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Antidepressants

Antidepressants 

Antidepressants 

Antidepressants are a type of medicine used to treat clinical depression.

Antidepressants are a class of medications used to treat major
depressive disorder, anxiety disorders, chronic pain, and addiction.

They are known as mood elevators. The first antidepressant drug to be discovered was a monoamine oxidase inhibitor by Crane (1957) and Kline (1958).

Depression, or major depressive disorder, is characterized by feelings of extreme sadness and hopelessness.

A patient may experience episodes that last for several days or even weeks.

Mechanism / Mode of action

Anti depressants acts by preventing the re-uptake of amines/ neurotransmitters involved here are serotonin and nor adrenaline. There is reduced production of these neurotransmitters are prevented, there by building up their quantities to the normal body level resulting into good clinical effect. Anti-depressants commonly take 2-3weeks before their effects are realized.

They are generally indicated in the following;

Depression like:

  • Psychotic depression (major depression)
  • Agitated depression.
  • Neurotic depression.
  • Reactive depression.
  • Atypical depression.
  • Suicidal tendencies.
  • Unipolar depression.

N.B: can also be used in alcoholism.

  • Sleeping disorders i.e. specifically can be used in early morning awakening here he feels unrefreshed in mind, lack of energy, in morning, he feels weak to wake up i.e. diurnal variation.
  • Eating disorders i.e. anorexia nervosa; here they have appetite but deliberately refuses to eat bulimia nervosa- excessive eating.
  • Chronic body complaints without pathology.
  • Nocturnal enuresis: bedwetting, if this follows no pathology i.e. physical, anti-depressants can be used in small doses.
  • Panic disorder.
  • Agora phobia, social phobia, school phobia.
  • Obsessive-compulsive disorder with or without depression.
  • Migraine headache.
  • Attention deficit disorder.
Classes of antidepressants

Classes of Antidepressants

  1. Selective Serotonin Re-uptake Inhibitors.(SNRI’s)
  2. Tricyclic  Antidepressants.(TCA’s)
  3. Tetracyclic Antidepressants.(TetCA’s)
  4. Monoamine Oxidase Inhibitors.(MAOI’s)
  5. Serotonin Norepinephrine Reuptake Inhibitors.(SNRI’s)
SELECTIVE SEROTONIN RE-UPTAKE INHIBITORS (SSRI’s)

These are antidepressants which target specific neurotransmitter receptor i.e. serotonin, and works on those without causing cholinergic effects. They are much safe to be used as they cause less side effects compared to other antidepressants.

Common antidepressants could fuel the rise of superbugs, study finds - ABC News

  1. Fluoxetine (Prozac).

Dose: 20mg-60mg, o.d/ mane. (‘mane’ stands for morning)

Indications

  • Obsessive compulsive disorder.
  • Depression.
  • Premenstrual dysphoric disorder.
  • Bulimia nervosa.

Side effect

  • Nausea 
  • Weight loss
  • Agitation.
  • Dryness of the mouth
  • Constipation 
  • Insomnia
  • Headache
  • Sexual dysfunction
  • Nervousness.

Contraindications

  • Hepatic/renal disease
  • Pregnancy 
  1. Paroxetine (Paxil, Aropax)

Dosage: 20mg-60mg o.d/nocte. ( ‘nocte’ stands for night)

Indications:

  • Depression
  • Anxiety
  • OCD
  • PTSD
  • Social phobia 
  • Panic disorder.

Side effects

  • Sedation.
  • Dryness of mouth 
  • Constipation.

Contra indication:

As for fluoxetine.

  1. Sertraline (Zoloft).

Dosage: 50-200mg/day

Indications:

  • PTSD
  • OCD
  • Depression
  • Panic disorders
  • Premature ejaculation.
  • Premenstrual dysphoric disorder.

Side effects

Contra indications

  • As for fluoxetine.
TRICYCLIC ANTIDEPRESSANTS (TCA’s)

MODE OF ACTION

They are well absorbed by mouth. Act by increasing the availability of the biogenic amine neurotransmitters. Noradrenaline and 5-hydroxytryptamine (5-HT) in the synaptic cleft through blocking their re-uptake into the pre-synaptic neuron. TCAS have along half-life; they are therapeutically effective if given once a day. The onset of their antidepressant action is relatively slow and variable, 2-4 weeks elapsing before any noticeable improvement in mood occurs. 

Examples:

Amitriptyline | Elavil Prescribing Information - MedWorks Media

  1. Amitriptyline (laroxyl)

It is tricyclic with high sedating properties. It is usually started in smaller doses and keeps on increasing. It is usually given as a single dose. Dosage: 25-75mg nocte. Maximum dose up to 200mg nocte. It is a very good anti depressant in agitated depression i.e. with restlessness.

       2.   Imipramine (tofranil)

It is a tricyclic with less sedating property.  The dose is the same as that of amitriptyline. It is a very good drug for depressive patients with psychomotor retardation.

       3. Clomipramine (Anafranil)

It is mainly indicated in obsessive compulsive neurosis with an underlying depression. 

Dose: 50mg, increase gradually up to 250mg nocte.

TETRACYCLIC ANTIDEPRESSANTS.(TetCA’s)

Example: 

Maprotiline (Ludiomil) - Uses, Dose, Side effects

Maprotiline( ludiomil) 

A tetracyclic antidepressant with an advantage of working on 

  • Agitated and retarded depression. 

Dose: 50mg-75mg b.d or tds in 24hrs or day 

Side effects of tricyclics and  tetracyclics: 

  • Causes mania.
  • Mild postural hypotension (orthostatic hypotension)
  • Tarchycardia.
  • Cardiac arrhythmias 
  • May cause heart block
  • Sedation
  • Dry mouth
  • Nausea & vomiting
  • Constipation. 
  • Weight gain 
  • Bone marrow depression
  • Blurred vision
  • Urticaria (rash)
  • Sexual dysfunction
  • Anti-histamininic: sedation and weight gain
  • Anti-cholinergic: dry mouth, dry eyes, constipation
  • Anti-adrenergic: orthostatic hypotension, sedation, sexual dysfunction
MONO AMINE OXIDASE INHIBITORS (MAOI).

The earliest antidepressant, but currently rarely used due to its gross side effect, and has been replaced by tricyclic and serotonin selective re-up take inhibitors.

INDICATIONS

It is indicated in depressive- neurosis, anxiety, phobic states, depressive illness which had failed to respond to other therapies.

It works by increasing the concentration of monoamines especially the nor adrenaline and serotonin.

Nardil Tabs (Phenelzine) | InternationalPharmacy.com

  1. Phenelzine ( Nardil)

Dosage: 15mg- 30mg bid /tds –maximum dose 60mg in 24hours.

Indications:

  • Anxiety states.
  • Obsessive compulsive disorder.

Side effects:

  • Weight gain.
  • Hypotension.
  • Oedema.
  •  Nervousness

Contra –indications:

  • Diabetes
  • CVS disease.  
  • Liver disease.
  1. Iso carboxazide(Marplan)

Dosage: 20mg-60mg single or divided doses.

Indications 

As for phenelzine.

Side effects:

  • Weight loss
  • Hypotension.
  • Drowsiness
  • Sexual dysfunction.
  • Mania 
  • Jaundice
  • Nausea 

Contra indications

As for phenelzine.

  1. Tranyl (cypromine ‘’parnate’’).

Dosage: 20mg-40mg bid

Side effects: 

  • Insomnia 
  • Weight gain but less common

Contra indications

As for phenelzine.

Mono-amine oxidase inhibitors (MAOI) interact with certain foods and drugs. These drugs interact with some foods and drugs to cause the following:

Hypertensive crisis: this is usually life threatening (fatal). This is usually caused by the MAOI combining with a substance called tyramine which is usually found in certain foods e.g. cheese, yeast extracts like wine, smoked fish, beans with broad pods, avocado, left over food which is decomposing.

Drugs

  • Amphetamine.
  • Barbiturates.
  • Ephedrine
  • Phenytoin
  • Tricyclic anti- depressants 

Note: Anti-depressants be given to the patients for 6months after improvement i.e. if has been on treatment for 3months and improves, now count 6months ahead without defaulting the treatment.  

SEROTONIN NORADRENALINE REUPTAKE INHIBITORS.(SNRI’s)

These work by affecting chemical messengers(neurotransmitters) used to communicate between brain cells, hence regulating mood and relieving depression. 

Examples

  • Duloxetine
  • Venlafaxine
Duloxetine® 30 - شرکت داروسازی تسنیم

Duloxetine (  Cymbalta, Yentreve)

Duloxetine is a type of antidepressant medicine known as a serotonin-noradrenaline reuptake inhibitor tha are thought to work by increasing the amount of mood-enhancing chemicals, serotonin and noradrenaline, in your brain.

Dose: the starting dose is 60mg, taken once a day and this can be increased to 120mg, taken once a day

Indications

  • depression
  • anxiety.
  • nerve pain such as fibromyalgia,
  • used to treat stress
  • urinary incontinence in women.

Side effects

  • Difficulty sleeping
  • Headaches
  • Feeling dizzy
  • Blurred vision
  • Constipation
  • Diarrhoea
  • Feeling or being sick
  • (nausea or vomiting)
  • Dry mouth
  • Sweating
  • Tiredness
  • Less appetite than usual and weight loss
  • Feeling less interested in sex, or having problems keeping an erection or reaching orgasm

CONTRA INDICATIONS

  • A bleeding disorder.
  • Type 1 diabetes or type 2 diabetes.
  • Epilepsy – SSRIs should only be taken if your epilepsy is well controlled, and the medicine should be stopped if the epilepsy gets worse.
  • kidney disease.
  • heart problems, or a thyroid disorder.
  • Have glaucoma.
  • Have a liver disease.
  • Have a history of seizures.

Antidepressants  Read More »

Medical Instruments for nurses revision

Medical Instruments For Nurses

MEDICAL INSTRUMENTS AND OTHER EQUIPMENTS

Instrument/ Appliance

Functions

Sand bags

It prevents movement of a limb in the treatment of special conditions.

Bed block

To elevate the bed

Mouth gag

To open the mouth of unconscious patient



Air ring and its pump

To prevent friction on the bed.

Cardiac table

Used by cardiac patients to lean forward.

Bed pan

Used for toileting of bedridden patients.

Dirty linen container

For collecting dirty bed linen.

Male urinal

For male bladder elimination

Kidney dish

Used for receiving soiled dressings and other medical wastes.

Sponge holding forceps

Used to grasp and hold sponges while conducting medical and surgical procedures.

Cheatle forceps

For picking sterile instruments.

Ampoule

Stores air sensitive medications and solutions.

Vial

Stores liquid or powdered medicine intended for parenteral administration.

Episiotomy scissors

Used for episiotomy

Auriscope/ Otoscope

For examining the ear.

Ear syringe

For performing ear syringing.



Tuning fork

For examination of sense of hearing.

Specimen bottles

For collecting laboratory specimens.

Calibrated medicine cup

For giving oral medication to the patient.

Dental probe

To measure the depth of a tooth’s pocket.

Mosquito artery forceps

To clamp small blood vessels to control haemorrhage.

Curved artery forceps

Used to compress arteries.

Straight artery forceps

To clamp arteries to arrest bleeding

Long artery forceps

Used as a cord clamp

Dental spatula

Used for mixing cement powder and denture powder.

Ovum forceps

Used to remove tissue from inside the uterus.

Towel clip

To hold sterile towels close to the inscision

Uterine curette

To remove the contents of the uterus.

Cord clamp

To clamp the cord.

Patella hammer

To examine the knee reflex.

Probe

To measure the depth of the wound.

Air way piece

To rescue ventilation.

Trapeze

Helps the patient lift himself off the mattress.

Bed cradle

To lift the weight of the bed linen.

Backrest

To help the patient sit upright in bed

Screens

For providing patients privacy



Trays

To carry medical supplies

Trolley

Used for transporting medical supplies

Double Sims vaginal spectrum

Used for examining the vagina and cervix.

Cusco’s vaginal spectrum

Used to inspect the cervix

Dissecting forceps

Used for grasping and holding objects.

Sputum mug

For collecting sputum.

Colostomy bag

For collecting fecal matter from a colostomy.

Motor and pestle

To crush medicine for children.

Footrest

To prevent foot drop

Bulb syringe

For sucking excess mucus from the baby’s nostrils and the mouth.

Manual suction machine

Used for suctioning.



Vulsellum

Used for gripping the cervix during surgical procedure.

Cord scissor

For cutting baby’s cord.

Kocher forceps

Used to grasp heavy tissue or clamp large blood vessels

Protoscope

For rectal examination.

Uterine packing forceps

Used to grasp the uterus during uterine birthing.

Tenaculum forceps

For holding the cervix

Uterine sound

For measuring the depth of the uterus.

Sterile drums

To store sterile equipment.

Ophthalmoscope

For examination of the eye.

Tracheostomy tube

To provide an alternative airway for breathing after tracheostomy.

Inhaler

Used to deliver medicine to the lungs and the airway.

Crocodile forceps

To remove small objects from small cavities in the body.

Nebulizer

To turn liquid medicine into a very fine mist to be inhaled by a patient through a face mask or mouthpiece.

Tongue depressor

To prevent back flow of the tongue in unconscious patients.

Fetal scope

To listen to the baby’s heart rate.

Allis tissue forceps

To hold or grasp heavy tissues.

Auvard vaginal spectrum

Opens the walls of the vagina and examine the vagina and cervix.

Cervical dilator

To dilate the cervix.

Enema can

Used to administer enema to the patient.

Endoscope

To visualize the interior of a hollow organ of part.

Penlight

To assess the pupil diameter.

Mucus extractor

To aspirate secretions from the oropharynx of new born babies.



Laryngoscope

To examine the interior of the larynx.

Tonsil holding forceps

To hold the tonsil during tonsillectomy.

Tonsil scissors

For blunt dissection and cutting of soft tissues during ENT procedures.

Nasal dressing forceps

To perform anterior nasal packing.

Tracheal dilator

To enlarge the airway in cases of subglottic stenosis and tracheal stenosis.

Hot water bottle

To warm the patient.

Pulse oximeter

To estimate the oxygen saturation of the blood and the pulse rate.

Glucometer

To check glucose levels.

Height board

To measure patient’s height.

Urinometer

To measure the specific gravity of urine.

Medical goggles

To shield the eyes against liquid or chemical splash.

Drape

To cover any unappealing area or space.

Babcock forceps

To grasp delicate tissues during laparotomy.

Needle holder forceps

To hold the needle while applying sutures.

Dressing forceps

Used when dressing wounds.

Amnihook

To rupture the amniotic sac.

Bladder sound

To locate stones in the bladder.

Teeth extractor

To extract the teeth.

Root elevator

To elevate the root of the tooth before extraction.

Wrigley forceps

Used in deliveries in which the baby is far along in the birth canal.

Nasogastric tube

To administer food and medicine to the stomach through the nose.

Giving set

For administering intravenous fluids and medicines to the patient.

Snellen chart

To assess monocular and binocular visual acuity.

Aneurysm needle

To pass ligatures around blood vessels.



Vomit bowl

To collect patient’s vomit.

Endotracheal tube

To keep the trachea open so that air can get into the lung.

Manual vacuum aspiration (MVA) set

Medical termination of pregnancy

Four prong retractor

To pull back soft tissue during surgery

Metallic catheter

For short term urinary tract catheterization for adult patients

Foley catheter

To drain out urine from the bladder

Three way foley catheter

Used for bladder irrigation

Penile sheath

To provide relief to men with intractable urinary incontinence.

Sterilization forceps

To remove sterilized instruments from boilers and formalin cabinets

Right angle forceps

Clapping, dissection or grasping tissue

Lane’s tissue holding forceps

To hold tough tissue such as fascia and cartilage

Duval intestinal grasping forceps

Used to grip internal tissues for manipulation.

Sinus forceps

To pack sinuses, remove foreign bodies from the sinuses and insert drains into the nasal or oral cavities

Blade holder

To hold the blade in place.



Medical Instruments For Nurses Read More »

Systemic Lupus Erythematosus

Systemic Lupus Erythematosus (SLE)

Systemic Lupus Erythematosus

Systemic Lupus Erythematosus is a chronic autoimmune disease in which the immune system attacks its own tissues, causing widespread inflammation and tissue damage in the affected organs.

 It can affect the joints, skin, brain, lungs, kidneys, and blood vessels.

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 »

Gout

Gout

Gout

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

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

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

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

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

Cause

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

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

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

Risk Factors

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

Signs & Symptoms of Gout

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

Other signs and symptoms include,

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

Stages/ Phases of Gout

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

ASYMPTOMATIC HYPERURICEMIA

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

ACUTE GOUTY ARTHRITIS

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

INTERCRITICAL GOUT

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

RECURRENT GOUTY ARTHRITIS (Chronic or Tophaceous Gout)

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

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

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

gout pathophysiology

Pathophysiology of Gout.

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

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

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

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

Diagnostic Tests / Investigations

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

Management of Gout

Aims

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

Medical Management.

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

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

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

Combination Therapy

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

Lowering uric acid in the body

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

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

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

 

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

Assessment: Acute Pain

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

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

Expected Outcome:

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

Interventions:

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

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

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

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

Assessment: Impaired Physical Mobility

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

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

Expected outcomes:

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

Interventions:

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

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

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

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

Gout Read More »

Osteoarthritis

Osteoarthritis

Osteoarthritis

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

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

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

osteoarthritis

Types of Osteoarthritis

  • Primary Osteoarthritis

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

  • Secondary Osteoarthritis

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

Kellgren-Lawrence Classification of Osteoarthritis

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

Osteoarthritis is deemed present at grade 2 although of minimal severity

Pathophysiology of Osteoarthritis

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

Cause

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

Predisposing Factors

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

Signs and Symptoms

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

Investigations and Diagnosis

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

Management of Osteoarthritis

Aims 

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

Management according to classification/ severity.

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

Treatment 

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

Grade 2-mild

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

Treatment

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

Grade 3- moderate

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

Treatment

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

Supportive treatment

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

Grade 4-  Severe

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

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

Treatment.

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

Prevention

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

Complications

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

Osteoarthritis Read More »

Rheumatoid Arthritis

Arthritis

Arthritis

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

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

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

Types of arthritis

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

Etiology of arthritis

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

Predisposing factor

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

Rheumatoid Arthritis

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

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

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

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

Pathophysiology of rheumatoid arthritis

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

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

Summary of pathophysiology.

The pathophysiology of rheumatoid arthritis is brief and concise.

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

Signs and symptoms of rheumatoid arthritis

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

Other signs and symptoms include;

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

Assessment and Diagnostic Findings

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

Management of rheumatoid arthritis

Aims

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

There is no specific cure for Rheumatoid arthritis

Nursing care

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

MEDICAL MANAGEMENT

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

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

Surgical Management.

SURGERY

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

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

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

Conservative measures

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

Nursing Diagnosis

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

Arthritis Read More »

Tendonitis

Tendonitis

Tendonitis or Tendinitis

Tendonitis is the inflammation or irritation of a tendon. 

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

tendon anatomy tendonitis

Anatomy Review

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

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

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

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

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

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

Common Types of Tendonitis 

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

Causes of Tendonitis 

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

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

Risk factors  

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

Pathophysiology 

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

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

Signs and symptoms 

★ Redness and Hotness at the site. 

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

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

★ Mild swelling

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

★ Tightness that makes it difficult to move the area 

Diagnostic management 

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

Pharmacological / Medical Management 

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

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

Nursing interventions (specific) 

★ Enough rest from activities 

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

★ Wrapping the area in a compression bandage until  swelling subsides 

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

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

★ Resting or elevating the tendon 

★ supports such as splints, braces, or a cane 

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

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

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

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

Complications 

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

Tendonitis Read More »

Osteogenesis Imperfecta

Osteogenesis Imperfecta

Osteogenesis Imperfecta

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

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

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

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

Osteogenesis Imperfecta bone 2

Aetiology 

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

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

❑ Certain gene changes or mutations cause the collagen defects 

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

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

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

Epidemiology 

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

Pathophysiology 

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

Clinical Manifestations

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

Classification of OI

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

❖ Osteogenesis imperfecta Type I (mild) 

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

❖ Osteogenesis imperfecta Type II (Perinatal Lethal)

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

❖ Osteogenesis imperfecta Type III (Progressive Deforming) 

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

❖ Osteogenesis imperfecta Type IV (moderately severe) 

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

Classification of OI

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

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

Assessment and Diagnostic Findings

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

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

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

Treatment and Management

There is no cure for OI 

Aims of management  

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

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

Medications: 

▪ Bisphosphonate therapy 

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

▪ Intravenous pamidronate 

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

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

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

– NOTE : Pre-treatment evaluation and monitoring  

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

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

Surgical intervention 

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

Physical and occupational therapy 

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

Experimental therapies 

  • Growth hormone

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

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

  • Cell replacement therapies

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

Complications.

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

Nursing Care

Nursing Diagnosis 

Desired Outcomes 

Intervention 

Rationale

Deficient  

Knowledge related  new diagnosis of  

osteogenesis  

imperfecta, as  

evidenced by  

patient’s  

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

At the end of the  health teaching  

session, the patient  will be able to  

demonstrate  

sufficient knowledge  of his/her condition and its  

management.

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

diagnosis or poor  lifestyle habits)

To address the  

patient’s cognition  and mental status  towards disease  

management and to  help the patient  

overcome blocks to  learning

Activity  

intolerance related  to bone pain, as  

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

disinterest in ADLs  due to pain,  

verbalization of  

tiredness and  

generalized  

weakness

The patient will  

demonstration  

active participation  in necessary and  

desired activities and  demonstrate  

increase in activity  levels

Assess the patient’s  activities of daily  

living, as well as  

actual and perceived  limitations to  

physical activity. Ask  for any form of  

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

Encourage  

progressive activity  through self-care  and exercise as  

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

Administer  

analgesics as  

prescribed prior to  exercise/ physical  activity.  

Teach deep  

breathing exercises  and relaxation  

techniques. 

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

fatigue and activity  intolerance. 

To gradually  

increase the  

patient’s tolerance  to physical activity. 

To provide pain  

relief before an  

exercise session.  

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

effective stress  

management. 

  

Provide adequate  ventilation in the  

room.

To allow enough  

oxygenation in the  room.

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

guarding sign on the  affected areas  

especially long  

bones, facial  

grimace, crying, and  restlessness

The patient will  

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

signs, and absence  of restlessness.

Administer  

prescribed pain  

medications. 

Assess the patient’s  vital signs and  

characteristics of  

pain at least 30  

minutes after  

administration of  medication. 

Place the patient in  complete bed rest  during severe  

episodes of pain.

To alleviate  

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

To monitor  

effectiveness of  

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

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

administered. 

To enable to patient  to rest and to  

provide comfort.

Risk for injury  

related to fragile  

bones

The patient will be  able to prevent  

injury by means of  exercising falls  

prevention protocols  and maintaining  

his/her treatment  regimen in order to  regain normal  

balance and healing.

Complete a falls risk  assessment, which  includes: 

Factors contributing  to falls risk 

Functional ability 

Use of mobility  

devices 

Use of bedrails 

Put the bed at the  lowest level. 

Place items within  the patient’s reach.

The use of a  

standard tool will  help identify the  

status of the  

patient’s risk for  

falling and will help  determine the  

factors contributing  to the falls risk. 

Low set beds reduce  the possibility of  

injuries related to  falls. 

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

  

Refer to  

physiotherapy and  occupational  

therapy.

Patients with  

fracture may need  therapies to help  them regain  

independence and  lower their risk for  injury.

Impaired Physical  Mobility related to  vertebral and joint  inflammation as  

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

fatigue

Patient will maintain  or regain functional  mobility.

Perform a mobility  assessment. Assess  the patient’s  

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

bathing, oral and  perineal care. 

Refer the patient to  the physiotherapist.

To identify patient’s  current strengths  and problems  

related to  

performing ADLs 

To provide  

specialized care and  individualized  

exercise program.

Practice Test: Osteogenesis Imperfecta

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

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

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

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

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

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

2. Answer: A.  Likes to play football.

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

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

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

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

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

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

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

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

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

4. Answer: A. Osteogenesis imperfecta.

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

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

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

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

5. Answer: D. Pamidronate.

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

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

Osteogenesis Imperfecta Read More »

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