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Psoriasis

Psoriasis

Psoriasis

Psoriasis is a chronic non contagious auto immune disease of the skin in which the epidermal cells are produced at an abnormal rate.

It results from over production of immature epidermal
cells. It affects many parts. Its cardinal sign is scaly skin that looks like silver fish which may not go away with rubbing.

Causes of Psoriasis

Psoriasis is caused by complex interactions between genetics, the immune system, and environmental factors. These include;

  •  Immune reactions.
  •  Genetic factors.
  •  Infections like strep throat, Streptococcal infections
  •  Injury to the skin such as cut or scrape.
  •  Stress.
  •  Smoking.
  •  Heavy alcohol consumption.
  •  Vitamin D deficiency.
  • Medications including high blood pressure medications and antimalarial drugs and lithium.
  • Withdrawal systems of oral or systemic corticosteroids
  • Cold weather and dry conditions

Clinical Presentations

  • A long-term history of erythematous, scaly area, which may involve. multiple areas of the body.
  • Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma.
  • Pruritus (especially in eruptive, guttate psoriasis)
  • Red scaly, white patches
  • Small scaling spots mostly in children
  • Dry, cracked skin
  • Ocular symptoms include redness and tearing due to conjunctivitis or blepharitis
  • Pain, which has been described by patients as unpleasant, superficial, sensitive, itchy, hot, or burning.
  • High fever in erythrodermic and pustular psoriasis
  • Pitted or cracked nails, Dystrophic nails
  • Avoidance of situations requiring social interaction
  • Arthralgia: Joint pain without any visible skin findings
  • Stiff joints
  • Itching sensation
types of psoriasis

Types of Psoriasis

  1. Guttate Psoriasis; It is caused by streptococcal infection (pharyngitis or perianal). It appears as small, scaly red, tear-drop shaped called papules. It is mainly seen in children and young adults.
  2. Postular Psoriasis; Its symptoms include pustules which are yellow, pus-filled lesions. They can be Generalized pustular psoriasis (GPP) which covers many parts of the body, or Localized pustular psoriasis covering smaller areas on the palms of the hands or the soles of the feet.
  3. Plaque Psoriasis; It is the common form of psoriasis and appears as raised, inflamed, red scaly patches with a silvery-white coating at the top. It can be tender, itchy and painful. They appear on the back, elbows, knees, and scalp.
    • Affects >70 % of the body surface area

Diagnosis / Investigation

  • History, age, family history of psoriasis, past medical history from streptococcal infections, bacterial or viral infection.
  • Physical examination; Common physical examination findings of psoriasis include erythematous, scaling papules, and plaques.
  • Enzyme linked immunosorbent assay (ELISA);
    In patients with severe psoriasis, increased levels of Long Pentraxin 3 protein (PTX3) can be observed in plasma and in monocytic cultures by enzyme linked immunosorbent assay (ELISA).
  • Skin biopsy may be helpful in the diagnosis of psoriasis. Common findings include perivascular and dermal inflammatory cell infiltration, vascular dilation, and absent granular layer.
  • Blood test; blood test to rule out any other health conditions relating to the development of psoriasis.

Management of Psoriasis

Nursing management;

  •  Body hygiene; Bathing daily helps to take off scales and soothes the inflamed skin.
  • Apply moisturizers. Moisturizing the skin smooths the roughness and reduces itching and swelling.
  • Avoid psoriasis triggers; Find out what triggers your psoriasis, and take precautions to avoid them.
  •  Care for pressure areas to avoid pressure sores.
  • Avoid alcohol consumption; Drinking alcohol may make some psoriasis treatments ineffective. So avoid drinking alcohol during psoriasis treatment.
  •  Give psychological care to allay anxiety.
  • Follow a healthy lifestyle by eating nutritious food and avoiding smoking. Stay away from pollution and dirt because pollution leads to flaring up of psoriasis symptoms. Consult your dermatologists to choose the right type of shampoo or soap, that does not cause any harm to your skin.
  • Advise against exposure to sun light.
  • Physiotherapy.

Pharmacological management;
First line treatment;

Medicated creams and ointments applied directly to psoriatic lesions can help decrease inflammation, remove built-up scale, reduce skin turnover, and clear affected skin of plaques.

  •  Apply topical drugs like corticosteroids like betamethasone cream, Vitamin D analogues like calcipotriol
  • Topical betamethasone plus calcipotriene  12 hourly for 1 week.

Second line;

  •  Expose the patient to photo therapy. It has long been recognized that daily, short, non-burning exposure to sunlight can help clear or improve psoriasis.
  • Steroids; Triamcinolone topical steroid can relieve psoriasis symptoms such as itching, crusting, scaling, redness, inflammation, dryness, and discomfort. It also serves as a dental medicine (paste) to relieve the discomfort of mouth sores. 
  • Retinoids;  Oral retinoids known as Acitretin are pills to slow down the production of skin cells. Doctors prescribe Acitretin to manage severe cases of psoriasis. Its side effects are dry skin and muscle soreness. They are not allowed during pregnancy or breastfeeding.
  • Methotrexate; It is a powerful drug. Prescribed to treat adults with severe, disabling psoriasis that cannot be cured with skin medicines applied or phototherapy. Methotrexate suppresses the overactive immune system that leads to psoriasis.
  • Biologics; These are new and strong drugs. They target only that area of the immune system that is hyperactive due to psoriasis. Therefore they cause no damage to other body organs, as compared to other strong medicines.
Psoriatic arthritis

This is a form of inflammatory arthritis affecting people having psoriasis.

Causes/predisposing factors.

  • Auto immune reactions.
  • Physical trauma
  • Microbial infestation.
  • Psoriasis.
  • Family history.
  • Age; affects people with30-50 years of age though any one can suffer from it.

Signs and symptoms.

  • It can affect joints on one side or both sides of your body.
  • Symptoms almost resemble those of rheumatic arthritis. I.e. hotness, redness, tenderness, swelling, joint stiffness.

However one is most likely to develop;

  • Lower back pain.
  • Foot pain.
  • Swollen finger and toes.

Diagnosis

  • History taking.
  • Physical examination.
  • X ray.
  • MRI.
  • Rheumatic factor test.
  • Joint fluid test.

Management/treatment.

Nursing management; 

  • Apply moisturizers.
  • Use of warm compress.
  • Care for pressure areas to avoid pressure sores.
  • Ensure general hygiene to do away with funny smells.
  • Give psychological care to allay anxiety.
  • Diet; encourage taking a balanced diet.
  • Advise against exposure to sun light.
  • Physiotherapy.

 

Pharmacological management.

  • Give analgesics like paracetamol for pain.
  • NSAIDS like ibuprofen to soothe inflamation.
  • Immune suppressants like imuran, azafan, cyclosporine.
  • Biological agents like DMARDS.
  • New oral medication like apremilast to decrease the activity of the enzyme in the body that controls the activity of inflamation in the body.

Surgical treatment.

  • Joint replacement may be done.



 Complications.

  • Arthritis mutilan.( Severe painful and disability form of a disease for over time; it destroys small bones of the hands e.g. fingers).
  • Conjunctivitis.
  • Uveitis.
  • High risk of cardiovascular diseases.

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Onychomycosis

Onychomycosis

Onychomycosis

Onychomycosis means fungal infection of the nails. It represents up to 20% of all nail disorders.

Onychomycosis may affect toe- or fingernails, but toenail infections are particularly common.

  • The most common type of onychomycosis (80-90%), caused by dermatophytes, is  known as tinea unguium (tinea of the nails).

 It can result in

  • discoloration,
  • thickening,
  • chalkiness, 
  • crumbling of the nails and is often treated by powerful oral medications 
onychomycosis classifications

Classification of Onychomycosis

Onychomycosis is classified according to the clinical pattern of nail bed involvement. The main types are:

  1. Distal and lateral subungual onychomycosis (DLSO); The most common form of tinea unguium usually caused by Trichophyton rubrum, which invades the nail bed and the underside of the nail plate.
  2. Superficial white onychomycosis; Caused by fungal invasion of the superficial layers of the nail plate to form “white islands” on the plate. Accounts for only 10 percent of onychomycosis cases.
  3. Proximal subungual onychomycosis; Fungal penetration of the newly formed nail plate through the proximal nail fold. It is the least common form of tinea unguium in healthy people but found more commonly when the patient is immunocompromised.
  4. Endonyx onychomycosis; Fungal penetration through the full thickness of the nail from directly under the skin. The nail bed is not infected. Commonly found in immunocompromised conditions.
  5. Total dystrophic onychomycosis; Total destruction of the nail plate. It is the end result of any of the above four types.

Causes of Onychomycosis

  • Dermatophytes are the fungi mostly responsible for onychomycosis
  •  Trichophyton rubrum is the most common dermatophyte fungi.
  • Others include, Trichophyton interdigitale and Epidermophyton floccosum, can be causes as well.
  • The dermatophytes are identified in 90% of the toenail and 50% of fingernail onychomycosis. 
  • Candida albicans accounts for 2% of onychomycosis, occurring especially in fingernails.
  • Yeasts mainly cause fingernail onychomycosis in people whose hands are often submerged in water.

Risk Factors

  1. Age; The most common risk factor for onychomycosis is aging. Reason may be due to nail trauma, poor nail care, poor peripheral circulation e.t.c.
  2. Family history of onychomycosis
  3. Warm and moist conditions of the fingers like wearing tight fitting shoes
  4. Walking with barefoot in public places such as swimming pool, public baths and showers.
  5. Nail conditions such as tinea pedis, nail injury, nail damage, psoriasis .
  6. Conditions that are related with poor peripheral circulation such as diabetes or peripheral arterial disease.
  7. Immunodeficient conditions like cancer , post transplant care , HIV , patients on chemotherapy and radiotherapy

Clinical Presentation.

  •  Always presents with distorted nails .
  • Change in nail texture and discoloration.
  • The nail plate can have a thickened, yellow, or cloudy appearance.
  • The nails can become rough and crumbly, or can separate from the nail bed.
  • Malodor; slight foul smelling of the infected nail.

Complications.

  • Cellulitis
  • Sepsis
  • Osteomyelitis
  • Tissue damage
  • Loss of nail

Management / Treatment of Onychomycosis

Oral medications such as Oral antifungal medications such terbinafine , itraconazole and fluconazole , Treatment Options

Preferred treatment regimen: 

Terbinafine 250 mg orally OD (children <20 kg: 67.5 mg/day, 20–40 kg: 125 mg/day, >40 kg: 250 mg/day) for 6 weeks OR Itraconazole 200 mg orally O.D for 3 months OR Fluconazole 150–300 mg orally weekly for 6–12 months

Fungal laser therapy; Laser treatments aim at either stopping fungal reproduction (fungistatic) or killing fungus (fungicidal).

 

Prevention of Onychomycosis

  1. Wear appropriate fitting shoes. Both, shoes that are too tight and or too loose can cause trauma to the toenails, creating a portal of entry for fungal organisms.
  2. Avoid being barefoot in public or communal areas that are shared by other barefoot people. These areas may include public swimming pools, locker rooms, showers, and hotel rooms.
  3. Do not pick or tear at your toenails. Use clean instruments to cut the toenails straight across, avoiding rounding the edges. Trauma or aggressive cutting can create portals of entry for fungus.
  4. Thoroughly dry your feet, including between your toes after showering.
  5. Maintain dry feet throughout the day and do not wear damp shoes.
  6. If you have family members with foot or toenail fungal infections, avoid sharing common spaces barefoot.
  7. If you have diabetes or reduced blood flow to the feet, maintain foot exercises and guidelines from the healthworker.

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Herpes zoster

Herpes zoster

Herpes zoster

Herpes zoster, also called shingles, is an infectious condition caused by varicella zoster virus (VZV), the same virus that causes varicella zoster (chickenpox).

  • The incubation period ranges from 7 to 21 days.
  • The total course of the disease is 10 days to 5 weeks from onset to full recovery.

Risk Factors

  • Older age- risk increases with age especially after age of 50
  • Suppressed immunity due to certain conditions like cancer, HIV and drugs
  • Stress due to prolonged unresolved emotional or physical stress

Pathophysiology

  • After a case of chickenpox run its course,
  • The virus lies dormant in the ganglia of the spinal nerve tracts.
  • Then the virus reactivates and travels along the peripheral nerves to the skin,
  • It then multiplies and produces painful vesicular eruptions.
  • It is most common in older adults and people who have weak immune systems.
  • Although VZV typically affects the trunk of the body,
  • It can also be noted on the buttocks or face.
  • If an ophthalmic nerve is involved, the client may potentially experience keratitis, ulceration and possibly blindness.
  • Secondary infection resulting from scratching the lesions is common.

Clinical Features

  • The initial symptom is usually a tingling sensation in the affected area.
  • Painful blisters form in the area supplied by one nerve root. This usually affects only one side of the body.
  • Pain and discomfort, which can be severe, begins about five days before the rash emerges.
  • Red papules develop into blisters, which crust over and heal within three to four weeks.
  • Malaise and fever are common and this, coupled with pain, makes shingles a debilitating condition.

Diagnosis

  • Past history of chickenpox.
  • The pain and rash of shingles is characteristically unilateral.
  • May start after a period of debility.
  • Culture and sensitivity in case of secondary infection

Assessment

Subjective Data:

  • Pain, burning
  • Numbness, tingling
  • Itching
  • Headache
  • Sensitivity to light
  • Fatigue

Objective Data:

  • Rash that develops in clusters of vesicles
  • Rash follows dermatome (nerve pathway
Nursing Management
  • Assess pain level
  • Note location and quality of pain
  • Duration
  • Non-verbal clues
  • Relieving factors
  • Severe nerve (burning) pain is the primary complaint with preceding sensations of tingling or itching.
  • Assess for signs / symptoms of bacterial infections on skin and obtain culture and sensitivity test as indicated
  • Assess for changes in vision and rash on forehead or nose

Specific Nursing care

  • Apply cool, moist dressings to pruritic lesions
  • Avoid temperature extremes, in both the air and bathwater.
  • Avoid rubbing or scratching the skin or lesion.
  • Wear loose, nonrestrictive clothing made of cotton.
  • Keep rash dry;
  • Rest, especially while malaise is a problem
  • Encourage herpes zoster vaccination
  • Explain to the patient the need for Isolation.
  • Restrict visitors
  • Keep finger nails short
  • Wear protective gears while caring for the patient

Medical Management

  • Antivirals (acyclovir, valacyclovir)  are given to decrease the severity and duration of symptoms
  • Oral analgesics (opioids) are given to treat severe pain of acute phase;
  • Antidepressants and antiepileptic medications may be given to treat post herpetic neuralgia;
  • Topical steroids provide an anti-inflammatory effect;
  • Antihistamines help with itching, especially at bedtime;
  • Topical analgesics provide pain relief
Complications
  • Ear complications such as ringing in ears, vertigo, hearing loss, one sided facial paralysis
  • Post herpes nerve pain (neuralgia) which can be very severe and persist for even years after healing
  • Eye complications such as erosion or ulceration of cornea, dryness of eyes, inflammation of optic nerve etc
Nursing Diagnosis
  1. Acute Pain or Chronic Pain related to Nerve pain (most commonly cervical, lumbar, sacral, thoracic, or ophthalmic division of trigeminal nerve) as evidenced by Alteration in muscle tone, Facial mask of pain, Reports of burning, dull, or sharp pain, Reports of pain localized to affected nerve.
  2. Deficient Knowledge related to Complexity of treatment, Herpes zoster outbreak, 
    as evidenced by Inadequate follow-up of instructions, Questioning members of healthcare team, Verbalizing inaccurate information.
  3. Risk for Infection related to Crusted-over lesions,
    Itching and scratching Skin lesions (papules, vesicles, pustules)
  4. Risk for Disturbed Body related to
    Preoccupation with changed body part and Visible skin lesions.

Nursing Interventions

1. Teach the patient about contact isolation. VZV is spread by contact with fluid from lesions containing viruses.

2. Instruct the client to avoid contact with pregnant women and immunocompromised individuals. Active lesions can be infectious, and immunosuppressed individuals are more susceptible.

3. Use universal precautions in caring for the client to prevent transmission of disease to self or other clients. VZV can be transmitted to others and cause chickenpox in a person who has not previously had the disease.

4. Suggest the use of gauze to separate the lesions in skin folds. This reduces irritation, itching, and cross-contamination.

5. Discourage the scratching of lesions. Encourage the client to trim fingernails. These measures prevent the inadvertent opening of lesions, cross-contamination, and bacterial infection.

6. Instruct the client on the use of antiviral medications, as prescribed. Antiviral agents are most effective during the first 72 hours of an outbreak when viruses are proliferating. Drugs of choice are acyclovir, famciclovir, or valacyclovir.

7. Instruct the client in the use of systemic steroids, if ordered, for anti-inflammatory effect.
The use of steroids is controversial; they are most commonly used in severe cases

8. Assist the client in articulating responses to questions from others regarding lesions and infectious risk. Clients may need some guidance in determining what to say to people who comment on the appearance of their skin. The rehearsal of set responses to anticipated questions may provide some reassurance.

9. Suggest the use of concealing clothing when lesions can be easily covered. This approach may help the client who is having problems adjusting to body image changes.

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Acne Vulgaris

Acne Vulgaris

Acne Vulgaris

Acne Vulgaris is an inflammatory skin disease caused by changes in the pilosebaceous units (skin structures comprising a hair follicle and its related sebaceous gland) of the skin.

The term acne comes from a Greek word acme meaning a skin eruption) 

Acne vulgaris is the most common cutaneous disorder affecting adolescents and young adults. Patients with acne can experience significant psychological morbidity and, rarely, mortality due to suicide.

The psychological effects of embarrassment and anxiety can impact the social lives and employment of affected individuals. 

Scars can be disfiguring and lifelong.

Acne Vulgaris Classification

Classification of Acne

It is classified as mild, moderate, or severe. 

Mild acne is defined as non-inflammatory lesions (comedones), a few inflammatory (papulopustular) lesions, or both. 

Moderate acne is defined as more inflammatory lesions, occasional nodules, or both, and mild scarring. 

Severe acne is defined as widespread inflammatory lesions, nodules, or both, and scarring, moderate acne that has not settled with 6 months of treatment, or acne of any “severity” with serious psychological upset. 

Causes of Acne Vulgaris

Acne occurs by hypersensitivity of the sebaceous glands to a normal circulating level of androgens, which are aggravated by P. acnes and inflammation.

 Causes of acne include the following:

  • Propionibacterium acnes infection, Staphylococcus epidermidis
  • Use of medications like lithium, steroids, and anticonvulsants
  • Exposure to excess sunlight
  • Use of occlusive wear like shoulder pads, headbands backpacks, and underwire brassieres
  • Endocrine disorders like polycystic ovarian syndrome and even pregnancy
  • Accumulation of dead skin cells.
  • Any medication containing halogens (iodides, chlorides, bromides), lithium, barbiturates, or androgens.
  • Conditions like Congenital adrenal hyperplasia, Cushing’s syndrome, polycystic ovary syndrome
  • Puberty
Pathophysiology of acne vulgaris

Pathophysiology of Acne

Four factors are involved:

  1. Follicular hyper keratinization .
  2. Increased sebum production .
  3. Propionic bacterium acnes (P. acnes) within the follicle. An anaerobic diphtheroid that is a normal component of skin flora.
  4. Inflammation.

During puberty, under the influence of androgens, sebum secretion is increased as 5-alpha reductase converts testosterone to more potent DHT, which binds to specific receptors in the sebaceous glands increasing sebum production. This leads to an increased hyperproliferation of follicular epidermis, so there is retention of sebum.

Distended follicles rupture and release pro-inflammatory chemicals into the dermis, stimulating inflammation.

C. acnes, Staphylococcus epidermis, and Malassezia furfur induce inflammation and induce follicular epidermal proliferation

Risk Factors

  • Role of androgens  — stimulating the growth and secretory function of sebaceous glands.
  • External factors  — Soaps, Oil-based cosmetics and facial massage, detergents,  Repetitive mechanical trauma caused by scrubbing with these agents may worsen the disorder by rupturing comedos, promoting the development of inflammatory lesions. Thus, patients with acne should refrain from rubbing their faces or picking their skin.
  • Turtlenecks, bra straps, shoulder pads, orthopedic casts, and sports helmets cause acne mechanical, in which occlusion of pilosebaceous follicles leads to comedone formation.
  • Diet  — The natural hormonal components of milk or other bioactive molecules in milk could exacerbate acne.
  • Family history  — Individuals with close family members with acne are at increased risk for the disorder. Has a more than three-fold risk among individuals with affected first-degree family members.
  • Stress  — Psychological stress can exacerbate acne. Receptors for corticotrophin releasing hormone (CRH), a hormone involved in the stress response, are present in human sebaceous glands. Severe anxiety and anger may aggravate acne, probably by stimulating stress hormones.
  • Body mass index  — There is an association between rising BMI and increased risk for acne only among females
  • Premenstruation — A premenstrual flare-up in acne seems to follow edema of the pilosebaceous duct. This occurs in 70% of female patients.

Signs and symptoms of Acne.

  • Acne vulgaris typically affects those areas of the body that have the largest, hormonally-responsive sebaceous glands, including the face, neck, chest, upper back, and upper arms.
  • Typical lesions of acne vulgaris (e.g, open comedones, closed comedones, and inflammatory lesions),
  • Scarring
  • Post inflammatory hyperpigmentation is common in patients with darker complexions, and take several months or more to resolve without treatment.
  • Adult women present with acne involving the lower face and neck that is often associated with premenstrual flares.

Management of Acne Vulgaris

Aims

  • To reduce bacterial colonies.
  • To decrease sebaceous gland activity, prevent the follicles from becoming plugged.
  • Reduce inflammation, combat secondary infection.
  • To minimize scarring and eliminate factors that predispose the person to acne.

Medical Management

  1. Topical Pharmacologic Therapy
    • Benzoyl peroxide 5% Topical bid
    • Topical antibiotics e.g. Clindamycin 1% gel 
    Systemic Pharmacologic Therapy
    • Antibiotics e.g. Doxycycline 100 mg PO bid
    • Oral Retinoids
    • Hormone Therapy,  Oral contraceptives: May help in women; estrogen decreases androgens and thereby suppresses sebum secretion.
    Surgical treatment
    • Extraction of comedo contents
    • Drainage of pustules and cysts
    • Excision of sinus tracts and cysts
    • Intralesional corticosteroids for anti-inflammatory action
    • Cryotherapy
    • Dermabrasion for scars
    • Laser resurfacing of scars
    Nursing Diagnosis
    • Impaired skin integrity
    • Deficient knowledge
    • Disturbed body image
    Nursing Management
    1. Administer prescribed medications, which may include acne products containing benzoyl peroxide (explain that these products initially cause skin redness and scaling but that the skin adjusts quickly); topical agents, such as vitamin A acid; and antibiotics such as tetracycline.
    2. Provide client and family teaching

    o    Advise the client that heat, humidity, and perspiration exacerbate acne. Explain that uncleanliness, dietary indiscretions, menstrual cycle, and other myths are not responsible for acne.

    o    Explain that it will take 4 to 6 weeks of compliance with the treatment regimen to obtain results.

    o     Instruct the client to wash his face gently (do not scrub) with mild soap twice daily.

    o    Instruct the client not to squeeze blackheads, not to prop hands on or rub the face, to wash hair daily and keep it off the face, and to use cosmetics cautiously because some may exacerbate acne.

    o    Instruct the female client to inform her health care provider if she is possibly pregnant. Some medication, such as systemic retinoic acid, have teratogenic effects, therefore a pregnancy test is required prior to treatment and strict birth-control measures are use throughout pregnancy.

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Dermatitis

Dermatitis

Dermatitis

 Dermatitis is an inflammation of the skin.

The word dermatitis is used to describe a number of different skin rashes that are caused by infections, allergies, and irritating substances.

The rashes range from mild to severe and can cause the following skin conditions depending on their cause.

Itchiness, Swelling, Painful ulcer, Reddening Thickening, Discoloration, Scaling, Crusting, Blisters, Creasing, Marking.
There are several different types. Usually all of them have in common an allergic reaction to specific allergens

Types of Dermatitis

  • Contact dermatitis. Caused by an allergen or an irritating substance. 
  • Atopic dermatitis. It presents usually with intense pruritus and is often associated with elevated levels of immunoglobulin E (IgE). Individuals who live in urban areas with low humidity are more prone to develop this type of dermatitis.
  • Dermatitis herpetiformis. Appears as a result of a gastrointestinal condition, known as celiac disease.
  • Seborrheic dermatitis. More common in infants and in individuals between 30 and 70 years old. It appears to affect primarily men and it occurs in 85% of people suffering from AIDS.
  • Nummular dermatitis. Also known as discoid dermatitis, it is characterized by round or oval-shaped itchy lesions. (The name comes from the Latin word “nummus,” which means “coin.”)
  • Stasis dermatitis. An inflammation on the lower legs which is caused by buildups of blood and fluid and it is more likely to occur in people with varicose veins.
  • Perioral dermatitis. Inflammation of the skin around the mouth 
  • Infective dermatitis. Dermatitis secondary to a skin infection
contact dermatitis of the face

Contact Dermatitis

Contact dermatitis is an acute or chronic skin inflammation that occurs when the skin comes in contact with a substance that causes a type IV delayed hypersensitivity reaction(allergic contact dermatitis) or when there is an injury to the skin’s surface (irritant contact dermatitis), or when the allergen or irritant is activated by sunlight hence Phototoxic dermatitis occurs.

Types of Contact Dermatitis
  1. Allergic dermatitis. Allergic dermatitis results from direct contact with substances called allergens, such as nickel, chlorine, presenting with; Skin reddening, Blisters that ooze, Itching which can become intense., Swelling in eyes, face and genital areas in severe cases.
  2. Irritant contact dermatitis. This is the most common form of contact dermatitis, Irritant contact dermatitis develops when your skin comes into contact with an irritating substance. Irritant contact dermatitis is either acute or chronic, according to the strength of the irritant, such as acids, kerosene. Stiff, tight feeling skin. May present with mild swelling, Dry, cracking skin, Blisters, Painful ulcers.
  3. Phototoxic contact dermatitis.  It is further divided into two categories, phototoxic and photoallergic contact dermatitis. Phototoxic contact dermatitis is a sunburn-like skin disorder resulting from direct tissue damage following the ultraviolet light-induced activation of a phototoxic agent. It is usually associated only with areas of skin which are left uncovered by clothing especially during scans and x-rays.
Causes of Contact Dermatitis

Contact dermatitis is caused by exposure to a substance that irritates your skin or triggers an allergic reaction, such irritants include;

  • Soaps. Most kinds of soaps, detergents, shampoos and other cleaning agents have harmful substances that could possibly irritate the skin.
  • Solvents. Solvents such as turpentine, kerosene, fuel, and thinners are strong substances that are harmful to the sensitive skin.
  • Extremes of temperature. There are people who are highly sensitive even when exposed to extremes of temperature and could cause contact dermatitis. 
  • Products that cause a reaction when you’re in the sun (photoallergic contact dermatitis), such as some sunscreens and cosmetics
  • Formaldehyde, which is in preservatives, cosmetics and other products
  • Personal care products, such as body washes, deodorants, hair dyes and cosmetics
  • Plants such as poison ivy and poison oak, cashew nuts, which contain a highly allergenic substance called urushiol
  • Airborne allergens, such as pollen and spray insecticides
  • Nickel, which is used in jewelry, and many other items
  • Medications, such as antibiotic creams, and there side effects such as diazepam, ceftriaxone.
  • Latex and long exposure to wet surfaces such as staying in a wet diaper for a long time.
Signs and Symptoms

Allergic dermatitis is usually affects the area where the trigger has touched the skin, while irritant dermatitis may be more widespread on the skin. Clinical features of both forms include the following:

  • Red rash. This is the commonest reaction. The rash appears immediately in irritant contact dermatitis and later in allergic.
  • Blisters or hives. Blisters and hives     may present in a pattern where skin was directly exposed to the allergen or irritant.
  • Burning skin. Irritant contact dermatitis tends to be more painful than itchy, causing swelling, burning or tenderness
  • Itching. Once the patient is exposed to an irritating substance, the patient presents with severe itching.
  • Crusting. The vesicles start to form a crust as it slowly becomes dry, cracked, and scaly skin.
  • Hyperpigmentation. Leathery patches that are darker than usual often because of scratching from irritation.
Diagnosis of Contact Dermatitis
  • Diagnosis is done by performing patch test. In this test, small samples of a chemical are placed on an area of skin to see if a rash develops.
  • Thorough history taking where the child mentions of use of certain products that are in contact with his or her skin.
  • Note; There are no tests for irritant contact dermatitis, only history of irritating substance that a child regularly come into contact with will prove that a child has irritant contact dermatitis.
Treatment of Contact dermatitis
  • The form of treatment will depend on the cause of dermatitis. Common treatments include;
  1. Cortisone-type creams. In severe cases, drugs containing cortisone may be given orally.
  2. Antihistamines. These are itching relievers.
  3. Dry skin care by use of lotions and creams.
  4. Oatmeal baths also to relieve itching.
  5. Barrier cream. These products can provide a protective layer for the skin.
  6. Avoiding the irritant. The key is to identify the substance that causes the rash so that it could be avoided.

Prevention

      For allergic contact dermatitis,

  • Avoid contact with substances that cause the skin rash.
  • Wash any child’s area that comes into contact with allergic substances.
  • Learn to recognize and remove poison oak and poison Ivy plants from playing areas of children

   For irritant contact dermatitis,

  • You can also use petroleum jelly to protect the child’s skin. Reapply the petroleum jelly two to three times a day and after washing hands.
  • Avoid contact with substances that irritate the child’s skin.
  • Use mild soaps.
  • Use hand creams frequently.

Question.

 Contact dermatitis is a type of hypersensitivity: 

A. Type I.
B. Type II.
C. Type III.
D. Type IV.

4. Answer: D. Type IV.

  • D: Type IV hypersensitivity is a delayed hypersensitivity reaction that are inflammatory in nature initiated by mononuclear leukocytes.
  • A: Type I hypersensitivity is triggered by an innocuous foreign substance (like dust, pollen or animal dander) that would cause no problems in the majority of people.
  • B: Type II hypersensitivity is the process by which IgG or IgM binds to a cell to cause injury or death (Antibody Dependent Cytotoxicity).
  • C: Type III hypersensitivity is tissue damage created by immune complexes, which are aggregations of antigen and antibodies.

Atopic Dermatitis

Atopic dermatitis, often referred to as eczema, is a chronic (long-lasting) disease that causes inflammation, redness, and irritation of the skin.

Cause
  • Unknown, idiopathic
  • Atopic dermatitis is the result of either skin barrier dysfunction
  • or immune dysregulation due to genetic defects
Clinical Features

In infancy

  • Severe pruritus: Can cause sleep disturbances in children. Red, very itchy dry patches of skin.
  • Rash on the cheeks that often begins at 2 to 6 months of age.
  • Rash oozes when scratched. Symptoms can become worse if the child scratches the rash. 
  • Chronic or relapsing skin lesions

 In adolescence and early childhood

  • Rash on creases of hands, elbows, wrists, and knees and sometimes on the feet, ankles and neck.
  • Dry, scaly, brownish grey skin rash.
  • Thickened skin with markings.
  • Skin rash may bleed and crust after scratching. 
  • Itch when sweating
Diagnosis
  • There are no reliable diagnostic laboratory findings associated with atopic dermatitis.
  • Although there is sometimes elevated total and/or allergen-specific serum IgE level.
Management of Atopic Dermatitis

Atopic dermatitis is a chronic condition which means that it can not be cured. Treatments however, are very effective in reducing the symptoms of itching and dry skin. It has also been found out that provision of prescribed lotions and oral medications can be helpful. These treatments include, corticosteroid creams and antihistamines.

  • You can also do the following to help the Child.
  • Avoid long, hot baths, which can dry the skin.
  • Use Luke warm water instead and give a spong bath to a child.
  • Apply lotion immediately after bathing while the skin is still moist. This will help trap moisture in the skin.
  • Keep the room temperature as regular as possible. Changes in room temperature and humidity can dry the skin.
  • Keep the Child dressed in a cotton. wool silk, and man made fabrics such as polyester can irritate the skin.
  • Use mild laundry soap and make sure that clothes are well rinsed.
  • Watch for skin infections. These should be dealt with immediately.
  • Avoid rubbing or scratching the rash.
  • Use moisturizers several times daily.

Nursing Diagnosis

  • Impaired skin integrity related to contact with irritants or allergens as evidenced by Inflammation
    Dry, flaky skin Erosions, excoriations, fissures, Pruritus, pain, blisters.
  • Disturbed body image related to visible skin lesions as evidenced by patient verbalizing feelings about the change in body appearance, negative feelings about the skin condition, fear of rejection or reactions from others.
  • Risk for infection related to excoriations and breaks in the skin.
  • Risk for impaired skin integrity related to frequent scratching and dry skin.

Nursing interventions

  1.  Assess skin, noting color, moisture, texture, and temperature; note erythema, edema, and tenderness. Specific types of dermatitis may have characteristic patterns of skin changes and lesions.
  2. Identify aggravating factors. Inquire about recent changes in the use of products such as soaps, laundry products, cosmetics, wool or synthetic fibers, cleaning solvents, and so forth.
    Patients may develop dermatitis in response to changes in their environment. Extremes of temperature, emotional stress, and fatigue may contribute to dermatitis.
  3. Skin care. Encourage the patient to bathe in warm water using a mild soap, then air dry the skin and gently pat to dry.
  4. Bathe or shower using lukewarm water and mild soap or non soap cleansers. Long bathing or showering in hot water causes drying of the skin and can aggravate itching through vasodilation.
  5. Topical application. Usual application of topical steroid creams and ointments is twice a day, spread thinly and sparingly.
  6. Acknowledge patient’s feelings. Allow patient to verbalize feelings regarding their skin condition.
  7. Proper hygiene. Encourage the patient to keep the skin clean, dry, and well lubricated to reduce skin trauma and risk for infection.
  8. Assist the patient in articulating responses to questions from others regarding lesions and contagiousness. Patients may need guidance in determining what to say to people who comment about the appearance of their skin. Dermatitis is not a contagious skin condition.
  9. Educate the patient about the skin condition, including triggers, treatment options, and measures to treat symptoms. Providing education regarding these topics can help patients with atopic dermatitis better understand the disease condition and manage the symptoms more effectively.
  10. Encourage the patient to engage in activities that can boost their self-esteem, such as hobbies or exercise. By engaging in enjoyable and fulfilling activities, patients can improve their self-esteem and mood, which can help them adjust with the emotional effects of the skin condition.

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Paget’s disease

Paget’s disease

Paget’s disease

Paget’s disease of bone also known as osteitis deformans is a chronic disease of the skeleton characterized by focal excessive bone remodeling. and is the second most common bone disease worldwide after osteoporosis.

Paget’s disease of bone is a disorder in which there’s a lot of bone remodeling that happens in some regions of the bone. Typically there’s excessive bone resorption followed by excessive bone growth, and that leads to skeletal deformities and potential fractures.

Pathophysiology of Paget’s Disease

In normal bone, there is a normal process called remodeling. Bone is absorbed and then reformed in response to the normal stresses on the skeleton.

  • Osteoclasts: cells that absorb bone.
  • Osteoblasts: cells that make new bone.

In Paget’s disease, osteoclasts are more active than osteoblasts. This means that there is more bone absorption than normal. The osteoblasts try to keep up by making new bone, but they overreact and make excess bone that is abnormally large and deformed.

Pathophysiology occurs in 3 stages, ie

  • Osteolytic Phase
  • Mixed Osteoclastic – Osteoblastic Phase
  • Osteoblastic Phase. 

Osteolytic phase, and as lytic mean destruction , So osteolytic phase presents with osteoclasts that destroy the bone and this destruction of bone results in formation of pits in the Bony matrix that are called resorption pits and these osteoclast will be visible as multinucleated large size cells.

Mixed (Osteoclastic – Osteoblastic) Phase, In the phase, there is both destruction as well as formation of new bone, where osteoclasts are destroying while osteoblasts are forming a new bone. Osteoblasts do not form enough bone compared to what osteoclasts are destroying.

Osteoblastic Phase. In this phase, there is excessive bone formation, and this excess quantity  is in form of mosaic pattern  of lamellar bone( jigsaw puzzle appearance)

Causes of Paget’s Disease

The causes of Paget’s disease are still unknown, idiopathic. But its thought to be a combination of environmental and genetic factors.

Risk Factors;

  • Age; common in elderly.
  • Viral; Paget’s disease may be caused by a slow virus infection, such as respiratory syncytial virus, and the measles virus.
  • Genetics. In around 15-40% of affected patients had a first-degree relative with Paget disease. 
  • Autoimmune, connective tissue, and vascular disorders are also rick factors.
signs and symptoms of paget's disease

Signs and Symptoms of Paget’s Disease

  • Bone Pain – commonly affected areas are pelvis, spine, skull, shoulders, and legs
    • is usually dull or aching pain
    • it is felt deep within the affected part of the body
    • the pain is constant and is at its worst at night
    • affected area may also feel warm
  • Joint pain, stiffness, and swelling -especially in the hips, back, and knees
  • Nerve Problems
    • pain travelling from the spine to the legs
    • pain travelling from the neck to arms and chest
    • numbness or tingling in the affected limbs
    • partial loss of movement in the affected limbs
    • problems in balance
    • loss of bladder or bowel control
  • Enlargement and bowing of femurs and lower legs
  • Enlargement of the skull around the forehead

Skull involvement may manifest these symptoms:

  • Development of hearing loss
  • Loss of vision
  • Hydrocephalus
  • Somnolence (drowsiness) due to vascular steal syndrome of the skull.

Diagnosis / Investigations.

  • X-rays – usually done to diagnose Paget’s disease. Bones may appear larger, denser, and also have a deformed shape
  • Blood tests – may reveal elevated levels of the alkaline phosphatase enzyme  with normal calcium, phosphate, and aminotransferase levels in an elderly patient are suggestive of Paget’s disease
  • Bone scan – may reveal the severity of abnormalities in the bones
  • Urine tests – Urinary Hydroxyproline is found to be elevated

Treatment and Management of Paget’s Disease

There is no cure for Paget’s disease and no way to reverse its effects on bone.

Aims;

  • To relieve bone pain and prevent the progression of the disease
  • Treatment focuses on the relief of symptoms
  • Prevention of future complications

Non-pharmacological Therapy. Physical therapy for the improvement of muscle strength and pain relief in some types of pain.

  • While there are no known ways to prevent Paget’s disease from occurring, eating a healthy diet with sufficient calcium and vitamin D, and getting regular exercise, are important components in maintaining skeletal health and joint mobility. 

Pharmacological Treatment. The medications used in the management of Paget’s disease include:

    • Biphosphonates (check more on osteoporosis)– suppress or reduce the resorption of bone by osteoclasts. Currently, there are 6 approved bisphosphonates for the treatment of Paget’s disease. Prior to the start of the therapy, patients undergo a regimen of calcium and vitamin D every day for two weeks. This is for the reduction of risk of low blood calcium after infusions. This drug is not indicated for those with low blood calcium or those with vitamin D deficiency and those with compromised renal function. Calcium supplements need to be taken with bisphosphonates to reduce the risk of hypocalcemia.
    • Calcitonins. They  decrease symptoms of bone pain, reduce inflammation over bones, improve neurological complications, and promote healing of lytic lesions. Calcitonins are used mostly by patients who cannot tolerate bisphosphonates.
  • Pain Management. Pain due to Paget’s disease may be the result of bone deformity, arthritic, or neurological complications. Acetaminophen, NSAIDs, are used for the management of pain associated with Paget’s disease.
  • Surgery. Surgical procedures used to treat fractures, malalignment, or arthritis in patients with Paget’s disease.
    • Internal fixation. This is used to treat fractures in the bone affected by the disease. In internal fixation, bone fragments are first repositioned into their normal alignment, then immobilized through the use of screws, wires, pins, or metal plates attached to the outside of the bone.
    • Osteotomy. This can help relieve pain and restore alignment to weight-bearing joints especially the hip and knee. The procedure involves the removal of a wedge of bone near the damaged joint in order to shift weight to a healthier, more stable part of the joint.
    • Total joint replacement. In this procedure, parts of a damaged or arthritic joint are removed and replaced with a metal, ceramic, or plastic device called a prosthesis. The prosthesis is designed to replicate the movement of a healthy joint.

Nursing Diagnosis

  1. : Acute pain related to joint inflammation secondary to Paget’s disease, as evidenced by pain score of 10 out of 10, guarding sign on the affected fingers, restlessness, and irritability
  2.  Activity intolerance related to joint inflammation and pain secondary to Paget’s disease, as evidenced by pain score of 8 to 10 out of 10, fatigue, disinterest in ADLs due to pain, verbalization of tiredness and generalized weakness.
  3.  Deficient Knowledge related new diagnosis of Paget’s disease, as evidenced by patient’s verbalization of “I want to know more how to manage my illness.”

Nursing Interventions.

  1. 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.
  2. 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. Alternate periods of physical activity with 60-90 minutes of undisturbed rest.
  3. Administer analgesics as prescribed  prior to exercise/ physical activity. Teach deep breathing exercises and relaxation techniques. Provide adequate ventilation in the room.
  4. Refer the patient to physiotherapy / occupational therapy team as required. This is to provide a more specialized care for the patient in terms of helping him/ her build confidence in increasing daily physical activity.
  5. Assess the patient’s readiness to learn, misconceptions, and blocks to learning (e.g., denial of diagnosis or poor lifestyle habits).
  6. Inform the patient the details about the prescribed medications (e.g., drug class, use, benefits, side effects, and risks) to treat acute pain. Ask the patient to repeat or demonstrate the self-administration details to you.
  7. If the patient is for surgery, explain the surgical procedure related to Paget’s to the patient and caregiver. The doctor may recommend surgery to resolve unbearable joint pain due to Paget’s disease.

Paget’s disease Read More »

Osteoporosis

Osteoporosis

Osteoporosis

Osteoporosis a musculoskeletal disorder which bones deteriorate or become brittle and fragile due to low bone mass as a result of bone
tissue loss.

 Osteoporosis occurs as a result of an imbalance between bone resorption and bone formation. Major contributing factors in the development of osteoporosis include estrogen deficiency and aging.

Classification of Osteoporosis

On the basis of etiology, osteoporosis can be classified into:

Primary Osteoporosis

Primary osteoporosis develops as a result of aging or menopause-related bone demineralization. In patients with primary osteoporosis, the bone density decreases as the age progresses. It is not merely a consequence of aging but of failure to develop optimal peak bone mass during childhood, adolescence, and young adulthood.

Secondary Osteoporosis

Secondary osteoporosis results from more severe loss of bone mass due to pathologies associated with immobilization, medications (iatrogenic), endocrine dysfunction, cancer, and chronic kidney disease.

Causes of Osteoporosis

Osteoporosis may be caused by conditions that can lead to the disturbed balance between bone formation and bone resorption.

Common causes of osteoporosis include

  •  Aging: Osteoporosis occurs at an older age, as it is believed that testosterone and estrogen are important in achieving and maintaining bone mass, so risk for osteoporosis increases with increasing age.
  • Menopause
  • Nutritional: A low calcium intake, low vitamin D intake, high phosphate intake, and inadequate calories reduce nutrients needed for bone remodeling. deficiency of calcium and vitamin D
  • Chronic renal failure
  • Immobility
  •  Hyperparathyroidism
  • Medications. Such as intake of corticosteroids, anti seizure medications, heparin, and thyroid hormone affects calcium absorption and metabolism.
  • Chronic glucocorticoid abuse.

Common risk factors

  • Age > 50
  • Menopause (lack of estrogen)
  • Family history of fracture or osteoporosis
  • History of at least two fractures
  • Alcohol consumption
  • Smoking (inhibits activity of osteoblasts)
  • Insufficient physical activity (lack of bone remodeling)
  • Glucocorticoids (steroid-induced osteoporosis)
  • Proton pump inhibitors.

Pathophysiology of Osteoporosis

Normally, The two main cells involved in bone production pathway are osteoblasts and osteoclasts.

  • Bone resorption is caused by osteoclasts, after which new bone is deposited by osteoblasts.
  • Osteoclasts determine the final outcome of bone resorption.
  • Normal balance between osteoblast and osteoclast activities within a bone is influenced by macrophages and innate adaptive immunity. This leads to the formation of a normal bone.

In Osteoporosis,  there is a disturbance of this balance leading to increased osteoclastic activity relative to osteoblastic activity, the result is resorption, and eventual bone mass loss.

  • Reduced total bone mass. Normal homeostatic bone turnover is altered; the rate of bone resorption that is maintained by osteoclasts is greater than the rate of bone formation that is maintained by osteoblasts, resulting in a reduced total bone mass.
  • Progression. The bones become porous, brittle, fragile; they fracture easily under stresses that would not break normal bone.
  •  The consequence of these changes is net loss of bone mass over time.

Role of Hormones

  • In addition to estrogen, calcium plays a significant role in bone turnover.
  • Deficiency of calcium and vitamin D leads to impaired bone deposition.
  • The parathyroid glands react to low calcium levels by secreting parathyroid hormone (parathormone, PTH) increasing bone resorption in a bid to ensure adequate calcium levels in the blood.
  • The role of calcitonin, a hormone produced by the thyroid that increases bone deposition, is less clear and probably less significant

Clinical Features of Osteoporosis

  • Fractures. The first clinical manifestation of osteoporosis may be fractures, which occur most commonly as compression fractures.
  • Kyphosis. The gradual collapse of a vertebra is asymptomatic, and is called progressive kyphosis or “dowager’s hump” associated with loss of height.
  • Decreased calcitonin. Calcitonin, which inhibits bone resorption and promotes bone formation, is decreased.
  • Decreased estrogen. Estrogen, which inhibits bone breakdown, decreases with aging.
  • Increased parathyroid hormone. Parathyroid hormone increases with aging, increasing bone turnover and resorption.

Diagnosis / Investigations

The most common test for measuring bone mineral density is;

  • Dual-energy X-ray Absorptiometry (DXA). It is a quick, painless, and noninvasive test. DXA uses low levels of x-rays as it passes a scanner over your body while you lie on a cushioned table. The test measures the BMD(bone mineral density) of your skeleton and at various sites that are prone to fracture, such as the hip and spine. Bone density measurement by DXA at the hip and spine is generally considered the most reliable way to diagnose osteoporosis.

Management of Osteoporosis

Aims

  •  To prevent further bone loss
  • To reduce your risk of bone fractures.
  •  For reduction in fracture risk with an increase in bone mass density.

Medical Management;

  1. Exercise: Exercise promotes the mineralization of bone and bone deposition particularly during growth. High impact exercise, in particular, has been shown to prevent the development of osteoporosis. However, it isn’t recommended in cases of poor nutrition, such as anorexia nervosa and celiac disease.
  2. Physical activity; Multiple studies have shown that aerobics, weight lifting, and resistance exercises can all maintain or increase BMD(bone mineral density) in postmenopausal women.
  3. Nutrition: A diet high in calcium and vitamin D prevents bone loss. Patients at risk for osteoporosis, such as persons with chronic steroid use are generally treated with vitamin D and calcium supplementation.
  4. Diet: Sufficient protein intake is necessary to maintain the function of the musculoskeletal system and to decrease the complications that occur after an osteoporotic fracture. 
  5. Smoking cessation may prevent osteoporosis. The use of tobacco products is detrimental to the skeleton as well as to overall health. 
  6. Avoiding excessive alcohol intake, or drinking only in moderation.
  7. Medications: Taking the least possible doses of certain medications associated with osteoporosis (anticonvulsants or corticosteroids).

  8. Fall prevention; by mitigating risk factors for falls are shown below:

    • Lack of assistive devices in bathrooms, by assisting with hygiene or use of hip protectors.
    • Obstacles in the walking path, Appropriate correction of visual impairment may improve mobility and reduce risk of falls.
    • Slippery conditions, by using cotton rugs and ensuring there environment is dry.

Pharmacological Management;

  • Calcium supplements with vitamin D. To ensure adequate calcium intake, a calcium supplement with vitamin D may be prescribed and taken with meals or with a beverage high in vitamin C to promote absorption, but these supplements should not be taken at the same day as bisphosphonates. • Dietary calcium 1200 ( Calcium supplement≤ 500 mg, if dietary calcium not met) mg/day and Vitamin D  800–2000 IU/day.
  • Bisphosphonates. Bisphosphonates are the first line treatment for osteoporosis. These include oral preparations of;
  1. Alendronate(70mg weekly orally.) or
  2. Risedronate(35mg weekly or 150mg monthly orally), 
  3. Ibandronate(150mg monthly orally, or 3mg every 3 months through intravenous (IV) route.), or yearly intravenous infusions of
  4. Zoledronic acid ( 5mg annually through IV route.) increase bone mass and decrease bone loss by inhibiting osteoclast function.
  • Calcitonin. Calcitonin directly inhibits osteoclasts thereby reducing bone loss and increasing bone mineral density. It is used for postmenopausal women with osteoporosis. The dosing is 100units subcutaneous daily; or 200 units intranasal daily.
  • Selective estrogen receptor modulators (SERMs). SERMs such as raloxifene which is a second line treatment, reduce the risk of osteoporosis by preserving bone mineral density without estrogenic effects on the uterus. The dosing is 60mg daily orally.

  • Parathyroid hormone: Such as Teriparatide (20mcg subcutaneous daily,) and as a recombinant PTH, it stimulates osteoblasts to build bone matrix and facilitates overall calcium absorption. Abaloparatide(80mcg subcutaneous daily) can also be used.

Surgical Management;

Surgery is not the first-line treatment option, Vertebroplasty, kyphoplasty, lordoplasty, and vesselplasty are the procedures that are usually reserved for patients with either pathological or osteoporotic vertebral fractures

Causes of Systemic Lupus Erythematosus

Idiopathic, but believed to result from a combination of genetics, hormones and the environment. It appears that people with a genetic predisposition to the condition may develop it when they come in contact with potential triggers in the environment, these triggers may include;

  • sunlight
  • infections
  • medications
  • physical or emotional stress
  • female hormone may play a role in causing the condition, this explains why the condition is 8 times more common in women, especially of child-bearing age.

Pathophysiology of Systemic Lupus Erythematosus

The pathophysiology of SLE may be related to the cell death process, which is called apoptosis.

Apoptosis may not be occurring as it is supposed to be, which leads to an immune system attack, and the creation of antinuclear antibodies. These antinuclear antibodies are formed because the immune system sees the proteins found in the nucleus of the cells as nuclear antigens. Normally, when a cell gets sick or old it’s time to die will have approached, and the normal process that it follows to die and get cleared out of the body is called apoptosis, also known as Programmed Cell Death.

In patients with lupus, cells begin to die when the patient is exposed to SLE risk factors such as UV Light. These risk factors cause damage to the body cell, badly damaging the cell DNA material leading to programmed cell death ( apoptosis). After cell death, it produces tiny apoptotic bodies that expose the inside of the dead cell, especially the nucleus, its DNA, histone and proteins too the rest of the body.

So, the immune system of the patient ( susceptibility genes) have an effect on this patients immune system that they take the apoptotic bodies to be nuclear foreign bodies or nuclear antigen (since they are from the nucleus of the apoptotic cell), hence the body starts an attack and also the susceptibity genes reduce the bodies ability to clear the apoptotic particles leading to an increase of these nuclear antigens.

The body’s B-Cells start the production of Anti-bodies(Antinuclear Antibodies) against these nuclear antigens, and so the antinuclear antibodies bind to the nuclear antigens forming Antigen-Antibody Complexes.

These Complexes get access to the blood stream and stick to blood vessel walls, and all other body organs and tissues like the kidney, the skin, joints and the heart. These deposited complexes initiate a local inflammatory reaction which causes damage to the complement system, which after a cascade of activation leave cells with channels that let fluid and molecules in and out of the cell, causing the cell to burst and die. This damage should normally affect foreign or infected cell, but in SLE, it affects normal cells leading tissue damage.

This tissue damage due to immune complexes it is referred to as a TYPE 3 HYPERSENSITIVE REACTION.

If the patient develops antibodies targeting other cells like Red and White blood cells, and phospholipid molecules, which can mark them for Phagocytosis and Destruction, this, then, is a TYPE 2 HYPERSENSITIVITY REACTION.

Systemic Lupus Erythematosus signs and symptoms unmeb

Clinical Feature of Systemic Lupus Erythematosus

 Often there are periods of illnesses called flares and periods of remission where there are only a few symptoms.

Symptoms may be mild or severe, may come on slowly or develop suddenly, and may be temporary or permanent. The symptom experienced will depend on the body system affected by the disease.

The most common symptoms include;

  • fever
  • fatigue
  • shortness of breath
  • chest pain
  • dry eyes
  • a facial rash that covers the bridge of the nose and the cheeks which is called a butterfly rash
  • headaches
  • confusion and memory loss
  • fingers and toes that turn white or blue with cold exposure or during stressful periods known as Raynaud’s phenomenon
  • hair loss, Diffuse thinning or hair fragility with visible broken hairs (in the absence of other causes)
  • anemia
  • joint swelling and joint pain
  • unusual sensitivity to sunlight.

Diagnosis and Investigations

No single test can establish a diagnosis, the combination of blood and urine tests imaging tests biopsy and SLE criteria established by the American rheumatism association may help improve the accuracy of the diagnosis.

  • blood and urine tests :  may include complete blood count, urinalysis, erythrocyte sedimentation rate, antinuclear antibody or a ANA test.
  • imaging tests such as chest X-ray, echocardiogram

Systemic Lupus International Collaboration Criteria (SLICC) for the diagnosis of SLE

With the criteria set by the American Rheumatism Association a person has the disease If any four(4) out of the eleven(11) symptoms are present simultaneously or on two separate conditions.

  1.  malar rash: over the cheeks of the face
  2.  discoid skin rash or red patches on the skin that can cause scarring 
  3. photosensitivity: skin rash as a result of unusual reaction to sunlight.
  4. oral ulcers sores or ulcers of the lining of the mouth or throat 
  5. arthritis 
  6. pleuritis or inflammation of the membrane around the lungs or pericarditis inflammation of the lining tissue around the heart 
  7. kidney abnormalities more than 0.5 grams per day amounts of protein in urine or clumps cellular elements called Casts seen in urine under a microscope
  8. neurologic disorder manifested by seizures or psychosis
  9. antinuclear antibody or positive ANA antibody testing
  10. immunologic disorder or abnormal immune tests including positive anti Smith anti dsDNA or false positive serological test for syphilis
  11. blood hematologic disorder such as low red blood count or white blood count treatment

Management of Systemic Lupus Erythematosus.

Aims

  • Ensure long-term survival
  • Achieve the lowest possible disease activity
  • Prevent organ damage
  • Minimize drug toxicity
  • Improve quality of life
Nurse’s Role in the management Systemic Lupus Erythematosus

L.U.P.U.S

L stands for Labs to help diagnose and monitor flares

Antibody Labs:

  • Positive ANA (anti-nuclear antibodies)
  • Anti-dsDNA (anti-double stranded DNA anti-body)
  • Anti-Sm antibody (Anti-Smith antibody)
  • Elevated ESR (erythrocyte sedimentation rate) and CRP (c-reactive protein)
  • CBC, metabolic panel etc.

U stands for Use Medications: to decrease occurrence of flares, protect organs/tissues/joints from damage, and improve quality of live.

Steroids: Prednisone, Prednisolone etc.

  • Decreases inflammation quickly, but causes side effects
  • Used when patient is not experiencing relief from other medications (severe cases)

NSAIDs (non-steroidal anti-inflammatory drugs): Ibuprofen, Naproxen etc.

  • Decreases inflammation (helpful with fever, joint pain)

Antimalarial: Hydroxychloroquine (very common medication for patients with severe lupus)

  • Decreases antibodies attacking the body, helps control the disease long term (preventing flares)

Immunosuppressant: Azathioprine or Mycophenolate Mofetil etc.

  • Suppresses immune system (increases risk for infection and certain cancers)
  • For severe cases of lupus and sometimes you may hear them referred to as “steroid-sparing” meaning the use of them helps lower the amount of steroids the patient may have to take. 
  • Educate about preventing infection and monitoring self for infection because the medication regime for lupus (example: taking steroids as well) can prevent the signs and symptoms of infection appearing (example: fever).
  • Vaccines up-to-date but no live vaccines (shingles, MMR, intranasal flu, smallpox, rotavirus)

Biologics: Belimumab

  • Binds with a protein that supports the activity of B-cells to decrease the activity of B-cell ,result: decreases antibody attacks and decreases inflammation
    • No LIVE vaccines

P for Pregnancy (many patients are childbearing age and need education):

Women who want to become pregnant need to make sure their lupus has been in control for at least 6 months before conceiving. Pregnancy and the post-partum period can cause flares.

U for Understanding Flares

Triggers: sunlight, stress, sickness, not taking medications correctly or needing an adjustment

Prevention: “LESS” Flares

  • Lower stress (avoid overworking, emotional, illness, and use techniques to help prevent stress)
  • Exercise (helps joints and manages weight)
  • Sleep (need more than 8 hours to prevent the body from getting too exhausted)
  • Sun Protection (sunscreen and large-brimmed hats…sunlight can activate a flare)

S for Signs of a flare of lupus: educate patient to keep diary of symptoms to monitor for flares

  • Fatigue
  • Low grade fever
  • Achy joints
  • Rash
  • Edema of the legs and hands
Medical Management

The treatment choice for systemic lupus erythematosus (SLE) is varied based on the severity of the disease and symptoms:

  • Mild cases are defined as disease pattern with one or two organ involvement.
  • Moderate cases are defined as more than 2 organ involvement during disease flares with low grade of involvement and complications or one or two organ involvement with more extensive involvements.
  • Severe cases are defined as presentation of the disease with life threatening complications and multiple (more than 2) organ involvements.
  • Hydroxychloroquine: 200 to 400 mg daily as a single daily dose or in 2 divided doses. Generally, all patients with any type of SLE manifestation should be treated with hydroxychloroquine regardless of the severity of the disease.

In most cases,

  •  Hydroxychloroquine PO 200 to 400 mg daily as a single daily dose or in 2 divided doses AND methylprednisolone as intravenous  0.5 to 1 g/day for three days in acutely ill patients, or 1 to 2 mg/kg/day in more stable patients
  • Alternatively; Hydroxychloroquine PO 200 to 400 mg daily as a single daily dose or in 2 divided doses AND prednisone oral; 40-60 mg/day.

Fever management

  •  Celecoxib PO 100 to 200 mg twice daily
  • Alternatively; Acetaminophen 1000 mg every 6 hours; maximum daily dose: 3000 mg daily 

Raynaud’s phenomenon treatment

  • Calcium channel blocker (nifedipine) 10 to 30 mg 3 times daily

Chronic pain management

  • Moderate pain should be treated with mild prescription opiates such as:
    • Co-codamol (Acetaminophene+opioid): Acetaminophen (300 to 1,000 mg/dose)/codeine (15 to 60 mg/dose) every 4 hours as needed; adjust dose according to severity of pain and response of patient (maximum: acetaminophen 4,000 mg/codeine 360 mg per 24 hours)
  • Moderate to severe chronic pain should be treated with stronger opioids such as:
    • Hydrocodone: Single doses >40 mg or >60 mg with a total daily dose ≥80 mg

Cutaneous lupus erythematosus

  • High potency topical steroid twice daily for patients with CLE 
    • Hydrocortisone 1% or 2.5% for facial involvement.

Lupus nephritis treatment

  • Aggressive antihypertensive therapy with blood pressure goal of 130/85
  • In patients with proteinuria, antiproteinuric therapy with blockade of the renin-angiotensin system include ACEIs and ARBs:
    • ACE inhibitors; captopril PO 25 mg 3 times daily
    • ARBs; losartan PO initial: 50 mg once daily; can be increased to 100 mg once daily based on blood pressure response.

Other considerations.

    • Vitamin D and calcium supplements for preventing osteoporosis in patients using corticosteroids
    • Antihypertensive drugs and statins are also recommended in patients using corticosteroids
Nursing Interventions and Rationales

1. Encourage adequate nutrition and hydration to promote healthy skin and healing in the presence of wounds.

2. Instruct the client to clean, dry, and moisturize intact skin; use warm (not hot) water, especially over bony prominences; use unscented lotion. Use mild shampoo. Scented lotions may contain alcohol, which dries the skin. Prescribed solutions reduce dryness of the scalp and maintain skin integrity.

3. Instruct the client to avoid contact with harsh chemicals and to wear appropriate protective gloves, as needed. Avoid hair dye, permanent solution, and curl relaxers. Chemicals aggravate this condition.

4. Recommended prophylactic pressure-relieving devices (e.g., special mattress, elbow pads). Such devices aid in the prevention of skin breakdown.

For skin rash:

  • Wear protective eyewear.
  • Wear a wide-brimmed hat and carry an umbrella.
  • Avoid ultraviolet rays.

The sun can exacerbate a skin rash or precipitate a disease flare. Special lotions, glasses, and other items may be required to protect the skin from sunlight exposure.

5. Inform the client of the availability of special makeup to cover rashes, especially facial rashes.
These preparations are specially formulated to completely cover rashes, birthmarks, and darkly pigmented areas. This will help the client who is having problems adjusting to body image changes.

6. Introduce or reinforce information about the use of hydroxychloroquine.
This antimalarial drug is a slow-acting medicine used to relieve or reduce inflammation and rash. It may take 8 to 12 weeks to effect. A potential side effect is a retinal toxicity. The client must follow up with an ophthalmologist every 6 months. Topical cortisone medication may likewise be used.

For oral ulcers:

  • Instruct the client to avoid spicy or citrusy foods.
    These foods might irritate fissures or ulcers in the mucous membranes.
  • Instruct the client to rinse the mouth with half-strength hydrogen peroxide three times per day.
    Hydrogen peroxide helps keep oral ulcers clean.
  • Instruct the client to keep ulcerated skin clean and dry. Apply dressings as needed.
    Skin is necessary to prevent infection and promote healing.
  • Instruct the client to apply topical ointments as prescribed.
    Vitamins A and E may be useful in maintaining skin health.

For hair loss:

  • Instruct the client that scalp hair loss occurs during the exacerbation of disease activity.
    Scalp hair loss may be the first sign of impending disease exacerbation. Scalp hair loss may not be permanent. As disease activity subsides, scalp hair begins to regrow.
  • Instruct the client that scalp hair loss may be caused by high-dose corticosteroids (prednisone) and immunosuppressant drugs.
    Hair will regrow as the dose decreases.
  • Encourage the client to investigate ways (e.g., scarves, hats, wigs) to conceal hair loss.
    Hair loss may interfere with lifestyle and self-image.
Complications.
  • Skin scarring
  • Joint deformities
  • Kidney failure
  • Stroke
  • Heart attack
  • Pregnancy complications
  • Hip destruction (also called avascular necrosis)
  • Cataracts
  • Bone fractures

Systemic Lupus Erythematosus (SLE) Read More »

Ankylosing Spondylitis

Ankylosing Spondylitis

Ankylosing Spondylitis

Ankylosing spondylitis (AS) is a medical condition that involves the inflammation (spondylitis) and fusion/stiffening (ankylosis) of the vertebrae or small bones in the spine.

Ankylosing spondylitis (AS) is a chronic inflammatory condition mainly affecting the spine that causes progressive stiffness and pain.

Also known as Bechterew disease, ankylosing spondylitis is described as a rare type of arthritis. The disease is found to be more common in men than in women, and is usually found in adult patients more than younger people.

Causes and Risk Factors of Ankylosing Spondylitis

Ankylosing spondylitis has no known etiology, but some experts believe that the gene HLA-B27 increases the risk for developing this disease. 

  • Heredity: People who are positive for HLA-B27 gene are more prone to develop ankylosing spondylitis.
  • Sex: When compared to women, men are more likely to develop ankylosing spondylitis.
  • Age: Most commonly seen in adolescence.
  • Race: Ankylosing spondylitis is more common in Native American tribes.

Pathophysiology

Ankylosing spondylitis (AS) is a potentially disabling form of seronegative spondyloarthritis. The main symptom of AS is inflammatory spinal pain; with time, some patients develop ankylosis and spinal immobility. The pathology mainly affects the entheses, where ligaments, tendons and capsules are attached to the bone.

Three processes are observed at the entheses: inflammation, bone erosion and syndesmophyte (spur) formation. Tumor necrosis factor is an important mediator of the inflammatory processes, but this proinflammatory cytokine is not closely involved in bone erosion or syndesmophyte formation. The major causative factors of AS are genetic, with the gene encoding HLA-B27 being the most important genetic factor. 

Several other susceptibility genes have also been identified. 

Signs and Symptoms

  • Lower back and/or hip pain – early sign of ankylosing spondylitis; usually worse in the morning and when the person is inactive (e.g. after watching TV, sitting, or taking a nap); may be accompanied with stiffness
  • Inflammation in other body parts – over time, the disease may aso affect other areas of the body such as shoulder joints, ribs, breastbone, back of the heel, and the eyes
  • Hunched-forward posture, Stooped posture in response to back pain (bending forward tends to relieve the pain)
  • Difficulty of breathing
  • Swelling of joints
  • Tiredness or fatigue
  • Straight and stiff spine
  • Inability to take a deep breath, if the joints between the ribs and spine are affected
  • Appetite loss
  • Weight loss
  • Fatigue
  • Fever
  • Anemia
  • Joint pain
  • Mild eye inflammation
  • Organ damage, such as to the heart, lungs, and eyes
  • Skin rashes

Diagnosis / Investigations.

  • Physical exam – involves checking for the spine’s range of motion by asking the patient to bend in various directions as well as palpation of the spinal and pelvic areas
  • X-ray. This test uses a small amount of radiation to create images of internal tissues, bones, and organs onto film.
  • MRI may show more detailed pictures of the soft tissues and bones; AS might not be detected easily during its early stages despite performing imaging tests
  • Erythrocyte sedimentation rate (ESR ). This test looks at how quickly red blood cells fall to the bottom of a test tube. When swelling and inflammation are present, the blood’s proteins clump together and become heavier than normal. They fall and settle faster at the bottom of the test tube. The faster the blood cells fall, the more severe the inflammation. Up to 7 in 10 people with AS have a high ESR.
  • Genetic testing. Genetic testing is done to find if a person carries a copy of an altered gene for a disease. The gene HLA-B27 is found in more than 19 in 20 people with AS.

Management.

Aims

  • There is no cure for AS yet and the goals of treatment for this disease is the relief of stiffness and pain,
  • delaying of its progression, and
  • prevention of complications.

Nursing management;

  • Physical Therapy. Staying active is the number one management for ankylosing spondylitis. Sitting, lying, and staying in one position for long periods of time increase the pain and stiffness of joints. An AS patient will benefit from an urgent referral to a physical therapist (PT) who will create an exercise and activity plan for him or her. Stretching and range-of-motion (ROM) exercises, as well as proper posture, walking, and sleeping positions will be discussed by the PT to the patient.
  •  Use warm compress to increase blood circulation to the affected part and relieve pain.
  •  Proper positioning of the patient while sleeping and walking.
  •  Exercise.
  •  Stretching.
  • Massaging the affected part.
  • Diet; patient should take balanced diet and food rich in calcium.
  • Send patient to a physiotherapist who will design suitable exercises.

Pharmacological management;

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) – commonly utilized to relieve pain, inflammation, and stiffness of joints.
  • Give prescribed analgesics like paracetamol and ibuprofen for pain.
  •  Biological medication like tumor necrosis factor.
  • Steroids – to slow down the damage of the joints, reducing inflammation and pain; they can be in oral form or injectables directly to the inflamed joint, like dexamethasone. 
  •  An interleukin 17 inhibitor (which targets the protein cells that cause inflammation in the body) helps to reduce pain, tenderness, and swelling of the joints. This is administered by IV or injecting under the skin. E.g. adalimumad (humira) and certolizumab-pegel (cimzia).
  • Tumor necrosis factor (TNF) blockers – alternative to NSAIDs if the latter are not effective; usually administered via subcutaneous injection or intravenous infusion; involves the use of monoclonal antibodies (MABs)

Surgical treatment.

  • Most people with this condition don’t require surgery but though the doctor may suggest surgery if there’s severe pain/ joint damage where there’s need for replacement.
  • Home remedy.
  •  Stay active. Exercise can help to ease pain, increase flexibility and
    improve posture.
  •  Apply hot or cold compress.
  •  Avoid smoking to prevent other related problems coming in e.g. further hampering breathing.
  •  Practice good posture while moving, standing or sitting.

Complications.

  •  Ineffective breathing.
  •  Uveitis (inflammation of the eye).one of the most complication resulting into blurred vision and photo phobia.
  •  Compressed fractures in early stages.
  •  Weakening in the vertebra.
  •  Heart problems majorly on the aorta.( if its inflamed the valves are involved too hence affecting the function).
Nursing Diagnosis
  1. Acute pain related to vertebral and joint inflammation secondary to ankylosing spondylitis, as evidenced by pain score of 10 out of 10, guarding sign on the affected area (commonly lower back, hip, shoulders), joint swelling, hunched-forward posture, restlessness, and irritability
  2.  Activity intolerance related to vertebral and joint inflammation and pain secondary to ankylosing spondylitis, as evidenced by pain score of 8 to 10 out of 10, fatigue, disinterest in ADLs due to pain, verbalization of tiredness and generalized weakness.
  3. Impaired Physical Mobility related to vertebral and joint inflammation as evidenced by severe pain rated 10/10, failure to perform ADLs, and verbalization of fatigue.

Ankylosing Spondylitis Read More »

Bursitis

Bursitis

Bursitis

Bursitis is inflammation of a bursa, a small fluid-filled sac that acts as a cushion between bone and muscle, skin or tendon.

Bursitis can also be defined as a painful medical condition characterized by inflammation of the bursae found in large joints.

Bursae are fluid-filled sacs that act as a cushion between bones, tendons, joints, and muscles. When these sacs become inflamed it is called bursitis.

There are over 150 bursae in the human body. They cushion and lubricate points between the bones, tendons, and muscles near the joints. 

The bursae are lined with synovial cells. Synovial cells produce a lubricant that reduces friction between tissues. This cushioning and lubrication allows our joints to move easily. 

Causes of Bursitis

Bursitis often results from sport injuries or repetitive movements. But it can also be caused by:

  • Autoimmune disorders 
  • Crystal deposition (gout and pseudo gout) 
  • Infectious diseases 
  • Traumatic events 
  • Hemorrhagic disorders 
  • Being secondary to overuse. Overuse and repetitive injuries to the joint, abnormal bony structure can cause bursitis.
  • Stress on soft tissues from an abnormal or poorly positioned joint or bone
  • Some types of arthritis and related conditions (rheumatoid arthritis, osteoarthritis or gout.)
  • Metabolic conditions such as diabetes.
  • Septic bursitis can be caused by bacterial infection of the bursa through skin injury following repetitive trauma.

Pathophysiology of Bursitis 

Repetitive injury within the bursa results in local vasodilatation and increased vascular permeability, which stimulate the inflammatory cascade. One study suggests that this process may be mediated by cytokines, metalloproteases, and cyclooxygenases. 

Trauma or infection leads to inflammation of the bursa which causes synovial cells to multiply and thereby increases collagen formation and fluid production. A more permeable capillary membrane allows entrance of high protein fluid. The bursal lining may be replaced by granulation tissue followed by fibrous tissue. The bursa becomes filled with fluid, which is often rich in fibrin, and the fluid can become hemorrhagic.

Types of Bursitis, with Signs and Symptoms

(a) According to duration.

  1. Acute Bursitis: (0months to 3months) During the acute phase of bursitis, local inflammation occurs and the synovial fluid is thickened, and movement becomes painful as a result.
  2. Chronic Bursitis:  (3months and above): leads to continual pain and can cause weakening of overlying ligaments and tendons and, ultimately, rupture of the tendons. Because of the possible adverse effects of chronic bursitis on overlying structures, bursitis and tendinitis may occur together.

(b) According to presence of infection.

  1. Septic Bursitis: Septic (or infectious) bursitis occurs when infection from either direct inoculation (usually superficial bursa) or hematogenous or direct spread from other sites (deep bursa involvement) causes inflammatory bursitis. Septic bursitis can be acute, subacute, or recurrent/chronic. Fluid may present with , White blood cell count (WBC) greater than 100,000/µL with a predominance of neutrophils, High protein and lactate, Positive culture and Gram stain.
  2. Aseptic Bursitis. A non-infectious condition caused by inflammation resulting from local soft-tissue trauma or strain injury. Fluid may present with White blood cell count (WBC) range from 2000 to 100,000/µl, Negative culture and Gram stain.

(c) According to Anatomy/Affected body part.

1. Subacromial bursitis.

Subacromial bursitis is a common etiology of shoulder pain. It results from inflammation of the bursa, a sac of tissue present under the acromion process of the shoulder. It is usually brought about by repetitive overhead activities or trauma.

Subacromial bursitis

  • Mid-shoulder pain early in the course of bursitis, which gradually increases over time; eventually pain may be felt even at rest
  • Pain after repetitive activity such as painting, throwing a ball, or playing tennis
  • Pain worsens at night
  • Popping sensation with shoulder movements.
2. Olecranon bursitis

The olecranon bursa is synovial membrane located immediately posterior to the olecranon bone of the elbow. The bursa’s function is to allow the bony olecranon to glide smoothly across the overlying tissues with flexion and extension of the elbow.

Olecranon bursitis

  • Painful or painless focal swelling at the posterior elbow
3. Trochanteric bursitis

 Trochanteric bursitis is inflammation (swelling) of the bursa at the outside (lateral) point of the hip known as the greater trochanter. When this bursa becomes irritated or inflamed, it causes pain in the hip. This is a common cause of hip pain.

Trochanteric bursitis

  • Pain in the lateral side of the hip with walking, running, or stair-climbing
  • Weakness of the lower extremities
  • Pain with active and passive motion.
4. Prepatellar bursitis

Prepatellar bursitis is an inflammation of the bursa in the front of the kneecap (patella). It occurs when the bursa becomes irritated and produces too much fluid, which causes it to swell and put pressure on the adjacent parts of the knee.

Prepatellar bursitis

  • Reduced range of motion at the knee
  • Focal swelling, pain, and redness
  • Difficulty kneeling and walking.
5. Retrocalcaneal bursitis

Retrocalcaneal bursitis (also known as ankle bursitis or Achilles tendon bursitis) is a condition in which the retrocalcaneal bursa, a small cushioning sac between the heel bone and the Achilles tendon, becomes inflamed.

Retrocalcaneal bursitis

  • Swelling at the back of heel
  • Pain at the back of the heel, especially when running uphill
  • Pain while standing on tiptoes

Diagnosis and Investigations.

  1. History and symptoms.
  2. Physical examination.
  3. Lab tests. There are no diagnostic lab findings associated with bursitis. However, patients with septic bursitis may present with elevated ESR, CRP, and white blood cells.
  4. X-ray. X ray may be used as a diagnostic measure to support a clinical diagnosis of bursitis. Joint x ray is generally reserved for patients with history of significant trauma. A plain x ray may be helpful in the diagnosis of fracture or dislocation
  5. CT Scan.  It is usually reserved for the patients who do not respond to initial treatment. On CT scan, superficial bursitis may be characterized by fluid density at the subcutaneous tissue. Additionally, a CT scan will detect any foreign bodies.
  6. Ultrasound Scan. Useful in confirming the diagnosis of bursitis. On ultrasound, bursitis may be characterized by bursal wall distention with the presence of local hypoechoic or anechoic intra-bursal material, synovial proliferation, calcifications, and rheumatoid nodules.

Management and Treatment of Bursitis

Aims

  • To reduce the inflammation and pain.
  • To identify and treat the cause.
  • To prevent complications.
Nursing Management
  1. Most patients with bursitis are treated conservatively to reduce inflammation.  
  2. Conservative treatment involves control of pain and inflammation, which may be guided by the PRICEMM acronym, as follows: 
    • P rotect – Use padding, braces, or changes in technique 
    • R est – Avoid activities that exacerbate pain 
    • I ce – Cryotherapy can relieve pain and decrease inflammation 
    • C ompression – Elastic dressings can ease pain, as in olecranon bursitis 
    • E levation – Raise the affected limb above the level of the heart 
    • M odalities – Employ electrical stimulation, ultrasonography, or phonophoresis 
    • M edications – Administer nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, or corticosteroid injections, bursal aspiration, and intra-bursal steroid injections (with or without local anesthetic agents). 
  3. Patients who have bursitis secondary to overuse should be educated about the importance of regular periods of rest and possible alternative activities to prevent recurrence. 
  4. Applying cold treatments for 20 minutes every several hours may be of value in the first 24-48 hours. Such treatments may be followed by heat treatments.  
  5. Elevation is useful, particularly in lower-limb bursitis. Consider site-specific therapy (eg, cushions for ischial bursitis, well-fitting padded shoes for calcaneal bursitis). 
  6. Patients with suspected septic bursitis should be treated with antibiotics while awaiting culture results. Superficial septic bursitis can be treated with oral outpatient therapy.  
  7. Those with systemic symptoms or who are immunocompromised may require admission for intravenous (IV) antibiotic therapy. 
  8. Surgical excision of bursae may be required for chronic or frequently recurrent bursitis however Surgery is reserved as a last resort for patients in whom conservative treatment fails.
Medical Management.

Medical management for  bursitis depends on the involved bursa.

Septic

  • Systemic antibiotics
  • Staphylococcus aureus, bursitis often resolves with antibiotics alone
  • Sporothrix schenckii bursitis often requires bursectomy
  • Most patients respond to oral antibiotics alone, although some require intravenous therapy

Antimicrobial Regimens

Standard antimicrobial regimens for septic bursitis are as follows:

1. Staphylococcus aureus, methicillin-susceptible (MSSA)

  • Oxacillin 2g IV q.i.d
  • Dicloxacillin 500 mg PO q.i.d
  • Dicloxacillin Sodium Capsules, USP

2. Staphylococcus aureus, methicillin-resistant (MRSA)

  •  Vancomycin 1g IV b.d

Aseptic

  • Usually managed with PRICEMM regimen 
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Local corticosteroid injections may be used in some patients who do not respond to initial therapy

Subacromial Bursitis

Conservative measures that are recommended among all patients who develop subacromial bursitis include:

Physical therapy (PT)

  • Scapular strengthening and postural reeducation
  • Shoulder exercise
  • Nonsteroidal anti-inflammatory medications (NSAIDs)

Prepatellar Bursitis

Conservative measures that are recommended among all patients who develop prepatellar bursitis include: 

  • Nonsteroidal anti-inflammatory medications (NSAIDs) is often used as a first choice
  • Reduce physical activity
  • PRICEMM regimen in the first 72 hours after the injury
  • Physical therapy
  • Local corticosteroid injections may be used in some patients who do not respond to initial therapy

Olecranon Bursitis

Conservative measures that are recommended among all patients who develop olecranon bursitis include:

  • PRICEMM regimen in the first 72 hours after the injury.
  • Avoidance of aggravating physical activity
  • Most patients improve significantly with these measures, so physical and occupational therapy are not usually necessary
  • Early aspiration (with or without corticosteroid injection) may be helpful among patients with bothersome fluid collections
  • Diagnostic aspiration should be performed among patients who do not respond to treatment in order to rule out possible infection

Trochanteric Bursitis

Conservative measures that are recommended among all patients who develop trochanteric bursitis include:

  • Modification of physical activity
  • Weight loss
  • Physical therapy
  • Nonsteroidal anti-inflammatory medications (NSAIDs)
  • Local glucocorticoid injections are reserved for patients with refractory symptoms

Physical therapy and NSAIDs are the most effective therapies for trochanteric bursitis. Most patients do not require any surgical intervention.

Retrocalcaneal Bursitis

Conservative measures that are recommended among all patients who develop retrocalcaneal bursitis include:

  • PRICEMM regimen in the first 72 hours after the injury.
  • Maneuvers that stretch the Achilles tendon may be helpful
  • Limitation of activity and modification of footwear to avoid posterior heel irritation
  • Nonsteroidal anti-inflammatory medications (NSAIDs) 
  • Physical therapy 

Corticosteroid injections are not recommended as they may have adverse effects on the Achilles tendon.

Surgical Management

Bursectomy

Surgical intervention is not usually recommended for the management of bursitis. Bursectomy is generally reserved for patients with chronic, recurrent, or septic bursitis.

Indications for surgical intervention (open incision/endoscopic bursectomy) in patients with bursitis include:

  • Inability to drain the infected bursa effectively with needle aspiration
  • Presence of a foreign body in superficial bursa
  • Adjacent skin or soft tissue infection requiring debridement
  • Critically ill patients who are immunocompromised
  • Chronically infected and thickened bursa
  • Severe refractory and recurrent bursitis

Prevention of Bursitis.

  • Regular exercise
  • Doing warm-ups or stretches before physical activity
  • Maintaining a healthy weight
  • Strengthening muscles around the joint
  • Taking breaks from repetitive tasks
  • Using foam for kneeling or elbow pads
  • Refraining from sitting still for long periods of time
  • Practicing good posture and positioning the body properly when going about daily activities

Complications of Bursitis.

  • Chronic pain: Untreated bursitis can lead to a permanent thickening or enlargement of the bursa, which can cause chronic inflammation and pain. 
  • Muscle atrophy: Long term reduced use of joint can lead to decreased physical activity and loss of surrounding muscle.

Bursitis Read More »

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