Postwound Care

Postwound care is an essential part of total burn management to ensure adequate

follow-up subsequent to wound healing, including psychological support. Good burn

care that helps to alleviate physical discomfort, pain, and scarring and that promotes

good wound healing will also provide psychological benefits for the patient. Healed

wounds should be moisturized on a regular basis. Pruritus can be a major problem

after burn injury. To reduce itching, moisturizers can be applied, and oral

antihistamines may be necessary.

172 Protection from the sun will help to prevent

further thermal damage or pigmentation changes to the affected area. Patients in this

population should avoid the sun after a burn injury whenever possible, with use of a

sunscreen with an SPF of at least 50 recommended.

173

If surface changes occur (e.g.,

skin becomes hypertrophic, or blisters or new wounds appear), the patient should be

advised to return for evaluation.

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E19.

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Osteoarthritis (OA) is a chronic, progressive condition, primarily

affecting women, that causes loss of articular cartilage in hands, knees,

hips, and cervical and lumbar spine. OA causes significant pain and

functional disability, and increases costs to our healthcare systems.

Case 43-1 (Question 1)

The evolving role of cytokines and the resultant imbalance between

cartilage maintenance and destruction contribute to the pathophysiology

of OA. There are no current disease-mitigating therapies.

Case 43-1 (Questions 2, 3),

Figure 43-1

The typical presentation includes stiffness and pain unilaterally in one or

more joints lasting less than 30 minutes after a period of immobility. This

causes significant limitations in activities of daily living as well as overall

quality of life.

Case 43-1 (Questions 1, 2)

Conservative treatment strategies include weight loss, self-management,

aerobic exercise, strength training, and physical and occupational

therapies to best maintain optimal functionalstatus.

Case 43-1 (Question 4)

Initial trials of routine dosing of acetaminophen, topical agents,

nonsteroidal

anti-inflammatory drugs (NSAIDs), and intra-articular glucocorticoid

injections represent initial pharmacologic interventions of osteoarthritis.

Case 43-1 (Questions 5, 6),

Case 43-2 (Questions 1–4),

Tables 43-1–43-3, Figure 43-

2

Intra-articular hyaluronan, tramadol, and duloxetine may be considered in

those patients with insufficient relief in symptoms and worsening

function after initial pharmacologic strategies have been attempted.

Case 43-2 (Questions 1–6)

A consistent and systematic approach to the management of chronic

pain caused by OA can help identify patients with limitations in activities

of daily living (ADLs) and prevent further disability. Then, the

effectiveness of current therapies can be more appropriately evaluated,

and the treatment plan can be updated.

Case 43-1 (Questions 5, 7),

Case 43-2 (Questions 1–6),

Case 43-3 (Questions 1, 2)

INCIDENCE, PREVALENCE, AND

EPIDEMIOLOGY

Osteoarthritis (OA) is a chronic, progressive disorder characterized by the changes

to articular cartilage and bone primarily in hands, knees, hips, and spine. Incidence

rates for OA of the hand have been estimated to be 100 per 100,000 person-years,

hip OA, 88 per 100,000 person-years, and knee OA, 240 per 100,000 person-years.

Incidence rates increase with advancing age until the 8th decade of life. The Centers

for Disease Control and Prevention (CDC) reported in 2005 that approximately 26.9

million people older than 65 years of age are affected, particularly after the age of

50.

1 Women seem to be affected by more severe OA of the knees than men,

particularly after the age of 50.

2 Additionally, women experience more severe

disease radiographically; however, severity of radiologic disease may not predict

severity of subjective symptoms of pain or disability. Men have a lower incidence of

knee and hip OA than women.

1 More recently, in 2013, it had been reported that

arthritis was the most common cause of disability in U.S. adults, and was noted to

co-occur in persons with multiple chronic conditions such as heart disease and

diabetes mellitus. This report illustrated that 52.5 million (22.7%) of adults older

than 18 years had self-reported provider-diagnosed arthritis,

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and 22.7 million (9.8% of all adults, 43.2 with arthritis) reported arthritisattributable activity limitations.

3 Arthritis contributes significant costs to the

healthcare system through hospitalizations, joint-related surgeries, and inability to

work. An estimated 200 billion US dollars is attributed to OA annually as either

direct medical costs or lost productivity.

4

Arthritis patients perceive lower health-related quality of life. The physical

limitations in arthritis-related activities and the subsequent effects on the

comorbidities related to obesity are current areas of research.

3 Considering the

morbidity and mortality associated with type 2 diabetes mellitus and coronary artery

disease is significant. The development of disease-mitigating interventions may

benefit not only those with OA but also in cases where inactivity contributes to or

worsens obesity-related conditions and complications.

ETIOLOGY

Osteoarthritis has been previously described as disease of cartilage that has

undergone significant wear and tear. It is now known to be a more complex and

dynamic process. Primary OA cannot be traced to any particular identifiable cause.

In secondary OA, a known etiology or cause has been determined. We know

osteoarthritis affects not only articular cartilage but also periarticular muscles,

subchondral bone and ligaments, synovial membranes, and the entire joint capsule.

The interplay of cellular, biochemical, and mechanical processes underlies the

disease. Various risk factors have been identified and can be classified as modifiable

and nonmodifiable. Modifiable risk factors of OA include obesity and joint trauma.

Increased body weight has been correlated with increased risk of OA of the knee, but

not the hip. Excess weight contributes to the biomechanical forces and stresses on the

knee joints. The cascade of increased pain leading to decreased function and further

worsening of obesity can be a difficult cycle to break. Weight loss and moderate

amounts of activity improve symptoms of OA of the knee and improve overall health.

Nonmodifiable risk factors are advancing age, sex, genetics, and joint location.

Typically, the development of symptomatic OA occurs with increased age

predominantly in the weight-bearing joints, although many women are affected by

localized inflammation of the proximal and distal interphalangeal joints known as

Bouchard and Heberden nodes, respectively. Approximately 80% of patients older

than 75 years are affected by OA.

Epidemiologic studies provide support for a genetic component to the

development of OA as well as the characteristic Heberden and Bouchard nodes.

Studies in twins have also supported the influence of genetics and the development of

OA. Multiple genes have been identified that are associated with increased risk for

OA as well as some genetic mutations associated with OA of early onset. With the

increasing development of isolating specific genotypes and pharmacogenomics, more

targeted interventions could be implemented to arrest disease progression. OA is

particularly more common in the hips and knees than in the ankle joint. Joint trauma

can result in the evolution of OA. Biochemical and mechanical changes can occur,

resulting in the characteristic joint pain and stiffness. The consequences are articular

cartilage with less functionality and resultant characteristics of cartilage, joint

capsule, and subchondral bone that are distinctively different from those of normal

bone. Regular exercise and physical activity do not increase the risk of OA in normal

joints and are necessary to maintain cartilage.

5

The development of radiologic evidence of OA precedes the clinical symptoms;

thus, the initial presentation may not always correlate with disease prognosis.

Diminished ability of chondrocytes to maintain and repair articular cartilage has been

correlated with resultant cartilage degradation. These age-related changes in

chondrocyte function are associated with a decreased response to anabolic stimuli

such as insulin-like growth factor-1 (IGF-1). Thus, the biochemical signal to spur

production of proteoglycans and collagen that maintain the strength of cartilage

decreases and results in an imbalance between breakdown and repair. The effect of

age on chondrocyte apoptosis seems to be strongly related. Perhaps, because of

occupational or recreational injury, men tend to have more OA before the age of 50.

5

Figure 43-1 Schematic representation of the convergence of modifiable, nonmodifiable risk factors, and

morphologic changes associated with osteoarthritis.

PATHOGENESIS

In the early stages of OA, changes occur that appear to begin the complex

abnormalities seen in the joint capsule, subchondral bone and ligaments, periarticular

muscles, and synovial membranes. Initial insult to the articular cartilage can result

from repetitive damage with time. Alternatively, another theory has been proposed

that examines articular damage after superficial or deep penetration injury. Either

repetitive or traumatic injury to articular surfaces initiates the cascade leading to

release of inflammatory cytokines (tumor necrosis factor [TNF], IL-1), nitric oxide,

and enzymes that break down the extracellular matrix. The breakdown of

extracellular matrix results in cartilage that is less elastic and less able to support

joint loads, and stiffening of subchondral bone. The cartilage is less able to support

forces, with diminished efficacy for providing joint lubrication and weight

distribution across the joint. Cartilage is avascular, however, and contains

chondrocytes that under normal conditions are responsible for cartilage breakdown

and repair. In early osteoarthritis, chondrocytes attempt to repair joint damage by

forming osteophytes, which try to stabilize the joint or alter the biochemical

properties of cartilage. The formation of osteophytes may provide an increased

surface area over which to distribute the forces across the joint. Cyst formation likely

arises via synovial fluid pressure exerted on the fissures or other structural defects in

subchondral bone.

5

Early in the disease process, the water content of the cartilage is increased.

However, this less viscous cartilage is structurally weaker than normal cartilage.

There are many structural alterations that contribute to the weakened collagen

network. One of the early changes is a smaller diameter of type II collagen, in

comparison with that in the more structurally intact disease-free joint. With disease

progression, the proteoglycan concentrations

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