Introduction to Septic Arthritis

A medical emergency, septic (infectious) arthritis is caused by bacterial invasion of a joint, resulting in inflammation of the synovial lining. If the organisms enter the joint cavity, effusion and pyogenesis follow, with eventual destruction of bone and cartilage.
Septic arthritis can lead to ankylosis and even fatal septicemia. However, prompt antibiotic therapy and joint aspiration or drainage cures most patients.

Pathophysiology
In most cases of septic arthritis, bacteria spread from a primary site of infection, usually in adjacent bone or soft tissue, through the bloodstream to the joint.
Common infecting organisms include four strains of gram-positive cocci—Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Streptococcus viridans—and two strains of gram-negative cocci—Neisseria gonorrhoeae and Haemophilus influenzae. Various gram-negative bacilli—Escherichia coli, Salmonella, and Pseudomonas, for example—also cause infection.
Anaerobic organisms such as gram-positive cocci usually infect adults and children older than age 2. H. influenzae most often infects children younger than age 2.

Risk factors
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as cancer, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, alcoholics and elderly people run a higher risk of developing septic arthritis.
Of course, susceptibility increases with diseases that depress the autoimmune system or with prior immunosuppressant therapy. I.V. drug abuse (by heroin addicts, for example) can also cause septic arthritis.
Other predisposing factors include recent articular trauma, joint surgery, intra-articular injections, and local joint abnormalities.

Introduction to Osteoarthritis

Osteoarthritis, also known as hypertrophic osteoarthritis, osteoarthrosis, and degenerative joint disease, is the most common form of arthritis. A chronic disease, it causes deterioration of the joint cartilage and formation of reactive new bone at the margins and subchondral areas of the joints. This degeneration results from a breakdown of chondrocytes, usually in the hips and knees.

Causes
Osteoarthritis is widespread, occurring equally in both sexes until age 55. After age 55, incidence is higher in women. Incidence is after age 40; its earliest symptoms generally begin in middle age and may progress with advancing age.
The degree of disability depends on the site and severity of involvement; it can range from minor limitation of the fingers to severe disability in persons with hip or knee involvement. The rate of progression varies, and joints may remain stable for years in an early stage of deterioration.
Primary osteoarthritis, a normal part of aging, results from many things, including metabolic, genetic, chemical, and mechanical factors. Secondary osteoarthritis usually follows an identifiable predisposing event—most commonly trauma, congenital deformity, or obesity—and leads to degenerative changes.

Signs and symptoms
The most common symptom of osteoarthritis is a deep, aching joint pain, particularly after exercise or weight bearing, usually relieved by rest. Other symptoms include:

• stiffness in the morning and after exercise (relieved by rest)
• aching during changes in weather (joint pain in rainy weather)
• “grating” of the joint during motion
• altered gait contractures
• limited movement.

These symptoms increase with poor posture, obesity, and occupational stress.
Osteoarthritis of the interphalangeal joints produces irreversible changes in the distal joints (Heberden’s nodes) and proximal joints (Bouchard’s nodes). These nodes may be painless at first but eventually become red, swollen, and tender, causing numbness and loss of dexterity.

Introduction To Ankylosing Spondylitis

Introduction: This is a chronic inflammatory arthritis especially affecting sacroiliac joints and spine and characterized by progressive stiffening and fusion of the axial skeleton. It is one of the seronegative spondyloarthropathies.

Incidence:  It is most commonly seen in the age range of 20 to 30 years and male to female ratio is   4: 1 . More than 90% of affected persons carry the histocompatibilty antigenHLA B27

Clinical Signs and Symptoms
Onset is usually insidious. There are recurring episodes of low back pain and stiffness sometimes radiating to the buttocks or thigh. Pain is worse in early morning and after inactivity.

Some patients complian of chest pain aggravated by breathing that is due to involvement of costovertebral joints. There is occasionally heel pain due to plantar fasciitis .

On examination there is failure to obliterate lumbar lordosis on forward flexion. There is pain on sacroilliac compression and tenderness over bony prominenece such as illiac crest, ischial tuberosity and greater trochanter.

There is restriction of movement of lumbar spines in all directions. As the disease progresses stiffness increases throughout the spine.

Associated Clinical findings

• Iritis occurs in about 25% of patients.
• Aortic regurgitation, heart blocks and anterior uveitis
• Pulmonary fibrosis of the upper lobes with progression to cavitation mimicking tuberculosis.

Investigations

• ESR is often raised.
• RA factor is absent.
• HLA B 27 seen in 90% of cases

X Ray Lumbar spine

Treatment Options For Rheumatoid Arthritis

Patients with rheumatoid arthritis need proper management and control of their symptoms to improve the quality of life. Although taking analgesic medicines for a long duration of time leads to gastric problems but it is important to give patient some relief from disturbing pain and inflammation.

Non Pharmacological Management

• Encourage regular exercise, physio and occupational therapy.
• Provide household aids and personal aids e.g wrist splints.
• Good mental and social support to improve life style and cope up with the disease.

Pharmacological Management
NSAIDs
If there is no contraindication e.g an active peptic ulcer start with an NSAID, such as ibuprofen. There is no single NSAID that is superior to other agents, and newer agents have not been shown to have a decreased incidence in toxicity. If patient cannot tolerate NSAIDs then consider COX2 inhibitors that prevents gastrointestinal side effects.

Steroids
Steroids may decrease joint damage and control difficult symptoms but using them for prolonged period of time leads to decreased bone density and predisposition to osteoporosis as well as other side effects related to prolonged steroid use.

Introduction To SLE

Definition
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disorder that affects the connective tissues. SLE is characterized by recurring remissions and exacerbations, which are especially common during the spring and summer.

Incidence
It strikes women 8 times as often as it does men, increasing to 15 times as often during childbearing years.

Etiology: 

The direct cause is unknown but it can be predisposed by certain factors

Predisposing factors

• Physical or mental stress
• Streptococcal or viral infections
• Exposure to sunlight or ultraviolet light
• Immunization
• Pregnancy
• Abnormal estrogen metabolism
• Drugs, including procainamide, hydralazine, anticonvulsants; less commonly, penicillins, sulfa drugs, oral contraceptives

Pathophysiology
Autoimmunity is believed to be the prime mechanism in SLE. The body produces antibodies against components of its own cells, such as the antinuclear antibody (ANA), and immune complex disease follows. Patients with SLE may produce antibodies against many different tissue components, such as red blood cells (RBCs), neutrophils, platelets, lymphocytes, or almost any organ or tissue in the body.

Differential Diagnosis Of Joint Disorders

Disorders of joint is one of the common problem a family physician comes across. Here is a list of differential diagnosis for joint disorders with brief description of each disorder:

1. Congenital Causes

– Achondroplasia: Premature osteoarthritis may occur in achondroplasia.

– Ehlers-Danlos syndrome: a genetic disorder of connective tissues in which patients have hypermobile joints and hyperextensible skin. they may present with joint subluxation, dislocations and swelling due to effusions.

– Marfan Syndrome: Patients have generalized joint laxityand present with joint pain and swelling due to effusions.

– Osteogenesis Imperfecta: Patients have brittle bones that lead to easy joint dislocations.

2. Accquired Causes

– Infective:

• Septic or pyogenic arthritis usually present as a monoarthritis with a red , swollen, painful, immobile joint. Usually a single joint is involved.
• Viral arthritis may occur following viral illness like rubella, mumps, hepatitis etc.
• In rheumatic fever which usually follows a streptococcal infection. There is a migratory poly arthritis together with carditis, erythematous skin lesions and sub cutaneous nodules.

– Inflammatory:

•  Rheumatoid arthritis presents initially with swollen, painful, stiff hands and feet. Later characteristic deformities develop. Most commonly swelling is seen at metacarpophalangeal joints.
• Psoriatic arthropathy usually follows several years after skin lesions.
• Reiter’s disease may present with arthritis in a single or few joints. There will be a history of sexual contact, urethritis and conjunctivitis.
• Ankylosing spondylitis presents in young males and initially presents with morning stiffness in the spine. The sacroilliac joints are involved.
• SLE presents with malaise arthralgia, myalgia, a butterfly rash on the face, raynaud’s syndrome, splenomegaly, pleurisy, pleural effusion, pericarditis.
• Polymyalgia rheumatica is associated with tender muscles, mild polyarthritis and there may be associated temporal arteritis.

Raynaud’s Disease - Definition, Causes, Symptoms, Diagnosis And Treatment

Introduction: One of several primary arteriospastic disorders, Raynaud’s disease is characterized by episodic vasospasm in the small peripheral arteries and arterioles, precipitated by exposure to cold or stress. This condition occurs bilaterally and usually affects the hands or, less often, the feet.
Raynaud’s disease is most prevalent in women, particularly between puberty and age 40. A benign condition, it requires no specific treatment and has no serious aftereffects.

Raynaud’s phenomenon, however, a condition often associated with several connective tissue disorders—such as scleroderma, systemic lupus erythematosus, and polymyositis—has a progressive course, leading to ischemia, gangrene, and amputation. 

Differentiating the two disorders is difficult because some patients who experience mild symptoms of Raynaud’s disease for several years may later develop overt connective tissue disease—most commonly, scleroderma.

Causes
Although the cause is unknown, several theories account for the reduced digital blood flow: intrinsic vascular wall hyperactivity to cold, increased vasomotor tone resulting from sympathetic stimulation, and antigen-antibody immune response (the most probable theory, because abnormal immunologic test results accompany Raynaud’s phenomenon).

Signs and symptoms

After exposure to cold or stress, the skin on the fingers typically blanches, then becomes cyanotic before changing to red and before changing from cold to normal temperature. Numbness and tingling may also occur but are usually relieved by warmth.