbycusis refers to sensorineural hearing impairment in elderly individuals.
Characteristically, presbycusis involves bilateral high-frequency hearing loss associated with
difficulty in speech discrimination and central auditory processing of information.
In patients with presbycusis, no abnormalities are found on physical examination.
-

Presbycusis is a diagnosis of exclusion that should not be made until all other possible
etiologies of hearing loss in elderly individuals have been evaluated and excluded.

Etiologies as simple as cerumen impaction and as complex as otosclerosis or

cholesteatoma must not be overlooked in the elderly patient with hearing loss because
these are amenable to treatment.

Imaging Studies
Evaluation may entail a variety of tests, including CT scanning or MRI to exclude anatomic
abnormalities or mass lesions that may cause hearing loss.
Other Tests
-

Audiometric testing with pure-tone average and speech discrimination forms the
cornerstone of diagnostic testing for presbycusis.

The need for additional testing can usually be determined from the audiometric test
results. For example, individuals with asymmetric hearing loss (ie, more than 10 dB
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difference at any 2 consecutive frequencies) and individuals with a conductive

component require further evaluation.
-

Evaluation may entail a variety of tests, including tests of central auditory processing
to exclude abnormal processing of auditory information in the central nervous system.

Medical Care
Presbycusis is not curable, but the effects of the disease on patients lives can be mitigated.
-

Amplification devices: Properly fitted hearing aids may contribute to the

rehabilitation of a patient with presbycusis. Older patients with arthritis in their
fingers and visual difficulties need extra help in learning to use hearing aids. Patients
using hearing aids may still experience difficulties with speech discrimination in
noisy situations.

Lip reading: Lip reading may help patients with diminished speech discrimination and
may help hearing aid users who have difficulty in noisy environments.

Assistive listening devices: These range from a simple amplification of the telephone
signal to a device on the television that sends a signal across the room to a headset
worn by a patient with hearing loss. The patient can amplify the sound without
disturbing other people with normal hearing who are in the same room.

Cochlear implants: Some patients with presbycusis benefit from cochlear implants.
Patients with cochlear changes and relatively intact spiral ganglia and central
pathways appear to be the best candidates.

HIPERTENSI
Hypertension is defined as a systolic blood pressure (SBP) of 140 mm Hg or more, or a
diastolic blood pressure (DBP) of 90 mm Hg or more, or taking antihypertensive medication.
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Based on recommendations of the Seventh Report of the Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), the classification
of BP for adults aged 18 years or older has been as follows:

Diagnosis
The evaluation of hypertension involves accurately measuring the patients blood pressure,
performing a focused medical history and physical examination, and obtaining results of routine
laboratory studies.
Management
Lifestyle modifications
JNC 7 recommendations to lower BP and decrease cardiovascular disease risk include the
following, with greater results achieved when 2 or more lifestyle modifications are combined.

Weight loss (range of approximate systolic BP reduction [SBP], 5-20 mm Hg per 10 kg)
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Reduce sodium intake to no more than 100 mmol/day (2.4 g sodium or 6 g sodium chloride;
range of approximate SBP reduction, 2-8 mm Hg)

Maintain adequate intake of dietary potassium (approximately 90 mmol/day)

Maintain adequate intake of dietary calcium and magnesium for general health

Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall
cardiovascular health

Engage in aerobic exercise at least 30 minutes daily for most days (range of approximate SBP
reduction, 4-9 mm Hg)

The AHA/ASA recommends a diet that is low in sodium, is high in potassium, and promotes
the consumption of fruits, vegetables, and low-fat dairy products for reducing BP and lowering the
risk of stroke. Other recommendations include increasing physical activity (30 minutes or more of
moderate intensity activity on a daily basis) and losing weight (for overweight and obese persons).
The 2013 European Society of Hypertension (ESH) and the European Society of Cardiology
(ESC) guidelines recommend a low-sodium diet (limited to 5 to 6 g per day) as well as reducing
body-mass index (BMI) to 25 kg/m 2 and waist circumference (to < 102 cm in men and < 88 cm in
women).
Pharmacologic therapy
If lifestyle modifications are insufficient to achieve the goal BP, there are several drug options
for treating and managing hypertension. Thiazide diuretics are the preferred agents in the absence of
compelling indications.
Compelling indications may include high-risk conditions such as heart failure, ischemic heart
disease, chronic kidney disease, and recurrent stroke, or those conditions commonly associated with
hypertension, including diabetes and high coronary disease risk. Drug intolerability or
contraindications may also be factors. An angiotensin-converting enzyme (ACE) inhibitor, angiotensin
receptor blocker (ARB), calcium channel blocker (CCB), and beta-blocker are all acceptable
alternative agents in such compelling cases.

The following are drug class recommendations for compelling indications based on
various clinical trials:

Heart failure: Diuretic, beta-blocker, ACE inhibitor, ARB, aldosterone antagonist

Postmyocardial infarction: Beta-blocker, ACE inhibitor, aldosterone antagonist

High coronary disease risk: Diuretic, beta-blocker, ACE inhibitor, CCB

Diabete : Diuretic, beta-blocker, ACE inhibitor, ARB, CCB

Chronic kidney disease: ACE inhibitor, ARB

Recurrent stroke prevention: Diuretic, ACE inhibitor

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The JNC 8 recommendations include the following:

In patients aged 60 years or older, initiate therapy in those with systolic BP levels at
150 mm Hg or greater or whose diastolic BP levels are 90 mm Hg or greater; treat to
below those thresholds
In patients younger than 60 years as well as those older than 18 years with either
chronic kidney disease (CKD) or diabetes, the BP treatment initiation and goals
should be 140/90 mm Hg

Do not use an ACE inhibitor in conjunction with an ARB in the same patient

If a patient's goal BP is not achieved within 1 month of treatment, increase the dose of
the initial agent or add an agent from another of the recommended drug classes; if 2drug therapy is unsuccessful for reaching the target BP, add a third agent from the
recommended drug classes

In patients whose goal BP cannot be reached with 3 agents from the recommended
drug classes, use agents from other drug classes and/or refer the patients to a
hypertension specialist

A joint AHA/ACC/CDC algorithm in the report includes the following recommendations:

BP: Recommended goal of 139/89 mm Hg or less

Stage 1 hypertension (systolic BP 140-159 mm Hg or diastolic BP 90-99 mm Hg): Can be
treated with lifestyle modifications and, if needed, a thiazide diuretic
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Stage 2 hypertension (systolic BP >160 mm Hg or diastolic BP >100 mm Hg): Can be treated

with a combination of a thiazide diuretic and an ACE inhibitor, an angiotensin receptor
blocker, or a calcium channel blocker

Patients who fail to achieve BP goals: Medication doses can be increased and/or a drug from a
different class can be added to treatment

Prognosis
Most individuals diagnosed with hypertension will have increasing blood pressure (BP) as
they age. Untreated hypertension is notorious for increasing the risk of mortality and is often
described as a silent killer. Mild to moderate hypertension, if left untreated, may be associated with a
risk of atherosclerotic disease in 30% of people and organ damage in 50% of people within 8-10 years
after onset.
Death from ischemic heart disease or stroke increases progressively as BP increases. For
every 20 mm Hg systolic or 10 mm Hg diastolic increase in BP above 115/75 mm Hg, the mortality
rate for both ischemic heart disease and stroke doubles.
Hypertensive retinopathy was associated with an increased long-term risk of stroke, even in
patients with well-controlled BP. Nephrosclerosis is one of the possible complications of longstanding hypertension.
It is estimated that 1 death is prevented per 11 patients treated for stage 1 hypertension and
other cardiovascular risk factors when a sustained reduction of 12 mm Hg in systolic BP over 10 years
is achieved. However, for the same reduction is systolic BP reduction, it is estimated that 1 death is
prevented per 9 patients treated when cardiovascular disease or end-organ damage is present.

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KYPHOSIS

Preoperative lateral of a patient with an 85 thoracic deformity secondary to Scheuermann

kyphosis.
Normal kyphosis is defined as a Cobb angle of 20-40 measured from T2-T1.
Pathologic kyphosis can affect the cervical and lumbar spine as well the thoracic spine, but
cervical and lumbar involvement is uncommon. Any kyphosis in these areas is abnormal.
Kyphosis can cause pain and potentially lead to neurologic deficit and abnormal
cardiopulmonary function.
Congenital abnormalities, such as failure of formation or failure of segmentation of the spinal
elements, can cause a pathologic kyphosis. Autoimmune arthropathy, such as ankylosing
spondylitis, can cause rigid kyphosis to develop as the spinal elements coalesce. Kyphosis
can also develop as a result of trauma, a spinal tumor, or an infection. Iatrogenic causes of
kyphosis include the effects of laminectomy and irradiation, which lead to incompetence of
the anterior or posterior column. Finally, metabolic disorders and dwarfing conditions can
lead to kyphosis.
Treatment
Indications for treatment of kyphosis include unremitting pain, neurologic changes,
progression of deformity, and cosmesis.
Other possible indications in severely affected patients are problems with balance while
sitting and skin problems due to pressure at the apex of the deformity.
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Surgical intervention for posttraumatic kyphosis is recommended if the patient's neurologic

status changes, if the condition progresses, if the kyphosis is 30 or more, or if the loss of
anterior vertebral height is more than 50%
Medical therapy for kyphosis consists of exercise, medication, and bracing. Physical therapy,
which usually consists of extension-focused activities, may be of some benefit; however, this
has not been proven.
Medications to treat discomfort associated with kyphosis should be limited to NSAID and,
possibly, muscle relaxants.
If a patient has an active infection, such as diskitis or vertebral osteomyelitis, appropriate
antibiotics based on culture results should be started as soon as possible.
Bracing is effective in some skeletally immature patients with Scheuermann kyphosis.
However, the correction obtained may diminish as patients approach and pass skeletal
maturity. Brace treatment seemed to be least effective when the curve was more than 74 at
the beginning of treatment. Bradford et al reported modest success in treating adults with a
brace, with some correction of their deformities.
Surgical planning for kyphosis is crucial to a successful operation. The goal of surgery is to
correct the deformity and remove any neural compression, if present. The correction can be
done anteriorly, posteriorly, or both. Posterior surgery is most commonly described and
performed. Posterior arthrodesis for kyphosis can be an extensive operation, with many spinal
segments typically included in the fusion mass.This procedure is most helpful for long,
sweeping, flexible curves.
In cases of rigid deformity, osteotomies can be performed to improve the correction.
Combined anterior-posterior surgery may be required for severe deformities.

Follow Up

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Standing posteroanterior and lateral full-length radiographs of the spine should be obtained as
soon as possible after surgery and serially for follow-up. Full-length scoliosis films obtained
yearly allow evaluation of the patient's curve over time.
Comparison of the postoperative and follow-up images with the preoperative images helps in
defining the amount of correction achieved and in determining if correction is being lost over
time. Loss of correction should prompt a careful evaluation for implant pull-out or breakage,
for subsidence of an anterior strut (if any), or for the lack of adequate fusion mass.
Postoperative measurements of the C7 plumb line should be at or within a few centimeters of
S1.

OBESITY
World Health Organization (WHO), based on body mass index (BMI):

Grade 1 overweight (commonly and simply called overweight) - BMI of 25-29.9

kg/m2

Grade 2 overweight (commonly called obesity) - BMI of 30-39.9 kg/m2

Grade 3 overweight (commonly called severe or morbid obesity) - BMI 40 kg/m2

Screening questions to exclude severe or untreated depression are vital because depression
may be a consequence or a cause of excessive dietary intake and reduced activity.
Because almost 30% of patients who are obese have eating disorders, screen for these in the
history. The possibility of bingeing, purging, lack of satiety, food-seeking behavior, nighteating syndrome, and other abnormal feeding habits must be identified because management
of these habits is crucial to the success of any weight-management program.
When taking the history, the clinician should investigate whether other members of the
patient's family have weight problems, inquire about the patient's expectations, and estimate
the patient's level of motivation.
The clinician should also determine whether the patient has had any of the comorbidities
related to obesity, including the following :
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Respiratory - Obstructive sleep apnea, greater predisposition to respiratory infections,

increased incidence of bronchial asthma, and Pickwickian syndrome (obesity
hypoventilation syndrome)

Malignant - Association with endometrial, prostate, colon, breast, gall bladder, and,
possibly, lung cancer

Psychological - Social stigmatization and depression

Cardiovascular - Coronary artery disease, essential hypertension, left ventricular

hypertrophy,

cor

pulmonale,

obesity-associated

cardiomyopathy,

accelerated

atherosclerosis, and pulmonary hypertension of obesity

Central nervous system (CNS) - Stroke, idiopathic intracranial hypertension, and

meralgia paresthetica

Obstetric and perinatal - Pregnancy-related hypertension, fetal macrosomia, and

pelvic dystocia

Surgical - Increased surgical risk and postoperative complications, including wound

infection, postoperative pneumonia, deep venous thrombosis, and pulmonary
embolism

Pelvic - Stress incontinence

Gastrointestinal (GI) - Gall bladder disease (cholecystitis, cholelithiasis), nonalcoholic

steatohepatitis (NASH), fatty liver infiltration, and reflux esophagitis

Orthopedic - Osteoarthritis, coxa vera, slipped capital femoral epiphyses, Blount

disease and Legg-Calv-Perthes disease, and chronic lumbago

Metabolic - Type 2 diabetes mellitus, prediabetes, metabolic syndrome, and

dyslipidemia

Reproductive - In women : Anovulation, early puberty, infertility, hyperandrogenism,

and polycystic ovaries; in men: hypogonadotropic hypogonadism

Cutaneous - Intertrigo (bacterial and/or fungal), acanthosis nigricans, hirsutism, and

increased risk for cellulitis and carbuncles

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Extremity - Venous varicosities, lower extremity venous and/or lymphatic edema

Miscellaneous - Reduced mobility and difficulty maintaining personal hygiene

Include questions to exclude secondary causes of obesity, some of which are rare.
Secondary causes of obesity.
In the clinical examination, measure anthropometric parameters and perform the standard,
detailed examination required in evaluating patients with any chronic, multisystem disorder,
such as obesity.
Waist and hip circumference are useful surrogates in estimating visceral fat; serial tracking of
these measurements helps in estimating the clinical risk over time. Neck circumference is
predictive of a risk of sleep apnea, and its serial measurement in the individual patient is
clinically useful for risk stratification.
Examination of organ systems should include the following:

Cutaneous - Search for intertriginous rashes from skin-on-skin friction; also search for
hirsutism in women, acanthosis nigricans, and skin tags, which are common with
insulin resistance secondary to obesity

Cardiac and respiratory - Exclude cardiomegaly and respiratory insufficiency

Abdominal - Attempt to exclude tender hepatomegaly, which may suggest hepatic

fatty infiltration or NASH, and distinguish the striae distensae from the pink and
broad striae that suggest cortisol excess

When examining the extremities, search for joint deformities (eg, coxa vara), evidence of
osteoarthritis, and any pressure ulcerations. Localized and lipodystrophic fat distribution
should also be identified, because of their common association with insulin resistance.
Weight-loss programs
The 3 major phases of any successful weight-loss program are as follows:

Preinclusion screening phase

Weight-loss phase
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Maintenance phase - This can conceivably last for the rest of the patient's life but
ideally lasts for at least 1 year after the weight-loss program has been completed

Evidence supports the use of commercial weight-loss programs. A 12-week randomized,

controlled trial found that commercially available weight-loss programs are more successful
and more affordable than primary care practicebased programs led by specially trained staff.
Pharmacologic therapy
Few drugs are available for the treatment of obesity, and their effectiveness is limited to
palliation (ie, production and maintenance of weight loss) rather than cure, with benefits
fading when the drugs are stopped. Because all medications inherently have more risks than
diet and exercise do, pharmacologic therapy should be used only in patients in whom the
benefit justifies the risk.
Surgery
In patients with morbid obesity associated with comorbidities, bariatric surgery is the only
available therapeutic modality associated with clinically significant and relatively sustained
weight loss. Well-performed bariatric surgery, in carefully selected patients and with a good
multidisciplinary support team, substantially ameliorates the morbidities associated with
severe obesity.

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DAFTAR PUSTAKA

Soepardi, Arsyad Efiaty, dkk. Telinga, Hidung, Tenggorok, Kepala & Leher FKUI.
Ed VI. Jakarta : 2007

Ilyas, Sidharta, et al. Ilmu Penyakit Mata FKUI. Ed IV. Jakarta : 2013

www.medscape.com

www.nhlbi.nih.gov

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