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Erectile dysfunction medications

Erectile Dysfunction Medications

Erectile Dysfunction

Erectile dysfunction, ED is the inability of the male to attain and maintain an erection sufficient to permit satisfactory sexual intercourse.

Penile erectile dysfunction is a condition in which the corpus cavernosum does not fill with blood to allow for penile erection. This can result from the aging process and in vascular and neurological conditions.

So, what is impotence?

Impotence, a term often used synonymously with ED, many involve a total inability to achieve erection, an inconsistent ability to achieve or ability to sustain only brief erections.

Physiology of an Erection

This begins with stimulus such as sight and touch. This stimulates the parasympathetic nervous division that transmits nerve impulses to the erectile tissue of the penis (corpus carvernosum). The nerve endings release nitric oxide(NO) which binds on muscle cells in the penis leading to generation of cyclic GMP (Cyclic Guanosine monophosphate) which relaxes the muscle cells in the corpus cavernosum leading to creation of larger intracellular spaces and sinusoids. More blood flows into the erectile tissues, the tissue expands compresses the veins leaving the penis, thus increased blood volume in the organ and one erects.

      Erection is continuously maintained during sexual intercourse by the release of NO, and prostaglandin E1 (PGE1).

Termination of erection( Detumescence ) is brought about by 2 events i.e.

  • Activity of enzyme phosphodiesterase type 5 enzyme (PDE-5) which catalyzes the breakdown of GMP into inactive form.
  • Stimulation of sympathetic nervous division to bring about the contraction of the penile muscles terminating ejaculation.

 

Pharmacology application of the above;

  • Erection relies on the penile blood flow thus an event that interferes with penile blood flow results into penile dysfunction.
  • Any factor which interferes with neuro-transmitters such as acetylcholine may end with Erectile Dysfunction.
  • Psychological factors e.g. stress may as well interfere initiation of erection.

Classification of Erectile Dysfunction.

Primary Erectile Dysfunction; is where a man has never  been able to attain and maintain an erection for sexual intercourse

Secondary Erectile Dysfunction: is where impotence occurs in a man who has past history of satisfactory sexual performance.

Causes of Erectile Dysfunction

  • Erectile Dysfunction mainly occurs past middle age and is common after the age of 65 years.

A variety of vascular, Neurological, hormonal or endocrinal, pharmacological or psychological and genetic causes may underly the disorder, i.e.

  • Vascular diseases: Blood supply to the penis can become blocked or narrowed as a result of vascular disease such as atherosclerosis (hardening of the arteries).
  • Neurological disorders (such as multiple sclerosis): Nerves that send impulses to the penis can become damaged from stroke, diabetes, or other causes.
  • Psychological states: These include stress, depression, lack of stimulus from the brain and performance anxiety.
  • Trauma: An injury could contribute to symptoms of Erectile Dysfunction.
  • Cancer treatments;  near the pelvis can affect the penis’ functionality.
    Surgery and or radiation for cancers in the lower abdomen or pelvis can cause Erectile dysfunction. Treating prostate, colon-rectal or bladder cancer often leaves men with Erectile dysfunction.
  • Drugs;  used to treat other health problems can negatively impact erections such as Cimetidine (Tagamet), Ranitidine (Zantac)

Classification of Drugs used to treat Erectile Dysfunction.

There are divided into 4 groups;

  • Central inhibitors
  • Peripheral inhibitors
  • Central conditioners
  • Peripheral conditioners

PDE 5 Inhibitors/Peripheral Inhibitors.

These are agents which act in the penile tissue to maintain the environment of erection. They include phosphodiesterase-5 inhibitors e.g. sildenafil, tadalafil, and vardenafil are selective PDE-5 inhibitors developed drugs in the past decade and found effective in a majority of patients with Erectile Dysfunction.

SILDENAFIL:

 It is an orally active drug

Classification:

Therapeutic– ED agent, vasodilator

Pharmacological– phosphodiesterase type 5 inhibitor

Brand names:
  • Kamagra
  • Penegra
  • viagra
  • Caverta
  • Edegra 25, 50, 100mg tablets
Indications:         
  • Erectile Dysfunction
  • Pulmonary Hypertension.
Mechanism of action;

 Sildenafil acts by selectively inhibiting an enzyme phosphodiesterase-5 and enhancing nitric oxide action in corpus cavernosum thus preventing the breakdown of GMP produces smooth muscle relaxation of the corpus cavernosum which in turn promotes increased blood flow and subsequent erection hence sex intercourse and exercise tolerance is improved but it has no effect on penile (swelling) tumescence in the absence of sexual activity. It doesn’t cause priapism in most patient.

 Dosage:

  It is recommended in the dose of

  • 50mg for men less than 65 years,
  • elderly 25mg if not effective then 100mg 1 hour by intercourse.

Duration and degree of penile erection is increased in 74-82% of men with Erectile Dysfunction including diabetic Neuropathy cases.

However, Sildenafil is effective in men who have lost libido or when ED is due to spinal cord injury or damaged Nervic eregantis since Nitric Oxide is an important regulator of pulmonary vascular resistance, PDE-5 inhibitor lower pulmonary circulation than vardenafil and is only PDE-5 inhibitor shown to improve arterial   oxygenation in pulmonary Hypertension. It has now become the drug of choice for this condition

N.B.; it should be given once a day.  

Adverse effects/ side effects:

These are mainly due to preservation of nitric oxide which causes vasodilatation in the brain.

  • Dizziness and headache
  • Nasal congestion
  • Hypotension and palpitation
  • Loose emotion
  • A feeling of dependency/ addiction
  • Flushing
  • Tachycardia
  • Muscle pain
  • Diarrhoea
  • Sildenafil in addiction, weakly inhibits the isoenzyme PDE-5 which is involved in photoreceptor transduction in the retina. As such impairment of colour vision especially, blue-green discrimination occurs in some recipients.
  • Hormones and related drug neuropathy among users of PDE-5 inhibitors have be reported.
Contraindications:
  • In patients with coronary heart diseases.
  • Those taking nitrates. Though sildenafil remains effective for less than 2hours, it is advised that nitrates should be avoided for 24hours
  • Presence of liver or kidney disorder
  • Peptic ulcer, bleeding disorder
  • Patients of leukemia, sickle cell anemia, myocardial infarction etc.
Drug interactions:
  •  Sildenafil markedly potentiates the vasodilator action of nitrates, precipitates fall in Blood Pressure and myocardial infarction may occur.
  • Inhibitors of CYP3A4 like erythromycin, Ketoconazote, cemetidine may potentiate its action i.e. may increase Sildenafil plasma concentration.
  • Vitamin k antagonist may increase the risk of bleeding.
  • Concomitant use with alpha- blockers may lead to hypotension.

N.B: men even without Erectile Dysfunction are going for it to enhance sexual satisfaction.

Nursing implications:
  • Determine Erectile Dysfunction before administration.
  • Monitor hemodynamic parameters and exercise before and after therapy
Patient/ family teaching:
  • Instruct the patient to take drugs at least 1 hour before sexual activity
  • Not more than once a day.
  • Instruct the patient that sexual stimulation is required for erection to occur.
  • Advise the patient that the drug is not indicated for women.
  • Advise the patient not to concurrently take the drug with nitrates or alpha-adrenergic blockers
  • Instruct the patient if chest pain occurs after taking the drug to report to the PHC practioners immediately.
  • Advise the patient to avoid excess alcohol intake in combination with PDE-5 since it can increase the risk of orthostatic hypotension
TADALAFIL:
  Brand names;
  • Megalis,
  • Tadarich,
  • Tadalis,
  • Cialis and Apcalis 10, 20mg tablets

            It is a more potent and longer acting congener of Sildenafil, duration of action is 24-36 hours. It is claimed to act faster, though peak plasma levels are attained between 30-120minutes.

Indication;
  • Erectile Dysfunction
Mechanism of action
  • As for Sildenafil

Side effects, risks, contraindications and drug interactions are similar to Sildenafil

  • Because of its longer lasting action, nitrates are contraindicated for 36-48hours after Tadalafil.
  • Due to its lower affinity for PDE-6, visual disturbances occur less frequently
Dosage:
  •  10mg o.d. at least 30minutes before sexual intercourse (max 20mg)

Peripheral Initiators of Erection

They include Alprostadil administered intra cavernously (injected) directly into the corpus cavernosum using a fine needle or introduced into the urethra as a small pellet, produces erection in few hours to permit intercourse  .  It is more used in patients taking anti-hypertensive drugs, those with cardiac diseases e.g Coronary artery disease and patients who do not respond to PDE-5 inhibitors.

Mode of Action

It is a prostaglandin E1 analog thus relaxes the penile muscles bringing about erection.

Contraindications
  1.  Presence of any anatomical obstruction or condition that might predispose to priapism. The risk could be exacerbated by these drugs.
  2.  Penile implants.
  3.  Bleeding disorders, CV diseases, optic neuropathy, severe hepatic and renal disorders.
Adverse effects
  • Priapism
  • Thrombo-embolism
  • Local tenderness
  • Penile fibrosis

Central initiators:

 These initiate neuronal path ways for erection e.g.

  • Apomorphine administered orally
Mechanism of action:

Apomorphine is a dopamine agonist  which acts centrally to stimulate an erectile neuronal path way.

It is also for known for Parkinsonism and induction of vomiting thus rarely used for this indication

Adverse effect:
  • Nausea and vomiting
  • Head ache and dizziness
  • Decreased milk production if taken by lactating mothers for another use

Central conditioners:

These provide a central mood condition of erection. They include;

(a). Trazodone which is a CNS anti-depressant due to massive adverse effects

(b). Androgens: e.g. testosterone

Click here to read more about Androgens.

Erectile Dysfunction Medications Read More »

androgens

Androgens

Androgens

Androgens are male sex hormones

Androgens include Testosterone, which is produced in the testes, and the Androgens, which are produced in the Adrenal glands.

Androgens are chiefly produced in the testes and small amounts in adrenal cortex. In female, small amounts are produced in the ovary and adrenal cortex.

        Testosterone is the most important natural androgen and in adult male, 8-10mg is produced daily. Its secretion is regulated by gonadotropins and gonadotrophic releasing Hormone (GnRH).  Inadequate production of androgens is due to pituitary malfunction or atrophy, injury to or removal of testicles. Androgens stimulate the development of male characteristics.

Naturally occurring androgens hormones are;

  • Testosterone, the principal androgenic hormone produced by the leydig cells of the testes.
  • Dehydroepiandrosterone (DHEA) produced by adrenal cortex.

Common Terms

Anabolic steroids: androgens developed with more anabolic or protein-building effects than androgenic effects.
Androgenic effects: effects associated with development of male sexual characteristics and secondary characteristics (e.g., deepening of voice, hair distribution, genital development, acne)
Androgens: male sex hormones, primarily testosterone; produced in the testes and adrenal glands
Hirsutism: hair distribution associated with male secondary sex characteristics (e.g., increased hair on trunk, arms, legs, face)
Hypogonadism: underdevelopment of the gonads (testes in the male)
Penile Erectile Dysfunction: condition in which the corpus cavernosum does not fill with blood to allow for penile erection; can be related to aging or to neurological or vascular conditions

Examples of Androgens

Drug NameUsual DosageUsual Indications
danazol (Danocrine)100–600 mg/d PO, depending on use and responsePrevent ovulation for treatment of endometriosis; prevention of hereditary angioedema
fluoxymesterone (Androxy)5–20 mg/d PO for replacement therapy; 10–40 mg/d PO for certain breast cancersTreatment of delayed puberty in male patients and certain breast cancers in postmenopausal women
testosterone (Androderm, Depo-testosterone)50–400 mg IM every 2–4 weeks, dose varies with preparation (check more below)Replacement therapy in hypogonadism (check more below)
methyltestosterone (Testred, Virilon)Males: 10–50 mg/d PO Females: 50–200 mg/d POReplacement therapy in hypogonadism; treatment of delayed puberty in male patients and certain breast cancers in postmenopausal women

TESTOSTERONE (depo-testerone, androderm) 

Classification:

Therapeutic: Hormone

Pharmacological: Androgen

Pregnancy; Category-x

Schedule: III controlled substance.

Dosage: 50–400 mg IM every 2–4 weeks, dose varies with preparation; some long-acting depository forms are available; dermatological patch 4–6 mg/day, replace patch daily.

Effects of Testosterones.

Anabolic Effects (Growth and Metabolic Functions)

  • Maintains bone density.
  • Regulates fat distribution.
  • Helps in Red Blood Cell production.
  • Supports muscle growth, strength and body mass.
  • Speeds up recovery from injury.
  • They act to increase the retention of nitrogen, sodium, potassium, and phosphorus.
  • They decrease the urinary excretion of calcium.
  • Testosterones increase protein anabolism and
    decrease protein catabolism (breakdown).

Androgenic Effects ( Sexual Characteristics and Functions)

  • Enhances sex drive and libido.
  • Increases aggression.
  • Acne.
  • Beard and body hair.
  • Male pattern boldness.
  • Development and maintenance of male sex organs.
  • Spermatogenesis.
  • Increased size of the prostate.

Control of Testosterone Secretion.

Hypothalamus releases GnRH, which stimulates the Anterior Pituitary gland to secrete FSH an LH which in turn stimulate the Leydig cells to secrete testosterone. High levels of serum testosterone exerts a negative feedback i.e.

  • APG suppresses secretion of LH.
  • Hypothalamus suppresses the GnRH.

Indications of Testosterone.

  1. Hypogonadism and impotence in males due to testicular/pituitary/hypothalamic deficiency.
  2. Testosterone deficiency .
  3. Breast cancer treatment in post menopausal women, who cant be operated.
  4. Treatment of delayed male puberty.
  5. Prevention of postpartum breast engorgement.
  6. Illegally, sportsmen often use anabolic steroids for promoting their musculature and sporting abilities.
  7. Blockage of follicle-stimulating hormone and luteinizing
    response hormone release in women to prevent ovulation for
    treatment of endometriosis.
  8. Prevention of hereditary angioedema

Contraindications of Testosterone.

  •  Allergy to androgens or other ingredients in the drug. Prevent hypersensitivity reactions.
  •  Pregnancy, lactation. Potential adverse effects on the neonate. It is not clear whether androgens enter breast milk.
  •  Presence or history of prostate or breast cancer . Aggravated by the testosterone effects of the drug.
  •  Liver dysfunction, Cardiovascular disease. Can be exacerbated by the effects of the hormones.
  •  Topical forms of testosterone have a Black Box Warning alerting user to the risk of virilization (Female develops male characteristics) in children who come in contact with the drug.
  •  Danazol has Black Box warning regarding the risk of thromboembolic events, fetal abnormalities, hepatitis, and intracranial hypertension.
  • For use with caution in patients with Diabetes Mellitus, BPH and Sleep apnea.

Side Effects and Adverse Effects of Testosterone

                      In men,

  • Administration of an androgen may result in breast enlargement
  • (gynecomastia),
  • testicular atrophy,
  • inhibition of testicular function,
  • impotence,
  • enlargement of the penis,
  • nausea and vomiting,
  • jaundice,
  • headache,
  • anxiety,
  • male pattern baldness,
  • acne and depression,
  • fatigue,
  • abdominal cramps,
  • confusion,
  • deepening of the voice,
  • edema,
  • drug-induced hepatitis,
  • gingivitis.
  • hirsutism (increased hair distribution)

                         In women,

  • receiving an androgen preparation for breast carcinoma the most common adverse reactions are;
  • amenorrhea and virilization (acquisition of male sexual characteristics such as changes in body and facial hair, a deepening voice, acne, menstrual irregularities and enlargement of the clitoris).
Drug Interactions
  1. May increase action of warfarin (anti-coagulants),  oral hypoglycemic agents and insulin.

  2.  Concurrent use with corticosteroids may increase the risk of edema formation.

Nursing intervention/ involvement:

  •  If the androgen is to be administered as a buccal tablet, the nurse demonstrates the placement of the tablet and warns the patient not to swallow the tablet but to allow it to dissolve in the mouth.
  • The nurse reminds the patient not to smoke or drink water until the tablets is dissolved. Oral and parenteral androgens are often taken or given by injection outpatient basis.
  • When given by injection, the injection is administered deep I.M into the gluteus muscle.
  •   Oral testosterone is given with or before meal to decrease gastric upset.
  • When testosterone Trans -dermal system testostederm is prescribed, the nurse places the system on clean, dry scrotal skin. Optimal skin contact of the Trans dermal system is achieved by shaving scrotal hair before placing the system.
  • Monitor fluid input and output
  • Weigh the patient twice a week
  • Assess for edema and report
  • Monitor secondary sexual characteristics in men
  •  Monitor menstrual irregularities, deepening of the voice, in females.
  • Monitor Hemoglobin and hematocrit periodically
  • Monitor urine and serum calcium levels
Patient/family teaching:
  1.  Advise the patient to report signs of priapism, difficulty in urinating, hypercalcemia, edema, unexpected weight gain, swelling of the fee, hepatitis, unusual bleeding.
  2. Explain rationale for prohibiting use of testosterone for increasing athletic performance
  3.   Notify Doctor of pregnancy.
  4.   DM patients to monitor blood sugar.
  5. Regular follow up, laboratory tests and physical examination
  6.  For ladies to notify doctor if signs of body hair distribution, deepening of voice menstrual irregularities occur.

ANABOLIC STEROIDS

 These are agents that are not easily converted to the potent androgen 5 alpha o-dihydrotestosterone (DHT) hence their effects on sex are less but their anabolic effect are high.

Drugs commonly used by athletes include; nandolone, stanozolol, and mithenelone. All of this drugs are regulated as controlled substances, making their use by athletes illegal.

Clinical uses/indications of anabolic steroids.

  • Osteoporosis
  • Appetite improves and there is a feeling of well being.
  • To counteract osteoporosis seen in chronic glucocorticosteroid therapy.
  • Stimulates linear growth in prepubertal boys (height).
  • Used in renal diseases.
NANDROLONE

      This is another steroid naturally produced by body, it is often synthesized and sold under the trade names Deca- Durabolin and Durbolin.

Professional athletes like Berry Bonds and Roger Clemens alleged used nandrolone to illegally enhance their performance.

STANOZOLOL:

       This synthetic steroid goes by the brand name Winstrol. This steroid is unusual in that it can be taken orally. Base ball players like Rafael. Palmeiro have tested positive for illegal use of stanozolol and strength athletes often use it illegally to quickly get stronger.

OXANDROLONE:

          Is a synthetic steroid retailed as the drug Anavar, which is approved for use in osteoporosis. Body builders use this steroid illegally to create greater muscle.

Contraindications:

  • Male patients with cancer of the breast or with known or suspected carcinoma of the prostate.
  • Carcinoma of the breast in female with hypercalcemia; androgenic anabolic steroids may stimulate osteolytic resorption of bones.
  • Pregnant because of masculinization of the fetus.
  • Nephrosis or the nephritic phase of nephritis.

Side effects of anabolic steroids:

  • Severe acne, oily skin and hair – hair loss.(virilization)
  • Liver diseases resulting into complications such as heart attack and stroke.
  • Altered mood, irritability, increased aggression, depression or suicidal tendencies.
  • Alteration in cholesterol and other blood lipids
  • High blood pressure
  • Gynecomastia- abnormal development of mammary glands in men causing breast enlargement.
  • Shrinking of testicles.
  • Azoospermia (absence of sperm in semen)
  • Menstrual irregularities in women
  • Infertility
  • Excess facial or body hair, deeper voice in women.
  • Stunted growth and heat in teens
    risk of viral or bacterial un function due to unsterile injections
  • Edema
  • Prostate cancer
  • Injury from skin-to-skin transfer of topical testosterone

 

Drug interactions:

  • Anti-coagulants. Anabolic steroids may increase sensitivity to oral anti-coagulants. Dosage of the anti-coagulants may have to be decreased in order to maintain the prothrombin time at the desired therapeutic level. Patients receiving oral anti-coagulant therapy require close monitoring, especially when anabolic steroids are started or stopped.

Patient’s information:

  • The physician should instruct patients to report any of the following effects of androgenic anabolic steroids,
  • hoarseness,
  • acne,
  • changes in menstrual periods,
  • more hair on the face,
  • Nausea and vomiting,
  • changes in skin colour or ankle swelling.

ANTI ANDROGENS

Antiandrogens, also known as androgen antagonists or testosterone blockers, are a class of drugs that prevent androgens  from mediating their biological effects in the body.

They act by blocking the androgen receptor and/or inhibiting or suppressing androgen production. They include:

  • Danzol
  • Finasteride
  • Spironolactone
  • Flutamide
  • Cyproterone
  • Ketoconazote
  • Bicalutamide and Nilutamide

Finasteride

Available preparations:      Tablets 5mg

Available brands:                 Finest, Proscar

           The androgen hormone inhibitor finasteride is a synthetic drug that inhibits the conversion of testosterone into the  androgen 5 alpha o-dihydrotestosterone (DHT). The development of the prostate glands is dependent on DHT. The lowering of serum levels of DHT reduces the effect of this hormone on the prostate gland, resulting in decrease in the size of the gland and this synthesis associated with prostate gland enlargement.

Indications;

  • Benign Prostatic Hyperplasia(BPH)
  • Androgenetic alopecia (male pattern baldness) in men only

Mechanism of action:

 It inhibits the enzyme 5-alpha-reductase which is responsible for converting testosterone to its potent metabolite 5-alpha dihydrotestosterone in prostate, liver and skin since 5-alphs dihydrotestosterone is partially responsible for prostatic hyperpiesia and hair loss.

Dose:

  • In BPH 5mg o.d
  • Alopecia 1mg/day for 3 months or more. Available in tablets of mg and 5mg

Side effects;

  • Decreased libido
  • Decreased volume of ejaculation
  • Erectile dysfunction/impotence
  • Breast tenderness and enlargement
  • Testicular pain

Contraindications/precautions;

  • Known hypersensitivity to finasteride
  • Use with caution on hepatic impairment

Nursing implications:

  •   Assess for symptoms of prostatic hyperplasia e.g. feeling of incomplete bladder emptying, interruption of the urinary stream
  •   Digital rectal examination should be done before and periodically during BPH therapy.
  •   Laboratory tests of prostate specific antigen cancer concentration which is used to screen for cancer of prostate.
  • Take this drug without regard to meals.

Patient/ family teaching;

  1. Finasteride possesses risk to male fetus; tell males not to have sex with pregnant women to avoid the risk of absorption
  2. Inform the Doctor immediately if sexual partner is or may become pregnant because additional measures such as discontinuing the drug or use of condom may be necessary.

Androgens Read More »

Uterine Relaxants

Uterine Relaxants

Uterine Relaxants

Uterine Relaxants are drugs which inhibit uterine motility by decreasing the frequency and strength of contractions.

Uterine Relaxants are drugs that inhibit uterine contractions and prolong pregnancy to allow the fetus develop more fully, thereby increasing the chances of neonatal survival.

These drugs prevent premature labor. It can succeed if only the cervical dilatation is less than 4cm.
They include;

  • Salbutamol
  • Magnesium Sulphate
  • Nifedipine
  • Indomethacin
  • Terbutaline

SALBUTAMOL

Legal class; class B controlled drugs
Medical class; tocolysis
Form; tabs , sterile solution for injection
Dosage :tabs 4mg
Soluton for injection 50mg/ ml

Indications
  • Uncomplicated premature labour between 24 to 33 weeks of gestation
  • Asthma
Contraindications
  •  Cardiac diseases
  • APH
  • Intra uterine fetal death.
  • Intra uterine infections
  • Raptured membranes
  • Eclampsia and pre-eclampsia
  • 1st an 2nd trimester of pregnancy
Dose
  • For premature labour, intravenous, infusion 10mcg/ min, gradually increase according to response at 10 minutes intervals until contractions diminish, then increase rate until contractions have ceased, max dose : 45mcg/min
  • Maintain rate for 1hr then gradually reduce by intravenous or intramuscular injection 100-250mg repeated according to response, then orally 4mg every 6-8hrs
    Do not use for more than 48minutes
Side effects
  •  Hypoglycemia
  • Vomiting and nausea
  • Sweating
  • Tremors
  • Hypotension
  • Pulmonary oedema
  • Maternal and fetal tachycardia
  • Headache
  • Palpitations
  • Urticaria

Magnesium Sulphate ( MgSO4)

Legal class; class B controlled drugs
Medical class; tocolytic and anticonvulsant
Form; sterile solution for injection
Strength/dosage; 50% of 5 grams/10ml

uterine relaxants magnesium sulphate

Dosage
Loading dose (14g)

4g of MgSO are given slowly intravenously for over 15 to 20 minutes and is prepared as follows

  1. Take a 20ml syringe and draw 8 mils if 50% MgSO4 (4g)
  2. Add 12 mils of water for injection to make 20% of the solution
  3. Give intravenously slowly over 15 minutes.

Immediately this is followed by 10g intramuscular and  is  prepared as follows;

  1. Take 20mils syringe, draw 10mils of 50% MgSO4 (undiluted) which is equivalent to 5g in each syringe
  2. Then add one mil of 2% lignocaine in each syringe to reduce pain
  3. Give deep intramuscular on each buttock
Maintenance Dose

Give 5g of 50% MgSO4 deep intramuscular on alternate buttocks every 4hrs prepare as below.

  1. Take 10ml syringe and draw 10ml of 50% of MgSO4 (5g).
  2. Add 1ml of lignocaine 2% in a syringe and give deep intramuscular.
    The dose can be repeated after every 4hrs of alternate buttock.
  3. The treatment is continued for 24hrs from the time of starting treatment or last fit.
    >  Incase the mother gets fit before 4hours, she is given 2g slowly intravenous.
Useful Effects of MgSO4:
  • Prevent seizures which are associated with pre eclampsia and eclampsia
  • Reduces cerebral oedema
  • Relieves constipation by retaining some water in the lumen
Indications
  •  Severe eclampsia and pre eclampsia
  • Patients with hypomagnesemia
  • Patients with severe asthma
  • Used in short term treatment of constipation
  • Patients with myocardial infarction
Contraindications
  •  Patients with hypermagnesemia
  • Patients who are hypersensitive to MgSO4
  • Renal impairment
  • Hepatic failure
  • Hypotensive patients
  • Patients with epilepsy
Side effects
  •  Drop in blood pressure
  • Flushing of the skin
  •  Dizziness
  •  Confusion
  •  Muscle weakness
  •  Loss of knee jack reflex
  •  Prolonged bleeding time
  •  Excessive bowel activity
Adverse effects
  •  Shock in hypertensive patients
  • Hypermagnesemia
  • Respiratory depression and coma

NIFIDIPINE

Legal class; class B controlled drugs
Medical class; tocolytic and antihypertensive
Form; tablet


Dosage
  •  20mg and the dose is repeated after 30minutes if contractions persists.
  • If contractions continue after 3hrs give 20mg every 3-8hrs until ceased and the maximum dose is 160mg/day

Indications
  •  Threatened abortion
  • Preterm labour less than 34wks of pregnancy
  • Hypertension

Contraindications
  •  Maternal conditions like cardiac diseases
  •  Hypertension
  •  Intrauterine infections
  •  Any condition that make pregnancy to prolong
  •  Fetal death

Side effects
  •  Dizziness
  • Headache
  • Flushing
  • Oedema
  • Fatigue

Uterine Relaxants Read More »

Drugs used in labor

Drugs used in Labor

Drugs used in Labour

Drugs used in labour can be grouped according to the effect they have on the uterus.

  1. Uterine Stimulants/Uterine Mortility drugs. (Oxytocics)
  2. Uterine relaxants (Tocolytics)

Uterine Stimulants/Uterine Motility Drugs(Oxytocics)

Uterine motility drugs stimulate uterine contractions to assist labor (oxytocics) or induce abortion (abortifacients)

Oxytocics

Oxytocics stimulate contraction of the uterus, much like the action of the hypothalamic hormone oxytocin, which is stored in the posterior pituitary. These drugs include

  • Ergonovine (Ergotrate)
  • Methylergonovine (Methergine)
  • Oxytocin (Pitocin, Syntocinon).

Oxytocin

Legal class; class B controlled drugs
Medical class; oxytocic drugs
Form; sterile solution for injection
Strength; 10 IV per ampule.

Indications of Oxytocin
  1.  Induction of labor
  2.  Cases of inter-uterine fetal death.
  3.  Hypotonic uterine contractions
  4.  Mothers with hypertension
  5.  After delivery to control bleeding
  6. Pre-eclampsia and eclampsia
  7.  Congestive cardiac failure
  8.  Post term
  9. Prevent PPH
  10. Incomplete or missed abortion.
  11. Active management of third stage of labor.

Contraindications of Oxytocin
  •  Hypertonic uterine
  •  Fetal and maternal distress
  •  Multiple pregnancy
  •  Trial of labor
  •  Mal presentation like breech, brow
  •  Cephalo pelvic disproportion
  •  Low blood pressure
Dose
  1. Induction/argumentation of labour;  5 I.U into 500mls of solution for infusion, initially, 5 drops per min.
  2. Preventing of PPH after delivery of the placenta; Slow I.V, 5 I.U, increase rate during 3rd stage.

Route
  •  Intramuscular
  • Intravenously when mixed with normal saline or dextrose

Side Effects
  •  Dizziness
  • Nausea and vomiting
  • Rashes
  • Fetal brandy cardia
  • Hypotension

Adverse Effects
  •  Lead to ruptured uterus
  • Hypotension
  • Tachycardia
  • Intra uterine fetal anoxia and hypoxia to the fetus leading to birth asphyxia.
Pharmacokinetics
  •  Absorption is immediate following IV injections
  • Drug is distributed throughout the extracellular fluid. Some amount enters the fetal circulation.
  • It is metabolized rapidly in kidney and liver in small amount and are excreted in urine

Abortifacients

Abortifacients are used to evacuate uterine contents via intense uterine contractions. These drugs include;

  • Misoprostol
  • Carboprost (Hemabate)
  • Dinoprostone (Cervidil, Prepidil Gel, Prostin E2)
  • Mifepristone ( Mifeprex). 

Misoprostol

Legal class; class B controlled drugs
Medical class; oxytocic drugs/ cervical, rippening agent
Form; tablet
Strength; 200mcg/ 100mcg tablet

Indications
  •  Induction of labour
  • Control post partum hemorrhage due to uterine atony
  • Before cervical dilatation
  • Intra-uterine fetal death
  • Gastric and deudenal ulcerations
Contraindications
  •  Mal presentation
  • Placeta previa grade 3 and 4
  • Multiparous mothers
  • Cephalo pelvic disproportion
  • Hypersensitivity to misoprostol
Dose
  • Induction of labour; 100mcg vaginally every after 12hrs
  • NSAID ulcerations; 200mcg 4 times a day
Route
  • Sublingually
  • Rectally
  • Vaginally
Side Effects
  • Headache
  • Dizziness
  • Fever
  • Shivering
  • Vomiting
  • Uterine rupture
  • Fetal distress.
  • Constipation
Pharmacokinetics.

Absorbed in the GIT and distributed widely through out the body metabolised in the liver and is excreted in urine.

DINOPROSTOL

Available preparation – 3mg tab
Available brand – Prostin

Pharmacokinetics

Following vaginal insertion, it diffused slowly into the maternal blood.
There is also some local absorption into the uterus through the cervix
It is distributed widely in the molter, metabolized in the lungs, liver, kidney, spleen and other maternal tissues and excreted in urine with small amount in faeces.

Indications
  • Induction of labor
  • Missed abortion
Contraindications
  •  Active cardiac diseases
  • Multiple pregnancy
  • Hypersentivity to dinoprostol
  • Untreated pelvic infection
  • Caesarian section

Dose :  3 mg vaginally

Side Effects
  •  Abdominal pain
  • Nausea and vomiting
  • Hypotension
  • Shivering
  • Back pain
  • Rapid cervical dilatation

SYNTOMETRINE

Legal class; class B controlled drugs
Medical class; oxytocic drug
Form; sterile solution for injection
Strength; combination of ergometrine and Pitocin ( ergometrine 0.5 mg + Pitocin 5 IU) –It exists in an ampules of 1 mill

Dose
  • I ml as single dose but can be repeated where necessary if bleeding is not controlled
Route
  •    Intramuscular
  •    Intravenous
Indications
  1.  Give to multi gravidas after delivery
  2.   Mothers with a history of post partum hemorrhage
  3. Multiple or twin delivery because of large placental site
  4. Mothers with heavy lochia
  5. Abortion when fundal height is less than 12 weeks
Contraindications

Mothers with cardiac disease, pre eclampsia, eclampsia and hypertension.

Adverse Effects
  •  Retained placenta
  •  IUFD in undiagnosed second twin
  • Lead to retained 2nd twin
  • Uterine rapture if given in abortion, above 20 weeks of gestation products of conception are not fully out.
  • Causes hypoxia and anoxia
Side Effects
  • Nausea and vomiting
  • Headache
  • Hypotension
  • Dyspnea
  • Muscle pain

ERGOMETRINE

Legal class; class B controlled drugs
Medical class; oxytocic drug
Form; tablet and sterile solution
Strength/dosage; tabs 0.25 to 0.5mg tab
Injection 200mcg/ml
0.5mg/ml
EFFECTS
It causes sudden prolonged intermittent uterine contraction
INDICATION
Contra indications
Side effects
Dangers
(Are the same as for syntometrine)

Drugs used in Labor Read More »

Fertility Drugs/ Gonadotropin Drugs drugs

Fertility Drugs/Gonadotropin Drugs

Fertility Drugs

Fertility drugs are drugs that stimulate the female reproductive system.

Examples of Fertility drugs;

  • Cetrorelix (Cetrotide)
  • Chorionic gonadotropin (Chorex, Profasi, Pregnyl).
  • Chorionic gonadotropin alpha (Ovidrel).
  • Clomiphene (Clomid)
  • Menotropins
    (Pergonal, Humegon).

Therapeutic Actions and Indications.

Women without primary ovarian failure who cannot get pregnant after 1 year of trying may be candidates for the use of fertility drugs. Fertility drugs work either directly to stimulate follicles and ovulation or stimulate the hypothalamus to increase FSH and LH levels, leading to ovarian follicular development and maturation of ova.

Indications

  1. Given in sequence with human chorionic gonadotropin (HCG) to maintain the follicle and hormone production, these drugs are used to treat infertility in women with functioning ovaries whose partners are fertile.
  2. Fertility drugs also may be used to stimulate multiple follicle development for the harvesting of ova for in vitro fertilization.
  3. Menotropins also stimulate spermatogenesis in men with low sperm counts and otherwise normally functioning testes.
  4. Cetrorelix inhibits premature LH surges in women undergoing controlled ovarian stimulation by acting as a GnRH antagonist.
  5. Chorionic gonadotropin is used to stimulate ovulation by acting like GnRH and affecting FSH and LH release.

Contraindications of fertility drugs

  1. Allergy to fertility drug:  Prevent hypersensitivity.
  2.  Primary ovarian failure: These drugs only work to stimulate functioning ovaries
  3. Thyroid or adrenal dysfunction. Drugs have effects on the hypothalamic-pituitary axis.
  4. Ovarian cysts: Can be stimulated by the drugs and can become larger
  5. Pregnancy: Due to the potential for serious fetal effects
  6. Idiopathic uterine bleeding: Can represent an underlying problem that could be exacerbated by the stimulatory effects of these drugs.
  7. Lactation: Risk of adverse effects on the baby
  8. Thromboembolic disease. Increased risk of thrombus formation
  9. Women with respiratory diseases: Alterations in fluid volume and blood flow can overtax the respiratory system.

Adverse effects of fertility drugs

  • Greatly increased risk of multiple births and birth defects
  • Ovarian overstimulation: abdominal plain, distention, ascites, pleural effusion
  • Headache
  • Fluid retention
  • Nausea
  • Bloating
  • Uterine bleeding
  • Ovarian enlargement
  • Gynecomastia
  • Febrile reactions possibly due to stimulation of progesterone release.

Fertility Drugs

DrugIndicationDose
Clomifene Anovulatory infertility50mg daily for 5 days, starting within 5 days of onset of menstruation (preferably on the second day) or at any time if cycles have ceased
Bromocriptine Hyper prolactanaemic, infertility, Suppression of lactation, Hypogonadism, Galactorrhoea syndrome, Benign breast diseaseInitially 1.25mg at bed time increased gradually to the usual dose of 2.5mg 3 times a day with food increased if necessary to a max. dose 30mgdaily

Nursing Diagnosis

  • Acute pain related to headache, fluid retention, or GI upset
  • Sexual dysfunction related to alterations in normal hormone control
  • Disturbed body image related to drug treatment and diagnosis
  • Deficient Knowledge regarding drug therapy
  •  Risk for Impaired Tissue Perfusion (Cardiopulmonary, Peripheral) related to increased risk for thrombus formation
  •  Situational Low Self-Esteem related to the need for fertility drugs.

Fertility Drugs/Gonadotropin Drugs Read More »

Estrogen Receptor Modulators

Estrogen Receptor Modulators

Estrogen Receptor Modulators

Estrogen Receptor Modulators are agents that either stimulate or block specific estrogen receptor sites.

They are used to stimulate specific estrogen receptors to achieve therapeutic effects of increased bone mass without stimulating the endometrium and causing other less desirable effects i.e. these drugs stimulate the estrogen receptors in the body so as to produce estrogen as needed by the body.

Examples of Estrogen Receptor Modulators.

Two available estrogen receptor modulators are raloxifene (Evista) and toremifene (Fareston).

Raloxifene

Dose : 60 mg/day Orally.

Indications : Used therapeutically to stimulate specific estrogen receptor sites, which results in an increase in bone mineral density without stimulating the endometrium in women; reduces risk of invasive breast cancer in  postmenopausal women with osteoporosis who are at
high risk for invasive breast cancer

Toremifene

Dose : 60 mg/day orally until disease progression occurs.

Indications: Used as an antineoplastic agent because of its effects on estrogen receptor sites for treatment of advanced breast cancer in postmenopausal women with estrogen receptor–positive and estrogen
receptor–unknown tumors

Contraindications of Estrogen Receptor Modulators
  • Allergy to estrogen receptor modulators.
  • Contraindicated in pregnancy and lactation because of potential effects on the fetus or neonate. 
  •  History of venous thrombosis or smoking. Increased risk of blood clot formation if smoking and estrogen are combined.
Adverse Effects of Estrogen Receptor Modulators
  • Raloxifene has been associated with GI upset, nausea, and vomiting.
  • Changes in fluid balance may cause headache, dizziness, visual changes, and mental changes.
  • Specific estrogen receptor stimulation may cause hot flashes, skin rash, edema, and vaginal bleeding.
Clinically Important Drug–Drug Interactions
  •  Cholestyramine: reduced raloxifene absorption
  • Highly protein-bound drugs (e.g. diazepam, ibuprofen, indomethacin, naproxen): interference on binding sites
  • Warfarin: decreased prothrombin time if taken with raloxifene

Nursing Considerations

  1.  Assess for the mentioned cautions and contraindications (e.g. drug allergies, cardiovascular diseases, metabolic bone disease, history of thromboembolism, etc.) to prevent any complications.
  2. Perform a thorough physical assessment (e.g. bowel sounds, skin assessment, vital signs, mental status, etc.) to establish baseline data before drug therapy begins, to determine effectiveness of
    therapy, and to evaluate for occurrence of any adverse effects associated with drug therapy.
  3. Assist with pelvic and breast examinations. Ensure specimen collection for Pap smear and obtain a history of patient’s menstrual cycle to provide baseline data and to monitor for any adverse
    effects that could occur.
  4. Arrange for ophthalmic examination especially for patients who are wearing contact lenses because hormonal changes can alter the fluid in the eye and curvature of the cornea, which can
    change the fit of contact lenses and alter visual acuity.
  5. Monitor laboratory test results (e.g. urinalysis, renal and hepatic function tests, etc.) to determine possible need for a reduction in dose and evaluate for toxicity.

Nursing Diagnoses
  •  Ineffective tissue perfusion related to changes in the blood vessels brought about by drug therapy and risk of thromboemboli
  • Excess fluid volume related to fluid retention
  • Acute pain related to systemic side effects of gastrointestinal (GI) pain and headache


Implementation with Rationale
These are vital nursing interventions done in patients who are taking female sex hormones and estrogen receptor modulators:

  •  Administer drug with food to prevent GI upset.
  • Provide analgesic for relief of headache as appropriate.
  • Provide small, frequent meals to assist with nausea and vomiting.
  • Monitor for swelling and changes in vision or fit of contact lenses to monitor for fluid retention and fluid changes.
  • Provide comfort measures to help patient tolerate drug effects.
  • Provide safety measures (e.g. adequate lighting, raised side rails, etc.) to prevent injuries.
  • Educate client on drug therapy to promote understanding and compliance.


Evaluation

Here are aspects of care that should be evaluated to determine effectiveness of drug therapy:

  •  Monitor patient response to therapy (palliation of signs and symptoms of menopause, prevention of pregnancy, decreased risk factors for coronary artery disease, and palliation of certain cancers).
  • Monitor for adverse effects (e.g. GI upset, edema, changes in secondary sex characteristics, headaches, thromboembolic episodes, and breakthrough bleeding).
  • Evaluate patient understanding on drug therapy by asking patient to name the drug, its indication, and adverse effects to watch for.
  • Monitor patient compliance to drug therapy

Estrogen Receptor Modulators Read More »

Fertility Drugs/ Gonadotropin Drugs drugs

Gonadotropin drugs

GONADOTROPINS

Gonadotropins are fertility medications given by injection that contain follicle-stimulating hormone (FSH) alone or combined with luteinizing hormone (LH).

Gonadotropins are hormones that stimulate the gonads, which are the sex organs in the body

Gonadotropins are produced by the pituitary gland, which is a small gland located at the base of the brain. The release of gonadotropins is regulated by the hypothalamus.

 

In females, the gonads are the ovaries, and in males, they are the testes.

Gonadotropins are a class of medications used to treat infertility and disorders associated with reproductive functions.

Types of Gonadotropins

There are two main types of gonadotropins:

1. Follicle-stimulating hormone (FSH): This hormone stimulates the growth and development of follicles in the ovaries of females and sperm production in the testes of males.

Females

Males

– Normal Ovarian Function: FSH is useful for the development and maturation of follicles in the ovaries, which contain the eggs. This ensures regular ovulation and fertility.

– Estrogen Production: FSH stimulates the production of estrogen by the growing follicles. Estrogen is for the development of female secondary sexual characteristics, menstrual cycle regulation, and overall reproductive health.

– Improved Egg Quality: FSH contributes to the development of healthy eggs, increasing the chances of successful fertilization and pregnancy.

– Fertility Treatment: FSH is a key component of fertility treatments like in vitro fertilization (IVF) to stimulate multiple egg production.

– Sperm Production: FSH is essential for the production of sperm in the testes. It stimulates the Sertoli cells, which are responsible for nourishing and supporting sperm development.

– Improved Sperm Quality: FSH contributes to the production of healthy, motile sperm, increasing the chances of fertilization.

2. Luteinizing hormone (LH): This hormone triggers ovulation in females and testosterone production in males.

Females

Males

– Ovulation: LH triggers the release of the mature egg from the follicle (ovulation), which is essential for fertilization.

– Corpus Luteum Formation: After ovulation, LH stimulates the formation of the corpus luteum, which produces progesterone. Progesterone is for maintaining the uterine lining for potential pregnancy.

– Hormonal Balance: LH plays a role in regulating the production of estrogen and progesterone, contributing to hormonal balance in the female body.

– Fertility Treatment: LH is used in fertility treatments to trigger ovulation and support the development of the corpus luteum.

– Testosterone Production: LH stimulates the Leydig cells in the testes to produce testosterone. Testosterone is essential for male sexual development, sperm production, and overall health.

– Secondary Sexual Characteristics: LH-driven testosterone production is responsible for the development of male secondary sexual characteristics like facial hair, muscle mass, and deepening of the voice.

– Libido and Sexual Function: Testosterone, produced under the influence of LH, plays a crucial role in libido and sexual function.

GONADOTROPIN DRUGS (Fertility Drugs)

Gonadotropin Drugs/Fertility drugs are agents that stimulate the female reproductive system.

Fertility drugs are medications used to help women who are having trouble getting pregnant. They work by stimulating the ovaries to produce more eggs, increasing the chances of conception.

Indications for Fertility Drugs:

1. Treatment of infertility in women with functioning ovaries whose partners are fertile: This is a broad category encompassing various causes of infertility, including:

  • Anovulation: When a woman doesn’t ovulate regularly, fertility drugs can stimulate ovulation and increase the chances of pregnancy.
  • Polycystic Ovarian Syndrome (PCOS): PCOS often causes irregular ovulation. Fertility drugs can help regulate ovulation and improve fertility.
  • Endometriosis: This condition can affect ovulation and egg quality. Fertility drugs can help stimulate ovulation and improve chances of conception.
  • Premature Ovarian Failure: In some cases, women experience premature ovarian failure, leading to low egg reserves. Fertility drugs can help stimulate limited egg production.
  • Unexplained Infertility: When the cause of infertility is unknown, fertility drugs can be used to stimulate ovulation and see if it improves chances of pregnancy.

2. Used to stimulate multiple follicle development for harvesting of ova for in vitro fertilization (IVF): This is a crucial aspect of IVF, where multiple eggs are needed for fertilization and embryo transfer.

3. Menotropins are used to stimulate spermatogenesis in men with low sperm counts and otherwise normally functioning testes: While not directly related to female fertility, this highlights the broader application of fertility drugs in both men and women.

Contraindications for Fertility Drugs:
  1. Allergy to fertility drug: Prevent hypersensitivity reactions.
  2. Primary ovarian failure: These drugs only work to stimulate functioning ovaries.
  3. Ovarian cysts: Can be stimulated by the drugs and can become larger.
  4. Pregnancy: Due to the potential for serious fetal effects.
  5. Idiopathic uterine bleeding: Can represent an underlying problem that could be exacerbated by the stimulatory effects of these drugs.
  6. Lactation: Risk of adverse effects on the baby.
  7. Thromboembolic disease: Increased risk of thrombus formation.
  8. Women with respiratory diseases: Alterations in fluid volume and blood flow can overtax the respiratory system.
Adverse Effects:
  • Greatly increased risk of multiple births and birth defects.
  • Ovarian overstimulation: abdominal pain, distention, ascites, pleural effusion.
  • Others: headache, fluid retention, nausea, bloating, uterine bleeding, ovarian enlargement, gynecomastia, and febrile reactions possibly due to stimulation of progesterone release.
  • Fluid retention is a common side effect of fertility medications, because;

    Hormonal Changes: Fertility drugs increase estrogen levels, which can lead to fluid retention. Estrogen promotes sodium retention in the body, and sodium attracts water, causing fluid buildup.

    Increased Blood Flow: Fertility drugs increase blood flow to the ovaries and uterus, which can lead to fluid buildup in the pelvic area.

Drugs used in treatment of infertility

Name

Clinical uses and dosage

Contraindications

Clomifene


  • Available in tablet form of 50mg

  • Brand name Clomid

Infertility due to failure to ovulate.

Given 50 mg daily × 5/7

Starting from the 5th day of the cycle ,

Increase to 100mg ×5/7

From day 5-10 if no response.

Pregnancy.

Bromocriptine


  • Available in tablet form of 2.5mg

Female infertility associated with hyperprolactinemia

Dosage 1.25 – 2.5mg

Bid × 3-7 days with food.

Inhibition of lactation 2.5mg bid with meals × 14 days.

 

Severe ischemic heart disease

Uncontrolled hypertension

Pregnancy

Breast feeding.

FEMALE REPRODUCTIVE SYSTEM DRUGS

Drugs that affect the female reproductive system typically include hormones and hormonal-like agents.

These drug types include;

  1.  Female Sex Hormones
  2. Estrogen Receptor Modulators
  3. Fertility Drugs/gonadotropins
  4. Drugs used in labor
  5. Abortifacients
gonadotropin sites

Gonadotropin Sites of Action

Female Sex Hormones

The female sex hormones can be used to replace hormones that are missing or to act on the control mechanisms of the endocrine system to decrease the release of endogenous hormones.
Drugs that act like estrogen, particularly at specific estrogen receptors, are also used to stimulate the effects of estrogen in the body with fewer of the adverse effects.

Female sex hormones include;

  • Estrogens 
  • Progestins

Estrogens.

This hormone is naturally produced by the ovaries, placenta and adrenal glands. It stimulates the development of female sex characteristics, prepares the body for pregnancy, affects the release of FSH and LH, and is responsible for proliferation of the endometrial lining.

Low estrogen in the body is responsible for the signs and symptoms of menopause, in the uterus, vagina, breast and cervix.

Other Functions of estrogen include;

  1. Breast development.
  2. Increase cholesterol in bile, to prevent damaging effects of bile salts.
  3. Increases fat storage, such as in breast tissue.
  4. Maintains bone mineral density.
  5. Maintains muscle strength.
  6. Prevents atherosclerosis, by increasing HDL concentration and lowering LDL.
  7. Estrogen is responsible for maintaining libido, memory, and mental health. 
  8. It stimulates ovulation, maintains the uterine walls and is important in vaginal lubrication.
Indications of Estrogen Therapy.
  • Estrogens are used for hormone replacement therapy (HRT) when ovarian activity is blocked or absent.
  • Is used to control the signs and symptoms of menopause.
  • They can also be used in therapy for prostate cancer and inoperable breast cancer, also as palliative care.
  • Treatment of female hypogonadism(when the body produces little or no hormones).
  • Treat ovarian failure.
  • Oral contraceptives (estrogen and progestin)
  • Morning after pill (emergency pills)
  • Endometriosis
  • Dysmenorrhea, used with progestin.

Progestin/Progesterone.

This promotes maintenance of pregnancy and it is called a pregnancy hormone.

Its functions include;

  1. Transforms proliferative endometrium into secretory endometrium.
  2. Prevents follicle maturation, ovulation and uterine contractions.
  3. Used in contraceptives. It inhibits release of GnRH, FSH and LH, hence follicle development and ovulation are prevented.
Indications of Progestin.
  • Used as a contraceptive.
  • Maintains pregnancy and development of secondary sex characteristics.
  • Use to treat primary and secondary amenorrhea, and functional uterine bleeding.
  • Treatment of acne and premenstrual dysphoric disorder (PMDD).
  • For the relief of signs and symptoms of menopause .
Contraindications of Female Sex hormones.

Estrogen

  • Known allergies
  • Idiopathic vaginal bleeding.
  • Breast Cancer(Estrogen dependant cancer)
  • CVA since it increases clotting factor prodn.
  • Hepatic dysfunction.
  • Pregnancy.
  • Lactation.

Progestin/Progesterone

  • PID
  • STD
  • Endometriosis
  • Renal and hepatic disorders.
  • Epilepsy.
  • Asthma.
  • Migraine headaches
  • Cardiac Dysfunction —potential excerbation.
Adverse Effects.
  • Corneal Changes.
  • Photosensitivity.
  • Peripheral edema.
  • Chloasma ( patches on the face)
  • Hepatic adenoma.
  • Nausea
  • Vomiting.
  • Abdominal cramps.
  • Bloating.
  • Withdraw bleeding.
  • Changes in menstrual flow.

Important aspects/issues to remember.

  1.  Women receiving any of these drugs should receive an annual medical examination, including
    breast examination and Pap smear, to monitor for adverse effects and underlying medical
    conditions.
  2. Women taking estrogen should be advised not to smoke because of the increased risk of
    thrombotic events.
  3. Women who are receiving these drugs for fertility programs should receive a great deal of psychological support and comfort measures to cope with the many adverse effects associated
    with these drugs. The risk of multiple births should be explained.
  4. Drugs are used in treatment of specific cancers in males and they should be advised about the
    possibility of estrogenic effects.
  5. Not indicated during pregnancy or lactation because of potential for adverse effects on the fetus
    or neonate.
Examples of female sex hormones and dosages.

Estrogen

  1. Estradiol, 1–2 mg/day orally or  1–5 mg IM every 3–4 weeks or  2–4 g intravaginal cream daily.
  2. Estrogens, conjugated (C.E.S., Premarin), 0.3–1.25 mg/day orally.
  3. Estropipate (Ortho-Est, Ogen), 0.625–5 mg/day orally.

Progestin/Progesterone.

  1. Etonogestrel (Implanon) 68 mg implanted sub dermally for up to 3 yr, replaced or changed when needed.
  2. Medroxyprogesterone (Provera) 5–10 mg/day PO for 5–10 days for amenorrhea or 400–1000 mg/week IM for cancer therapy or 150 mg of deep IM every 3 months (13 weeks) for contraception.
Clinically important Drug Interactions

Estrogen

  •  Barbiturates, rifampin, tetracyclines, phenytoin: decreased serum estrogen levels
  • Corticosteroids: increased therapeutic and toxic effects of corticosteroids.
  • Nicotine: Increased risk of thrombi and emboli
  • Grapefruit juice: inhibition of metabolism of estradiols
  • St. John’s wort: can affect metabolism of estrogens and can make estrogen-containing
    contraceptives less effective.

Progestins

  •  Barbiturates, carbamazepine, phenytoin, griseofulvin, penicillin, tetracyclines, rifampin: reduced
    effectiveness of progestins
  • St. John’s wort: can affect the metabolism of progestins and can make progestin-containing
    contraceptives less effective..

Gonadotropin drugs Read More »

pneumonia in children

Pneumonia in Children

Pneumonia 

Pneumonia is an inflammation of the lung parenchyma characterized by cough, tachypnea and dyspnea.

The causative agent usually various microorganisms, including bacteria, mycobacteria, fungi, and viruses are introduced into the lungs through  inhalation or from  the blood stream.

pneumonia parenchyma

Causes of Pneumonia

  • Bacterial ; streptococcus pneumoniae, haemophilus influenzae ,mycoplasma pneumoniae, staphylococcus aureus, pseudomonas aeruginosa, klebsiella pneumoniae, Moraxella catarrhalis and legionella spp.
  • Viral; respiratory syncytial viruses, Influenza A and B, adeno viruses, parainfluenza virus etc.
  • Fungal; Histoplasma capsulatum, coccidioides immitis, pneumocystis jirovecii or cryptococcus neoformans.

Classifications of Pneumonia.

Classification is according to;

  1. Etiology
  2. Anatomical
  3. Duration
  4. Clinical grounds
1. Etiologic classification
  1. Infective pneumonia:

    –Viral pneumonia e.g Influenza A virus   –Bacterial pneumonia e.g S. Pneumonia   –Fungal pneumonia -Tuberculous pneumonia e.g M.TB

  2. Non Infective pneumonia: causes;  –Toxins  –Chemicals e.g. paraffin and vomitus   –Radiotherapy  –Allergic mechanisms
2.  Anatomical   
  1. Lobar pneumonia – Inflammation is localized on one or more lung lobes
  2. Bronchopneumonia – Pneumonia with inflammation of bronchi and bronchioles –Inflammation is diffuse and primarily affects lobules of the lung.
  3. Interstitial pneumonia – Pneumonia with inflammation of the lung interstitial tissue.
3.  Duration
  1. Acute pneumonia: Type of pneumonia that lasts only for a few days to and not more than two weeks.
  2. Chronic Pneumonia: –Lasts for more than two weeks.  –Common in Immune Suppressed  patients – TB is most common.
4. Clinical Grounds

Pneumonia is classified as:

1.  Community-acquired pneumonia (CAP):

  • CAP occurs either in the community setting or within the first 48 hours after hospitalization. The causative agents include streptococcus pneumoniaeH. influenzaLegionella, and Pseudomonas aeruginosa.
  • Pneumonia is the most common cause of CAP in people younger than 60 years of age.
  • Viruses are the most common cause of pneumonia in infants and children.

2Hospital acquired (Nosocomial pneumonia): 

  • Hospital Acquired Pneumonia is also called nosocomial pneumonia and is defined as the onset of pneumonia symptoms more than 48 hours after admission in patients with no evidence of infection at the time of admission.
  • HAP is the most harmful nosocomial infection and the leading cause of death in patients with such infections.
  • Common microorganisms that are responsible for HAP include Enterobacter speciesEscherichia coliinfluenzaKlebsiella speciesProteusSerratia marcescensS. aureus, and S. pneumonia.

3. Aspiration pneumonia:

  • Aspiration pneumonia refers to the pulmonary consequences resulting from entry of endogenous or exogenous substances into the lower airway.
  • The most common form of aspiration pneumonia is a bacterial infection from aspiration of bacteria that normally reside in the upper airways.
  • Aspiration pneumonia may occur in the community or hospital setting.
  • Common pathogens are S. pneumoniaH.influenza, andS. aureus.

4. Pneumonia in immunocompromised patients

  • Pneumonia in immunocompromised patients includes Pneumocystis pneumonia, fungal pneumonias and Mycobacterium tuberculosis.
  • Patients who are immunocompromised commonly develop pneumonia from organisms of low virulence.
  • Pneumonia in immunocompromised patients may be caused by the organisms also observed in HAP and CAP.

5. Primary or secondary pneumonia

  1. Primary pneumonia: Type that occurs in a previously healthy persons living in community. Its usually lobar pneumonia due to strep pneumoniae.
  2. Secondary pneumonia 
  • Develops in after;
  • History of prior respiratory disease
  • Immunocompromised e.g. AIDs patients
  • Surgical operation thus in post-operative patientts

Pathophysiology of Pneumonia

  • When the infective agents reach the alveoli , they adhere to the walls of bronchi and bronchioles
  • They multiply extracellularly , trigger inflammation and pouring of exudates into the air spaces.
  • WBCs migrates to alveoli, the alveoli become more thick due to filling with exudates (consolidation).
  • Due to inflammation, involved areas are not adequately ventilated, due to increased secretions and edema.
  • This will lead to partial occlusion of alveoli and bronchi causing a decrease in alveolar oxygen content.
  • Venous blood from the affected areas thus returns to the heart without being oxygenated.
  • This will lead to arterial hypoxemia and even death due to interference with gas exchange.

Clinical Features of Pneumonia

  • Fever with chills (Temperature 38-39◦c)
  • Cough (may be absent in neonates and infants) with sputum production in older children
  • Fast breathing (Tachypnea)
  • Nasal flaring (with inspiration, the side of the nostrils flares outwards)
  • Chest indrawing ( it is inward movement of the lower chest wall when the child is breathes in)
  • Altered consciousness
  • Irritability
  • Shortness of breath
  • Grunting respirations
  • Chest in-drawing
  • Stridor
  • Wheezing
  • Crackles
  • Decreased breath sounds

Diagnosis and Investigations

  • History taking. The diagnosis of pneumonia is made through history taking, particularly a recent respiratory tract infection.
  • Physical examination. Mainly, the number of breaths per minute and breath sounds is assessed during physical examination.
  • Chest x-ray. Identifies structural distribution (e.g., lobar, bronchial); may also reveal multiple abscesses/infiltrates, empyema (staphylococcus); scattered or localized infiltration (bacterial); or diffuse/extensive nodular infiltrates (more often viral). In mycoplasma pneumonia, chest x-ray may be clear. 
  • Arterial Blood Gas/pulse oximetry. Abnormalities may be present, depending on extent of lung involvement and underlying lung disease.
  • Gram stain/cultures. Sputum collection; needle aspiration of empyema, pleural, and transtracheal or transthoracic fluids; lung biopsies and blood cultures may be done to recover causative organism. More than one type of organism may be present; common bacteria include Diplococcus pneumoniae, Staphylococcus aureus, a-hemolytic streptococcus, Haemophilus influenzae; cytomegalovirus (CMV). Note: Sputum cultures may not identify all offending organisms. Blood cultures may show transient bacteremia.
  • CBC. Leukocytosis usually present, although a low white blood cell (WBC) count may be present in viral infection, immunosuppressed conditions such as AIDS, and overwhelming bacterial pneumonia. Erythrocyte sedimentation rate (ESR) is elevated.
  • Serologic studies, e.g., viral or Legionella titers, cold agglutinins. Assist in differential diagnosis of specific organism.
  • Pulmonary function studies. Volumes may be decreased (congestion and alveolar collapse); airway pressure may be increased and compliance decreased. Shunting is present (hypoxemia).
  • Electrolytes. Sodium and chloride levels may be low.
  • Bilirubin. May be increased.

Management of Pneumonia

  • Although viruses are major causes of pneumonia in infants and young children, pneumonia should always be considered potentially bacterial and patient treated with antibiotics.
  • Prompt treatment with appropriate antibiotics e.g.
  • Amoxicillin is the antibiotic of first choice in children with no serious pneumonia. In infants under 2 months with severe pneumonia, the first line treatment is a combination of ampicillin (150-200mg/kg/day in divided doses) plus gentamycin (5-6 mg/kg/day) intravenously for 10 days. If penicillin is not available, alternative may be cefotaxime. If child condition does not improve, add cloxacillin.
  • For older children 2 months to 5 years, ceftriaxone is first line treatment or ampicillin plus gentamycin.
  • Fever is treated with paracetamol. Tepid sponging when necessary.
  • Nurse patient in semi-sitting up position of head elevated to aid breathing.
  • In neonates, clear the airway or nasal irrigation with sodium chloride 0.9%
  • Monitoring for increased respiratory distress
  • Assist the patient to cough if unable clear the airway by suction
  • Administer broncho-dilators
  • Oxygen therapy where cyanosis has occurred.
  • Fluid- Promote adequate rehydration. In children with severe respiratory difficulty, place and i.v. line and give 70% of normal maintenance fluids. Resume oral fluids as soon as possible.
  • Well balanced nutrition, may be via NGT. In the absence of severe respiratory difficulty breastfeed on demand.
  • Observations of respiratory rate, temperature, and pulse rate.
  • Hygiene: This should be maintained.
  • Keep the patient warm and dry. Change position of the patient where indicated.
  • Physiotherapy: Chest exercises may be done.

Complications of Pneumonia

  • Bacteria in blood stream( bacteremia)/ sepsis
  • Lung abscesses
  • Empyema
  • Pleural effusion
  • Obstructive airway secretion
  • Shock and respiratory failure
  • Necrotizing pneumonia
  • Chronic lung disease
Nursing Diagnosis
  1. Impaired tissue oxygenation related to inflammatory process in airway passages evidenced by cyanosis
  2. Extreme anxiety related to the frequent life threatening asthmatic attacks evidenced by patient asking many questions
  3. Impaired breathing patterns related to inflammatory process in the lungs evidenced by use of accessory muscles/wheezing.
  4. Altered body temperature related to inflammatory process in the lungs evidenced by a high thermometer reading.
  5. Ineffective airway clearance related to copious tracheobronchial secretions.
  6. Risk for deficient fluid volume related to fever and a rapid respiratory rate.

Pneumonia in Children Read More »

Asthma in children

Asthma in Children

ASTHMA

Asthma is a  chronic reversible inflammatory disease of the airways characterized by an obstruction of airflow.

  • Inflammation causes recurrent typical characteristics of recurrent episodes of wheezing(occurs during expiration), breathlessness, chest tightness, and coughing, which respond to treatment with bronchodilators.
  • Many inflammatory mediators play a role; mast cells, eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cells.
  • No precise cause but genetic and triggers are associations

Classification of Asthma

Asthma can be divided into;

(a)Intrinsic asthma– when no causative agent can be identified.

(b)Extrinsic or cryptogenic asthma– implying a definite external cause. 

Levels of Asthma

These guidelines were established by the National Institutes of Health so that physicians and pediatricians can determine the extent of your child’s asthma.

1. Intermittent asthma

Asthma is considered intermittent if without treatment any of the following are true:

  • Symptoms (difficulty breathing, wheezing, chest tightness, and coughing):
  • Occur on fewer than 2 days a week.
  • Do not interfere with normal activities.
  • Nighttime symptoms occur on fewer than 2 days a month.

2. Mild persistent asthma

Asthma is considered mild persistent if without treatment any of the following are true:

  • Symptoms occur on more than 2 days a week but do not occur every day.
  • Attacks interfere with daily activities.
  • Nighttime symptoms occur more than twice a month.

3. Moderate persistent asthma

Asthma is considered moderate persistent if without treatment any of the following are true:

  • Symptoms occur daily. Inhaled short-acting asthma medication is used every day.
  • Symptoms interfere with daily activities.
  • Nighttime symptoms occur more than 1 time a week, but do not happen every day

4. Severe persistent asthma

Asthma is considered severe persistent if without treatment any of the following are true:

Symptoms:

  • Occur throughout each day.
  • Severely limit daily physical activities.
  • Nighttime symptoms occur often, sometimes every night
asthma triggers

Etiology/Risk Factors.

Multiple environmental factors and genetic determinants are implicated in the development of asthma.

 These include;

  1. Endogenous factors 

(a) Genetic predisposition; There is familial association of asthma and a high degree of occurrence of asthma in identical twins

(b) Atopy: A form of allergy in which there is a hereditary tendency to develop hypersensitivity reactions like; Hay fever/allergic rhinitis & atopic eczema /dermatitis & asthma. Atopy is due to the genetically determined production of specific IgE antibody, with many patients showing a family history of allergic diseases

        2. Infection and Diseases 

(a) Upper Respiratory Tract viral infections

  • Rhinitis  and Sinusitis
  • Postnasal drip
  • Respiratory syncytial virus infection in infancy
  1.   Drugs like;
  • Beta 2 blockers cause bronchoconstriction
  • ACEI like Captopril

        4.  Environmental Factors.

(a) Air Pollution

  • Air pollutants, such as sulfur dioxide, nitrogen dioxide, diesel particulates
  • Indoor air pollution; Leads to exposure to nitrogen oxides from cooking stoves and exposure to passive cigarette smoke

(b) Allergens;

  • Indoor allergens like cats ,cockroaches house, dust mites often found in pillows, mattresses, furniture, carpets and drapes
  • Outdoor allergens like pollen grains , animal fur
  • All these inhaled allergens are common triggers of asthma
  • Food: e.g. Nuts, chocolate, milk.

(c) Occupational Exposure;

  • Occupational asthma is relatively common
  • Over 200 sensitizing agents have been identified
  • Some chemicals, fungal amylase in wheat flour bakers

(d) Changes in the weather

(e) Irritants like household sprays, paint fumes

(i) Others may include;

  • Strong emotions: e.g. fear, laughing.
  • Exercise or hyperventilation,
  • Temperature and weather changes.
asthma pathophysiology

Pathophysiology of Asthma

Summary

The  pathophysiology in asthma is reversible and airway inflammation leads to airway narrowing.

  • Trigger Factor. When a person is exposed to a trigger, it causes airway inflammation and mast cells are activated.
  • Activation. When the mast cells are activated, it releases several chemicals called mediators.  These chemicals perpetuate the inflammatory response, causing increased blood flow, vasoconstriction, hypersecretion of mucus, the attraction of white blood cells to the area, airway muscle constriction and bronchoconstriction.
  • Narrow Breathing Passages. Acute bronchoconstriction due to allergens results from a release of mediators from mast cells that directly contract the airway.
  • Asthma features: As asthma becomes more persistent, the inflammation progresses and other factors may be involved in the airflow limitation, Signs include wheezing, cough, dyspnea, chest tightness. etc.
Full Pathophysiology Context
  • Exposure to a stimulus –Release of substances from immune cells: mast cells, eosinophils, basophils, neutrophils, and macrophages.
  • The initial step: T-cell activation. Lymphokines are produced which amplify the immune response, notably by the production of IgE antibodies and their induction of allergic reactions.
  • Early-phase reaction: Release of IgE and the activation of cells bearing allergen specific IgE receptors, particularly airway mast cells.
  • The activated cells produce proinflammatory mediators such as histamine, eicosanoids, and reactive oxygen species (ROS). 
  • Some of these substances, such as histamine, adenosine, bradykinin, and major basic protein, are stored in cells as granules.
  • Other substances are formed and immediately released in response to asthmatic stimuli, including lipid mediators derived from arachidonic acid, such as leukotrienes and prostaglandins.
  • Proinflammatory mediators induce contraction of airway smooth muscle, mucus secretion, and vasodilation.
  • Airflow obstruction is caused by inflammatory mediators that induce microvascular leakage and exudation of plasma into the airways.
  • Plasma protein leakage induces a thickened, engorged, and edematous airway wall and a narrowing of the airway lumen.
  • The late-phase reaction occurs 6 to 9 hours after the early-phase reaction and is characterized by recruitment and activation of eosinophils, CD4+ cells, basophils, neutrophils, and macrophages. Adhesive interactions occur among the various cell types.
  • T cells are recruited 24 hours after the early-phase reaction and are thought to play a role in the chronic phase of the response and the enhancement of non-specific bronchial hyper-responsiveness.
  • All of these substances contribute to inflammation of the airway,
    edema and desquamation of the bronchial epithelium, and
    hypertrophy of smooth muscles in the respiratory tract.
    • These chemical mediators also increase the responsiveness of
    smooth muscles and the permeability of bronchioles to
    allergens, infectious agents, mediators of inflammation, and
    other irritants.
    • As a result of these effects, mucus production increases and leads to mucus plugging of the airways, thereby decreasing the ability of the airways to remove noxious substances.
    • As a result, patients develop airway obstruction and must use
    accessory muscles to breathe.
  • Airway obstruction in asthma results from a combination of
    bronchial inflammation, smooth muscle constriction, and obstruction of the lumen with mucus, inflammatory cells, and epithelial debris.
  • Symptoms of obstruction include dyspnea (difficult breathing), coughing, wheezing, headache, tachycardia, syncope, diaphoresis, pallor, and cyanosis

Clinical Manifestations

  Principal symptoms

  • Wheezing attacks
  • Episodic shortness of breath

 Typical symptoms

  •  Wheezing
  • Chest tightness
  • Breathlessness
  • Non-productive cough 

Signs

  • Diaphoresis
  • Tachycardia
  • Widened pulse pressure
  • Hypoxemia
  • Central cyanosis
  • Tachypnoea (RR> 25BPM)
  • Cyanosis
  • Feeble respiratory effort
  • Bradycardia or arrhythmias
  • Hypotension
  • Exhaustion
  • Confusion
  • Coma

Acute severe asthma

  • Respiratory rate ≥ 25/min
  • Heart rate ≥ 110/min
  • Inability to complete sentences in 1 breath

Diagnosis and Investigations

To determine the diagnosis of asthma, the clinician must determine that episodic symptoms of airway obstruction are present.

  • Positive family history. Asthma is a hereditary disease, and can be possibly acquired by any member of the family who has asthma within their clan.
  • Physical Examination:  Auscultation, Wheezing allover the lung, Breathlessness, Cyanosis

  • Diagnostic techniques Chest x-ray ,Blood and sputum tests, Skin tests, CBC

management of asthma

Management of Asthma

Aims

  • Achieve and maintain control of symptoms
  • Prevent asthma exacerbations
  • Maintain pulmonary function as close to the normal as possible (Homeostasis)
  • Avoid adverse effects from asthma medications
  • Prevent development of irreversible airflow limitation
  • Prevent asthma mortality
  • Restore normal or best possible lung function
  • Reduce the risk of severe attacks
  • Enable normal growth to occur in children
  • Minimize absence from school

Step Ladder Management.

  • Step 1: Occasional use of inhaled short-acting β2-adrenoreceptor agonist bronchodilators
  • Step 2: Introduction of regular preventer therapy preferably inhaled corticosteroids-ICS
  • Step 3: Add-on therapy Long-acting β2-agonists (LABAs), such as salmeterol and formoterol.
  • Step 4: Poor control with step 3: addition of a fourth drug eg leukotriene receptor antagonists, theophyllines
  • Step 5: Continuous or frequent use of oral steroids
  • Reassure the patient
  • Keep patient in upright position
  • Oxygen 50-60%
  • Peak Flow Monitoring

    Peak Flow Meter
    • Peak flow meters. Peak flow meters measure the highest airflow during a forced expiration.
    • Daily peak flow monitoring. This is recommended for patients who meet one or more of the following criteria: have moderate or severe persistent asthma, have poor perception of changes in airflow or worsening symptoms, have unexplained response to environmental or occupational exposures, or at the discretion of the clinician or patient.
    • Function. If peak flow monitoring is used, it helps measure asthma severity and, when added to symptom monitoring, indicates the current degree of asthma control.

Pharmacological management

Quick response medicines

  • Bronchodilators
  • Short acting inhaled beta 2 agonists
  • Salbutamol (albuterol), Terbutaline, Levalbuterol, Pirbuterol
  • Anticholinergics (Ipratropium 500mcg)
  • Corticosteroids (Hydrocortisone)

Long term medicines

  • Anti-inflammatory drugs
  • Montelclust/levocetirizine
  • Corticosteroids
  • Bronchodilators
  • Long acting beta 2 agonists
  • Salmeterol, Formoterol
  • Theophylline 5-7mg/kg
Nursing Care after an Acute Attack
  1. Give high flow oxygen to patient to relieve hypoxemia.
  2. Prepare and give the patient a bed in a propped up position to help improve breathing patterns
  3. Start up an IV access for IV drugs
  4. Give IV fluids if the patient is dehydrated and encourage oral fluid intake by patient.
  5. Prepare a fluid balance chart if patient is on IV fluids
  6. Take all patient vitals to monitor response to treatment
  7. Give emergency treatment like nebulized salbutamol or IV aminophylline /hydrocortisone to relieve Difficult in Breathing
  8. Administer all prescribed drugs for the patient and monitor for any Side and effects of drugs

NURSING DIAGNOSIS

  • Impaired breathing patterns related to severe inflammatory process in the lungs evidenced by wheezing
  • Impaired tissue oxygenation related to inflammatory process in airway passages evidenced by cyanosis
  • Extreme anxiety related to the frequent life threatening asthmatic attacks evidenced by patient asking many questions
  • Ineffective airway clearance related to increased production of mucus and bronchospasm evidenced by wheezing and dyspnea
  • Impaired gas exchange related to altered delivery of inspired Oxygen.

Complications of Asthma.

  • Airway infection like bronchiolitis
  • Cor pulmonale; Rheumatic Heart Failure secondary to chronic chest disease
  • Pneumonia
  • Hypoxic respiratory failure in severe disease
  • Atelectasis
  • Pneumonia
  • Status asthmaticus
  • Pneumothorax /Air-leak syndromes (rare)
  • Death

Asthma in Children Read More »

Pericarditis

Pericarditis

Nursing Notes - Inflammatory Diseases of the Heart

PERICARDITIS

Introduction

Pericarditis is the inflammation of the pericardium,
a double-layered sac that encloses the heart and the roots of the great vessels (aorta, pulmonary artery, vena cavae). This sac provides protection, lubrication, and helps to anchor the heart within the chest cavity. When inflamed, the layers of the pericardium can rub against each other, causing characteristic pain and other symptoms.

The Pericardium

The pericardium is a thin, two-layered, fluid-filled sac that covers the outer surface of the heart.(normal volume of the fluid is around 50ml)

  • It also prevents the heart from over-expanding when blood volume increases, which keeps the heart functioning efficiently.
  • It shields the heart from infection or malignancy and contains the heart in the chest wall.
Etiology (Causes) of Pericarditis

Pericarditis can be caused by various factors, with idiopathic (unknown cause) being the most common, often suspected to be viral in origin.

  • Infections:
    • Viral: Most common cause of acute pericarditis (e.g., coxsackievirus, echovirus, influenza, HIV).
    • Bacterial: Less common but more severe (e.g., tuberculosis, staphylococcal, streptococcal).
    • Fungal and Parasitic: Rare, typically in immunocompromised individuals.
  • Autoimmune Diseases: Systemic inflammatory conditions like Systemic Lupus Erythematosus (SLE), rheumatoid arthritis, scleroderma, and inflammatory bowel disease.
  • Myocardial Infarction (Heart Attack):
    • Early Post-MI Pericarditis: Occurs within a few days of a heart attack due to inflammation from myocardial necrosis.
    • Dressler's Syndrome (Post-cardiac Injury Syndrome): An autoimmune reaction occurring weeks to months after a heart attack, cardiac surgery, or trauma.
  • Uremia: Occurs in patients with kidney failure due to the buildup of toxins (uremic pericarditis).
  • Malignancy: Cancer spreading to the pericardium (e.g., lung cancer, breast cancer, lymphoma).
  • Trauma: Injury to the chest or heart, including iatrogenic (due to medical procedures).
  • Radiation Therapy: Can lead to acute or chronic pericarditis.
  • Drugs: Certain medications (e.g., procainamide, hydralazine, isoniazid) can induce drug-induced lupus-like syndromes with pericardial involvement.
  • Metabolic Disorders: Hypothyroidism (myxedema).
  • According to Culprit

    Infectious Pericarditis

    Infections are a common cause, particularly viral, leading to acute pericarditis. Other pathogens are less frequent but can cause more severe disease.

  • Viral: This is the most common cause of acute pericarditis. Viruses directly infect and inflame the pericardium.
    • Common culprits: Coxsackievirus B (most frequent), Adenovirus, Echovirus, Influenza virus (A and B), Parvovirus B19, Herpesviruses (CMV, EBV, VZV), HIV.
    • Mechanism: Direct viral invasion and replication within pericardial cells, triggering an inflammatory response.
  • Bacterial: Less common in developed countries due to widespread antibiotic use, but can be severe, often leading to purulent (pus-filled) pericarditis.
    • Pyogenic (Pus-forming) Bacteria: Staphylococcus aureus, Streptococcus pneumoniae (Pneumococci), other Streptococci.
    • Routes of Infection: Hematogenous spread (from bloodstream, e.g., septicemia), direct extension from adjacent infections (e.g., pneumonia, empyema), or direct inoculation (e.g., cardiac surgery, trauma).
    • Tuberculosis (TB): A significant cause in endemic areas. Tuberculous pericarditis can lead to chronic, constrictive pericarditis.
  • Fungal: Rare, typically seen in immunocompromised individuals.
    • Examples: Histoplasma capsulatum, Candida species, Aspergillus.
  • Parasitic: Extremely rare in most regions, but important in specific geographic areas.
    • Example: Toxoplasma gondii, Entamoeba histolytica (amoebic pericarditis), Echinococcus (hydatid cyst).
  • Non-Infectious Pericarditis

    A significant proportion of pericarditis cases are not caused by direct infection but rather by systemic conditions, injury, or other inflammatory processes.

  • Autoimmune/Inflammatory Diseases: Conditions where the immune system mistakenly attacks the body's own tissues.
    • Systemic Lupus Erythematosus (SLE): Pericarditis is a common manifestation of lupus.
    • Rheumatoid Arthritis (RA): Less common, but can cause pericardial involvement.
    • Scleroderma (Systemic Sclerosis): Can lead to pericardial effusion and thickening.
    • Ankylosing Spondylitis: A chronic inflammatory disease primarily affecting the spine, but can have cardiac manifestations.
    • Inflammatory Bowel Disease (IBD): (Crohn's disease, Ulcerative colitis) can have extra-intestinal manifestations, including pericarditis.
    • Rheumatic Fever: An inflammatory disease that can develop as a complication of untreated streptococcal infection, affecting the heart (rheumatic carditis), joints, brain, and skin. Pericarditis is one component of carditis.
  • Post-Cardiac Injury Syndromes: Inflammatory reactions following damage to the heart or pericardium.
    • Dressler's Syndrome (Post-Myocardial Infarction Syndrome): An immune-mediated inflammation of the pericardium that occurs weeks to months after a myocardial infarction (heart attack).
    • Post-Pericardiotomy Syndrome (PPS): Occurs after cardiac surgery (e.g., bypass surgery, valve replacement, pacemaker insertion) due to inflammation from surgical trauma.
    • Trauma: Direct chest trauma (e.g., blunt force, penetrating injuries) can cause pericardial injury and inflammation.
  • Metabolic Disorders:
    • Uremia: Occurs in patients with severe kidney failure (end-stage renal disease) due to the accumulation of metabolic toxins that irritate the pericardium. It typically does not respond to anti-inflammatory drugs and requires dialysis.
    • Myxedema (Severe Hypothyroidism): Can lead to pericardial effusion due to increased capillary permeability and fluid retention.
  • Malignancy (Cancer):
    • Metastatic Cancer: Cancer cells can spread to the pericardium from primary tumors (e.g., lung cancer, breast cancer, lymphoma, leukemia, melanoma). This often leads to malignant pericardial effusion.
    • Primary Pericardial Tumors: Very rare (e.g., mesothelioma).
  • Radiation-Induced Pericarditis: Can occur as a complication of radiation therapy to the chest for cancer treatment (e.g., breast cancer, Hodgkin's lymphoma). Can manifest acutely or years after treatment.
  • Acute Myocardial Infarction (MI): Early pericarditis can occur in the first few days after a transmural (ST-elevation) MI due to inflammation over the necrotic myocardial tissue.
  • Aortic Dissection: If an aortic dissection extends into the pericardial sac, it can cause hemopericardium (blood in the pericardial sac) and acute pericarditis-like pain. This is a medical emergency.
  • Drug-Induced Pericarditis: Certain medications can trigger a lupus-like syndrome or direct pericardial inflammation.
    • Examples: Isoniazid, Procainamide, Hydralazine, Phenytoin, Minoxidil, Cyclosporine, Anthracyclines (some chemotherapy drugs).
  • Idiopathic Pericarditis: When no specific cause can be identified despite thorough investigation, it is termed idiopathic. This is the most common diagnosis for acute pericarditis, often presumed to be viral.
  • Pathophysiology of Pericarditis

    • The acute inflammatory response in pericardium can produce either serous or purulent fluid, or a dense fibrinous material. In viral pericarditis, the pericardial fluid is most commonly serous, is of low volume, and resolves spontaneously.
    • Neoplastic, tuberculous, and purulent pericarditis may be associated with large effusions that are exudative, hemorrhagic, and leukocyte filled.
    • Gradual accumulation of large fluid volumes in the pericardium, even up to 250 mL, may not result in significant clinical signs.
    Clinical Manifestations of Pericarditis
  • Beck's triad is a collection of three medical signs associated with acute cardiac tamponade.
  • The signs are:-

    • Low arterial blood pressure
    • Distended neck veins
    • Distant, muffled heart sounds.

    Chest pain symptoms associated with pericarditis can be described as:

    • Sharp and stabbing chest pain (caused by the heart rubbing against the pericardium). May increase with coughing, deep breathing or lying flat.
    • Can be relieved by sitting up and leaning forward .
    • You may also feel the need to bend over or hold your chest to breathe more comfortably.

    Other clinical features include;

    The symptoms of pericarditis can range from mild to severe and may mimic other cardiac conditions. The classic symptoms include:

    1. Chest Pain:
      • Character: Typically sharp, stabbing, or pleuritic (worsens with deep breath, cough, or swallowing). Can also be dull, aching, or pressure-like.
      • Location: Usually substernal (behind the breastbone) or precordial (over the heart), often radiating to the left shoulder, neck, trapezius ridge (shoulder blade area), or back.
      • Aggravating Factors: Worsens with lying flat (supine position), deep inspiration, coughing, swallowing, and sometimes with movement.
      • Relieving Factors: Often eased by sitting up and leaning forward. This position reduces pressure on the inflamed pericardium.
    2. Pericardial Friction Rub: A characteristic scratching, grating, or squeaking sound heard during auscultation of the heart, caused by the inflamed pericardial layers rubbing against each other. It is best heard with the diaphragm of the stethoscope over the left sternal border, with the patient leaning forward and exhaling. This is a highly specific sign.
    3. Dyspnoea (Shortness of Breath): May be due to pleuritic chest pain limiting deep breaths, or in severe cases, due to pericardial effusion leading to cardiac tamponade.
    4. Low-Grade Fever: Common, especially in infectious causes.
    5. Fatigue and Malaise: Generalized symptoms due to the inflammatory process.
    6. Palpitations: Can occur if the inflammation irritates the heart muscle or conductive system.
    7. Cough: May be present due to irritation of the airways or associated pleural inflammation.
    8. Anxiety: Often results from the frightening nature of chest pain and other symptoms.
    Cardinal Signs and Symptoms of Pericarditis (Mnemonics)

    Remember “Friction” (as previously noted) and also consider the more comprehensive "PERICARDITIS" mnemonic for key features:

    • Friction rub pericardial (sounds like a grating, scratching sound), Fever
    • Radiating substernal pain to left shoulder, neck or back
    • Increased pain when in supine position (leaning forward relieves pain)
    • Chest pain that is stabbing (will feel like a heart attack)
    • Trouble breathing when lying down (supine position)
    • Inspiration or coughing makes pain worse
    • Overall feels very sick and weak
    • Noticeable ST segment elevation on ECG (often widespread concave up)

    P.E.R.I.C.A.R.D.I.T.I.S. Mnemonic:

    • Pleuritic chest pain (worsens with breathing)
    • ECG changes (widespread ST elevation, PR depression)
    • Rub (pericardial friction rub)
    • Increased pain with supine position
    • Cough, fever, malaise (flu-like symptoms)
    • Autoimmune disease history
    • Radiation to trapezius ridge (classic finding)
    • Difficulty breathing (dyspnoea)
    • Increased pain with inspiration
    • Treatment with NSAIDs (often effective)
    • Idiopathic or Infectious cause (viral most common)
    • Sitting up and leaning forward relieves pain
    Types of Pericarditis

    Pericarditis is classified based on its temporal course and characteristics:

    1. Acute Pericarditis:
      • Onset: Sudden and rapid.
      • Duration: Typically resolves within 3 weeks.
      • Characteristics: Often associated with severe chest pain and a pericardial friction rub. Usually self-limiting, but can recur.
      • Common Causes: Viral infections, idiopathic.
    2. Incessant Pericarditis:
      • Duration: Lasts for more than 4-6 weeks but less than 3 months, with continuous presence of symptoms and signs without remission.
      • Characteristics: Symptoms persist despite initial treatment, indicating ongoing inflammation.
    3. Recurrent Pericarditis:
      • Onset: Occurs after a symptom-free interval of at least 4-6 weeks following an acute episode.
      • Characteristics: Can be very distressing for patients, with repeated episodes of chest pain and inflammation. Often requires long-term management.
      • Causes: Often idiopathic, but can be associated with autoimmune conditions.
    4. Chronic Pericarditis:
      • Duration: Develops slowly and lasts for more than 3 months.
      • Characteristics: Can lead to pericardial thickening and fibrosis, potentially progressing to more serious conditions like constrictive pericarditis. Symptoms may be less acute but persistent.
    5. Constrictive Pericarditis:
      • Nature: A serious complication of chronic pericarditis where the pericardium becomes thick, rigid, and fibrotic.
      • Mechanism: This hardened sac restricts the heart's ability to expand and fill with blood properly during diastole.
      • Consequences: Leads to impaired cardiac filling, elevated venous pressures, and symptoms of right-sided heart failure (e.g., severe edema, ascites, jugular venous distension).
    Investigations for Pericarditis

    Diagnosing pericarditis involves a combination of clinical assessment, specific tests to confirm inflammation, identify the cause, and assess for complications.

    Medical History and Physical Exam:
    • History: Detailed inquiry about chest pain characteristics (onset, location, radiation, aggravating/relieving factors), fever, recent infections, autoimmune conditions, trauma, medications, and travel history.
    • Physical Exam:
      • Pericardial Friction Rub: The hallmark sign, a scratching or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border, with the patient leaning forward and holding their breath in expiration.
      • Signs of Pericardial Effusion/Tamponade: Muffled heart sounds, pulsus paradoxus, jugular venous distension, hypotension (late signs).
      • Signs of Systemic Disease: Rash, joint swelling (suggesting autoimmune disease).
    Electrocardiography (ECG):
    • Classic Findings: Widespread ST-segment elevation (concave upwards) in most leads (unlike MI, which is localized and convex), and PR-segment depression (especially in leads II, aVF, V5, V6). These changes reflect inflammation of the epicardium.
    • Evolution: ECG changes typically evolve over days to weeks, from ST elevation to T-wave inversion, then normalization.
    Echocardiography (Echo):
    • Purpose: The most important imaging test. It is essential for assessing for pericardial effusion (fluid around the heart) and its hemodynamic significance (e.g., signs of cardiac tamponade).
    • Information Provided: Can visualize the pericardium, quantify effusion size, assess cardiac chamber size and function, and identify signs of cardiac tamponade (e.g., right ventricular diastolic collapse, paradoxical septal motion).
    Cardiac CT scan/MRI:
    • Cardiac Computed Tomography (CT): Useful for visualizing pericardial thickening, calcification (in constrictive pericarditis), and large effusions. Can help differentiate pericardial disease from myocardial disease.
    • Cardiovascular Magnetic Resonance Imaging (MRI): Provides excellent soft tissue characterization. It is the gold standard for detecting pericardial inflammation, edema, and fibrosis. Can also differentiate constrictive pericarditis from restrictive cardiomyopathy.
    Blood Tests:
    • Inflammatory Markers:
      • C-reactive protein (CRP): Usually elevated and helps confirm inflammation. Serial CRP levels can monitor disease activity and response to treatment.
      • Erythrocyte Sedimentation Rate (ESR): Also typically elevated, another general marker of inflammation.
    • Cardiac Biomarkers:
      • Troponin (I or T): May be mildly elevated in pericarditis if there is associated myocardial inflammation (myopericarditis), indicating some degree of myocardial cell injury. Higher levels raise suspicion for myocarditis or myocardial infarction.
      • CK-MB and Myoglobin: Less specific than troponin for cardiac injury, but may be checked.
    • Infectious Workup: Depending on clinical suspicion, tests for specific pathogens:
      • Viral Serology: (e.g., Coxsackievirus antibodies) may be done but often not helpful for acute management.
      • Bacterial Cultures: Blood cultures if sepsis is suspected. Pericardial fluid culture if pericardiocentesis is performed.
      • TB Tests: Tuberculin skin test (PPD), interferon-gamma release assays (IGRAs), and acid-fast bacilli (AFB) stains/cultures on pericardial fluid.
    • Autoimmune Markers:
      • Antinuclear Antibodies (ANA), Rheumatoid Factor (RF), Anti-dsDNA: If autoimmune disease is suspected.
    • Renal Function Tests:
      • Blood Urea Nitrogen (BUN) and Creatinine: To assess for uremia in patients with kidney disease.
    Radionuclide Scanning (e.g., PET scan): May be used in complex cases to detect areas of active inflammation or malignancy, particularly if other tests are inconclusive.
  • Pericardiocentesis and Pericardial Biopsy:
    • Pericardiocentesis: A procedure to drain fluid from the pericardial sac. Indicated for large effusions, signs of cardiac tamponade, or for diagnostic purposes (e.g., to analyze fluid for infection, malignancy, or specific inflammatory markers).
    • Pericardial Biopsy: Rarely performed, but may be considered in cases of chronic or recurrent pericarditis with an unknown etiology, or suspicion of specific infiltrative diseases.
  • Nursing Interventions and Management of Pericarditis

    Nursing care for patients with pericarditis focuses on pain management, monitoring for complications, providing emotional support, and patient education.

    General Principles of Management
    • Goal: Relieve pain, reduce inflammation, prevent complications (e.g., cardiac tamponade, constrictive pericarditis), and treat the underlying cause.
    • Setting: Mild cases may be managed outpatient, while moderate to severe cases, or those with complications, require hospitalization.
    Management for Mild Pericarditis

    Patients with mild, uncomplicated pericarditis often respond well to conservative measures and oral medications.

    Pain Assessment and Management:
    • Assess Patient’s Pain: Characterize the pain (sharp, stabbing, dull), location, radiation, and aggravating/relieving factors. Use a pain scale (e.g., 0-10) to quantify severity. Pericarditis pain can be excruciatingly painful.
    • Positioning for Pain Relief: Keep patient in a high Fowler’s position (sitting upright) or encourage leaning forward. Avoid a supine (lying flat) position, as it exacerbates pericardial pain by increasing pressure on the inflamed pericardium.
    Monitoring for Complications (e.g., Cardiac Tamponade):
    • Constant Vigilance: Cardiac tamponade is a life-threatening complication that requires immediate recognition and intervention.
    • Key Signs to Monitor (Beck's Triad):
      • Muffled or Distant Heart Sounds: Due to fluid buildup around the heart.
      • Jugular Venous Distension (JVD) with Clear Lungs: Increased pressure in the right atrium due to restricted filling, but without pulmonary congestion typical of heart failure.
      • Hypotension: Decreased cardiac output due to compression of the heart.
    • Pulsus Paradoxus: A significant (typically >10 mmHg) drop in systolic blood pressure during inspiration. This is a classic sign of cardiac tamponade and severe restrictive filling.
    • Tachycardia: The heart attempts to compensate for reduced cardiac output by increasing its rate.
    • Other Signs: Narrowed pulse pressure, decreased urine output, cool extremities, altered mental status (signs of decreased perfusion).
    Administer Medications as Prescribed by Physician:
    • First-line Therapy:
      • High-dose Aspirin: Often used, especially for post-MI pericarditis. It has both anti-inflammatory and anti-platelet effects.
      • NSAIDs (Nonsteroidal Anti-Inflammatory Drugs): Such as Ibuprofen, Indomethacin. These are the cornerstone of treatment for acute pericarditis.
        • Nursing Considerations: Administer with food or milk to minimize gastrointestinal (GI) upset. Monitor for GI bleeding (e.g., black, tarry stools; coffee-ground emesis). Advise patients to take with a full glass of water.
    • Colchicine: An anti-inflammatory agent that works by inhibiting microtubule assembly, reducing inflammation. It is increasingly used as first-line therapy or in combination with NSAIDs, and is particularly effective in preventing recurrence.
      • Nursing Considerations: Do not take with grapefruit juice as it increases colchicine toxicity (nausea, vomiting, abdominal pain, diarrhea). Can be taken with or without food. Monitor for GI side effects.
    • Corticosteroids: Such as Prednisone. Reserved for patients who do not respond to NSAIDs/Colchicine, have contraindications to them, or have specific etiologies (e.g., autoimmune).
      • Nursing Considerations: Administer with food. Monitor for side effects (e.g., hyperglycemia, increased infection risk, fluid retention, mood changes). Taper slowly to prevent rebound inflammation.
    • IV Antibiotics: Administered if bacterial pericarditis is diagnosed or strongly suspected. Based on culture and sensitivity results.
    Management for Moderate to Severe Pericarditis / Hospitalized Patients

    These patients require more intensive monitoring and often invasive procedures.

    Comprehensive Assessment:
    • Establish Good Rapport: Essential for building trust and reducing patient anxiety.
    • Detailed History Taking: Include smoking history, anginal pain characteristics (differentiate from pericardial pain), and other presenting symptoms.
    • Continuous Observations: Monitor vital signs (temperature, pulse, respiration, blood pressure) frequently. Perform a thorough general examination, including cardiovascular, respiratory, and peripheral assessments.
    Pain Management Intensified:
    • Positioning: Continue to keep the patient in high Fowler’s position or encourage leaning forward to relieve pain.
    • Pain Level Monitoring: Continuously monitor patient pain level using a standardized scale and evaluate the effectiveness of analgesics within 30 minutes of administration.
    • Administer Prescribed Pain Medication: May include stronger analgesics such as morphine or other opioids if NSAIDs are insufficient.
    Intensive Cardiac Monitoring:
    • Monitor for Cardiac Tamponade: Hourly or more frequent assessment for signs of cardiac tamponade (pulsus paradoxus, JVD, muffled heart sounds, hypotension, tachycardia). Notify physician immediately if signs develop.
    • Continuous ECG Monitoring: To detect arrhythmias or worsening ST-T changes.
    Fluid Balance and Hemodynamic Support:
    • Careful Maintenance of Fluid Intake and Output (I&O): Essential, especially if there's a risk of fluid overload or if diuretics are used.
    • Daily Weight Check: To monitor for fluid retention.
    • Administer O2: Maintain SpO2 >90% to optimize oxygen delivery to tissues.
    • IV Antihypertensive Medication: If persistent blood pressure elevation is a concern (though hypotension is more common with tamponade).
  • Medication Administration and Monitoring:
    • Administer NSAIDs and Steroids with Food: To reduce GI side effects.
    • Ensure Timely Administration of Antibiotics: If bacterial infection is the cause.
    Patient Education and Psychological Support:
    • Disease Process Discussion: Explain pericarditis, its causes, and signs/symptoms. Reassure the patient that the chest pain is not a myocardial infarction (unless it is a co-existing condition).
    • Anxiety Reduction: Build a strong rapport with the patient to reduce anxiety associated with chest pain and hospitalization.
    • Preparation for Procedures: If surgical intervention (e.g., pericardiocentesis, pericardiectomy) is needed, provide psychological support and prepare the patient for the procedure.
    • Post-Surgical Education: For post-surgical patients, discuss warning signs of postoperative complications such as fever, inflammation at the surgical site, bleeding, and excessive swelling.
    • Activity Progression: Advise the patient to resume daily activities slowly and gradually to prevent symptom recurrence. Ensure bed rest until fever, chest pain, and friction rub disappear.
    • Warning Signs for Home: Educate on when to seek medical attention after discharge (e.g., recurrent chest pain, fever, increasing shortness of breath, swelling).
    Bowel and Bladder Care:
    • Provide a Bedside Commode: To reduce stress on the heart during defecation, especially if patient is on strict bed rest.
    • Assist with Bathing if Necessary: To conserve patient energy.
  • Monitoring for Specific Complications (less common but severe):
    • Persistent Cough, Vomiting, or Systolic BP >180 mmHg: Closely monitor and notify physician immediately, as these may increase risk for specific complications (e.g., hemorrhage in aortic dissection if not carefully managed).
  • Nursing Interventions for Pericarditis

    Nursing care for patients with pericarditis is crucial for symptom management, monitoring for complications, providing emotional support, and educating the patient and family. The following is a comprehensive list of nursing interventions:

    1. Pain Management and Comfort:
      • Assess the patient’s pain level regularly using a standardized pain scale (e.g., 0-10) and document findings.
      • Evaluate the effectiveness of administered analgesics (e.g., NSAIDs, aspirin, colchicine, opioids) within 30 minutes to 1 hour of administration.
      • Administer prescribed pain medication promptly and on schedule to maintain comfort.
      • Position the patient comfortably, typically in a high Fowler’s position (sitting upright) or leaning forward, as this position significantly alleviates pericardial chest pain. Avoid supine (lying flat) positioning.
      • Provide non-pharmacological pain relief measures, such as guided imagery, distraction, or quiet environment, as appropriate.
    2. Vital Signs and Hemodynamic Monitoring:
      • Monitor vital signs (temperature, pulse, respiration, blood pressure) frequently and continuously, especially during the acute phase or if complications are suspected.
      • Continuously monitor the patient's electrocardiogram (ECG) for rhythm disturbances, ST-T wave changes, or PR segment depression characteristic of pericarditis.
      • Assess for signs and symptoms of cardiac tamponade (e.g., muffled heart sounds, jugular venous distension [JVD] with clear lung sounds, hypotension, pulsus paradoxus [a significant drop in systolic BP during inspiration], tachycardia, narrowed pulse pressure) at least every 4-8 hours and as needed (PRN). Report any changes immediately to the physician.
      • Monitor for signs of decreased cardiac output and perfusion (e.g., cool extremities, decreased urine output, altered mental status).
      • Administer supplemental oxygen as prescribed to maintain oxygen saturation (SpO2) above 90% or as per target.
    3. Medication Administration and Monitoring:
      • Administer all prescribed medications (e.g., NSAIDs, colchicine, corticosteroids, antibiotics) as ordered, ensuring correct dosage, route, and timing.
      • Administer NSAIDs and corticosteroids with food or milk to minimize gastrointestinal irritation and reduce the risk of peptic ulcers.
      • Educate the patient about each medication, its purpose, potential side effects, and the importance of adherence.
      • Monitor for adverse effects of medications (e.g., GI bleeding with NSAIDs, hyperglycemia with corticosteroids, diarrhea with colchicine).
      • If antibiotics are prescribed, ensure timely administration and monitor for signs of infection resolution.
    4. Fluid Balance and Nutritional Support:
      • Maintain accurate intake and output (I&O) records, especially if the patient has a pericardial effusion or is receiving diuretics.
      • Monitor daily weights to assess for fluid retention or dehydration.
      • Encourage adequate oral fluid intake unless contraindicated.
      • Provide a diet that is easily digestible and well-tolerated. Assist with feeding if the patient is too weak or fatigued.
    5. Activity and Rest:
      • Ensure the patient has adequate bed rest during the acute inflammatory phase, usually until fever, chest pain, and pericardial friction rub have resolved.
      • Assist the patient with activities of daily living (ADLs) as needed to conserve energy and reduce cardiac workload.
      • Provide a bedside commode to reduce straining during bowel movements, which can increase intrathoracic pressure.
      • Educate the patient on the importance of gradual resumption of physical activity after the acute phase, advising avoidance of strenuous activities for several weeks to months to prevent recurrence.
    6. Patient Education and Psychological Support:
      • Explain the disease process of pericarditis, its causes, symptoms, and the rationale behind the treatment plan to the patient and family.
      • Reassure the patient that the chest pain, although severe, is typically not indicative of a myocardial infarction (heart attack), which can alleviate significant anxiety.
      • Build a trusting and empathetic rapport with the patient to reduce anxiety and promote open communication.
      • Provide psychological support, acknowledging the patient's fears and concerns related to chest pain and their condition.
      • If pericardiocentesis or other procedures are anticipated, explain the procedure clearly, address patient questions, and provide emotional support before, during, and after.
      • For post-surgical patients (e.g., after pericardiectomy or creation of a pericardial window), educate on warning signs of postoperative complications such as fever, signs of infection at the surgical site, unusual bleeding, or excessive swelling.
      • Educate the patient on warning signs of recurrence (e.g., return of chest pain, fever) and when to seek medical attention after discharge.
      • Discuss the importance of medication adherence, follow-up appointments, and lifestyle modifications.
    7. Monitoring for Other Complications:
      • Closely monitor for and report persistent cough, vomiting, or significant changes in blood pressure (e.g., systolic BP >180 mmHg), as these may indicate other underlying issues or increase the risk for certain complications.
      • Assess for signs of chronic or constrictive pericarditis in patients with recurrent or persistent symptoms (e.g., persistent JVD, ascites, peripheral edema, Kussmaul's sign).

    Nursing Diagnoses for Pericarditis

    Nursing diagnoses provide a framework for nursing care, identifying patient problems that nurses can independently address. For pericarditis, these diagnoses often revolve around pain, inflammation, potential cardiac complications, and the psychological impact of the illness. Here are several common and relevant nursing diagnoses, with supporting evidence:

    1. Acute Pain related to inflammatory process of the pericardium as evidenced by:
      • Verbalization of severe chest pain (e.g., "10 out of 10," sharp, stabbing, precordial pain radiating to neck/shoulder).
      • Facial grimacing, guarding behavior (e.g., clutching chest), restlessness.
      • Increased heart rate and blood pressure (unless in tamponade, where BP may drop).
      • Pain exacerbated by deep breathing, coughing, lying supine, or movement.
      • Pain relieved by leaning forward.
      • Shortness of breath (due to pain and/or effusion).

      Rationale: The hallmark of acute pericarditis is severe, often pleuritic, chest pain caused by the inflammation and irritation of the pericardial layers. This pain significantly impacts comfort and can trigger sympathetic responses.

    2. Hyperthermia related to inflammatory process (e.g., infection, autoimmune response) as evidenced by:
      • Body temperature above normal range (e.g., 38.0°C or higher).
      • Flushed skin, warm to touch.
      • Increased heart rate and respiratory rate.
      • Profuse sweating and/or chills.
      • Malaise and generalized weakness.

      Rationale: Inflammation, particularly if infectious (e.g., bacterial, viral), often leads to a systemic febrile response as the body attempts to combat the underlying cause and inflammatory mediators are released.

    3. Decreased Cardiac Output related to impaired ventricular filling due to pericardial inflammation and/or effusion as evidenced by:
      • Fatigue, weakness, and generalized malaise.
      • Inability to perform usual Activities of Daily Living (ADLs) or requiring increased rest.
      • Shortness of breath, dyspnea on exertion, or orthopnea.
      • Tachycardia (compensatory mechanism).
      • Hypotension (especially with significant effusion/tamponade).
      • Weak or thready peripheral pulses.
      • Cool, clammy skin.
      • Delayed capillary refill.
      • Decreased urine output.
      • Altered mental status (in severe cases).
      • Abnormal hemodynamic readings (e.g., low cardiac index, elevated central venous pressure).

      Rationale: Inflammation of the pericardium can lead to fluid accumulation (effusion) or thickening/constriction, both of which can impede the heart's ability to fill adequately, thereby reducing the amount of blood pumped out to the body.

    4. Activity Intolerance related to acute chest pain, decreased cardiac output, and systemic inflammation as evidenced by:
      • Verbalization of fatigue, tiredness, or weakness after minimal exertion.
      • Dyspnea on exertion.
      • Disinterest or inability to participate in activities of daily living (ADLs) due to pain or fatigue.
      • Reported need for increased rest periods.
      • Changes in vital signs (e.g., increased heart rate, respiratory rate, or blood pressure) with activity.

      Rationale: The pain associated with pericarditis makes movement difficult, and the systemic inflammatory response, coupled with potentially decreased cardiac output, reduces the patient's physiological reserve for physical activity.

    5. Excessive anxiety related to chest pain of unknown etiology (initially), fear of serious cardiac event (e.g., heart attack), or threat to health status as evidenced by:
      • Verbalization of feeling nervous, fearful, worried, or helpless.
      • Increased heart rate and respiratory rate (beyond that caused by pain/fever).
      • Restlessness, agitation, or irritability.
      • Crying or tearfulness.
      • Sleep disturbances.
      • Questioning about the prognosis or cause of illness.
      • Preoccupation with symptoms.

      Rationale: Chest pain is often associated with myocardial infarction, leading to significant anxiety for patients. The uncertainty of the diagnosis, the severity of symptoms, and the potential for complications can further exacerbate anxiety.

    6. Risk for Ineffective Health Management related to insufficient knowledge of the disease process, treatment regimen, and potential for recurrence as evidenced by:
      • (No subjective/objective data yet, as it's a risk diagnosis, but factors include:)
        • Lack of previous experience with pericarditis.
        • Complex medication regimen (e.g., multiple anti-inflammatory drugs).
        • Need for activity restrictions.
        • Potential for recurrent episodes.

      Rationale: Patients need comprehensive education on their condition, medications, symptom recognition, and activity modifications to prevent recurrence and manage the disease effectively post-discharge.

    7. Risk for Fluid Volume Deficit (in specific cases, e.g., if experiencing excessive sweating due to fever and inadequate fluid intake, or with aggressive diuretic therapy) related to:
      • Fever-induced diaphoresis.
      • Nausea/vomiting impacting oral intake.
      • Aggressive diuretic therapy for effusion management.

      Rationale: While fluid overload is a concern with effusions, certain interventions or symptoms can lead to dehydration, necessitating careful fluid balance monitoring.

    8. Risk for Impaired Gas Exchange (in cases of significant pericardial effusion leading to lung compression or severe cardiac compromise) related to:
      • Decreased lung expansion due to large pericardial effusion.
      • Reduced cardiac output impacting pulmonary perfusion.

      Rationale: While not a primary diagnosis for all pericarditis, a very large effusion can restrict lung expansion, and severe cardiac compromise can lead to ventilation-perfusion mismatch.

    9. Risk for Infection (post-procedural) related to invasive procedures (e.g., pericardiocentesis, pericardiectomy) as evidenced by:
      • Presence of surgical incision or puncture site.
      • Disruption of skin integrity.
      • Invasive lines (e.g., IV, drain).

      Rationale: Any break in skin integrity or invasive procedure introduces a risk of localized or systemic infection.

    Complications of Pericarditis

    While most cases of acute pericarditis are benign and self-limiting, complications can occur, ranging from mild to life-threatening.

    1. Pericardial Effusion:
      • Description: Accumulation of excess fluid within the pericardial sac. It is a common complication.
      • Severity: Can range from small and asymptomatic to large and rapidly accumulating, which can lead to cardiac tamponade.
    2. Cardiac Tamponade:
      • Description: A medical emergency where a large or rapidly accumulating pericardial effusion compresses the heart, severely restricting its ability to fill with blood during diastole.
      • Consequences: Leads to a significant decrease in cardiac output, hypotension, and shock if not treated promptly.
      • Treatment: Requires urgent pericardiocentesis (fluid drainage) or surgical drainage.
    3. Recurrent Pericarditis:
      • Description: Episodes of pericarditis that recur after a symptom-free interval following an initial acute episode. This can be very distressing for patients.
      • Management: Often requires long-term anti-inflammatory therapy, sometimes with colchicine.
    4. Chronic Pericarditis:
      • Description: Pericarditis that persists for more than 3 months. Can lead to thickening and fibrosis of the pericardium.
    5. Constrictive Pericarditis:
      • Description: A severe, long-term complication where the pericardium becomes thick, rigid, and fibrotic, preventing the heart from filling properly.
      • Consequences: Leads to symptoms of right-sided heart failure (e.g., severe peripheral edema, ascites, elevated JVD) and can be progressive.
      • Treatment: Often requires surgical pericardiectomy (removal of the pericardium).
    6. Myocarditis (Myopericarditis):
      • Description: Inflammation of the heart muscle occurring concurrently with pericarditis.
      • Consequences: Can lead to myocardial dysfunction, arrhythmias, and elevated cardiac biomarkers (e.g., troponin).
    7. Fatal Hemorrhage:
      • Context: This is a very rare but catastrophic complication, typically associated with traumatic pericardial injury, iatrogenic injury during procedures (e.g., central line insertion, pericardiocentesis), or rupture of a large vessel (e.g., aortic dissection) into the pericardial sac.
    8. Stroke and Paraplegia due to Interruption of the Anterior Spinal Artery, Abdominal Ischemia:
      • Context: These are not direct complications of typical pericarditis. They are severe complications specifically associated with Aortic Dissection, especially if it involves the great vessels originating from the aorta or compromises blood supply to the spinal cord or abdominal organs. If an aortic dissection leads to hemopericardium, it can mimic pericarditis. It's crucial to differentiate these conditions due to the vastly different prognoses and emergency management required for aortic dissection.

    Pericarditis Read More »

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