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Gout

Gout

Gout

Gout is a metabolic disorder characterized by elevated serum uric acid levels and deposits of urate crystals in synovial fluids and surrounding tissues.

It is derived from the Latin word “Gutta” meaning a “drop” (of liquid).

Gout also is a kind of arthritis that occurs when uric acid builds up in blood and causes joint inflammation, it can be acute or chronic.

Acute: The affected joints often appear reddened and swollen and are sensitive to touch. The pain is described as a burning sensation. The development of acute gout is typically triggered by trauma, alcohol use, surgery, and systemic infection. 

Chronic: This is characterized by visible deposits of urate crystals (tophi) that form nodules and may be painful during gout attacks.

Cause

Gout is associated with the presence of hyperuricemia (high blood levels of urate, or serum urate levels greater than ~6.8 mg/dl

  • Hyperuricemia: Gout occurs when urate crystals accumulate in your joint, causing the inflammation and intense pain of a gout attack. Urate crystals can form when you have high levels of uric acid in your blood.

NOTE: Not everyone with hyperuricemia develops gout as this condition requires two essential processes to develop – crystallization and inflammation. When uric acid levels become elevated, crystals will form in the joints, which will then trigger the inflammatory process. 

Risk Factors

  • Gender, common in males than females. Men have higher urate levels than women
  • Obesity
  • Age. Increased age is associated with reduced renal function & increased use of diuretics, which interfere with urate clearance. 
  • Having certain health conditions, including:
    • Congestive heart failure
    • Hypertension (high blood pressure)
    • Insulin resistance
    • Metabolic syndrome
    • Diabetes
    • Poor kidney function
  • Using certain medications, such as thiazides and loop diuretics since they interfere with urate clearance by effects on multiple transporters in the proximal renal tubule. Asprin, aspirin inhibits urate secretion and increases serum urate levels at commonly used doses,
  • Drinking alcohol. The risk of gout is greater as alcohol intake goes up.
  • Eating or drinking food and drinks high in fructose (a type of sugar). Plasma uric acid levels rise within minutes after fructose infusion
  • Having a diet high in purines, which the body breaks down into uric acid. Purine-rich foods include red meat.
  • Family history of Gout.
  • Chemotherapy-induced tumor lysis syndrome where the high rate of cancer cell death produces a large increase in urate.

Signs & Symptoms of Gout

  • Podagra – an acute episodes of arthritis associated with the big toe. The big toe is the most common target for painful gout related inflammation because the combination of decreased temperature, lower pH and level of dehydration.
temperature (the first metatarsal phalangeal joint has a lower temperature, which favors crystallization)
pH (physical trauma can cause acidosis & low pH favors crystallization)
level of joint hydration (nocturnal intra-articular dehydration may cause nocturnal crystallization, and explain the common nocturnal onset of pain)
  • Tophi (plural of tophus) which are deposits of urate that form in patients suffering from chronic hyperuricemia. They are most commonly found in joints, cartilage, bones.
  • Urate kidney stones forming in the ureter (urolithiasis). These usually occur in patients having an acidic urine pH.
  • Nephropathy caused by urate crystal deposition in the renal medulla in severe cases of the disease.

Other signs and symptoms include,

  • Onset is usually nocturnal, will sudden swelling and excruciating pain.
  • Joint pain usually begins over two to four hours and during the night.
  • May have low grade fever. 
  • Usually subside within 2 to 10 days.

Stages/ Phases of Gout

 The four phases of gout include asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout.

ASYMPTOMATIC HYPERURICEMIA

Asymptomatic hyperuricemia is the term for an abnormally high serum urate level, without gouty arthritis or nephrolithiasis. In this first stage of gout, the person has no joint pain, no red or swollen joints, just an elevated uric acid blood test.

ACUTE GOUTY ARTHRITIS

Acute gout is characterized by the sudden onset of pain, erythema, limited range of motion and swelling of the involved joint. This is when the urate crystals are released into the joint fluid and cause an inflammatory reaction, bringing in many white blood cells and releasing inflammatory chemicals that cause the pain, redness, and swelling.

INTERCRITICAL GOUT

Following recovery from acute gouty arthritis, the patient reenters an asymptomatic phase of the disease. This phase is referred to as “intercritical gout. This phase is where a person has already had a gout episode but is presently not having any joint pain or swelling, no signs and symptoms of gout.

RECURRENT GOUTY ARTHRITIS (Chronic or Tophaceous Gout)

 Because the uric acid deposits can form nodules called “tophi,” often at the bunion point of the big toe or at the elbow. This stage is where a person can have some joint pain from gout just about all the time, It usually takes many years of uncontrolled gout for someone to get into this stage.

During this stage, progressive joint damage develops, so patients with gout should be treated before this starts happening.

The frequency of subsequent acute attacks of gout usually increases over time. Approximately 60 percent of patients have a second attack within the first year, and 78 percent have a second attack within two years. Only 7 percent of patients do not have a recurrence within a 10-year period

gout pathophysiology

Pathophysiology of Gout.

Normal healthy joints are lined by a synovial membrane containing both fibroblast-like and macrophage-like cells that function to maintain joint homeostasis, including the supply of nutrients and the production of a clear viscous fluid to reduce friction between joint cartilage during movement.

When urate crystals form within the joint during periods of hyperuricemia, they become coated by proteins which increases their pro-inflammatory properties. Protein coating may also restrain urate crystals from leaving joint areas.

The presence of protein-coated urate crystals initiates a series of events including phagocytosis of urate crystals, activation of membrane signaling events from cells in the synovial membrane, and the release of multiple cytokines.

Cytokines released from cells within the joint (in particular IL-1β) cause chemotaxis and activation of neutrophils, monocytes and numerous other inflammatory cells. Once within the joint, neutrophils and other inflammatory cells interact with urate crystals, inducing the release of additional inflammatory mediators including prostaglandins, nitric oxide, leukotrienes and other mediators that contribute to both tissue damage and hypersensitivity of pain receptors.

Diagnostic Tests / Investigations

  • Joint fluid test. A needle is used to draw fluid from the affected joint. Urate crystals may be visible when the fluid is examined under a microscope. This is a more accurate way to confirm a gout diagnosis.
  • Blood test. Gout occurs when uric acid, a bodily waste product, builds up in the bloodstream and forms as crystals in the joints. A blood test that shows high levels of uric acid could help confirm a diagnosis of gout.  Not definitive.
  • X-ray imaging. Joint X-rays can be helpful to rule out other causes of joint inflammation.
  • Ultrasound. It  uses sound waves to detect urate crystals in the joints or deposits of uric acid crystals that form hard, visible lumps in or near the joints, called tophi.
  • Dual-energy computerized tomography (DECT). This test combines X-ray images taken from many different angles to visualize urate crystals in joints.
  • Creatinine. This test measures the levels of creatinine, a waste product made by your muscles, in a sample of blood or urine. Abnormal levels could be a sign of kidney disease.
  • Blood Urea Nitrogen (BUN). Often performed in conjunction with the creatinine test, this test checks for blood levels of urea nitrogen, a bodily waste product normally excreted through the kidneys. A high level could mean kidneys are not working properly.
  • Urinalysis. Your doctor may order check for high levels of uric acid in your urine, which could indicate a risk for kidney stones.

Management of Gout

Aims

  • To alleviate the pain and inflammation associated with acute attacks.
  • To decrease uric acid levels.
  • To prevent complications.

Medical Management.

  • The acute treatment of gout is focused on treating the pain & inflammation caused by the accumulation of urate crystals in joints (most commonly affecting the large toe).
  • However, because anti-inflammatory drugs have no effect on uric acid levels and do not prevent joint damage or renal stones, anti-inflammatory agents should not be used for long-term therapy in patients who are appropriate candidates for urate-lowering treatment.

  • There are 3 common anti-inflammatory treatment options for treatment of acute gout:

    1. NSAIDs
    2. COLCHICINE
    3. GLUCOCORTICOIDS (Corticosteroids)
  1. NSAIDs e.g
      • Naproxen, Ibuprofen (over the counter options)
      • Indomethacin (more potent prescribed NSAIDs)
    • Indication:
      • Treatment of inflammation & pain associated with acute attacks of gout
    • Mechanism of Action:
      • Non-selective inhibitors of cyclooxygenase (COX) 1 & 2
      • COX inhibition reduces the synthesis of prostaglandins that are involved in mediating inflammatory responses & pain associated with gout.
    • Relative contraindications:
      • Renal insufficiency (inhibiting prostaglandin synthesis can induce renal failure)
      • Peptic ulcer (increased risk for GI bleeding)
      • CV disease (increased risk of stroke or MI)
      • NSAID allergy
      • Treatment with other anticoagulants (increased bleeding risk)
  2. COLCHICINE
    • To reduce pain & inflammation associated with acute attacks of gout most effective when taken at the first sign of articular discomfort (at early stages of neutrophil chemotaxis & activation)
    • colchicine treatment is typically reserved for patients with NSAID contraindications, or who do not adequately respond to NSAIDs.
    • Can be combined with NSAID.
  3. GLUCOCORTICOIDS (Corticosteroids)
    • an alternative for patients with contraindications to both NSAIDs & colchicine.
    • can be given by intra-articular injection, oral or parenteral administration, with the route depending on the severity of symptoms and the number of joints affected

Combination Therapy

  • Combination therapy can be tried in patients with severe pain, or pain that is not adequately relieved by monotherapy. Common examples include:
    • Colchicine + NSAID
    • Colchicine + oral glucocorticoid
    • NSAID + intraarticular glucocorticoid
    • Colchicine + intraarticular glucocorticoid
    • Oral glucocorticoid + intraarticular glucocorticoid

Lowering uric acid in the body

XANTHINE OXIDASE INHBITORS
  • the recommended 1st line drug therapy, decrease the synthesis of uric acid from purines
    • Allopurinol (Zyloprim ®)
      • a purine analog
      • “not an innocuous drug”, and is recommended for symptomatic hyperuricemia only.
      • Concurrent treatment with colchicine or NSAIDs during the first 3-6 months of urate-lowering therapy has been shown to reduce the risk of flare-ups.
      • N.B. Allopurinol can cause relatively rare, but serious (life-threatening) drug hypersensitivity reactions (e.g. Stevens-Johnson & DRESS syndromes). Allopurinol is one of the most frequent causes of these reactions .
URICOSURICS
    • Uricosuric drugs are organic acids that inhibit the reabsorption of uric acid by inhibiting anionic transport sites of the renal proximal tubule; inhibiting renal reabsorption enhances uric acid clearance. The only uricosuric drug available in the Uganda is probenecid.
      • Probenecid
        • for patients who can’t tolerate allopurinol, or require additional urate lowering; can be combined with a xanthine oxidase inhibitor.
        • typically administered concomitantly with colchicine to reduce the likelihood of gouty flare-up
        • can lower mean serum uric acid by 30-40%
        • not effective in the setting of renal dysfunction
        • it can promote kidney-stone formation in patients with high urinary uric acid levels, and is contraindicated in patients with a history of kidney stones (nephrolithiasis)
URICOSLYTICS
    • converts uric acid to a water soluble metabolite
      • Pegloticase (Krystexxa ®)reserved for the treatment of severe, treatment-refractory chronic gout.
        • while Pegloticase is effective in lowering uric acid levels, little is known about its ability to reduce the frequency of recurrent attacks of gout, or the optimal duration of Pegloticase therapy.
        • uricase (uric oxidase) is an enzyme found in almost all organisms, but the gene for uricase is non-functional in humans (Wikipedia). It converts uric acid to a metabolite (allantoin) that is 5-10 times more water soluble than uric acid.
        • infusions every 2 weeks are effective in lowering uric acid levels, but cost, infusion reactions, and development of tolerance (which may be due to development of antibodies) have limited its use.
Surgical Management

If gout symptoms have occurred on and off without treatment, uric acid crystals may have built up in the joints to form gritty chalky nodules called tophi.

The tophi can cause infection, pain, pressure and deformed joints. Surgery is recommended to do excision and remove the tophi.

 

Patient advice.
Reduce fructose consumption
    • sweetened soft drinks & fruit juices
    • any foods containing high fructose corn syrup such as ice cream, desserts, syrup
Avoid high purine foods
    • avoid consuming organ meats (kidney, liver, sweetbreads)
    • limit serving sizes of beef & pork
Reduce alcohol intake
    • reduce wine & spirits, and avoid all alcohol intake during gout attacks.
    • beer contains purines & alcohol consumption can produce lactic acid that interferes with urate clearance
Weight loss for obese patients
    • modify diet & increase exercise to achieve a healthy BMI
    • weight loss can enhance the renal excretion of urate.
Encourage consumption of
    • low fat or non-fat dairy products
    • vegetables
Eliminating unnecessary drugs
    • Many drugs including thiazides, loop diuretics, niacin, & aspirin may contribute to producing hyperuricemia. In some cases adequate substitutes, or dosage reductions are feasible, but therapeutic benefits must be considered.
Nursing Management using Nursing Process.

Assessment: Acute Pain

Sudden and severe pain occurring in one or more joints, usually in the big toe, is the classic symptom of gout. This occurs due to the accumulation of uric acid, forming sharp crystals in the joints.

Nursing Diagnosis: Acute Pain related to Inflammatory process as evidenced by:
Reddened, swollen joints, Distraction behavior, Expressive behavior, Guarding behavior, Positioning to ease pain, Limited range of motion, Reports pain characteristics and intensity 

Expected Outcome:

  • The patient will verbalize pain relief and perform activities of daily living without discomfort
  • The patient will display an absence of redness, swelling, and warmth to the affected joints

Interventions:

1. Administer pain medications as indicated.
NSAIDs are usually prescribed to help relieve pain and reduce joint inflammation in patients with gout. Steroids can also help reduce damage to the joints.

2. Elevate the limb.
Elevating the affected joint can help reduce inflammation.

3. Apply cool compresses.
Nonpharmacologic interventions such as the application of cool compresses and ice can reduce inflammation and soothe burning sensations.

4. Adjust lifestyle behaviors.
Gout attacks can be minimized by reducing risk factors such as the intake of alcoholic beverages, sugary drinks, and high-purine foods such as red meats and some seafood.

Assessment: Impaired Physical Mobility

Patients with gout often find it difficult to walk or stand when they are having flare-ups in their feet, knees, or ankles because of severe and sudden pain and swelling. When there is joint swelling, the joints can become stiff, and painful when moved, and the range of motion will become more limited.

Nursing Diagnosis: Impaired Physical Mobility related to: Pain, Inflammatory process, Limited range of motion , Joint tenderness, Joint stiffness as evidenced by:
Altered gait, Decreased range of motion, Difficulty turning, Slowed movement, Spastic movement, Uncoordinated movement, Hesitancy to move.

Expected outcomes:

  • The patient will be able to ambulate with minimal discomfort
  • The patient will participate in activities to improve their range of motion

Interventions:

1. Encourage weight loss.
Obesity places extra stress on joints and also increases the incidence of diabetes, hypertension, and other chronic conditions that are risk factors for gout.

2. Encourage active and passive ROM exercises.
Range of motion exercise can help preserve the flexibility and mobility of affected joints. Gout causes joint stiffness and patients can be provided with exercises they can do themselves or with someone else to maintain their mobility.

3. Refer to PT or OT.
A physical therapist or occupational therapist can help evaluate the extent of impaired physical mobility in patients with gout.

4. Encourage the use of mobility aids when necessary.
Mobility aids like handrails, canes, and shower benches promote patient safety during gout flare-ups and prevent accidental falls and other injuries.

Gout Read More »

Osteoarthritis

Osteoarthritis

Osteoarthritis

Osteoarthritis is a type of arthritis that occurs when flexible tissue at the ends of bones wears down.
The wearing down of the protective tissue at the ends of bones (cartilage) occurs gradually and worsens over time.
Therefore, Osteoarthritis can also be defined as a gradual decrease of the cartilage covering of the bone ends within joints.

Osteoarthritis is a degenerative joint disease or sometimes called osteoarthrosis even though inflammation may be present.

It is the most common among the joint disorders and also the most disabling.

osteoarthritis

Types of Osteoarthritis

  • Primary Osteoarthritis

it’s the most common and it affects the spine, fingers, hips, knees and great big toes and it has no obvious cause 

  • Secondary Osteoarthritis

occurs with a pre existing abnormality e.g  injury or trauma. This can be due to septic arthritis and congenital abnormalities.

Kellgren-Lawrence Classification of Osteoarthritis

Kellgren-Lawrence osteoarthritis classification
  • grade 0 (none): definite absence of x-ray changes of osteoarthritis
  • grade 1 (doubtful): doubtful joint space narrowing and possible osteophytic lipping
  • grade 2 (mild/minimal): definite osteophytes and possible joint space narrowing
  • grade 3 (moderate): moderate multiple osteophytes, definite narrowing of joint space and some sclerosis and possible deformity of bone ends
  • grade 4 (severe): large osteophytes, marked narrowing of joint space, severe sclerosis and definite deformity of bone ends

Osteoarthritis is deemed present at grade 2 although of minimal severity

Pathophysiology of Osteoarthritis

  • Osteoarthritis occurs when the cartilage that cushions the ends of the bone in the joints gradually decreases.
  • Cartilage is a firm slippery tissue that permits nearly frictionless joint motion. In osteoarthritis, the slick surface of the cartilage becomes rough eventually and if  the cartilage wears down completely, bones will be left rubbing onto another bone.
  • Mechanical injury. OA starts from an injury of the articular cartilage, subchondral bone, and synovium.
  • Chondrocyte response. Factors that initiate chondrocyte response include previous joint damage, genetic and hormonal factors, and others.
  • Cytokines. After the chondrocyte response, the release of cytokines occurs.
  • Stimulation of enzymes. Proteolytic enzymes, metalloproteases, and collagenase are stimulated, produced, and, released.
  • Damage. The resulting damage predisposes to damage further as the chondrocyte is triggered to respond again.

Cause

  • Increased age. Most elderly people experience osteoarthritis because the ability of the articular cartilage to resist microfracture with repetitive loads diminishes with age.
  • Obesity. Obese people easily wear out their weight-bearing joints because of their increased weight.
  • Previous joint damage. Having previous joint damage predisposes the patient to secondary OA.
  • Repetitive use. Repetitive use due to occupational or recreational factors also causes OA.

Predisposing Factors

  • Age. the risk increases with age
  • Diabetes or other rheumatic diseases
  • Genetics
  • Hormonal imbalance
  • Bone deformities
  • Increased cholesterol levels
  • Obesity 
  • Sex more common in females than males
  • Joint injuries

Signs and Symptoms

  • Limited movements of the joints
  • Pain and tenderness
  • Swelling
  • Stiffness lasting for a short time after a  period of inactivity or when waking up
  • Crackling noise
  • Enlarged distorted joints
  • Bone spurs- these are extra bits of bone which feel like hard lumps may form around the affected joint.

Investigations and Diagnosis

  • Physical assessment. Physical assessment of the musculoskeletal system reveals the tender and swollen joints.
  • X-ray. Osteoarthritis  characterized by a progressive loss of joint cartilage, which appears on x-ray as a narrowing of the joint space.
  • Routine blood tests can be useful to exclude infective causes and inflammatory causes.
  • MRI use of radio waves and strong magnetic fields to produce detailed images of bone and soft tissues including cartilages.
  • Joint fluid analysis : Use of a needle to draw fluid out of the affected joints. This helps to determine if there is inflammation or if pain is caused by gout or an infection.

Management of Osteoarthritis

Aims 

  • To relief pain
  • To minimize progress of the condition
  • To restore normal functions of the bones.

Management according to classification/ severity.

  • Grade 1- doubtful: patients will develop very minor wear and tear and bone spur growth at the end of the knee joints. Pain and discomfort are rarely felt.

Treatment 

  • If the patient is not predisposed to O.A, orthopedic physicians may not recommend any special treatment
  • Supplement such as glucosamine may be recommended.
  • Exercises are also recommended

Grade 2-mild

  • A diagnostic images or x-rays of the knee joint will show more bone spur growth and through the space between the bones appear normal, people will begin experiencing symptoms of the joint pain. The area around the knee joint will feel stiff and uncomfortable mainly when sitting for a long time or in the morning after waking up after a period of inactivity.

Treatment

  • non pharmacological therapies to relieve pain and discomfort
  • exercise and strength training for increased joint stability.
  • Helping devices

Grade 3- moderate

  •  obvious erosion to the cartilage surface between bones and fibrillation narrow the gap between the bone
  • Crepitus sounds

Treatment

  • Over counter NSAIDS or pain relief therapies.
  • If not effective, doctor may prescribe codeine and oxycodeine.

Supportive treatment

    • Physical therapy if it does not work, patient is given articular cortisone.
    • Hyaluronic acid over 3-5 weeks time.

Grade 4-  Severe

The joint space is reduced causing cartilage to wear off, leaving the joint stiff which leads to a chronic inflammatory response, with decreased synovial fluid that causes friction, greater pain and discomfort when walking or moving the joint.

There is increased production of synovial metalloproteinases, cytokines and TNF(Tumour necrosis factor ) that can diffuse back into the cartilage to destroy soft tissue around the knee.

Treatment.

  • Incase of severe O.A of the knee, an option is performing osteotomy or bone realignment surgery where the orthopedic surgeon cuts the bone above or below the knee to shorten the length and help realign it for less stress on the  joint. 
  • Another surgical option is total knee replacement or arthroplasty.
  • Arthroplasty. Diseased joint components are replaced in arthroplasty.

Prevention

  • Weight reduction. To avoid too much weight upon the joints, reduction of weight is recommended.
  • Prevention of injuries. As one of the risk factors for osteoarthritis is previous joint damage, it is best to avoid any injury that might befall the weight-bearing joints.
  • Perinatal screening for congenital hip disease. Congenital and developmental disorders of the hip are well known for predisposing a person to OA of the hip.
  • Keeping a healthy body weight
  • Reduce on sugar intake.

Complications

  • Bone death
  • Bleeding inside the joint
  • Rapid complete break down of cartilage
  • Infection of the joint
  • Rupture of tendons and

Osteoarthritis Read More »

Rheumatoid Arthritis

Arthritis

Arthritis

Arthritis is the swelling and tenderness of one or more joints.

Inflammatory arthritis includes a large number of arthritic conditions in which the predominant feature is a synovial inflammation.
This includes post viral arthritis, rheumatic arthritis, seronegative spondyloarthropathy, / arthritis and Lyme arthritis.

  •  Disease presenting as an inflammatory mono arthritis include crystal arthritis e.g. gout, pseudo gout.
    Septic arthritis and arthritis due to Juxta – articular bone tumors
  •  Disease presenting as an inflammatory polyarthritis include rheumatoid arthritis, reactive arthritis and Seronegative arthritis associated with psoriasis.

Types of arthritis

  1.  Rheumatoid arthritis
  2.  Osteoarthritis
  3.  Goutily arthritis
  4.  Traumatic arthritis
  5.  Septic arthritis
  6.  Hemophilic arthritis
  7.  Gonococcal arthritis
  8.  Syphilitic arthritis
  9.  Tubercular arthritis

Etiology of arthritis

  •  Trauma
  •  Infection like staphylococci and streptococci
  •  Extrapulmonary TB
  •  Late syphilis
  •  Deposition of crystal like urate crystals in uric acid metabolic disorder arthritis, reactive
  • Degeneration of articular parts like cartilages
  • Autoimmunity due to rheumatic fever
  • Hemorrhage into the joint

Predisposing factor

  •  Gender – women before the menopause are affected three times more often than men
  •  Familial – history
  •  Genetic factors
  •  Age
  •  Renal failure

Rheumatoid Arthritis

Rheumatoid arthritis an autoimmune inflammatory disorder of unknown origin that primarily involves the synovial membrane of the joints

Rheumatoid arthritis is a chronic inflammatory joint condition of un known origin characterized by persistent bilateral proportional small joints involvement resulting in cartilage destruction and bony erosion
with subsequent joint deformities.

The disease affects many systems including articular and non articular structures
It is called seropositive arthritis because of rheumatoid factor that is present in 80% of the cases.
Rheumatology deals with a heterogeneous group of disorder of joint, bones and connective  tissues.
Rheumatic diseases affect people of all sexes, ethnic groups, and ages.

The frequency increases with age so that as many as 40% of persons over the age of 50 years have Rheumatic complaints.

Pathophysiology of rheumatoid arthritis

Rheumatoid arthritis is an autoimmune disease where by body tissues are destroyed by its own immune system. The exact cause is not yet known. The disease target the synovium and involves two pathological changes i.e. inflammation and proliferation
The joints are acutely inflamed due to inflammatory changes in the synovial membrane. The synovium becomes thicker, very vascular and the site of increased cell infiltration which may cause an effusion within the joint that manifests as a swollen tender and painful joint with
restriction of its movements. Extra-articular structures lead to rheumatoid nodules (subcutaneous nodules)
The proliferative tissue spreads as pannus over the articular cartilage leading to its slow erosion.

Systemic inflammatory changes can affect many body organs leading to pericarditis, pleuritis, bowel vasculitis, general malaise and anemia
The condition can occur in children less than 16 years as juvenile rheumatoid arthritis or still disease presenting with poly articular arthritis assuming a flexed position, refusing to work, lymphadenopathy, hepatosplenomegaly, pericarditis and pleuritis.

Summary of pathophysiology.

The pathophysiology of rheumatoid arthritis is brief and concise.

  • Autoimmune reaction. In RA, the autoimmune reaction primarily occurs in the synovial tissue.
  • Phagocytosis. Phagocytosis produces enzymes within the joint.
  • Collagen breakdown. The enzymes break down collagen, causing edema, proliferation of the synovial membrane, and ultimately pannus formation.
  • Damage. Pannus destroys cartilage and erodes the bone.
  • Consequences. The consequences are loss of articular surfaces and joint motion.
  • Degenerative changes. Muscle fibers undergo degenerative changes, and tendon and ligament elasticity and contractile power are lost.

Signs and symptoms of rheumatoid arthritis

  • Joint pain. One of the classic signs, joints that are painful are not easily moved.
  • Swelling. Limitation in function occurs as a result of swollen joints.
  • Warmth. There is warmth in the affected joint and upon palpation, the joints are spongy or boggy.
  • Erythema. Redness of the affected area is a sign of inflammation.
  • Lack of function. Because of the pain, mobilizing the affected area has limitations.
  • Deformities. Deformities of the hands and feet may be caused by misalignment resulting in swelling.
  • Rheumatoid nodules. Rheumatoid nodules may be noted in patients with more advanced rheumatoid arthritis, and they are nontender and movable in the subcutaneous tissue.

Other signs and symptoms include;

  •  Gradual onset of pain and morning stiffness
  • Loss of appetite and weight
  • Swelling and progressive loss of joint function
  • Mild pyrexia and fatigue
  • Other prodromal signs like anorexia, weakness and vague joint pains that persist for weeks or months followed by pain, tender swollen joints
  • Inflammation involves three or more joints including small joints
  • Symmetrical bilateral arthritis involving ankles, knee, wrists, elbows, shoulders, spine and temporomandibular joints
  • Pain increases with joint movement and may disturb sleep
  • Subcutaneous nodule
  • Extra articular manifestation includes splenomegaly, lymphadenopathy, pericarditis, carpal tunnel syndrome, neuropathy, ulcers, pancytopenia and nephritic syndrome
  • Erythmatous boggy joints
  • The condition is precipitated by stress, emotions, infections and physical exertion
  • The condition is characterized by relapses and remissions
  • There may be hemorrhagic infarcts in the nails and finger pulps.
  • Inflammation in the eye and ulceration of the white portion of the eye.
  • Axial joint leading to fetal cervical cord compression.

Assessment and Diagnostic Findings

  • Physical examination.
  • History taking.
  • X-rays of involved joints: Reveals soft-tissue swelling, erosion of joints, and osteoporosis of adjacent bone (early changes) progressing to bone-cyst formation.
  • Rheumatoid factor (RF): Positive in more than 80% of cases (Rose-Waaler test).
  • Synovial membrane biopsy: Reveals inflammatory changes and development of pannus (inflamed synovial granulation tissue).
  • Synovial/fluid aspirate: May reveal volume greater than normal; opaque, cloudy, yellow appearance (inflammatory response, bleeding, degenerative waste products).
  • Erythrocyte sedimentation rate (ESR): Usually greatly increased (80–100 mm/hr). May return to normal as symptoms improve.
  • CBC: Usually reveals moderate anemia. WBC is elevated when inflammatory processes are present.
  • Immunoglobulin (Ig) (IgM and IgG): Elevation strongly suggests autoimmune process as cause for rheumatoid arthritis.
  • Direct arthroscopy: Visualization of area reveals bone irregularities/degeneration of joint.

Management of rheumatoid arthritis

Aims

  • To control pain
  • To prevent joint damage
  • Control systemic symptoms
  • Stop inflammation[put disease in remission] wellbeing
  • Restore physical function and overall
  • Reduce long term complications
  • Relieve symptoms

There is no specific cure for Rheumatoid arthritis

Nursing care

  1. Provide adequate rest of the painful swollen joints in acute phase. Use a bed cradle to lift linen from affected joints
  2. Firm back support should be used during the day
  3. The legs must be kept straight and the pillow placed behind the knees, this prevents flexion deformities
  4. Encourage the patient to do active exercise under the guidance of a physiotherapist.
  5. Diet should hence a high protein content with aplenty of milk and eggs
  6. Iron should be given to correct anemia which is common.
  7. Vitamin D, calcium supplements may help to reduce osteoporosis
  8. Should be immobilized in light plastic splints on even plaster of paris.
  9. Relieve pain and discomfort. Provide comfort measures like application of heat or cold massage, position changes, supportive pillows etc
  10. Encourage verbalization of pain. Administer anti inflammatory and analgesic as prescribed.
  11. FACILITATING SELF CARE, Assist patient to identify self care deficit. Develop a plan based on patient perception and priorities.
  12. IMPROVING BODY IMAGE AND COPING SKILLS, Identify areas of life affected by the disease and answer questions., Develop a plan for managing symptoms and enlisting support of family and friends to promote daily function
  13. INCREASING MOBILITY, Asses need for occupational or physical therapy consultation., Encourage independence in mobility and assist as needed
  14. REDUCING FATIGUE, Encourage adherence on treatment programs., Encourage adequate nutrition, Encourage on how to use energy conservation techniques like delegation, setting prioties etc
  15. PROMOTE HOME AND COMMUNITY BASED CARE, Focus on teaching on the disease and possible changes related to it, prescribed drugs and their side effect ., Strategies to maintain independence and safety at home.

MEDICAL MANAGEMENT

There is no cure for rheumatoid arthritis. But recent discoveries indicate that remission of symptoms is more likely when treatment begins early with strong medications known as disease-modifying antirheumatic drugs (DMA). The types of medications recommended will depend on the severity of your symptoms and how long you’ve had rheumatoid arthritis.

  1. NSAIDs. Nonsteroidal anti-inflammatory drugs (NSAIDs) can relieve pain and reduce inflammation. Over-the-counter
    NSAIDs include ibuprofen (Advil, Motrin IB) and naproxen sodium (Aleve). 
    • Acetyl salicylic acid (aspirin) 80 – 100mg/kg daily 4-60
    •  Other alternative to aspirin, Indomethacin, Naproxen
    , Diclofenac Piroxicam. Stronger NSAIDs are available by prescription. Side effects may include ringing in your ears, stomach irritation, heart problems, and liver and kidney damage.
  2. Steroids. Corticosteroid medications, such as prednisone, reduce inflammation and pain and slow joint damage. Side effects may include thinning of bones, weight gain and diabetes. Doctors often prescribe a corticosteroid to relieve acute symptoms, with the goal of gradually tapering off the medication.
  3. Disease-modifying antirheumatic drugs (DMARDs). These drugs can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage. Common DMARDs include methotrexate (Trexall, Otrexup, Rasuvo), leflunomide (Arava), hydroxychloroquine (Plaquenil) and sulfasalazine (Azulfidine). Side effects vary but may include liver damage, bone marrow suppression and severe lung infections.
  4. Biologic agents. Also known as biologic response modifiers, this newer class of DMARDs includes abatacept (Orencia), adalimumab (Humira), anakinra (Kineret), certolizumab (Cimzia), etanercept (Enbrel), golimumab (Simponi), infliximab (Remicade), rituximab (Rituxan), tocilizumab (Actemra) and tofacitinib (Xeljanz). These drugs can target parts of the immune system that trigger inflammation that causes joint and tissue damage. These types of drugs also increase the risk of infections. Biologic DMARDs are usually most effective when paired with a non biologic DMARD, such as methotrexate.

Surgical Management.

SURGERY

If medications fail to prevent or slow joint damage, you and your doctor may consider surgery to repair damaged joints. Surgery may help restore your ability to use your joint. It can also reduce pain and correct deformities.

Rheumatoid arthritis surgery may involve one or more of the following procedures:

  1. Synovectomy. Surgery to remove the inflamed synovium (lining of the joint). Synovectomy can be performed on knees, elbows, wrists, fingers and hips.
  2. Tendon repair. Inflammation and joint damage may cause tendons around your joint to loosen or rupture. Your surgeon may be able to repair the tendons around your joint.
  3. Joint fusion. Surgically fusing a joint may be recommended to stabilize or realign a joint and for pain relief when a joint replacement isn’t an option.
  4. Total joint replacement. During joint replacement surgery, your surgeon removes the damaged parts of your joint and inserts a prosthesis made of metal and plastic.
  5. Osteotomy. 
  6. Tenorrhaphy. Tenorrhaphy is the suturing of a tendon.
  7. Arthrodesis. Arthrodesis is the surgical fusion of the joint.
  8. Arthroplasty. Arthroplasty is the surgical repair and replacement of the joint.

Conservative measures

  • Weight reduction
  • Joint rest
  • Avoidance of joint over use
  • Orthotic devices to support inflamed joints[braces and splits].
  • Isometric and postural exercises and aerobic exercises
  • Occupation and physical therapy.

Nursing Diagnosis

  1. Acute and chronic pain related to inflammation and increased disease activity, tissue damage, fatigue, or lowered tolerance level.
  2. Fatigue related to increased disease activity, pain, inadequate sleep/rest, inadequate nutrition, and emotional stress/depression
  3. Impaired physical mobility related to decreased range of motion, muscle weakness, pain on movement, limited endurance, lack or improper use of ambulatory devices.
  4. Self-care deficit related to contractures, fatigue, or loss of motion.
  5. Disturbed body image related to physical and psychological changes and dependency imposed by chronic illness.

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Tendonitis

Tendonitis

Tendonitis or Tendinitis

Tendonitis is the inflammation or irritation of a tendon. 

Tendinitis can occur in any of your body’s tendons, it’s most  common around your shoulders, elbows, wrists, knees and  heels.

tendon anatomy tendonitis

Anatomy Review

A tendon is a fibrous connective tissue that attaches muscle to  bone.

Tendons let us move our limbs. They also help prevent  muscle injury by absorbing some of the impact your muscles  take when you run, jump or do other movements. Your body  contains thousands of tendons. 

The tendon plays an extraordinary role in mechanics and  movement. They transmit the force produced by the muscular  contraction to the skeletal levers, thus allowing the movement  and the maintenance of the body posture. 

The primary cell types of tendons are the spindle-shaped tenocytes (fibrocytes) and tenoblasts (fibroblasts). Tenocytes  are mature tendon cells that are found throughout the tendon  structure, typically anchored to collagen fibers. Tenoblasts are  spindle-shaped immature tendon cells that give rise to  tenocytes. Tenoblasts typically occur in clusters, free from  collagen fibers. They are highly proliferative and are involved in  the synthesis of collagen and other components of the  extracellular matrix. 

Tendon sheath is a membrane like structure surrounding the  tendon, which separates the tendon from surrounding tissue  and allows tendon to glide smoothly inside the sheath.

Tendons are stiffer than muscles, have greater tensile strength  and can withstand very large loads with minimal deformations. They differ from ligaments because ligament are fibrous  connective tissue that connects bones to other bones and  tendinosis – a chronic condition that causes the tendons to  break down over time. 

Common Types of Tendonitis 

  • Achilles tendonitis is a common sports injury. Additionally,  people with rheumatoid arthritis are at a higher risk of  Achilles tendinitis.
  • Tennis elbow – Tennis elbow (lateral epicondylitis) is a  painful condition that occurs when tendons in your elbow  are overloaded, usually by repetitive motions of the arm  and wrist. Wrist tendonitis can affect anyone who  repeatedly performs the same movements with their  wrists. It is common in people who do a lot of typing,  writing, and sports like tennis. 
  • Golfer’s elbow – Medial epicondylitis is also known as  golfer’s elbow, baseball elbow, suitcase elbow, or  forehand tennis elbow. It’s characterized by pain from the  elbow to the wrist on the inside (medial side) of the elbow 
  • Pitcher’s shoulder – When a muscle or tendon is  overworked, it can become inflamed. The rotator cuff is  frequently irritated in throwers 
  • Swimmer’s shoulder – Swimmer’s shoulder, also called  shoulder impingement, is a condition where swimmers  often aggravate their shoulders while they swim due to the  constant joint rotation. In supraspinatus tendonitis the  tendon at the top of the shoulder joint becomes inflamed.  This causes pain when moving the arm
  •  Jumper’s knee – Jumper’s knee, also known as patellar  tendonitis, is a condition characterized by inflammation of  your patellar tendon

Causes of Tendonitis 

Tendinitis can be caused by a sudden injury, the condition is  much more likely to stem from the repetition of a particular  movement over time. 

  • Strain – stretching or tearing of a muscle or a tissue  connecting muscle to bone (tendon). 
  • Overuse of the tendons or excessive exercises
  •  Injury or trauma.

Risk factors  

  • Age – in elderly the tendons get less flexible. 
  • Sports and exercises 
  • Diabetes 
  • Rheumatoid arthritis
  •  Antibiotics like quinolones ( Cipro , levofloxacin ) • Trauma or injury

Pathophysiology 

The cause of inflammation is irritation of the sheaths by  prolonged or abnormal use of the tendons. These sheaths are  composed of thin, filmy tissue that permits the sliding motion of  tendons within them. Less often it may follow invasion of the  tendon sheaths by bacteria with subsequent infection. 

Inflammation in the sheath of the tendon produces swelling,  redness, and pain along the course of the involved tendon, and  motion of the tendon produces severe pain. Swelling of the  sheath narrows the space through which the tendon may slide,  causing stiffness in the involved area. A grating sensation may  be felt as the tendon moves.  

Signs and symptoms 

★ Redness and Hotness at the site. 

★ Pain often described as a dull ache, especially when  moving the affected limb or joint. It increases when you  move the injured area. 

★ Tenderness – The area will be tender, and you’ll feel  increased pain if someone touches it. 

★ Mild swelling

★ feeling a grating or crackling sensation when you move  the tendon 

★ Tightness that makes it difficult to move the area 

Diagnostic management 

  • Physical examination.  
  • MRI scans to help determine tendon thickening,  dislocations and tears 
  • X ray 
  • Ultrasound 

Pharmacological / Medical Management 

  • NSAIDs to relieve pain  
  • Platelet-rich plasma (PRP) – PRP treatment involves  taking a sample of your own blood and spinning the blood  to separate out the platelets and healing factors. The  solution is then re-injected into the area of chronic tendon  irritation. 
  • Corticosteroid injections to reduce inflammation – Corticosteroids are not recommended for chronic tendinitis (lasting over three months), as repeated injections may  weaken a tendon and increase your risk of rupturing the  tendon. 
  • Treat underlying conditions like rheumatoid arthritis and  diabetes. 
Surgical management 

For chronic tendon inflammation, focused aspiration of scar  tissue (FAST) is a minimally invasive treatment option using  ultrasound guidance and very small instruments designed to remove tendon scar tissue without disturbing the surrounding  healthy tendon tissue. 

Nursing interventions (specific) 

★ Enough rest from activities 

★ Encourage the patient to use heat or cold therapy as  prescribed. Teach the patient to use a barrier between the  skin and heat or to use cold therapy to prevent burning or  frostbite. 

★ Wrapping the area in a compression bandage until  swelling subsides 

★ Applying heat or ice – Teach the patient how to apply ice  and heat properly to prevent burning or chilling. 

★ Fluid removal by aspiration and physical therapy to  prevent “frozen” joints and preserve motion constitute  supplementary treatment 

★ Resting or elevating the tendon 

★ supports such as splints, braces, or a cane 

★ Explain the importance of anti-inflammatory medications,  and teach the patient to take them with milk to minimize  gastrointestinal (GI) distress.  

★ You may be advised to wear a shoe insert that will place  your foot in the correct position for walking and running.

★ Physical therapy – Stretching , Massage , Ultrasound ,  Strengthening exercises 

★ Stretches and exercises to build strength and improve  mobility in the area 

Complications 

  • Contractures (or tightening) of the tendon 
  • Scarring (called adhesions) 
  • Muscle wasting
  •  Disability.

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Osteogenesis Imperfecta

Osteogenesis Imperfecta

Osteogenesis Imperfecta

Osteogenesis imperfecta (OI) also known as brittle bone disease, is a genetic disorder characterized by fragile bones that break easily.

 OR
Osteogenesis imperfecta is a disorder of bone fragility chiefly caused by mutations is the COL1A1 and COL1A2 that encode type I procollagen.

Osteogenesis imperfecta (OI) is a genetic disorder that results in fragile bones.

▪ OI affects both bone quality and bone mass
▪ It is a genetic disorder
▪ OI is the most common cause of osteoporosis and it is a generalised disorder of
connective tissue.
▪ Osteoporosis is fragility of the skeletal system and a susceptibility to fractures of the
long bones or vertebral compressions from mild or inconsequential trauma.

Osteogenesis Imperfecta bone 2

Aetiology 

❑ OI is caused by a mutation on a gene that affects the body’s production of collagen  found in bones and other tissues. People with OI have less collagen than normal or a  poorer quality than normal 

❑ OI is caused by defects in or related to a protein called type 1collagen. Collagen is an  essential building block of the body. The body uses type 1 collagen to make bones  strong and to build tendons, ligaments and teeth.  

❑ Certain gene changes or mutations cause the collagen defects 

❑ About 80%-90% of OI cases are caused by autosomal dominant mutations in type 1  collagen genes, COL1A1 and COL1A2. These mutations cause the body to make  either abnormally formed collagen or too little collagen 

❑ The remaining cases of OI are caused by autosomal recessive mutations in any of the  six genes ( SERPINF1 ,CRTAP ,LEPRE 1 ,PPIB ,SERPINH1 ,and FKBP10) 

❑ These gene changes are inherited, or passed down from parents to their children. 

Epidemiology 

  • The autosomal dominant forms of OI occur equally in all racial and ethnic groups  whereas recessive forms occur predominately in ethnic groups with consanguineous  marriages. 
  • The west African founder mutation for type VIII OI has a carrier frequency of 1 in 200- 300 among African-Americans. 
  • The incidence of OI detectable in infancy is approximately 1 in 20,000

Pathophysiology 

  • People with OI are born with defective connective tissue or without ability to make it,  usually because of deficiency of type 1 collagen. This deficiency arises from an amino  acid substitution of glycine to bulkier amino acids in the collagen triple helix  structure. 
  • The larger amino acid side-chains create steric hindrance that creates bulge in the  collagen complex, which in turn influences both the molecular Nano mechanics and  the interaction between molecules which are both compromised 
  • As a result, the body may respond by hydrolyzing the improper collagen structure. 
  • If the body doesn’t destroy the improper collagen, the relationship between the  collagen fibrils and hydroxyapatite crystals to form bone is altered, causing  brittleness.

Clinical Manifestations

❑ Short stature
❑ Weak tissues, fragile skin, muscle weakness and loose joints
❑ Bone deformities such as bowing of the legs
❑ Hearing loss
❑ Discolouration of the sclera, may be blue, purple in colour
❑ Curvature of the spine
❑ Breathing problem
❑ Easy bruising of skin
❑ Soft, discoloured teeth

Classification of OI

The silence classification divides OI into 4 types based on clinical and radiographic criteria.  Types V and VI were later proposed based on histologic distinctions.  

❖ Osteogenesis imperfecta Type I (mild) 

OI type 1 is sufficiently mild that is often found in large pedigrees. Many type 1 families have  blue sclerae, recurrent fractures in childhood and presenile hearing loss (30%-60%). Other  possible connective tissue abnormalities include hyperextensible joints, easy bruising, thin  skin, scoliosis, hernia and mild short stature compared with family members. 

❖ Osteogenesis imperfecta Type II (Perinatal Lethal)

  • Infants with OI type II maybe stillborn or die in the first year of life. Birth weight and  length are small for gestational age. There is extreme fragility of the skeleton and  other connective tissues. There are multiple intrauterine fractures of long bones  which have a crumpled appearance on radiographs. 
  • There are striking micromyelia and bowing of extremities; the legs are held abducted  at right angles to the body in the frog leg position. The skull is large for body size,  with enlarged anterior and posterior fontanels. Sclerae are dark blue-grey. 

❖ Osteogenesis imperfecta Type III (Progressive Deforming) 

  • OI type III is the most severe non-lethal form of OI and results in significant physical  disability. Birth weight and length are often low normal. Fractures usually occur in  utero. There is a relative macrocephaly and triangular faces. 
  • Disorganization of the bone matrix results in a “popcorn” appearance at the  metaphysis 
  • All type III patients have extreme short stature 
  • Dentinogenetic imperfecta, hearing loss and kyphoscoliosis may be present or  develop over time  

❖ Osteogenesis imperfecta Type IV (moderately severe) 

  • Patients with OI type IV can present with utero fractures or bowing of lower long  bones. They can also present with recurrent fractures after ambulation and have  normal to moderate short stature. 
  • Most children have moderate bowing even with infrequent fractures • Children with OI type IV requires orthopaedic and rehabilitation intervention. 
  • Fracture rates decrease after puberty. Radiographically they are osteoporotic and  have metaphyseal flaring and vertebral compressions. 
  • Patients with type IV have moderate short stature. Scleral hue maybe blue or white. 

Classification of OI

Forlino and Marini in 2015 offered an alternate way of understanding the genetics of  osteogenesis imperfecta by sorting into five functional categories as follows: 

  • Group A. These are the primary defects in collagen structure and function. 
  •  Group B. These are the collagen modification defects.
  • Group C. These are the collagen folding and crosslinking defects.
  • Group D. This group includes ossification or mineralization defects.
  • Group E. The group includes osteoblast development defects with collagen  insufficiency.

Assessment and Diagnostic Findings

Results of diagnostic tests on people with osteogenesis imperfecta are useful in ruling out  other metabolic bone diseases. 

  • Collagen synthesis analysis. Collagen synthesis analysis is performed by culturing dermal fibroblasts obtained during skin biopsy.
  • Prenatal DNA mutation analysis. Prenatal DNA mutation analysis can be performed in pregnancies with the risk of osteogenesis imperfecta to analyze uncultured chorionic villus cells.
  • Bone mineral density. (DEXA scan). A scan of the bones to check for softening. Bone mineral density, as measured with dual-energy radiographic absorptiometry, is generally low in children and adults with osteogenesis  imperfecta. 
  • X-ray. Images may reveal thinning of the long bones with thin cortices or it may reveal beaded ribs, broad bones and numerous fractures with deformities of the long bones. 
  • Biochemical testing which may include a skin sample to examine the collagen 
  •  Blood tests or urine tests; usually to rule out other conditions such as rickets

Differential Diagnosis
• Child abuse
• Rickets
• Scurvy
• Osteopetrosis
• Leukaemia
• Cushing syndrome

Treatment and Management

There is no cure for OI 

Aims of management  

  • To reduce fracture rate
  • prevent long bone deformities
  • minimize chronic pain
  • maximize functional capacity.

The main modalities of treatment can be grouped into medications, surgical intervention,  physical therapy, and experimental therapies.

Medications: 

▪ Bisphosphonate therapy 

It is the mainstay of pharmacologic fracture prevention therapy for most forms of OI.  Observational studies show that bisphosphonates for children reduced fracture frequency up  to 100%.  

▪ Intravenous pamidronate 

– For patients with all forms of OI, IV pamidronate is advised, except Type VI, in whom clinical  benefits are likely to outweigh potential long-term risks (i.e., those with long bone  deformities, vertebral compression fractures, and ≥3 fractures/year)  

– Pamidronate is administered IV in cycles of 3 consecutive days at 2–4-month intervals  with doses ranging from 0.5–1 mg/kg/day, depending on age, with a corresponding  annual dose of 9 mg/kg.  

– Smallest effective dose should be used, with careful monitoring of vertebral geometry  and long-bone fractures 

– NOTE : Pre-treatment evaluation and monitoring  

– Calcium and vitamin D intake are based on recommended dietary allowance for  child’s age (700–1300 mg/day calcium and 400–600 IU vitamin D) should be  supplemented before treatment is initiated if dietary intake is inadequate. Indices of  calcium homeostasis (e.g., calcium, phosphorous, and parathyroid hormone) and  renal function test should be assessed before initiation of treatment and followed  every 6–12 months.  

– Calcium levels are to be assessed before each IV bisphosphonate infusion to assure  that child is not hypercalcaemic. 

Surgical intervention 

  • Management of fractures (with quick mobilization to prevent bone loss due to inactivity) and placement of intramedullary rods to prevent or correct long-bone deformities are advised. Telescoping rods is advised for patients older than >2 years  who are actively growing. Those with severe scoliosis may benefit from surgery.  
  • Intramedullary rod replacement. In patients with bowed long bones, intramedullary rod replacement may improve weight bearing and, thus, enable the child to walk at an earlier stage than he or she might otherwise. 
  • Surgery for basilar impression. This procedure is reserved for cases with neurologic deficiencies, especially those caused by compression of brain stem.
  • Correction of scoliosis. Correction of scoliosis may be difficult because of bone fragility, but spinal fusion injury may be beneficial in patients with severe disease. • In utero bone marrow transplant. In utero bone marrow transplantation of adult bone marrow has been shown to decrease perinatal lethality. 

Physical and occupational therapy 

  • Physical therapists are instrumental in designing physical activity program that minimizes fracture risk, ensuring mobilization to prevent contractures and bone loss from immobility. 
  • Occupational therapists can address impairments in activities of daily living secondary to upper or lower limb deformities.  

Experimental therapies 

  • Growth hormone

In a single randomized trial, thirty prepubertal children with OI (Types I, III, and IV) were  observed for 12 months during ongoing neridronate therapy and then randomized to  recombinant growth hormone (GH) plus neridronate or neridronate alone. 

Growth velocity were found to be significantly higher in the group that received GH  compared with control group, but no differences were observed in the fracture risk. 

  • Cell replacement therapies

Pilot study of allogeneic hematopoietic cell transplantation was performed in five children  with OI; three children had successful engraftment, and in these 3, improvements in growth  velocity and reduction in fracture rate were noted following transplantation. More clinical  research is needed for exploring this modality.

Complications.

➢ Respiratory infections such as pneumonia
➢ Kidney stones
➢ Joint problems
➢ Hearing loss
➢ Eye conditions and vision loss
➢ Basilar invagination
➢ Brain stem compression
➢ Hydrocephalus

Nursing Care

Nursing Diagnosis 

Desired Outcomes 

Intervention 

Rationale

Deficient  

Knowledge related  new diagnosis of  

osteogenesis  

imperfecta, as  

evidenced by  

patient’s  

verbalization of “I  want to know more  how to manage my  illness.”

At the end of the  health teaching  

session, the patient  will be able to  

demonstrate  

sufficient knowledge  of his/her condition and its  

management.

Assess the patient’s  readiness to learn,  misconceptions, and  blocks to learning  (e.g. denial of  

diagnosis or poor  lifestyle habits)

To address the  

patient’s cognition  and mental status  towards disease  

management and to  help the patient  

overcome blocks to  learning

Activity  

intolerance related  to bone pain, as  

evidenced by bone  pain score of 7 out  of 10, fatigue,  

disinterest in ADLs  due to pain,  

verbalization of  

tiredness and  

generalized  

weakness

The patient will  

demonstration  

active participation  in necessary and  

desired activities and  demonstrate  

increase in activity  levels

Assess the patient’s  activities of daily  

living, as well as  

actual and perceived  limitations to  

physical activity. Ask  for any form of  

exercise that he/she  used to do or wants  to try. 

Encourage  

progressive activity  through self-care  and exercise as  

tolerated. Explain  the need to reduce  sedentary activities  such as watching  television and using  social media in long  periods. 

Administer  

analgesics as  

prescribed prior to  exercise/ physical  activity.  

Teach deep  

breathing exercises  and relaxation  

techniques. 

To create a baseline of activity levels and  mental status related  to chronic pain,  

fatigue and activity  intolerance. 

To gradually  

increase the  

patient’s tolerance  to physical activity. 

To provide pain  

relief before an  

exercise session.  

To allow the patient to relax while at rest  and to facilitate  

effective stress  

management. 

  

Provide adequate  ventilation in the  

room.

To allow enough  

oxygenation in the  room.

Acute Pain related to  the fragility of the  bones evidenced by  pain score of 7 out  of 10, verbalization  of sharp pain,  

guarding sign on the  affected areas  

especially long  

bones, facial  

grimace, crying, and  restlessness

The patient will  

demonstrate relief of  pain as evidenced by  a pain score of 0 out  of 10, stable vital  

signs, and absence  of restlessness.

Administer  

prescribed pain  

medications. 

Assess the patient’s  vital signs and  

characteristics of  

pain at least 30  

minutes after  

administration of  medication. 

Place the patient in  complete bed rest  during severe  

episodes of pain.

To alleviate  

acute/chronic bone  pain. Pain is usually  described as sharp  and spasmic. 

To monitor  

effectiveness of  

medical treatment  for the relief of bone  pain. The time of  

monitoring of vital  signs may depend  on the peak time of  the drug  

administered. 

To enable to patient  to rest and to  

provide comfort.

Risk for injury  

related to fragile  

bones

The patient will be  able to prevent  

injury by means of  exercising falls  

prevention protocols  and maintaining  

his/her treatment  regimen in order to  regain normal  

balance and healing.

Complete a falls risk  assessment, which  includes: 

Factors contributing  to falls risk 

Functional ability 

Use of mobility  

devices 

Use of bedrails 

Put the bed at the  lowest level. 

Place items within  the patient’s reach.

The use of a  

standard tool will  help identify the  

status of the  

patient’s risk for  

falling and will help  determine the  

factors contributing  to the falls risk. 

Low set beds reduce  the possibility of  

injuries related to  falls. 

Items far away from  the patient’s reach  may contribute to  falls and fall-related  injuries.

  

Refer to  

physiotherapy and  occupational  

therapy.

Patients with  

fracture may need  therapies to help  them regain  

independence and  lower their risk for  injury.

Impaired Physical  Mobility related to  vertebral and joint  inflammation as  

evidenced by severe  leg pain rated 8 out  of 10, leg muscle  weakness, failure to  perform ADLs, and  verbalization of  

fatigue

Patient will maintain  or regain functional  mobility.

Perform a mobility  assessment. Assess  the patient’s  

function ability to  perform activities of  daily living (ADLs)  such as eating,  

bathing, oral and  perineal care. 

Refer the patient to  the physiotherapist.

To identify patient’s  current strengths  and problems  

related to  

performing ADLs 

To provide  

specialized care and  individualized  

exercise program.

Practice Test: Osteogenesis Imperfecta

1. The nurse is teaching the parents of a newborn with osteogenesis imperfecta. The nurse should tell the parents:

A. That the baby will need daily calcium supplements.
B. To lift the baby by the buttocks when diapering.
C. That the condition is a temporary one.
D. That only the bones are affected by the disease.

1. Answer: B. To lift the baby by the buttocks when diapering.

  • Option A is incorrect because children with osteogenesis imperfecta have normal calcium and phosphorus levels.
  • Option C is incorrect because the condition is not temporary.
  • Option D is incorrect because the teeth and the sclera are also affected.

2. The home health nurse is visiting an 18-year-old with osteogenesis imperfecta. Which information obtained on the visit would cause the most concern? The client:

A. Likes to play football.
B. Drinks several carbonated drinks per day.
C. Has two sisters with sickle cell trait.
D. Is taking acetaminophen to control pain.

2. Answer: A.  Likes to play football.

The client with osteogenesis imperfecta is at risk for pathological fractures and is likely to experience these fractures if he participates in contact sports.

  • Options B, C, and D are not factors for concern.

3. A patient presents with multiple fractures and blue sclera of the eye. The same disease in infants would result in:

A. Death.
B. A, C, D.
C. Fractures.
D. Blue sclera.

3. Answer: B. A, C, D.

Death, fractures, and blue sclera can all occur in a patient with osteogenesis imperfecta.

  • Options A, C, D: All options can be found in a patient with osteogenesis imperfecta.

4. What bone disorder is caused by an autosomal dominant defect in the synthesis of collagen type 1?

A. Osteogenesis imperfecta.
B. Achondroplasia.
C. Osteopetrosis.
D. Osteomyelitis.

4. Answer: A. Osteogenesis imperfecta.

Osteogenesis imperfecta can be caused by an autosomal dominant defect in the synthesis of collagen type 1.

  • Option B: The FGFR3 gene instructs your body to make a protein necessary for bone growth and maintenance. Mutations in the FGFR3 gene cause the protein to be overactive. This interferes with normal skeletal development.
  • Option C: Osteopetrosis, literally “stone bone”, also known as marble bone disease and Albers-Schönberg disease, is an extremely rare inherited disorder whereby the bones harden, becoming denser, in contrast to more prevalent conditions like osteoporosis, in which the bones become less dense and more brittle, or osteomalacia, in which the bones soften. Osteopetrosis can cause bones to dissolve and break.
  • Option D: Most cases of osteomyelitis are caused by staphylococcus bacteria, types of germs commonly found on the skin or in the nose of even healthy individuals.

5. Which drug reduces the incidence of fracture and increases bone mineral density, while reducing pain levels and increasing energy levels?

A. Risedronate.
B. Gentamycin.
C. Tramadol.
D. Pamidronate.

5. Answer: D. Pamidronate.

Cyclic administration of intravenous pamidronate reduces the incidence of fracture and increases bone mineral density while reducing pain levels and increasing energy levels.

  • Option A: Oral biphosphates such as risedronate may have some effect in reducing fractures in patients with osteogenesis imperfecta.
  • Option B: Gentamycin is an antibiotic that reduces the signs and symptoms of infection.
  • Option C: Tramadol is an opioid pain medication used to treat moderate to moderately severe pain.
 

Osteogenesis Imperfecta Read More »

Osteomyelitis

Osteomyelitis 

Osteomyelitis 

Osteomyelitis is a pus forming infection of the bone.

It is among the commonest conditions in children, decreasing as the child grows, and it increases in patients who are immune compromised, mainly affecting older children.

Cause

Children develop infection in a long bone metaphysis. The commonest causative organism is Staphylococcus aureus, following infection elsewhere in the body despite the infrequency of staphylococcal
bacteremia, presumably because of that organism’s particular ability to infect bone

Common causes 

Age group

Most common organism

Newborns (less than 4 months 

S. aureus ,Enterobacter species & group A&B streptococcus species.

Children (aged 4months to 4yrs )

S. aureus, group A streptococcus species, haemophilus influenza and enterobacter species.

Children 4yrs to adult

S. aureus (80%), groupA streptococcus species, H influenza and enterobacter species

Adult

S. aureus and occasionally Enterobacter or streptococcus species

Sickle cell anemia patients

Salmonella species are the most common in patients with sickle cell disease

Note;

  • In children the long bone are usually affected. in adults, the vertebrae and the pelvis are most commonly affected.
  •  Acute osteomyelitis invariably occurs in children because of rich blood supply to the growing bones. 
  • When adults are affected it may be because of compromised host resistance due to debilitation, intravenous drug abuse, infectious root canaled teeth or other disease like immunosuppressive.

Wald Vogel Classification of Osteomyelitis

Osteomyelitis can be classified according to;

  1. Duration of Infection
  2. Mechanism of bone infection

Duration of Infection

  • Acute osteomyelitis ( suppurative osteomyelitis) is usually regarded as that which occurs before there is actual bone death. Initial episodes of  Edema, formation of pus, vascular congestion, thrombosis of small vessels, e.t.c
  •  Chronic osteomyelitis (suppurative osteomyelitis phase ) osteomyelitis involves infection both, within and around, the bone that has died.  Recurrence of acute cases, Large areas of ischemia, necrosis, and bone sequestra.

N.B.: Acute osteomyelitis can lead to chronic osteomyelitis because without treatment, the infection and inflammation block the blood vessels and causes the bone to die. Chronic osteomyelitis is harder to treat Sequestra= a fragment of dead bone attached to healthy bone

Mechanism of Bone Infection

  •  Hematogenous: Secondary to bacterial transport through the blood. Majority of infections in children
  • Associated with vascular insufficiency: Infections in patients with diabetes affecting the feet, or peripheral vascular insufficiency
  •  Contiguous: Bacterial inoculation from an adjacent focus. E.g. Posttraumatic Osteomyelitis like from neighboring tissue, infections from prosthetic devices

Pathophysiology of Osteomyelitis

  • Causative bacteria enters bone causing an infection. Bacteria can enter bone via bloodstream, from a nearby infection, or direct contamination Risk factors include: Open wound over a bone, Open fracture, Recent surgery, Injection around bone, Medications that weaken immune system, Pre-morbid conditions (diabetes).
  • In general, microorganism may infect the bone through one or more of the three basic methods.
  • Via the blood stream. (haematogeneously) the most common method. From nearby areas of infection (as in cellulitis )
  • Penetrating trauma including Iatrogenic causes such as joint replacement or internal fixation of fractures or secondary peripheral periodontitis in teeth
  • The area usually affected when the infection is contracted through the blood stream is the metaphysis of the bone. Once the bone is infected, leukocytes enter the infected area and in their attempt to engulf the infectious organisms, release enzymes that lyse the bone.
  • Pus spreads into the bone’s blood vessels, impairing their flow and areas of devitalized infected bone known as sequestra, form basis of chronic infection. Often the body will try to create new bone around the area of necrosis. The resulting new bone is often called an involucium.
  • On histologic examination these areas of necrotic bone are the basis for distinguishing between acute osteomyelitis and chronic OM
  • The history is usually short, 48 hours or less. Initially, there is bone pain and marked tenderness without visible inflammation. When infection spreads sub periosteally, local and systemic signs of infection appear. Pus then forms in bone and soft tissues. The appearance of the bone does not change for 10–14 days so radiographs are a baseline for future change and to exclude differential diagnoses (Ewing’s sarcoma, leukaemia). Softening of soft-tissue planes may be seen.  OM is all infective process of bone (osseous) component including the bone marrow. When it is chronic, it can lead to bone sclerosis and deformity.

PREDISPOSING FACTORS

  • Pyomyositis (bacterial infection of muscle)
  • Cellulitis
  •  Sickle-cell disease (thrombotic crisis)(causative agent mostly S.Aureus, Salmonella also common)
  • Diabetes
  • Intravenous drug use
  • Prior removal of spleen
  • Age
  • Immune suppression
  • Autoimmune disorder
  • Systemic infections

Signs and Symptoms of Osteomyelitis.


Acute osteomyelitis

  •  Onset is usually over several days
  •  Fever, usually high but may be absent, especially in neonates
  •  Pain (usually severe) in the affected limb
  •  Tenderness and increased “heat” at the site of infection, swelling of the surrounding tissues and joint
  •  Reduced or complete loss of use of the aected limb
  •  The patient is usually a child of 4 years or above with reduced immunity, but adults may also be afected.
  •  History of injury may be given, and may be misleading, especially if there is no fever
  •  Malaise 
  • Redness of the limb 
  • Edema of the limb

Chronic osteomyelitis

  • May present with pain, erythema, or swelling, sometimes in association with a draining sinus tract
  •  Deep or extensive ulcers that fail to heal after several weeks of appropriate ulcer care (e.g. in diabetic foot), and non-healing fractures, should raise suspicion of chronic osteomyelitis

Deferential diagnosis

  •  Infection of joints
  • Injury (trauma) to a limb, fracture (children)
  • Bone cancer (osteosarcoma, around the knee) and adults.

Management of Osteomyelitis

Management can be medical or surgical or both.

Aims of management

  1. To preserve limb and joint function
  2. To prevent further complications

Admission

  • Child is admitted to pediatric ward.
  • Patient’s history is taken of including name, sex, address, nationality. Past medical history, past surgical history are taken

Assessment

  • Vital observation T,P,R and BP and recorded in patients chart 
  • Assessment of patient limb for redness, hotness, edema, general examination of the patient from head to toe
  • Doctor is informed who will order the following investigations.

Investigations / Diagnosis

  • Diagnosis is through physical examination, laboratory findings and radiological findings.
  • ¾ X-ray shows
  • – Nothing abnormal in first 1-2 weeks
    – Loss of bone density (rarefaction) at about 2 weeks
    – May show a thin “white” line on the surface of the infected part of the bone (periosteal reaction)
    – Later, may show a piece of dead bone (sequestrum)
  • ¾ Blood: CBC, ESR, C&S: Type of bacterium may be detected

Medical Management

  •  Immobilize the limb, splint
  •  Elevate the  affected limb 
  • Provide pain and fever relief with paracetamol, or ibuprofen 
  • Typically patient need antibiotic for several weeks to properly treat the infections.
  • Drain the infected site.
  • Immobilize or stabilize the bone if necessary.
  • Administer intravenous antibiotics like Cloxacillin Child: below 12yrs  50 mg/kg every 6 hours; Above 12year 500 mg IV every 6 hours for 2 weeks. Then Continue orally for at least 4 weeks (but up to 3 months) if  it fails; then, 
  • Ceftriaxone 50mg-100mg/kg for about 10 days, vancomycin, penicillin and ciprofloxacin can also be used depending on results from culture and sensitivity.
  • Administer analgesics depending on severity like, ibuprofen acetaminophen, morphine for pain relief. 
  • Failure to improve after 48-72 hours of antimicrobial therapy surgical intervention is considered by;
  • Surgical intervention may be indicated in the following cases: Drainage of subperiosteal , soft tissue abscesses, and intramedullary purulence
  • Removal of necrotic bone tissue and local pus or drainage is often necessary to speed up healing.
  • – Debridement of contiguous foci of infection (which also require antimicrobial therapy)
    – Excision of sequestra (i.e. weak and lifeless bone) Debridement of the area to remove necrotic tissue.
  • Failure to improve after 48-72 hours of antimicrobial therapy

Chronic osteomyelitis
Surgery and antibiotics

  • Continue with the Administration of intravenous antibiotics like ceftriaxone 50mg-100mg/kg for about 10 days, vancomycin, penicillin and ciprofloxacin can also be used depending on results from culture and sensitivity

Nursing Care

Nursing Diagnosis
  1. Ineffective Tissue Perfusion Related to: Inflammatory reaction, Thrombosis of vessels, Tissue destruction, Edema, Abscess formation As evidenced by: Bone necrosis, Continuation of the infectious process, Delayed healing, Pain, Erythema, Swelling, Altered sensation in the affected area, Weak peripheral pulses.

Ineffective Tissue Perfusion Interventions:

1. Establish blood flow at the site.
Blood circulation distributes nutrients throughout the body, aids in controlling waste production, enhances site recovery, and speeds up the healing process. Healthy blood flow across vessels, arteries, veins, and capillaries maximizes perfusion.

2. Manage chronic conditions and lifestyle factors.
Diabetes, peripheral vascular disease, sickle cell disease, neuropathy, smoking, malnutrition, and more affect the revascularization of the affected area. These need to be addressed before surgical intervention.

3. Provide DVT prophylaxis.
Anticoagulants should be administered as ordered to promote circulation and prevent the development of blood clots.

4. Prepare for possible surgery.
Depending on the degree of vascular insufficiency, procedures to restore adequate blood flow, such as debridement or vascular surgery may be necessary.

5. Prevention through pressure ulcer prophylaxis.
Patients who are immobile or bed-bound are at an increased risk of experiencing osteomyelitis due to pressure ulcers. By implementing appropriate interventions such as turning schedules and skin care, this can be prevented.

      2.  Hyperthermia Related to: Increased metabolic rate, Infection, Inflammatory response, Trauma As evidenced by: Increased body temperature, Warmth to touch, Flushed skin, Tachypnea, Tachycardia

Hyperthermia Interventions:

1. Provide a tepid sponge bath.
Tepid sponge baths lower body temperature and provide comfort to the patient.

2. Apply a cooling blanket.
A cooling blanket can lower the internal body temperature by surface cooling. Monitor closely to prevent a rapid drop in body temp.

3. Initiate antibiotics.
Long-term antibiotics are required for the treatment of osteomyelitis to control the infectious process. Instruct patients that antibiotic therapy may be required for weeks. 

4. Instruct on symptoms.
Teach the patient and family that if fever, chills, warmth to the skin, or skin flushing is observed that the body is attempting to fight off infection and to seek immediate assistance.

  3. Acute pain Related to: Inflammation, Tissue necrosis As evidenced by: Verbalization of pain, Tenderness with palpation, Guarding behaviors, Facial grimacing, Increased vital signs.

Acute Pain Intervention

1. Reposition as needed.
Repositioning and turning can decrease the stimulation of the pain and pressure receptors.

2. Administer pain medication as prescribed.
Mild or moderate pain may be controlled with non-steroidal anti-inflammatory drugs (NSAIDs). More severe pain or pain related to debridement or surgical intervention may require oral or IV opioid medications.

3. Elevate or immobilize the site.
Elevation or splinting of an extremity may improve pain by increasing circulation.

4. Collaborate with physical and occupational therapists.
Physical and occupational therapists assist in pain management through exercise, stretching, and other techniques.

5. Anticipate referral to a pain specialist.
Osteomyelitis and its treatment can be very painful and prolonged. Acute pain can turn into chronic pain depending on the severity and pain tolerance of the patient, which may need a referral to a pain specialist.

Complications
  • Necrosis 
  • Gangrene
  • Amputation
  • Sepsis
  • Cancer of the bone.

Osteomyelitis  Read More »

Osteopenia of Prematurity

 Osteopenia of Prematurity

Osteopenia of Prematurity

Osteopenia of prematurity is the decrease in the amount of calcium and phosphorus in bones which makes the bones weak and brittle resulting into broken bones.

Prematurity affects bone mineralization and bone growth—thus the condition osteopenia of prematurity;

Normal bone is formed by the deposition of minerals, predominantly calcium (Ca+2) and phosphorus (P), onto an organic matrix (osteoid) secreted by the osteoblasts. Osteoclasts play an important role in bone resorption and remodeling.

Osteopenia of prematurity is principally a result of inadequate calcium intake to meet bone growth demands.

Causes

  •  Lack of vitamin D (vitamin D helps in absorption of calcium from intestines and kidneys) by the mother during pregnancy which has to be transferred from the mother to the fetus.
  • Prematurity these neonates lose much more phosphorous in their urine than babies that are born full-term
  •  Liver problems which may lead to deficiency of vitamin D e.g
    cholestasis(obstruction of bile flow).

Signs and symptom

Clinically, osteopenia manifests between 6 and 12 weeks of age and is usually asymptomatic; however, severe manifestations may include the following:

Severe manifestations

    1. Poor weight gain and growth failure.

    2. Rickets-like findings may include growth retardation, frontal bossing,  and epiphyseal widening.

    3. Fractures may manifest as pain on handling.

    4. Respiratory difficulties or failure to wean off ventilator support due to poor chest wall compliance.

Consequences of osteopenia. Osteopenia can result in myopia of prematurity due to alterations in the shape of the skull. In childhood, infants remain thinner and shorter with a decreased total BMC(Bone Marrow Concentration) and density. Increased urinary calcium excretion has also been reported.

  • Decreased movements
  • Swelling of the arm or legs due to unknown fractures.

Pathophysiology

  • Bone mineralization begins during embryonic phase of human development, but the large part of this process occurs in the third trimester of gestation, during this period .
  •  The most of placental transfer of calcium and phosphorous  occurs in the third trimester at  the 34th  week of gestation .when 80% of the mineral content is stored.
  •  By the 28th week of gestation mineral accumulation is about 60mg/day then  increases  to more 300mg /day between 35-38th week .
  • The osteoblast produce the  organic bone matrix for deposition of calcium and phosphate  with a progressively expansion of bone volume through an increase in trabecular thickness. This This activity is thought  to be important for bone development and it helps the baby to grow,  If this doesn’t occur the child develops osteopenia of prematurity. Which leads to fractures of long bones including ribs resulting into respiratory insufficiency.
  • A premature infant may not receive the proper amount of calcium and phosphorus needed to form strong bones.
  • Premature babies lose much more phosphorus in their urine and they have limited physical activities  which lead to weak bones.

Risk Factors

Fetal and neonatal causes

    1. Prematurity and birthweight. Preterm birth results in Calcium and Phosphorus deficiency. The frequency of osteopenia is inversely related to gestational age and birthweight. Both conditions predispose these infants to mineral deficiencies in the face of increased nutritional and growth requirements.

    2. Feeding practices. Delayed enteral feeding, prolonged use of parenteral nutrition, use of unfortified human milk, enteral feeding restrictions, and malabsorption states can result in mineral deficiencies.

    3. Human milk is low in Phosphorus, and donor milk content is even lower compared with preterm maternal milk. Prolonged use can result in low serum phosphate levels and decreased incorporation into the organic bone matrix. Unfortified human milk cannot match the mineral accretion that can be achieved across the placenta.

    4. Drugs. Corticosteroids, furosemide, and methylxanthines are commonly used in preterm infants and cause mobilization of Calcium from the bone, resulting in decreased bone mineral content.

    5. Lack of mechanical stimulation. Bone growth requires mechanical stimulation that is interrupted by preterm birth, illness, sedation, and paralysis. Neurologically impaired infants with spina bifida  have limited mobility and poor bone growth.

    6. Vitamin D.  Postnatal vitamin D deficiency may occur in breast-fed infants without fortification due to low levels (25–50 IU/L) in breast milk. Other causes of vitamin D deficiency in preterm infants include the following:

      1. Renal (osteodystrophy) disorders.

      2. Drugs such as phenytoin and phenobarbital increase vitamin D metabolism.

    7. Aluminum contamination of parenteral nutrition.

    8. Malabsorption of vitamin D and Ca+2 can occur in infants with prolonged cholestasis and short gut syndrome.

  2. Maternal factors

    1. Maternal deficiency of vitamin D results in low fetal levels. 

    2. Maternal smoking, thin body habitus, low Calcium intake, and increased physical activity in the third trimester result in a decreased Calcium in the fetus.

    3. Exposure to high doses of magnesium in utero, preeclampsia, chorioamnionitis, and placental infections are associated with osteopenia.

    4. Higher incidence of postnatal rickets is seen in infants with intrauterine growth restriction (chronic damage to the placenta may alter phosphate transport).

    5. Increased maternal parity and boys have higher incidence.

    6. Placental hormones including estrogen and parathyroid hormone (PTH) and PTH-related protein also play a role.

Predisposing factors

  • Prematurity ;Gestation period of less than 30 weeks
  • Chronic use of medication that increase mineral excretion e.g diuretics ,theophylline.
  • Vitamin D deficiency.
  • Low parathyroid hormone during pregnancy which suppresses the fetal calcium and phosphorous levels.
  • A less effective intake  of calcium and phosphorous occurs in infants with Poor tolerance to Enteral feeds with low mineral content who require total parenteral nutrition.
  • Common neonatal morbidities like sepsis, acidosis, necrotizing enterocolitis can impair bone remodeling by reducing osteoclast  activity, decreasing calcium absorption and increasing calcium renal excretion.
  • Paralysis may increase calcium renal excretion.
  • Short gut syndrome(malabsorption of vitamin D and calcium

Diagnosis and Investigations

Radiographs. Most commonly, osteopenia is recognized on radiographs, which are often subjective.

Calcium levels may remain normal until late in the course.

Phosphorous. Serum phosphate levels are low (<3 mg/dL). 

Ultrasound.  Ultrasound offers several advantages, including easy accessibility and lack of exposure to ionizing radiation. It uses peripheral sites such as the calcaneus and tibia. It measures both qualitative and quantitative bone properties, such as bone mineralization and cortical thickness, respectively, in addition to bone mass (osteopenia), elasticity, and microarchitecture.

Dual-energy x-ray absorptiometry (DEXA). DEXA is the gold standard used to assess both bone size and bone mineral status and can predict risk of fractures in newborn infants. However, limitations in its use and interpretation of data preclude wide clinical application.

Management

Aims

  1. To  restore normal calcium and phosphorus in the body
  2. To prevent further complications or disease progress

Admission

The child is admitted to pediatric ward in case the child is referred from outside the hospital.

Assessment 

  • A demographic data of patient is taken which includes name, age, sex, etc 
  • A detailed medical and obstetric  history,prenata and natal data,birth weight, APGAR score at birth history are taken
  • Physical examination is done from head to toe putting more emphasis on bone formation to notify any abnormalities. 

Immediate care

  • Baby is put in a comfortable, warm bed to prevent hypothermia.
  • Analgesics like paracetamol 2.5mg 8hourly for three days are administered to relieve pain which may be due to unknown fractures.
  • In case of fractures immobilisation is done which helps to maintain the bone in position.
  • Meanwhile the doctor is called who will come and perform a quick assessment and order for investigastions which will help him make a diagnosis depending on the results.

Investigations will include: 

  • Blood to detect calcium and phosphorus levels and a protein called alkaline phosphate.
  • Ultra sound to rule out fractures.
  • X-rays to rule out the extent of fractures.

TREATMENT

  • The following treatment is administered to the patient as prescribed by the doctor.
  •  Calcium 1.25mmol/kg /dose added to iv fluids  like normal saline and ringers lactate given until the condition is stable.
  • Iv Phosphorus 1mmol/kg/dose  added to iv fluids until the condition stabilizes.
  • Vitamin D supplements are given to children with liver problems.

Nursing interventions

  • Ensure the baby is warm and comfortable.
  • Monitoring of vital observations i.e. TPR 
  • Ensure the patient is getting a diet rich in calcium and phosphorus. By feeding the baby with fortified milk
  • Physical exercises by the physiotherapists are encouraged
  • Ensure the baby is getting adequate rest and sleep by providing a conducive environment.
  • Psychological care is done to the mother to allay the anxiety
  • Both environmental and personal hygiene is promoted to prevent cross infection.
  • Administration of medicine to the patient as prescribed by the doctor.
  • Weekly monitoring of urine calcium, phosphorus.
  • When the patient improves  discharge is considered.

Advise on discharge

  • Mother is advised to continue feeding the baby on a diet containing calcium and phosphorus.
  • Mother is also advised to handle the baby gently since there is a risk of broken bones.
  • A return date is given to help in the follow up and to know the prognosis of the disease 

 Osteopenia of Prematurity Read More »

fractures

Fractures

Fractures

  • Fractures are complete or incomplete disruption in the continuity of the bone.
  • A fracture is a break in the continuity of a bone tissue, when subjected to excessive abnormal force or
  • A fracture is a break in the bone that occurs when more force is applied to the bone than the bone can withstand.
  • Fractures are also known as broken bones.

Common Childhood Fractures.

  • Arm bones are fractured more often than other bones.
  • Collarbone or shoulder fractures
  • Elbow fractures
  • forearm, wrist, or hand fracture
  • Leg, foot, or ankle fracture.

Causes of Fractures

  • Direct Force: in which the fracture occurs at the point of contact.
  • Torsion: in which the fracture occurs at the point opposite the location of the force, e.g. twisting of the foot may lead to break of bones of the leg.
  • Violent Contractions: e.g. forcibly throwing an object produces powerful muscle contractions which can fracture the humerus. Also in strong contractions in tetanus.
  • Disease Processes: cause weakening of the bone structure; osteoporosis, malnutrition, bone tumors

Risks for fractures

  • Sporting accidents
  • Falls from heights
  • Bike and car accidents
  • Poor nutrition; a diet low in calcium

Associated events following fractures.

When a bone is broken adjacent structures are also affected, resulting in;

  • Soft tissue edema
  • Joint dislocation
  • Ruptured tendons
  • Severed nerves
  • Damaged blood vessels
  • Hemorrhage into the muscles & joints

Classification of Fractures

Fractures can be grouped into 4 categories; i.e

  1. Communication with environment.
  2. By Anatomical Site
  3. By Pattern
  4. Miscellaneous

COMMUNICATION WITH ENVIRONMENT

  • Open/compound fracture: fractured part is exposed to the external environment. These are fractures where the bone is exposed  through the skin or mucous membrane.
  • Closed/simple fracture: fracture with the overlying skin intact. These are types of fractures that do not penetrate the skin.
  • Complete fracture/Incomplete: Foe complete, the fracture line runs entirely through the bone substance with the periosteum disrupted on both sides of the bone and 2 fragments are present on either side of the fracture line. In incomplete, the fracture doesn’t entirely destroy the continuity of the bone.
BY ANATOMICAL SITE.
  • Avulsion:  A fracture occurring from pulling effects of ligaments and tendons.
  • Potts Fracture : Type of fracture that occurs at the ankle joint.
  • Colles fracture(distal radius fracture): a fracture that occurs at the wrist joint.
BY PATTERN
  • Transverse : where the fracture in the bone is broken perpendicular to its length i.e. right angle to the bone.
  • Oblique: where the fracture extends in an oblique direction.
  • Spiral: fracture in which the born has been twisted apart.
MISCELLANEOUS
  • Green stick fracture: common in children and bone commonly bends or in severe cases, fracture line extends only half way across the bone substance. One side of the bone is broken, causing the other side to bend. A greenstick fracture resembles a broken tree branch. The branch cracks on one side but remains partially intact on the other.
  • Depressed fracture: a fracture having its edges driven below the surrounding bone surfaces, e.g. fractured skull.
  • Comminuted fracture: bone fragments are crushed or broken into small pieces. Occurs after high impact trauma eg a vehical road crash.
  • Displaced/overriding fracture: the bone fragments are separated away from the fracture line and bone ends are overlapping each other.
  • Impacted: where a bone fragment is moved into another.
  • Complicated fracture: that which is associated with many structures destroyed such as nerves, blood vessels, joints, muscles
  • Stress fracture: occurs on a normal or abnormal bone from constant exposure to stress e.g. running a long distance, jumping a rope
  • Pathological fracture: a fracture caused by a disease e.g bone cysts, paget’s disease.

Signs and symptoms of fractures

  • Pain at the site of injury : which is continuous and increases in severity until the bone fragments are immobilized.
  • Local tenderness.
  • Deformity : displacements, rotation of fragments in the fracture of the limb causes deformity(either palpable/visible). Is detectable when limb is compared with the uninjured extremity.
  • Soft tissue swelling
  • Loss of function : after the fracture, the extremity cannot function properly because normal function of muscles depends on the integrity of the bones to which they are attached.
  • Bruising
  • Involuntary muscle spasms.
  • Intense pain e.g. in the rib cage when a patient takes a deep breath or coughs.
  • Abnormal mobility
  • Involuntary muscle spasms
  • Crepitus – when the extremity is examined with the hands,  a grating sound or sensation is heard or felt when broken ends rub on each other and is called crepitus.
  • Bone may be visibly seen protruding through the skin.
  • Impaired sensation/numbness may occur if there is nervous damage
  • Shock results from blood loss
  • Swelling and discoloration: localized swelling and discoloration of the skin (Ecchymosis) occurs after a fracture, as a result of trauma and bleeding into the tissues.

Assessment and Diagnostic Findings

To determine the presence of fracture, the following diagnostic tools are used.

  • History taking.
  • Physical Examinations.
  • X-ray examinations: Determines location and extent of fracture.
  • Bone scans, computed tomography (CT)/magnetic resonance imaging (MRI) scans: Visualizes fractures, bleeding, and soft-tissue damage.
Illustration-of-stages-in-bone-healing-after-a-fracture

Process of Fracture Healing

This process varies according to the type of bone involved type of fracture and the amount of movement at the fracture site. In the absence of rigid fixation in tubular bones, healing proceeds in five stages as follows;

1.Tissue destruction & haematoma formation:

After tissue destruction, torn blood vessels result to hematoma formation (which is a collection of clotted blood between the ends of the bones and in surrounding soft tissues. Fibrin, red blood cells, debris and inflammatory exudates come together and form a fibrin clot.

 2.Inflammation & cellular proliferation:

This follows development of acute inflammation and accumulation of inflammatory exudate containing macrophages that phagocytose the hematoma and small fragments of bone without blood supply and this takes about 5 days. Fibroblasts migrate to the site, granulation  tissue and new capillaries develop.

3. Stage of Callus formation (Soft Callus)

New bone forms as large number of osteoblasts secrete spongy bone, which unites  the broken ends, osteoclasts begin mopping up the dead bone. The new deposits of  bone and cartilage are called callus. As the immature bone (soft callus) becomes more densely mineralized, movement of the site  progressively decreases.

4.Stage of consolidation(Hard callus)

Over the next few days, callus matures and the cartilage is gradually replaced with new bone.

5.Stage of remodelling

This is the reshaping of the callus by a continuous process of resorption and laydown. Internal callus is hollowed out into marrow cavity, while external callus is slowly removed. Reshaping of the bone continues and gradually the medullary canal is reopened through the callus, and callus tissue is completely replaced with mature compact bone. Often the bone is thicker and stronger at the repair site than originally and a second fracture is more likely to occur at a different site.

Healing of Fractures

Factors necessary for bone healing

  • Haematoma formation.
  • Contact of bone end and no interposition of other tissues
  • Continued immobilization until calus is able to withstand stress.
  • Good supply of blood
  • Enough rest of the fractured site
  • Good nutrition- calcium, proteins

Factors influencing bone healing.

(a). Systemic factors

  •   -Age ( healing is almost twice as fast in   children as in adults )
  •   -Activity level.( immobilization)
  •   -Nutritional status.
  •   -Hormonal factors (GH, corticosteroids )
  •   -Diseases e.g. DM, anaemia, neuropathies
  •   -Vitamin deficiencies e.g. A C D K
  •   -Drugs e.g. anti coagulants, anti inflammatory.

(b). Local factors.

  •   -type of bone( cancellous heals faster than   cortical bone)
  •   -type of fracture. Spiral better than transverse.
  •   -blood supply ( poor circulation-poor healing.)
  •   -reduction- faster when there’s perfect   reduction.
  •   -infection
  •   -soft tissue interposition
  •   -mobilization. Early vs late mobilization.

Management

Aims of management.

  1. To regain and maintain the normal alignment of the injured part.
  2. To regain normal function of the injured part.
  3. To achieve the above objectives for the patient in the shortest time possible

Basic principles of managing fractures

The principles of fracture management are:

  • Reduction
  • Immobilization
  • Rehabilitation

(1) Reduction: Reduction is the process of restoring the bone ends (and any fractured fragments) into their normal anatomical positions. This is accomplished by open or closed manipulation of the affected area, referred to as open reduction and closed reduction. 

  •  Closed reduction is accomplished by bringing the bone ends into alignment by manipulation and manual traction. X-rays are taken to determine the position of the bones. A cast is normally applied to immobilize the extremity and maintain the reduction.
  •  In open reduction, a surgical opening is made, allowing the bones to be reduced manually under direct visualization. Frequently, internal fixation devices will be used to maintain the bone fragments in reduction.

(2) Immobilization: Immobilization is necessary to maintain fracture reduction until healing occurs. Immobilization may be accomplished by external or internal fixation.

  • Methods of external fixation include casts, splints, and continuous traction.
  •  Internal fixation devices include pins, wires, screws, rods, nails, and plates.

(3) Rehabilitation: Rehabilitation is the regaining of strength and normal function in the affected area. Specific rehabilitation for each patient will be based upon the type of fracture and the methods of reduction and immobilization used.

First aid management

This can save the client’s life so it is crucial.  A B C D of life criteria is used as follows;

Ensure that the patient is breathing then do the following:

  • Airway should be clear
  • Breathing should be maintained.
  • Check pulse and control bleeding.
  • Deformity should immobilized, Immobilize the limb to avoid more harm and pain by using splints.

Emergency Management of Fractures

  • Immediately after injury, whenever a fracture is suspected, it is important to immobilize the body part before the patient is moved.
  • If an injured patient must be removed from a vehicle before splints can be applied, the extremity is supported above and below the fracture site to prevent rotation as well as angular motion.
  • Adequate splinting, including joints adjacent to the fracture,  is essential.
  • Movement of fracture fragments causes additional pain, soft tissue damage, and bleeding.
  • Temporary, well-padded splints, firmly bandaged over clothing, serve to immobilize the fracture. 
  • Immobilization of the long bones of the lower extremities may be accomplished by bandaging the legs together, with the unaffected extremity serving as a splint for the injured one.
  • In an upper extremity injury, the arm may be bandaged to the chest, or an injured forearm may be placed in a sling.
  • The neurovascular status distal to the injury should be assessed to determine adequacy of peripheral tissue perfusion and nerve function. 
  • With an open fracture, the wound is covered with a clean (sterile) dressing to prevent contamination of deeper tissues.
  • No attempt is made to reduce the fracture, even if one of the bone fragments is protruding through the wound.
  • Splints are applied for immobilization. 
  • In the emergency department, the patient is evaluated completely.
  • The clothes are gently removed, first from the uninjured side of the body and then from the injured side.
  • The patient’s clothing may be cut away. The fractured extremity is moved as little as possible to avoid more damage

Management in hospital

  • Care depends on class/type of fracture
  • Immobilization/ reduction and rehabilitation is done.
  • Pain relief
  • Anti biotics
  • Supportive treatment eg feso4,FA ,multivitamin
  • Bone x- ray
  • Fluid resuscitation
  • Infection prevention
  • Nutrition – calcium
  • Exercises/ physiotherapy
  • Nursing care

Nursing Care

  • Encourage patients with closed (simple) fractures to return to their usual activities as rapidly as possible.
  • Teach patients how to control swelling and pain associated with the fracture and with soft tissue trauma and encourages them to be active within the limits of the fracture immobilization.
  • It is important to teach exercises to maintain the health of unaffected muscles and to increase the strength of muscles needed for transferring and for using assistive devices (eg, crutches, walker, special utensils).
  • Teach patients to use assistive devices safely. Plans are made to help patients modify their home environment as needed and to secure personal assistance if necessary.
  • Patient teaching include self-care, medication information, monitoring for potential complications and the need for continuing health care supervision.
  • Flracture healing and restoration of full strength and mobility may take months

Managing Fractures at Specific Sites

Maximum functional recovery is the goal of management.

Clavicle

  • Fracture of the clavicle (collar bone) is a common injury that results from a fall or a direct blow to the shoulder.
  • Monitor the circulation and nerve function of the affected arm and compare with the unaffected arm to determine variations, which may indicate disturbances in neurovascular status. 
  • Caution the patient not to elevate the arm above shoulder level until the fracture has healed (about 6 weeks).
  • Encourage the patient to exercise the elbow, wrist, and fingers as soon as possible and, when prescribed, to perform shoulder exercises.
  • Tell the patient that vigorous activity is limited for 3 months.

Humeral Neck

  • With humeral neck fractures (seen most frequently in older women after a fall on an outstretched arm), perform neurovascular assessment of the involved extremity to evaluate the extent of injury and possible involvement of the nerves and blood vessels of the arm.
  • Teach the patient to support the arm and immobilize it by a sling and swathe that secure the supported arm to the trunk.
  • Begin pendulum exercises as soon as tolerated by the patient. Instruct the patient to avoid vigorous activity for an additional 10 to 14 weeks. 
  • Inform the patient that residual stiffness, aching, and some limitation of range of motion may persist for 6 or more months.
  • When a humeral neck fracture is displaced with required fixation, exercises are started only after a prescribed period of immobilization.

Humeral shaft fractures

  • The nerves and brachial blood vessels may be injured, so neurovascular assessment is essential to monitor the status of the nerve or blood vessels.
  • Use well-padded splints to initially immobilize the upper arm and to support the arm in 90 degrees of flexion at the elbow, use a sling or collar and cuff to support the forearm, and use external fixators to treat open fractures of the humeral shaft.
  • Functional bracing may also be used for these fractures.
  • Teach patient to perform pendulum shoulder exercises and isometric exercises as prescribed.

Elbow

  • Elbow fractures (distal humerus) may result in injury to the median, radial, or ulnar nerves.
  • Evaluate the patient for paresthesia and signs of compromised circulation in the forearm and hand.
  • Monitor closely for Volkmann’s ischemic contracture (an acute compartment syndrome) as well as for hemarthrosis (blood in the joint). 
  • Reinforce information regarding reduction and fixation of the fracture and planned active motion when swelling has subsided and healing has begun.
  • Explain care if the arm is immobilized in a cast or posterior splint with a sling. Encourage active finger exercises.
  • Teach and encourage patient to do gentle range of motion exercise of the injured joint about 1 week after internal fixation. 

Radial head fractures

  • They are usually produced by a fall on the outstretched hand with the elbow extended.
  • Instruct patient in use of a splint for immobilization.
  • If the fracture is displaced, reinforce the need for postoperative immobilization of the arm in a posterior plaster splint and sling.
  • Encourage the patient to carry out a program of active motion of the elbow and forearm when prescribed

Wrist

  • Wrist fractures (distal radius [Colles’ fracture]) usually result from a fall on an open, dorsiflexed hand.
  • They are frequently seen in elderly women with osteoporotic bones and weak soft tissues that do not dissipate the energy of a fall.
  • Reinforce care of the cast, or with more severe fractures with wire insertion, teach incision care. 
  • Instruct patient to keep the wrist and forearm elevated for 48 hours after reduction.
  • Begin active motion of the fingers and shoulder promptly by teaching patient to do the following exercises to reduce swelling and prevent stiffness:
  • Hold the hand at the level of the heart. Move the fingers from full extension to flexion. Hold and release. Repeat at least 10 times every hour when awake.
  • Use the hand in functional activities. 
  • Actively exercise the shoulder and elbow, including complete range-of-motion exercises of both joints
  • Assess the sensory function of the median nerve by pricking the distal aspect of the index finger, and assess the motor function by testing patient’s ability to touch the thumb tot he little finger.
  • If diminished circulation and nerve function is noted, treat promptly. 

Hand and Fingers

  • Hand trauma often requires extensive reconstructive surgery.
  • The objective of treatment is always to regain maximum function of the hand.
  • With a non displaced fracture, the finger is splinted for 3 to 4 weeks to relieve pain and protect the fingertip from further trauma, but displaced fractures and open fractures may require open reduction with internal fixation, using wires or pins. 
  • Encourage functional use of the uninvolved portions of the hand
  • Evaluate the neurovascular status of the injured hand.
  • Teach the patient to control swelling by elevating the hand.

Pelvis

  • Pelvic fractures may be caused by falls, motor vehicle crashes, or crush injuries. At least two thirds of these patients have significant and multiple injuries.
  • Monitor for symptoms, including ecchymosis; tenderness over the symphysis pubis, anterior iliac spines, iliac crest, sacrum, or coccyx; local edema; numbness or tingling of the pubis, genitals, and proximal thighs; and inability to bear weight without discomfort. 
  • Complete a neurovascular assessment of the lower extremities to detect injury to pelvic blood vessels and nerves.
  • As pain resolves, instruct patient to resume activity gradually, using assistive mobility devices for protected weight bearing. Patients with unstable pelvic fractures may be treated with external fixation or open reduction and internal fixation (ORIF).
  • Promote hemodynamic stability and comfort, and encourage early mobilization. 
  • Examine urine for blood to assess for urinary tract injury. In male patients, do not insert a catheter until the status of the urethra is known.
  • Monitor for diffuse and intense abdominal pain, hyperactive or absent bowel sounds, and abdominal rigidity and resonance (free air) or dullness to percussion (blood), which suggest injury to the intestines or abdominal bleeding. 
  • Monitor for hemorrhage and shock, two of the most serious consequences that may occur. Palpate both lower extremities for absence of peripheral pulses, which may indicate a torn iliac artery or one of its branches.
  • Assess for injuries to the bladder, rectum, intestines, other abdominal organs, and pelvic vessels and nerves. 
  • If patient has a stable pelvic fracture, maintain patient on bed rest for a few days and provide symptom management until the pain and discomfort are controlled.
  • Provide fluids, dietary fiber, ankle and leg exercises, antiembolism stockings to aid venous return, logrolling, deep breathing, and skin care to reduce the risk for complications and to increase comfort.
  • Monitor bowel sounds. If patient has a fracture of the coccyx and experiences pain on sitting and with defecation, assist with sitz baths as prescribed to relieve pain, and administer stool softeners to prevent the need to strain on defecation.

Femur and Hip

  • Femoral shaft fractures are most often seen in young adults involved in a motor vehicle crash or a fall from a high place.
  • Frequently, these patients have associated multiple trauma and develop shock from a loss of 2 to 3 units of blood.
  • Assess neurovascular status of the extremity, especially circulatory perfusion of the lower leg and foot (popliteal, posterior tibial, and pedal pulses and toe capillary refill time as well as Doppler ultrasound monitoring). 
  • Note signs of dislocation of the hip and knee, and knee effusion, which may suggest ligament damage and possible instability of the knee joint
  • Apply and maintain skeletal traction or splint to achieve muscle relaxation and alignment of the fracture fragments before ORIF procedures, and later a cast brace. 
  • Assist patient in minimal partial weight bearing when indicated and progress to full weight bearing as tolerated.
  • Reinforce that the cast brace is worn for 12 to 14 weeks
  • Instruct in and encourage patient to perform exercises of lower leg, foot, and toes on a regular basis. 
  • Assist patient in performing active and passive knee exercises as soon as possible, depending on the management approach and the stability of the fracture and knee ligaments.

Tibia and Fibula

  • Tibia and fibula fractures (most common fractures below the knee) tend to result from a direct blow, falls with the foot in a flexed position, or a violent twisting motion.
  • Provide instruction on care of the long leg walking cast or patellar-tendon-bearing cast.
  • Instruct patient in and assist with partial weight bearing,
  • usually in 7 to 10 days.
  • Instruct patient on care of a short leg cast or brace (in 3 to 4 weeks), which allows for knee motion.
  • Instruct patient in care of skeletal traction, if applicable.
  • Encourage patient to perform hip, foot, and knee exercises  within the limits of the immobilizing device.
  • Instruct patient to begin weight bearing when prescribed (usually in about 4 to 8 weeks).
  • Instruct patient to elevate extremity to control edema.
  • Perform continuous neurovascular evaluation.

Rib

  • Rib fractures occur frequently in adults and usually result in no impairment of function but produce painful respirations.
  • Assist patient to cough and take deep breaths by splinting the chest with hands or pillow during cough.
  • Reassure patient that pain associated with rib fracture diminishes significantly in 3 or 4 days, and the fracture heals within 6 weeks.
  • Monitor for complications, which may include atelectasis, pneumonia, a flail chest, pneumothorax, and hemothorax.
COMPLICATIONS OF FRACTURES

Early complications include;

  • Shock,
  • Fat embolism,
  • Compartment syndrome, and
  • Venous thromboembolism (deep vein thrombosis [DVT],
  • Pulmonary embolism [PE]).

Delayed Complications;

  • Delayed union,
  • Malunion,
  • Nonunion,
  • Avascular necrosis (AVN) of bone, reaction to internal fixation devices
  • Complex regional pain syndrome (CRPS, formerly called reflex sympathetic dystrophy (RSD), is chronic condition of severe burning pain affecting one of the extremities
  • Heterotopic ossification- is the presence of bone in the soft tissue where bone normally does not exist

MANIFESTATION OF COMPLICATIONS

Fat embolism syndrome:

  • Occurs with blockage of the small blood vessels that supply the brain, lungs, kidneys, and other organs.
  • Sudden onset, usually occurring within 12 to 48 hour but may occur up to 10 days after injury),
  • Signs & symptoms: hypoxia, tachypnea, tachycardia, and pyrexia; dyspnea, crackles, wheezes, precordial chest pain, cough, large amounts of thick white sputum.

Compartment syndrome

  • Acute compartment syndrome may produce deep, throbbing, unrelenting pain not controlled by opioids
  • It can be due to a tight cast or constrictive dressing or an increase in muscle compartment contents because of edema or hemorrhage.
  • Signs & symptoms include; Cyanotic (blue-tinged) nail beds and pale or dusky and cold fingers or toes are present; nail bed capillary refill times are prolonged (greater than 3 seconds); pulse may be diminished or absent; and motor weakness, paralysis, and paresthesia may occur.

DIC- disseminated intravascular coagulation is evidenced by;

  • Unexpected bleeding after surgery and
  • Bleeding from the mucous membranes,
  • Venipuncture sites, and
  • Gastrointestinal and urinary tracts.

Infection. symptoms include.

  • Tenderness on examination
  • Pain (patient history)
  • Redness,
  • Swelling,
  • Local warmth,
  • Elevated temperature, and
  • Purulent drainage.

Nonunion is manifested by

  • Persistent discomfort and abnormal movement at the fracture site.

Some risk factors include;

  • Infection at the fracture site
  • Interposition of tissue between the bone ends
  • Inadequate immobilization or manipulation that disrupts callus formation,

MANAGEMENT OF COMPLICATIONS

Treatment of shock :

  • Consists of stabilizing the fracture to prevent further hemorrhage
  • Restoring blood volume and circulation
  • Relieving the patient’s pain
  • Providing proper immobilization and
  • Protecting the patient from further injury and other complications.

Prevention and management of fat embolism:

  • Include immediate immobilization of fractures
  • Adequate support for fractured bones during turning and positioning
  • Maintenance of fluid and electrolyte balance
  • Prompt initiation of respiratory support with prevention of respiratory and metabolic acidosis
  • Corticosteroids as well as vasopressor medications may be given.

Compartment syndrome:

  • Is managed by controlling swelling by elevating the extremity to heart level or by releasing restrictive devices (dressings or cast).
  • A fasciotomy (surgical decompression with excision of the fascia) may be needed to relieve the constrictive muscle fascia.
  • The wound remains open and covered with moist sterile saline dressings for 3 to 5 days.
  • The limb is splinted and elevated.
  • Prescribed passive range-of-motion exercises may be performed every 4 to 6 hours.

Nonunion (failure of the ends of a fractured bone to unite)

  • Is treated with internal fixation
  • Bone grafting
  • Electrical bone stimulation, or a combination of these.

Related Question

Josephine a thirty year old female patient has been involved in a road traffic accident and sustained a compound fracture.

  1. Outline ten signs and symptoms of fracture.
  2. Discuss the negative factors that can influence healing of a bone.
  3. Describe the healing of a bone.
  4. Mention ten complications of fractures.

SOLUTIONS

  1. a) History from the patient or the on lookers.
  • Pain aggravated by movement
  • Tenderness over the fractured limb
  • Loss of function of the affected part or the whole limb
  • Deformity
  • Shortening of the limb
  • Abnormal mobility at the affected area
  • Creepers or grating of the bone ends as they move each other
  • Swelling of the affected part
  • Shock may occur
  • The bone may be seen out if it’s a compound fracture

b)

  • Tissue fragments between bone ends; Splinters of dead bone (sequestrate) and soft tissue fragments not removed by phagocytosis delay healing.
  • Deficient blood supply; this delays growth of granulation tissue and new blood vessels. Hypoxia also reduces the number of osteoblasts and increases the number of chondrocytes that develop from there common parent cells. This may lead to cartilaginous union of fracture which results in a weaker repair.
  • Poor alignment of bone ends: This may result in the formation of a callus that heals slowly and often results in permanent disability
  • Continued mobility of bone ends; Continuous movement results in fibrosis of the granulation tissue followed fibrous union of the fracture.
  • Miscellaneous; this include
  • Infection; pathogens enter through broken skin, although they occasionally be blood borne, healing will not occur until infection resolves
  • System illness 
  • Malnutrition
  • Drugs e.g. Corticosteroids
  • Aging

 

c)

  • Following a fracture the broken ends of a bone a joined by the deposition of a new bone. This occurs in several stages
  • Hematoma forms between the ends of the bone and in the surrounding soft tissues.
  • There follows development of acute inflammation and accumulation of inflammatory exudates, continuing microphages that phagocytosis the hematoma and small fragments of a bone without blood supply(this takes place about five days). Fibroblasts migrate to the site, granulation tissue and the new capillaries develop.
  • New bone forms as large numbers of osteoblasts secretes spongy bone, which unit the broken ends, and is protected by the outer layer of the bone and cartilage, this new deposits of bone and cartilage are called callus.
  • Over the next few weeks, the callus matures and the cartilage is gradually replaced by new bone
  • Reshaping of the bone continues and gradually the medullary canal is re –opened through the callus (in weeks or month). In time the bone heals completely with callus tissue replaced with mature compact bone. Often the bone is thicker and stronger at the repair site that originally, and the second is more likely to occur at a different site.

 

  1. d)                  Complications of fractures are divided in to two.
  • General complications.
  • Local complications
  • General complications are;
  • Hemorrhage which may lead in to shock.
  • Fat embolism
  • Infections
  • Hypostatic Pneumonia
  • Damage to the nearby structures
  • Local complications
  • Keloids
  • Loss of function
  • Damage to the nerves
  • Necrosis
  • Delayed union of bones; this may be as a result of incomplete reduction, inadequate immobilization, lack of blood supply to areas, infection which disrupt formation
  • Malunion of the bones; this when there’s failure of bone fragments to unit. This as a result of a big gap between the fragment

Fractures Read More »

Prevention and Control of HIV/AIDS

Prevention and Control of HIV/AIDS

Prevention and Control of HIV/AIDS

Prevention Framework in children and infants.

 

Prevention in Pediatrics 

  1. ∙ Behavioral change and risk reduction interventions 
  2. ∙ Biomedical prevention interventions 
  3. ∙ Structural intervention 

BEHAVIORAL CHANGE AND RISK REDUCTION INTERVENTIONS 

The priority of behavioral interventions is to delay sexual debut; reduce unsafe sex and multiple, especially  concurrent sexual partnerships; and discourage cross-generational and transactional sex.

Types of behavioral change 

  • ∙ Service delivery 
  • ∙ Risk assessment for client 
  • ∙ Provide socio-behavioral change Communication (SBCC) and link to services as appropriate ∙ Condom promotion and provision 

Service delivery 

The government of Uganda ensures that  

1 . ⇒ Each health facility/program should have a focal person for HIV prevention 

2. ⇒ All staff offering prevention services need to be trained 

3. ⇒ Outreaches for key and priority populations 

Risk assessment  

4. ⇒ Offer HTS to sexually active adolescents, pregnant mothers who have not tested in the last 12  months or have had unprotected sex in last three months. 

5. ⇒ HIV testing for infants born of HIV infected mothers.

6. ⇒ Assess sexual behavior of the in pregnant mothers and adolescents (ask if condoms are used,  frequency, the number of partners, transactional sex/sex work) and if the client is involved in  transactional sex/sex work encourage correct and consistent condom use. 

Provide socio-behavioral change Communication (SBCC) and link to services as appropriate

7. ⇒ Discuss delay of onset of sexual debut in children and adolescents (abstinence) ⇒ Discuss correct and consistent condom use and offer condoms as appropriate to adolescents ⇒ Discourage multiple, concurrent sexual partnerships to promote faithfulness with a partner of  known status. 

8. ⇒ Discuss with the adolescents about sexual and reproductive health services and link to services as  appropriate. 

9. ⇒ Discourage risky cultural practices such as childhood marriages 

10. ⇒ Identify, refer and link clients to other available facility and community programs

11. ⇒ Assess for violence, (physical, emotional, or sexual); if child discloses sexual violence, assess if the  client was raped and act immediately 

Condom promotion and provision 

12. ⇒ Discuss condom use as an option for risk reduction in pregnant mothers and adolescent ∙ Discuss barriers to condom use to pregnant mothers and adolescent 

13. ⇒ Clarify any questions and dispel myths around condoms

Biomedical prevention interventions 

The key biomedical interventions include; 

  • ∙ EMTCT 
  • ∙ Safe male circumcision (SMC) 
  • ∙ ART 
  • ∙ PEP, 
  • ∙ PrEP 
  • ∙ Blood transfusion safety 
  • ∙ STI screening and treatment  

Safe male circumcision (SMC) 

  • Male circumcision is the surgical removal of the foreskin of the penis. SMC reduces the risk of HIV  acquisition among circumcised men (adolescents) by approximately 60%.  

Blood transfusion safety 

  • Ensuring the screening of blood donors for HIV and hepatitis B 
  • Ensuring proper storage and administration 

STI screening and treatment 

  • Integration of STI services in all health programs e.g. YCC, MCH. 

EMTCT (Elimination of Mother-to-Child Transmission of HIV)

  • Measures of reducing the risk of HIV transmission to the child during pregnancy, labor, puerperium and  breastfeeding. 
Post-exposure prophylaxis (PEP)
  • Post-exposure prophylaxis (PEP) is the short-term use of ARVs to reduce the likelihood of acquiring HIV  infection after potential occupational or non-occupational exposure. 

Types of exposure: 

  1. ∙ Occupational exposures occur in the health care or laboratory setting and include sharps and  needlestick injuries or splashes of body fluids to the skin and mucous membranes. 
  2. Non-occupational exposures include unprotected sex, exposure following assault like in rape and  defilement, and road traffic accidents. 

Steps for providing Post Exposure Prophylaxis 

Step 1: Clinical assessment and providing first aid 

  • Conduct a rapid assessment of the client to assess exposure and risk and provide immediate care. Occupational exposure: 

After a needlestick or sharp injury 

  • ∙ Do not squeeze or rub the injury site 
  • ∙ Wash the site immediately with soap or mild disinfectant (chlorhexidine gluconate solution) ∙ Use antiseptic hand rub/gel if no running water 
  • ∙ Don’t use strong, irritating antiseptics (like bleach or iodine) 

After a splash of blood or body fluids in contact with intact skin 

  • ∙ Wash the area immediately 
  • ∙ Use antiseptic hand rub/gel if no running water 
  • ∙ Don’t use strong, irritating antiseptics (like bleach or iodine) 

Step 2: Eligibility assessment 

Provide PEP when: 

  • ∙ Exposure occurred within the past 72 hours; and 
  • ∙ The exposed individual is not infected with HIV; and 
  • ∙ The ‘source’ is HIV-infected, has unknown HIV status or is high risk 

Do not provide PEP when: 

  • ∙ The exposed individual is already HIV-positive 
  • ∙ The source is established to be HIV-negative 
  • ∙ Individual was exposed to bodily fluids that do not pose a significant risk (e.g. tears, non-blood stained saliva, urine, sweat) 
  • ∙ Exposed individual declines an HIV test 

Step 3: Counseling and support  

Counsel on: 

  • ∙ The risk of HIV from the exposure 
  • ∙ Risks and benefits of PEP 
  • ∙ Side effects of ARVs  
  • ∙ Enhanced adherence if PEP is prescribed 
  • ∙ Importance of linkage for further support for sexual assault cases 

Step 4: Prescription 

∙ PEP should be started as early as possible, not beyond 72 hours of exposure ∙ Recommended regimens include: 

  • ⇒ Pregnant mothers/adults: TDF+3TC+ATV/r
  • ⇒ Children: ABC+3TC+LPV/r 

∙ A complete course of PEP should run for 28 days 

∙ Do not delay the first doses because of lack of baseline HIV test 

∙ Document the event and patient management in the PEP register (ensure confidentiality of patient  data) 

Step 5: Provide follow-up 

  • ∙ Discontinue PEP after 28 days 
  • ∙ Perform follow-up HIV testing three months after exposure 
  • ∙ Counsel and link to HIV clinic for care and treatment if HIV-positive 
  • ∙ Provide prevention and education/risk reduction counseling if HIV-negative
ORAL PRE-EXPOSURE PROPHYLAXIS (PrEP) 

PrEP is the use of ARV drugs by people who are not infected with HIV to block the acquisition of HIV.  

The process of providing pre-exposure prophylaxis (PrEP) 

  1. ∙ Eligibility for PrEP 
  2. ∙ Screening for PrEP eligibility 
  3. ∙ Steps to initiation of PrEP 
  4. ∙ Follow-up/ monitoring clients on PrEP 
  5. ∙ Guidance on discontinuing PrEP 

Step 1: Eligibility for PrEP 

PrEP provides an effective additional biomedical prevention option for HIV-negative people at substantial  risk of acquiring HIV infection. These include people who: 

  • ∙ Have multiple sexual partners 
  • ∙ Engage in transactional sex including sex workers 
  • ∙ Use or abuse injectable drugs and alcohol 
  • ∙ Have had more than one episode of an STI within the last twelve months 
  • ∙ Are part of a discordant couple, especially if the HIV-positive partner is not on ART or has been on  ART for less than six months 
  • ∙ Are recurrent users of PEP (3 consecutive cycles of PEP) 
  • ∙ Engage in anal sex 

These risk factors are likely to be more prevalent in populations such as sex workers, fisher folk, long distance truck drivers, men who have sex with men (MSM), uniformed forces, and adolescents and young  women engaged in transactional sex. 

Step 2; Screening for PrEP eligibility 

After meeting the eligibility criteria: 

  • ∙ Confirm HIV-negative status 
  • ∙ Rule out acute HIV infection 
  • ∙ Assess for hepatitis B infection: if negative, patient is eligible for PrEP; if positive, refer patient for  management
  • ∙ Assess for contraindications to TDF/FTC 

Step 3: Steps to initiation of PrEP 

  • Provide risk-reduction and PrEP medication adherence counseling: 
  • ∙ Provide condoms and education on their use 
  • ∙ Initiate a medication adherence plan 
  • ∙ Prescribe a once-daily pill of TDF (300mg) and FTC (200mg) 
  • ∙ Initially, provide a 1-month TDF/FTC prescription (1 tablet orally, daily) together with a 1-month  follow-up date 
  • ∙ Counsel client on side effects of TDF/FTC 

Step 4: Follow-up/ monitoring clients on PrEP 

  • ∙ After the initial visit, the patient should be given a two-month follow-up appointment and  thereafter quarterly appointments 
  • ∙ Perform an HIV antibody test every three months 
  • ∙ For women, perform a pregnancy test based on clinical history 
  • ∙ Review the patient’s understanding of PrEP, any barriers to adherence, tolerance to the medication  as well as any side effects 
  • ∙ Review the patient’s risk exposure profile and perform risk-reduction counseling ∙ Evaluate and support PrEP adherence at each clinic visit 
  • ∙ Evaluate the patient for any symptoms of STIs at every visit and treat as needed 

Step 5: Guidance on discontinuing PrEP 

  • ∙ Acquisition of HIV infection 
  • ∙ Changed life situations resulting in lowered risk of HIV acquisition 
  • ∙ Intolerable toxicities and side effects 
  • ∙ Chronic non-adherence to the prescribed dosing regimen despite efforts to improve daily pill-taking ∙ Personal choice 
  • ∙ HIV-negative in a sero-discordant relationship when the positive partner has achieved sustained viral  load suppression (condoms should still be used consistently.

MOTHER-TO-CHILD TRANSMISSION OF HIV 

Approximately one-third of the women who are infected with HIV can pass it to their babies. 

Elements of elimination of mother to child transmission 

  1. ∙ : Primary prevention of HIV infection Women and men of reproductive age including  adolescents 
  2. ∙ : Prevention of unintended pregnancies among women living with HIV Women including  adolescents living with HIV and their partners. 
  3. ∙ : Prevention of HIV transmission from women living with HIV to their infants Pregnant and  breastfeeding women including adolescents living with HIV 
  4. ∙: Provision of treatment, care, and support to women infected with HIV, their children and  their families Women living with HIV and their families 

Cause 

Time of transmission; 

  • ∙ During pregnancy (15-20%) 
  • ∙ During time of labour and delivery (60%-70%) 
  • ∙ After delivery through breast feeding (15%-20%) 

Pre-disposing factors 

  • ∙ High maternal viral load 
  • ∙ Depleted maternal immunity (e.g. very low CD4 count) 
  • ∙ Prolonged rupture of membranes 
  • ∙ Intra-partum haemorrhage and invasive obstetrical procedures 
  • ∙ If delivering twins, first twin is at higher risk of infection than second twin 
  • ∙ Premature baby is at higher risk than term baby 
  • ∙ Mixed feeding carries a higher risk than exclusive breastfeeding or use of replacement feeding

Investigations 

 

  1. ∙ Blood: HIV serological test 
  2. ∙ HIV -DNA/ PCR testing of babies.

Management 

All HIV services for pregnant mothers are offered in the MCH clinic. After delivery, mother and baby will  remain in the MCH postnatal clinic till HIV status of the child is confirmed, then they will be transferred to  the general ART clinic. 

The current policy aims at elimination of Mother-to-Child Transmission (eMTCT) through provision of a continuum of care with the following elements: 

  • ∙ Primary HIV prevention for men, women and adolescents 
  • ∙ Prevention of unintended pregnancies among women living with HIV 
  • ∙ Prevention of HIV transmission from women living with HIV to their infants 
  • ∙ Provision of treatment, care and support to ALL women infected with HIV, their children and their families 

Management of HIV Positive Pregnant Mother 

Key Interventions for eMTCT ;

  • ∙ Routine HIV Counseling and Testing during ANC (at 1st contact. If negative, repeat HIV test in the  third trimester/ labour. 
  • ∙ Enrolment in HIV care if mother is positive and not yet on treatment
  • ∙ If mother already on ART, perform viral load and continue current regimen 
  • ∙ ART in pregnancy, labour and post-partum, and for life – Option B+ 

Treatment  

Recommended ARV for option B+ 

  • One daily Fixed Dose Combination (FDC) pill containing TDF + 3TC + EFV started early in pregnancy  irrespective of the CD4 cell count and continue during labour and delivery, and for life, Alternative regimen for women who may not tolerate the recommended option are: ∙ 
  • If TDF contraindicated: ABC+3TC+EFV 
  • If EFV contraindicated: TDF + 3TC + ATV/r 

Prophylaxis for opportunistic infections 

  • Cotrimoxazole 960 mg 1 tab daily during pregnancy and postpartum 

   NB.  Mothers on cotrimoxazole DO NOT NEED IPTp with SP for malaria 

Notes 

  • ∙ TDF and EFV are safe to use in pregnancy 
  • ∙ Those newly diagnosed during labour will begin HAART for life after delivery 

Caution 

∙ In case of low body weight, high creatinine, diabetes, hypertension, chronic renal disease, and  concomitant nephrotoxic medications: perform renal function investigations before starting TDF ∙ TDF is contraindicated in advanced chronic renal disease.

Prevention and Control of HIV/AIDS Read More »

Treatment of HIV/AIDS in Children (ARV therapy)

hiv / aids Treatment in Children

Treatment Modalities of HIV/AIDS

Treatment Modality

Description

Antiretroviral Therapy (ART)

Suppresses viral load to undetectable levels, reducing morbidity, mortality, and transmission of HIV.

Treatment of Acute Bacterial Infections

Addresses immediate bacterial infections.

Prophylaxis and Treatment of Opportunistic Infections

Prevents and manages opportunistic infections.

Maintenance of Good Nutrition

Ensures adequate nutrition to support overall health.

Immunization

Administers vaccines to prevent opportunistic infections.

Management of AIDS-Defining Illnesses

Addresses specific illnesses associated with advanced HIV infection.

Psychological Support for the Family

Provides emotional support and guidance for affected families.

Palliative Care for the Terminally Ill

Offers comfort and support for patients nearing the end of life.

ANTIRETROVIRAL DRUG TREATMENT 

The goal of ART 

Goal of ART: Suppress viral load to undetectable levels, reducing morbidity, mortality, and transmission of HIV.

When to Initiate ARV:

  • All HIV-infected children below 12 months.
  • Clinical AIDS
  • Mild to moderate symptoms and immunosuppression.

Process of Starting ART:

  •  Assess all clients for opportunistic infections especially TB and cryptococcal meningitis. If the patient has TB or cryptococcal meningitis, ART should be deferred and initiated after starting treatment for these OIs. Treatment for other OIs and ART can be initiated concurrently.
  •  For patients without TB or cryptococcal meningitis, offer ART on the same day through an opt-out approach. In this approach, the patients should be prepared for ART on the same day and assessed for readiness to start ART using the readiness checklist 
  • If a client is ready, ART should be initiated on the same day. If a client is not ready or opts out of same-day initiation, a timely ART preparation plan should be agreed upon with the aim of initiating ART within seven days for children and pregnant women, and within one month for adults. 

Principles for selecting the ARV regimens 

The first-line ART regimens for treating HIV infection in Uganda were selected based on the following  principles: 

  • ∙ Regimen with lower toxicity 
  • ∙ Better palatability and lower pill burden 
  • ∙ Increased durability and efficacy 
  • ∙ Sequencing: spares other available formulations for use in the 2nd line regimen ∙ Harmonization of regimen across age and population 
  • ∙ Lower cost 
  • ∙ Help the country to achieve a recommended regimen for the vast majority of PLHIV(People Living With HIV)

Available ARVs in Uganda

Drug Class

Examples

Nucleoside Reverse Transcriptase Inhibitors (NRTIs): Incorporate into the DNA of the  virus, thereby stopping the building process. 

 

Tenofovir (TDF), Zidovudine (AZT), Lamivudine (3TC), Abacavir (ABC)

Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs): stop HIV production by binding directly onto the reverse transcriptase enzyme, and prevent the conversion of RNA to DNA.

Efavirenz (EFV), Nevirapine (NVP), Etravirine (ETV)

Integrase Inhibitors: interfere with the HIV DNA’s ability to insert itself into the host DNA and copy  itself.

Dolutegravir (DTG), Raltegravir (RAL)

Protease Inhibitors (PIs): prevent HIV from being successfully assembled and released from the infected CD4 cell.

Atazanavir (ATV), Lopinavir (LPV), Darunavir (DRV)

Entry Inhibitors:  prevent the HIV virus particle from infecting the CD4 cell.

Enfuvirtide (T-20), Maraviroc

 

Uses of ART (Antiretroviral Therapy)

  1. Treatment of HIV/AIDS: ART is the primary treatment for managing HIV/AIDS, helping to control the viral load and maintain the health of the immune system.
  2. Prevention of Mother-to-Child Transmission (PMTCT): ART is crucial in preventing the transmission of HIV from an infected mother to her baby during pregnancy, childbirth, and breastfeeding.
  3. Post-Exposure Prophylaxis (PEP): ART is used as an emergency intervention for individuals who have been potentially exposed to HIV. It must be started within 72 hours of exposure to be effective.
  4. Pre-Exposure Prophylaxis (PrEP): ART can be taken by HIV-negative individuals at high risk of infection to prevent acquiring HIV. This is particularly useful for people with HIV-positive partners, among others.
  5. Treatment and Support for Children: Ensuring children with HIV receive ART is essential for their growth, development, and long-term health. Adherence to the treatment regimen is crucial for its effectiveness.
  6. Reducing Viral Load to Undetectable Levels: ART helps reduce the viral load in the body to undetectable levels, significantly lowering the risk of HIV transmission and improving overall health.
  7. Improving Quality of Life: Effective ART can improve the quality of life for people living with HIV by reducing the incidence of opportunistic infections and other HIV-related complications.
  8. Increasing Life Expectancy: ART has been shown to increase the life expectancy of people living with HIV, allowing them to live longer, healthier lives.
  9. Preventing Sexual Transmission of HIV: By reducing the viral load to undetectable levels, ART can prevent the sexual transmission of HIV, a strategy known as “treatment as prevention” (TasP).
  10. Reducing HIV-Related Stigma and Discrimination: Successful ART can help reduce stigma and discrimination associated with HIV by enabling individuals to lead healthy, productive lives, thereby changing perceptions about the disease.
  11. Managing Co-Infections: ART can help in managing co-infections such as hepatitis B and C, tuberculosis, and other conditions that are common in people living with HIV.

Recommended First Line Regimens in Adults, Adolescents, Pregnant Women and Children

HIV management guidelines are constantly being updated according to evidence and public policy decisions. Always refer to the latest official guidelines.

The 2022 guidelines recommend DOLUTEGRAVIR (DTG) an integrase inhibitor as the anchor ARV in the preferred first and second-line treatment regimens for all HIV infected clients; children, adolescents, men, women (including pregnant women, breastfeeding women, adolescent girls and women of child bearing potential).

Patient Category

Preferred Regimens

Alternative Regimens

Adults and Adolescents

  

Adults (including pregnant women, breastfeeding mothers, and adolescents ≥30Kg)

TDF + 3TC + DTG

– If DTG is contraindicated: TDF + 3TC + EFV400

– If TDF is contraindicated: TAF + FTC + DTG 

– If TDF or TAF is contraindicated: ABC + 3TC + DTG 

– If TDF or TAF and DTG are contraindicated: ABC + 3TC + EFV400 

 – If EFV and DTG are contraindicated: TDF + 3TC + ATV/r or ABC + 3TC + ATV/r

Children

  

Children ≥20Kg – <30Kg

ABC + 3TC + DTG

– If DTG is contraindicated: ABC + 3TC + LPV/r (tablets) 

 – If ABC is contraindicated: TAF + FTC + DTG (for children >6 years and >25Kg) 

 – If ABC and TAF are contraindicated: AZT + 3TC + DTG

Children <20Kg

ABC + 3TC + DTG

– If intolerant or appropriate DTG formulations are not available: ABC + 3TC + LPV/r granules 

– If intolerant to LPV/r: ABC + 3TC + EFV (in children >3 years and >10Kg) 

 – If ABC is contraindicated: AZT + 3TC + DTG or LPV/r

Notes:

  • Contraindications for DTG include known diabetics, patients on anticonvulsants (carbamazepine, phenytoin, phenobarbital) – use the DTG screening tool prior to DTG initiation.
  • Contraindications for TDF and TAF include renal disease and/or GFR <60ml/min, weight <30Kg.
  • TAF can be used in subpopulations with bone density anomalies.
  • Children will be assessed individually for their ability to correctly take the different formulations of LPV.

Notes from Ministry of Health

  1. For clients on an ABC-3TC-DTG based regimen weighing >25 kg, use the fixed-dose combination of Abacavir/Lamivudine/Dolutegravir 600/300/50 mg instead of the separate pills of Abacavir/Lamivudine 600/300 mg plus Dolutegravir 50 mg.
  2. Use Abacavir/Lamivudine 600/300 mg for patients on the following regimens: ABC-3TC-ATV/r, ABC-3TC-LPV/r, and ABC-3TC-DRV/r.
  3. Use the single pill of Dolutegravir 50 mg for patients on AZT-3TC-DTG based regimens.
  4. For eligible patients on ATV/r and LPV/r, optimize to Dolutegravir.
  5. For PrEP, while the guidelines provide options for the use of either TDF/3TC 300/300 mg or TDF/FTC 300/200 mg, use TDF/FTC 300/200 mg for PrEP in terms of programmatic implementation.

RECOMMENDED FIRST-LINE REGIMEN FOR INITIATION OF ART IN CHILDREN UNDER 3 YEARS OF AGE

Recommended first-line regimen: ABC+3TC+LPV/r 

All HIV-infected children under 3 years should be initiated on abacavir + lamivudine + ritonavir-boosted  lopinavir (ABC+3TC+LPV/r). 

NB: Children younger than 36 months have a reduced risk of discontinuing treatment, viral failure or death  if they start on an LPV/r based regimen instead of the NVP-based regimen. Also, surveillance of drug  resistance among vertically infected children younger than 18 months in 

Uganda has revealed high levels of resistance to NNRTIs and LPV/r is known to have a high barrier to  resistance. 

When to use alternative first-line regimens AZT+3TC+LPV/r 

AZT+3TC+ LPV/r should only be used in children who experience a hypersensitivity reaction to abacavir  (ABC), however, this is rare in African populations. 

WHAT REGIMEN TO SWITCH TO (SECOND-LINE AND THIRD-LINE ART) 

Second-line ARVS in adolescents/children above 10 years 

Recommended 2nd line regimen: 2 NRTIs +ATV/r 

HIV-infected adolescents/children above 10 years, initiating 2nd line ART should be initiated on 2 NRTIs and  ritonavir-boosted atazanavir (ATV/r). The choice of NRTI should be determined based on the regimen the  patient was on. 

The recommended sequence is: 

  1. After failing on TDF + 3TC or ABC+3TC based regimen, use AZT+3TC 
  2. After failing on AZT+3TC based regimen, use TDF + 3TC 

When to use alternative 2nd line regimen: 2 NRTIs +LPV/r 

LPV/r is should only be used to initiate adolescents/children who weigh less than 40kg. 

Second-line ARVS in children aged 3 years to less than 10 years 

RECOMMENDED 2nd line REGIMEN: 2 NRTIs +LPV/r 

HIV-infected children aged 3 to less than 10 years initiating 2nd line ART should be initiated on 2 NRTIs and  ritonavir-boosted lopinavir (LPV/r). The recommended formulation is the LPV/r 100/25mg tablet. The choice of NRTI should be determined based on the regimen the patient was on The recommended sequence of the NRTIs is below: 

∙ After failing on ABC+3TC based regimen, use AZT+3TC. 

∙ After failing on AZT+3TC based regimen, used ABC+3TC. 

Second-line ARVS in children under 3 years 

Recommended 2nd line regimen: 2 NRTIs +RAL 

HIV-infected children less than 3 years of age initiating 2nd line ART should be initiated on 2 NRTIs and RAL. The choice of NRTI should be determined based on the regimen the patient was on (Table 55). The recommended sequence of the NRTIs is: 

∙ After failing on ABC+3TC based regimen, use AZT+3TC. 

∙ After failing on AZT+3TC based regimen, used ABC+3TC. 

The rationale for using raltegravir

Raltegravir is the recommended drug of choice for the second line ARVs in children with prior exposure to  protease inhibitors because there is no data on safety and efficacy of dolutegravir in children under six  years, while darunavir is contraindicated in this age group. 

When to use alternative 2nd line regimen: 2 NRTIs + LPV/r 

LPV/r is recommended in children who have used NNRTI (NVP) in their first line regimen.

Monitoring of ARV Treatment

The monitoring of patients on antiretroviral therapy (ART) serves several purposes:

  1. Assess Response to ART and Diagnose Treatment Failure
  2. Ensure Safety of Medicines: Identify Side Effects and Toxicity
  3. Evaluate Adherence to ART

Methods of Monitoring ARV Treatment

1. Clinical Monitoring: Involves medical history and physical examination.

2. Laboratory Monitoring: Includes various laboratory tests.

  • Viral Load Monitoring: Preferred for assessing response to ART and diagnosing treatment failure.
  • CD4 Monitoring: Recommended in specific scenarios.
  • Other Minor Laboratory Tests: Includes tests for specific indications.

Viral Load Monitoring

  • Preferred method for monitoring ART response. A patient who has been on ART for more than 6 months and is responding to ART should have viral suppression (VL <1000 copies/ml) irrespective of the sample type (either DBS or plasma). 
  • Provides an early and more accurate indication of treatment failure and the need to switch from first line to second-line drugs, hence reducing the accumulation of drug resistance mutations and improving  clinical outcomes. 
  • Early and accurate indication of treatment failure.
  • Differentiates between treatment failure and non-adherence.
  • Recommended frequency: Every six months for children and adolescents under 19 years.

CD4 Monitoring

  • Baseline CD4 count is essential for assessing opportunistic infection risk.
  • Recommended for patients with high viral load or advanced clinical disease.

Other Laboratory Tests

Tests

Indication

CrAg

Screen for cryptococcal infection

Complete Blood Count (CBC)

Assess anaemia risk

TB Tests

Suspected tuberculosis

Serum Creatinine

Assess kidney function

ALT, AST

Evaluate liver function

Lipid Profile, Blood Glucose

Assess metabolic health

 

Problems Associated with ARV Treatment

Immune Reconstitution Inflammatory Syndrome (IRIS)

IRIS is a spectrum of clinical signs and symptoms linked to immune recovery triggered by ART. It occurs in 10–30% of individuals starting ART, usually within the first 4–8 weeks.

  • Serious Forms: Most severe cases happen in patients co-infected with TB, Cryptococcus, Kaposi’s sarcoma, and herpes zoster.
  • Risk Factors: Include low CD4+ cell count (<50 cells/mm3) at ART initiation and disseminated opportunistic infections.
  • Management: Usually self-limiting; treat co-infections to reduce symptoms and reassure patients to maintain ART adherence.

Steps to Reduce IRIS Development

  1. Early HIV Diagnosis: Initiate ART before CD4 declines to below 200 cells/mm3.
  2. Optimal Management of Opportunistic Infections: Screen and treat infections before starting ART, especially TB and cryptococcus.

ARV Drug Toxicity

  • Range of Toxicities: ARVs can cause mild to life-threatening side effects.
  • Challenges: Differentiating between ARV toxicity and HIV complications can be complex.
  • Management: Assess patients for side effects at every clinic visit and take appropriate actions based on severity.

Management of ARV Side Effects/Toxicities

Category

Action

Severe, Life-threatening Reactions (e.g., SJS/TEN, severe hepatitis)

– Discontinue all ARVs immediately. 

– Manage the medical event and substitute offending drug when stable.

Severe Reactions (e.g., Hepatitis and Anemia)

– Substitute offending drug without stopping ART.

Moderate Reactions (e.g., Gynaecomastia, Lipodystrophy)

– Substitute with a drug in the same class or different class with a different toxicity profile. 

– Do not discontinue ART; continue if feasible.

Mild Reactions (e.g., Headache, Minor Rash, Nausea)

– Do not discontinue or substitute ART. 

– Provide reassurance and support to mitigate adverse reactions. 

– Counseling about the events.

Management of HIV Positive Pregnant Mother

Key Interventions for eMTCT:

  • Routine HIV Counseling and Testing during ANC (at 1st contact. If negative, repeat HIV test in the third trimester/ labour).
  • Enrolment in HIV care if the mother is positive and not yet on treatment.
  • If the mother is already on ART, perform viral load and continue the current regimen.
  • ART in pregnancy, labour, post-partum, and for life – Option B+.

Recommended ARV for option B+:

One daily Fixed Dose Combination (FDC) pill containing TDF + 3TC + EFV started early in pregnancy irrespective of the CD4 cell count and continued during labor and delivery, and for life.

Alternative regimens for women who may not tolerate the recommended option are:

  • If TDF contraindicated: ABC+3TC+EFV
  • If EFV contraindicated: TDF + 3TC + ATV/r
  • TDF and EFV are safe to use in pregnancy.
  • Those newly diagnosed during labor will begin HAART for life after delivery.

Prophylaxis for Opportunistic Infections

Cotrimoxazole 960 mg 1 tab daily during pregnancy and postpartum –– Mothers on cotrimoxazole DO NOT NEED IPTp with SP for malaria.

Care of HIV Exposed Infant

HIV-exposed infants should receive care at the mother-baby care point together with their mothers until they are 18 months old. A mother-baby care point is a healthcare facility that provides comprehensive services to both HIV-exposed infants and their parents.

 The goals of HIV-exposed infant care services are:

  • To prevent the infant from being HIV infected.
  • Among those who get infected: to diagnose HIV infection early and treat it.
  • Offer child survival interventions to prevent early death from preventable childhood illnesses.

The HIV Exposed Infant and the mother should consistently visit the health facility at least nine times during that period i.e  (i.e., at 6, 10 and 14 weeks, then at 5, 6, 9,  12, 15 and 18 months). 

Nevirapine Prophylaxis

Provide NVP syrup from birth for 6 weeks: Give NVP for 12 weeks for babies at high risk, that is breastfeeding infants who mothers: 

  • Have received ART for 4 weeks or less before delivery; or 
  • Have VL >1000 copies in 4 weeks before delivery; or 
  • Diagnosed with HIV during 3rd trimester or breastfeeding period (Postnatal) 

Do PCR at 6 weeks (or at first encounter after this age) and start cotrimoxazole prophylaxis 

  • If PCR positive, start treatment with ARVs and cotrimoxazole and repeat PCR (for confirmation) 
  • If PCR negative and the baby never breastfed, the child is confirmed HIV negative. Stop cotrimoxazole, continue clinical monitoring and do HIV serology test at 18 months. 
  • If PCR is negative but the baby has breastfed/is breast feeding, start/continue cotrimoxazole prophylaxis and repeat PCR 6 weeks after stopping breastfeeding.
  • Follow up any exposed child and do PCR if they develop any clinical symptom suggestive of HIV at any  time and independently of previously negative results.
  • For negative infants, do serology at 18 months before final discharge.

Dosages of Nevirapine

Age Group

Weight Range

Dosage

Syrup Volume (10 mg/ml)

Child 0-6 weeks

2-2.5 Kg

10 mg once daily

1 ml

Child 0-6 weeks

>2.5 Kg

15 mg once daily

1.5 ml

Child 6 weeks – 12 weeks

Any weight

20 mg once daily

2 ml

Cotrimoxazole Prophylaxis: Provide cotrimoxazole prophylaxis to all HIV exposed infants from 6 weeks of age until they are proven to be uninfected.

  • Child <5 kg: 120 mg once daily  
  • Child 5-14.9 kg: 240 mg once daily 

Isoniazid (INH) Preventive Therapy (IPT): 

  • Give INH for six months to HIV-exposed infants who are exposed to TB.
  • Isoniazid 10 mg/kg + pyridoxine 25 mg daily 
  • For newborn infants, if the mother has TB disease and has been on anti-TB drugs for at least two weeks before delivery, INH prophylaxis is not required. 

Immunization

Immunise HIV exposed children as per national immunisation schedule.

In case of missed BCG at birth, do not give if the child has symptomatic HIV.

Avoid yellow fever vaccine in symptomatic HIV.  

Measles vaccine can be given even in symptomatic HIV.

Counselling on Infant Feeding Choice

  • Explain the risks of HIV transmission by breastfeeding (15%) and other risks of not breastfeeding (malnutrition, diarrhoea).
  • Mixed feeding may also increase the risk of HIV transmission and diarrhoea.
  • Tell her about options for feeding, advantages, and risks.
  • Help her to assess choices, decide on the best option, and then support her choice.

Feeding Options

  • Recommended option: Exclusive breastfeeding, then complementary feeding after the child is 6 months old.
  • Exclusive breastfeeding stopping at 3-6 months old if replacement feeding is possible after this.
  • If replacement feeding is introduced early, the mother must stop breastfeeding.
  • Replacement feeding with home-prepared formula or commercial formula and then family foods (provided this is acceptable, feasible, safe, and sustainable/affordable).

If Mother Chooses Breastfeeding

  • The risk may be reduced by keeping the breasts healthy (mastitis and cracked nipples raise HIV infection risk).
  • Advise exclusive breastfeeding for 3-6 months.

If Mother Chooses Replacement Feeding

  • Counsel and teach her on safe preparation, hygiene, amounts, times to feed the baby, etc.
  • Follow up within a week from birth and at any visit to the health facility.

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