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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 »

    Rheumatic Heart Disease

    Rheumatic Heart Disease

    Rheumatic Heart Disease

    Rheumatic heart disease is  a condition in which the heart valves have been permanently damaged by rheumatic fever.

    Rheumatic Heart Disease can also be defined as a chronic stage of Rheumatic Fever involving all the layers of the heart causing major cardiac sequelae

    So what is Rheumatic Fever?

    Rheumatic Fever is an autoimmune, systemic, post-streptococcal, inflammatory disease, principally affecting the heart, joints, central nervous system, skin and subcutaneous tissues.

    rheumatism licks the joint, 
    but bites the whole heart’.

    Causes/Etiology of Rheumatic Heart Disease

    • Infection: The heart damage may start shortly after untreated streptococcal throat infection referred to as strep throat or scarlet fever. The disease is caused by rheumatic fever and the bacteria responsible is group A beta-hemolytic streptococci. (Streptococcus pyogenes).

    >  The heart valve can be inflamed  and become scarred  over time.
    >  This can result in narrowing  or leaking (regurgitation) of the heart valve making it harder for the heart to function normally. 
     > The commonest valves affected are the mitral valve and the aortic valve however all 4 valves may be affected.  This may take years to develop and can result to heart failure.

    rheumatic heart disease

    Heart Valves

    Pathophysiology of Rheumatic Heart Disease.

    Causative agent (Group A Beta hemolytic streptococci) causing Strep throat, untreated strep throat infection leads to rheumatic fever several weeks after a sore throat has resolved (only infections of the pharynx have been shown to initiate or reactivate rheumatic fever.

    Severe scarring of the valves develops during a period of months to years after an episode of  rheumatic fever, and recurrent episodes may cause progressive damage to the heart valves. The mitral valve is affected most commonly and severely (65-70% of patients) followed by aortic valve. This eventually can lead to heart failure.

    Clinical features of Rheumatic Fever.

    • Fever (39 degrees Celcius)
    • Swollen, tender, red and extremely painful joint –particularly the knees and ankles. (Migrating Poly arthritis)
    • Nodules (lumps under the skin)
    • Shortness of breath and chest discomfort. Uncontrolled movement of arms, legs or facial muscle
    • General weakness
    • Carditis presenting with chest pain, dyspnea, palpitations, 

    Clinical features of Rheumatic Heart Disease.

    • Carditis: Carditis can involve the pericardium (pericarditis), myocardium (myocarditis), and endocardium (endocarditis) /
    • Polyarthritis: Acute pain and swelling in the joints, starting with one joint and onto the other(migratory polyarthritis),less often in kids.
    • Chorea: involuntary, irregular, unpredictable muscle movement
    • Erythema marginatum:  A long-lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance
    • Subcutaneous nodules:  Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees

    Diagnosis of Rheumatic Heart Disease

    • People with rheumatic heart disease will have or recently had strep throat infection ( throat culture / blood test may be used to check for streptococcus)
    • The patient may have the murmurs or rub that may  be heard during auscultation this may be due to blood leaking around the damaged valves
    • Along with complete medical history and physical examination, test to diagnosed rheumatic  heart disease may include:
    • Echocardiogram (cardiac echo).

      Electrocardiogram (ECG): valve insufficiency and ventricular dysfunction. are observed in patients with rheumatic heard disease.

      Cardiac MRI and Chest Radiography: Cardiomegaly, pulmonary congestion, and other findings consistent with heart failure may be observed on chest radiograph in individuals with rheumatic fever.

      Blood test:  C-reactive protein and erythrocyte sedimentation rate are elevated in individuals with rheumatic fever due to the inflammatory nature of the disease

    RHEUMATIC

    Modified JONES criteria guideline for the diagnosis of Rheumatic Heart Disease.

    (A)  Major  criteria

     Major criteria is a Jones criteria 

    • J – Joint involvement which is usually migratory and inflammatory joint involvement that starts in the lower joints and ascends to upper joints
    • O – (“O” Looks like heart shape) – indicating that patients can develop myocarditis or inflammation of the heart
    • N – Nodules that are subcutaneous
    • E – Erythema marginatum which is a rash of ring-like lesions that can start in the trunk or arms. When joined with other rings, it can create a snake-like appearance
    • S – Sydenham chorea is a late feature which is characterized by jerky, uncontrollable, and purposeless movements resembling twitches
    (B)  Minor Criteria

    Minor criteria include

    • C – CRP Increased (C-reactive Protein) High in cases of inflammation. (above 3mg/dl)
    • A – Arthralgia ( Joint pain)
    • F – Fever (> 38.5 degrees Celicius)
    • E – Elevated ESR (inflammation indicative) (>60mm/hr)
    • P – Prolonged PR Interval
    • A – Anamnesis (suggestive of rheumatism)
    • L – Leukocytosis

    Diagnostic

    • Evidence of Group A Streptococcal Infection + 2 major criteria
      or
    • 1 major + 2 minor criteria
    A prolonged PR interval 
    represents a delay in the time it takes for the
    signal to move across the atria at the top of the heart,
    which receive blood flowing in from the veins,
    into the ventricles at the bottom of the heart,
    which pump blood out into the arteries
    (C) Supportive evidence of preceding group A streptococcal infection including;

    Positive throat culture for group A streptococci, raised titers of streptococcal antibodies (ant streptolysin O and S, ant streptokinase), and recent scarlet fever.

    Investigations for rheumatic heart disease

    • Throat swab/ culture.
    • Rapid antigen detection test
    • Anti-streptococcal antibody titers.
    • CBC
    • Physical examination; murmurs? Abnormal rhythms?
    • Chest x-ray may show cardiomegaly, congestion.
    • Echocardiogram/ Doppler echocardiography may show effusion, vulvular dysfunction

    Management of Rheumatic Heart Disease.

    The treatment depends on how much damage has been done to the heart valves. In severe cases, treatment may include surgery to replace or repair the badly damaged valves. The  medical treatment is divided into three parts i.e.

    1.  Prevent and eradicate infection
    2. Maximize cardiac output
    3. Promote comfort

     1.   To prevent and eradicate infection

    ´The best treatment  is to prevent rheumatic fever by giving antibiotic for throat infection and keep rheumatic fever from developing hence prevent damage to the  valves.

    >   i.m benzathine penicillin 0.6-1.2 mu every 4 weeks, the same dose is given every 3 weeks in areas where rheumatic fever is endemic.
    > Note. patients with rheumatic fever and have developed carditis and valve damage should receive antibiotic for at least 10 years or until age of 40 years. Patients who had rheumatic fever without valve damage do not need this prophylaxis.

    2.  To maximize cardiac output

    • Anti-inflammatory. Treatment of the acute inflammatory manifestations of acute rheumatic fever consists of salicylates and steroids; aspirin in anti-inflammatory doses effectively reduces all manifestations of the disease except chorea.
    • Analgesics for pain relief such as Paracetamol are preferred to opioids.
    • Corticosteroids. If moderate to severe carditis is present as indicated by cardiomegaly, third-degree heart block, or Congestive Heart Failure, add orally prednisone to salicylate therapy.
    • Anticonvulsant medications. For severe involuntary movements caused by Sydenham chorea, prescribe an anticonvulsant, such as valproic acid or carbamazepine (Carbatrol, Tegretol, others).
    • Antibiotics. Such as penicillin or erythromycin or another antibiotic to eliminate remaining strep bacteria.
    • Surgical care. When heart failure persists or worsens after aggressive medical therapy for acute Rheumatic Heart Disease, surgery to decrease valve insufficiency may be lifesaving; approximately 40% of patients with acute rheumatic fever subsequently develop mitral stenosis as adults.
    • Diet. Advise nutritious diet without restrictions except in patients with Congestive heart failure, who should follow a fluid-restricted and sodium-restricted diet; potassium supplementation may be necessary because of the mineralocorticoid effect of corticosteroid and the diuretics if used.
    • Activity. Initially, place patients on bed rest, followed by a period of indoor activity before they are permitted to return to school or work; do not allow full activity until the PRs have returned to normal; patients with chorea may require a wheelchair and should be on homebound instruction until the abnormal movements resolve.
    • ACE Inhibitors e.g captopril, enapril, beta blockers e.g. bisoprolol, metoprolol, diuretics and digitalis e.g digoxin.
    • Therapy for congestive heart failure. Heart failure in Rheumatic heart disease probably is related in part to the severe insufficiency of the mitral and aortic valves and in part to pancarditis; therapy traditionally has consisted of an inotropic agent (digitalis) in combination with diuretics (furosemide, spironolactone) and afterload reduction (captopril).

    3.   To promote comfort

    • Patients with arthritic complication are given salicylate e.g. aspirin
    • Encouraged to have bed rest
    • Warm compress on the joints
    • And use of bed cradle to lift the weight of bed linen from the affected joints
    Complications of rheumatic heart disease
    • Heart failure: This occur from either narrowed or leaking heart valve.
    • Bacterial endocarditis .infection of the inner lining of the heart this occur when the rheumatic fever has damaged the heart valves.
    • Raptured heart valves. this is a medical emergency that require urgent surgery to replace or repair the damaged heart valve.
    • Cerebral stroke: this occur when  a piece of vegetation dislodges itself and join circulation to the cerebral vessels.
    • Pulmonary hypertension due to systemic congestion with blood.
    • Atrial fibrillation. happens when abnormal electrical impulses suddenly start firing in the atria. These impulses override the heart’s natural pacemaker, which can no longer control the rhythm of the heart. This causes you to have a highly irregular pulse rate.
    • Infective Endocarditis, pericarditis and myocarditis.
    Nursing Diagnosis
    1. Decreased cardiac output related to valve stenosis as evidenced by shortness of breath, fatigue, dizziness.
    2. Acute pain related to inflammation of synovial membranes as evidenced by patient verbalizing about painful joints.
    3. Hyperthermia related to inflammation of synovial membranes and heart valves as evidenced by a thermometer reading of 38 degrees Celsius.
    4. Activity intolerance related to muscle weakness as evidenced by prolonged bed rest.
    5. Self care deficit related to polyarthritis, therapy, bed rest.
    6. Impaired skin integrity related to skin inflammation as evidenced by subcutaneous nodules and skin rash.
    7. Risk for impaired Gas exchange related to blood accumulation in the lungs due to atrial filling.
    8. Risk for injury related to chorea.
    9. Risk for non-compliance with prophylactic drug therapy related to financial or emotional burden of lifelong therapy.

    Rheumatic Heart Disease Read More »

    Sickle Cell Disease

    Sickle Cell Disease

    Sickle Cell Disease/Sickle Cell Anaemia

    Sickle cell disease is an inherited red-blood cell disorder which causes the body to produce abnormally shaped red blood cells.

    Sickle cell disease is inherited as an autosomal recessive trait. Normal Hb A gets replaced with Abnormal Hb S.

    Children with this disorder have atypical haemoglobin  molecules called haemoglobin S which can distort red blood cells into a sickle or crescent shape.

    sickle cell normal and abnormal

    Red blood cells with normal hemoglobin are smooth, disk-shaped, and flexible, like doughnuts without holes. They can move through the blood vessels easily.

    Cells with sickle cell hemoglobin are stiff and sticky. When they lose their oxygen, they form into the shape of a sickle or crescent, like the letter C.

    These cells stick together and can’t easily move through the blood vessels. This can block small blood vessels and the movement of healthy, normal oxygen-carrying blood. The blockage can cause pain

    Classification of sickle cell disease

    Disease is broadly classified into;

    1.  Sickle Cell Anaemia (Homozygous): Are patients whose Red blood cells only contain abnormal beta chains leading to HbSS (SS). These patients are said to have sickle-cell anaemia and they have S+S of Sickle cell disease. Individuals with sickle cell anaemia inherit two copies of the faulty haemoglobin gene, one from each parent. This is denoted as HbSS or SS. Other names: HbSS, SS disease, Haemoglobin S.

    2. Sickle Cell Trait (Heterozygous): Patients whose Red blood cells contain a mixture of normal beta chains of HbA and abnormal beta chains of HbS. Thus patients have both HbA and HbS (HbAS). Individuals with sickle cell trait inherit one copy of the normal haemoglobin gene and one copy of the faulty haemoglobin gene. This is denoted as HbAS. People with sickle cell trait are usually asymptomatic, meaning they don’t experience the typical symptoms of SCD. They are carriers of the faulty gene and can pass it on to their children.

    To understand Homozygous and Heterozygous,

    SCD (Sickle Cell Disease): Think of this as a house built with a faulty instruction manual. The manual has instructions for building strong, healthy red blood cells (the “bricks” of your blood), but the instructions are messed up. This leads to problems with the shape and function of red blood cells, causing sickle cell disease.

    Autosomal: This refers to the chromosomes that determine most of your traits, except for sex (male or female). Imagine these chromosomes like the foundation of your house.

    Heterozygous: You have two copies of each autosomal chromosome, one from each parent. Imagine you received an instruction manual with good instructions from your mom and a manual with a faulty set from your dad. This means you have a good copy and a faulty copy of the gene that causes sickle cell disease. You are a “carrier” of the faulty gene, but you don’t have SCD.

    Homozygous: You received the same instruction manual from both parents. There are two possibilities:

    • Homozygous dominant: You received two good instruction manuals (from both parents). Your house is built strong and healthy, you don’t have SCD.
    • Homozygous recessive: You received two faulty instruction manuals (from both parents). Your house has serious problems, you have SCD.

    Recessive: A recessive gene only causes a disease when you have two faulty copies (like in the homozygous recessive case). Think of it as needing two faulty instruction manuals to build a house with problems.

    Dominant: A dominant gene always causes a disease, even if you only have one faulty copy (like in the heterozygous case). Imagine the faulty instruction manual overrides the good one.

    Summary:

    • SCD: A faulty instruction manual leads to problems with red blood cells.
    • Autosomal: The chromosomes that determine most traits (the house’s foundation).
    • Heterozygous: You have one good and one faulty copy of a gene (one good and one faulty instruction manual).
    • Homozygous: You have two identical copies of a gene (two good or two faulty instruction manuals).
    • Recessive: You need two faulty copies to express the disease (two faulty instruction manuals to build a bad house).
    • Dominant: You only need one faulty copy to express the disease (one faulty instruction manual is enough to build a bad house).
    • Red Blood Cells: These cells carry oxygen throughout the body.
    • Haemoglobin: A protein within red blood cells that binds to oxygen.
    • Haemoglobin Gene: A gene located on chromosome 11 that provides instructions for making haemoglobin.

    Possibility of Sickle cell Disease

    Problems in sickle cell disease begin around 5 to 6 months of age. Sickle-cell disease occurs when a person inherits two abnormal copies of the haemoglobin gene, one from each parent. This gene occurs in chromosome 11.

    Type of GeneNormalTraitDisease
    One Parent with Trait50%50%0%
    Both Parents with Trait25%50%25%
    One Parent with Disease50%50%50%
    Both Parents have Disease0%0%100%

    Cause of Sickle Cell Disease

    • It is caused by a defect in beta chains where a given amino acid is replaced by another (Substitution of valine for glutamic acid) at position 6 of the chain.
    • This change creates abnormal hemoglobin called HbS.

    Sickle cell disease is caused by a genetic mutation in the gene that produces haemoglobin, a protein in red blood cells that carries oxygen.

    • Normal Haemoglobin: Normal haemoglobin is made up of two alpha chains and two beta chains, denoted as HbA.
    • Sickle Cell Haemoglobin: In sickle cell disease, there’s a single point mutation in the beta chain of haemoglobin, replacing a glutamic acid with valine, at position 6 of the chain.This mutated haemoglobin is called HbS.

    Pathophysiology of Sickle Cell Disease.

    Normally each haemoglobin molecule consists of four molecules of haem folate into one molecule of globin.

    But in sickle cell disease this is altered and cells become sickle shaped, glutamine is replaced by valine. The sickle cells elongate under conditions of lower oxygen concentration, Acidosis takes place and dehydration.

    When red blood cells (RBCs) containing homozygous HbS are exposed to deoxygenated conditions, the sickling process begins. This distorts the membranes of red blood cells. The cell becomes easily entangled leading to blood viscosity, vessel occlusion and tissue necrosis.

    These cells fail to return to normal shape when normal oxygen tension is restored. As a result, these rigid blood cells are unable to deform as they pass through narrow capillaries, leading to vessel occlusion and ischemia. The actual anaemia of the illness is caused by haemolysis, the destruction of the red cells, because of their shape.

    Although the bone marrow attempts to compensate by creating new red cells, it does not match the rate of destruction. Healthy red blood cells usually function for 90–120 days, but sickled cells only last 10–20 days. Increased sequestration of Red blood cells in the spleen also cause anaemia

    Clinical Presentation of SCD 

    Children are rarely symptomatic until late in the first years of life related to increased amounts of fetal haemoglobin being cleared from blood. The severity of symptoms can vary from person to person. Sickle-cell disease may lead to various acute and chronic complications, several of which have a high mortality rate.

    • Painful swelling of hands and feet (Hand-foot syndrome): This is a common presentation in children, caused by vaso-occlusive crisis in the small blood vessels of the hands and feet.
    • Pain crisis (sickle crisis): This is a major complication characterized by intense pain due to blocked blood flow to a specific area of the body and can last for days or weeks. Pain in the chest, abdomen, limbs, and joints.
    • Anaemia: A consistent feature, as the lifespan of sickle red blood cells is shortened. This leads to fatigue, weakness, and paleness.
    • Jaundice: Caused by the breakdown of red blood cells, leading to a yellowish discoloration of the skin and eyes.
    • Haemoglobin levels: Usually low, ranging from 6 g/dL to 9 g/dL, indicating the severity of anaemia.
    • Shortness of breath: Caused by complications like pneumonia, acute chest syndrome, and pulmonary hypertension.
    • Fatigue and weakness: A common symptom due to the low oxygen levels caused by anaemia.
    • Priapism: A painful erection lasting for hours or days, caused by blocked blood flow in the penis. If not promptly treated, it can lead to impotence.
    • Abdominal swelling and pain: Often associated with spleen enlargement (splenomegaly) or blockages in the blood vessels supplying the intestines.
    • Unusual headache: May be a sign of stroke, as sickled cells can block blood flow to the brain.
    • Loss of appetite: A common symptom associated with anaemia and pain.
    • Irritability: Can be a response to pain, fatigue, or other symptoms.
    • Bossing of the bones of the skull: Indicates active erythropoiesis (red blood cell production) to compensate for the loss of sickle cells.
    • Intercurrent infections: Patients with sickle cell disease are more susceptible to infections like pneumonia, acute respiratory infections, and malaria, often complicated by severe anaemia.
    • Splenomegaly: Enlarged spleen, common in younger children, but often shrinks in older children due to splenic infarction.
    • Growth retardation: Can occur due to chronic illness, pain, and infections.
    • Stroke: A serious complication resulting from blocked blood flow to the brain, leading to brain damage.

    Newborns: May present with jaundice, delayed cord clamping, and possible failure to thrive.

    Children:

    • Dactylitis (Hand-foot Syndrome): Painful swelling of hands and feet due to vaso-occlusive crisis.
    • Splenomegaly: Often present in young children, but can be absent in older children due to splenic infarction (damage).
    • Delayed growth and development are common due to recurrent infections and pain crises.
    • Delayed puberty: Can be a feature, especially in males.

    Adults:

    • Chronic pain is a defining feature, often with unpredictable patterns.
    • Pulmonary complications: Pulmonary hypertension, acute chest syndrome, and pneumonia are frequent issues.
    • Osteonecrosis: Damage to bone due to lack of blood flow.
    • Avascular necrosis: Can affect bones, especially hips and shoulders.
    • Chronic kidney disease: Can develop over time due to repeated damage to the kidneys.
    Chronic Symptoms:
    • Jaundice: Yellowing of the skin and whites of the eyes due to the breakdown of red blood cells.
    • Gallstones: Formation of stones in the gallbladder, often caused by a build-up of bilirubin from red blood cell breakdown.
    • Progressive kidney impairment: Damaged blood vessels in the kidneys can lead to reduced kidney function over time.
    • Growth retardation: Slower growth of long bones and skeletal deformities, particularly in the spine, can occur.
    • Delayed puberty: The chronic illness can delay the onset of puberty.
    • Chronic painful leg ulcers: Related to chronic anaemia and poor blood flow to the extremities.
    • Decreased lifespan: While advancements in medical care have improved life expectancy, individuals with sickle cell disease still have a shortened lifespan compared to the general population.
    • Altered body structures: These include “bossing” of the skull (abnormal thickening of the skull bones), as well as septic necrosis (bone death due to infection) in the femur (thigh bone) and head of the humerus (upper arm bone).

    Sickle-cell crisis

    Sickle cell crisis is pain that can begin suddenly and lasts several hours to several days.

    The terms “sickle-cell crisis” or “sickling crisis” may be used to describe several independent acute conditions occurring in patients with Sickle Cell Disease. It happens when sickled red blood cells block small blood vessels that carry blood to bones. Children may present with pain in the back, knees, legs, arms, chest or stomach. The pain can be throbbing, sharp, dull or stabbing.

    Types of Sickle Cell Crisis.

    (i)  Vaso-occlusive Crisis: This is the most common form of crisis. Small blood vessels are occluded by the sickle cells causing distal ischemia and infarction, leading to pain, swelling, and inflammation.

    • Symptoms: Intense pain in the bones, joints, abdomen, chest, or head. Other symptoms may include fever, fatigue, and shortness of breath.
    • Extremities.  Bone destruction leading to osteoporosis or ischaemic necrosis.
    • Foot and hand syndrome due to aseptic infarction of metacarpals and metatarsals causing swelling and pains often this is seen in infants and toddlers.
    • Triggers: Dehydration, infection, cold weather, high altitude, and strenuous physical activity.
    • Treatment: Pain management with analgesics, intravenous fluids, and blood transfusions in severe cases.

    (ii)  Splenic sequestration Crisis:  Large amounts of blood become pooled to the spleen, leading to a decrease in blood volume and blood pressure. The spleen becomes massively enlarged.

    • Symptoms: Abdominal pain, swelling, fever, and shock. Great decrease in Red blood cells mass occurs within hours. Signs of circulatory collapse develop rapidly.
    • This is the most frequent cause of death in infants with sickle cell disease.
    • Treatment: Immediate medical attention with intravenous fluids, blood transfusions, and sometimes splenectomy.

    (iii) Aplastic Crisis:  The bone marrow ceases to produce RBCs. A sudden drop in red blood cell production, leading to severe anaemia and worsening of symptoms. There will be low blood cell circulation in blood hence anaemia.

    • Cause: Usually triggered by viral infections like parvovirus B19. Folic acid deficiency and Ingestion of bone marrow toxins (eg, phenylbutazone).
    • Symptoms: Fatigue, weakness, pallor, and shortness of breath.
    • Treatment: Blood transfusions to increase red blood cell count.

    (iv) Haemolytic CrisisHemolytic crisis occurs when large numbers of red blood cells are destroyed over a short time. The loss of red blood cells occurs much faster than the body can produce new red blood cells.

    • Cause: Often triggered by infections.
    • Symptoms: Fatigue, pallor, jaundice, and dark urine.
    • Treatment: Blood transfusions and treatment of underlying infections.

    Causes of hemolysis include:

    • A lack of certain proteins inside red blood cells
    • Autoimmune diseases
    • Certain infections
    • Defects in the haemoglobin molecules inside red blood cells
    • Defects of the proteins that make up the internal framework of red blood cells
    • Side effects of certain medicines
    • Reactions to blood transfusions.

    (v)  Acute chest syndrome. This occurs in the chest, when sickled red blood cells block blood flow to the lungs, leading to inflammation and damage. This can be life-threatening. It often occurs suddenly, when the body is under stress from infection, fever, or dehydration. 

    • Symptoms: Chest pain, fever, shortness of breath, cough, and rapid breathing.
    • Treatment: Oxygen therapy, antibiotics, pain management, and sometimes mechanical ventilation.

    Precipitating Factors of Sickle Cell Crisis

    Sickle cell crises are painful episodes that occur when sickle red blood cells block blood flow in the body. These crises can be triggered by various factors, including:

    Environmental and Physiological Factors:

    • Dehydration: Lack of fluids can thicken the blood, making it harder for sickle cells to flow through small blood vessels.
    • Infection: Infections can increase the body’s demand for oxygen, putting stress on already compromised red blood cells.
    • Trauma: Injury, including even minor cuts or bruises, can lead to localized blood clotting and trigger a crisis.
    • Extreme Temperature Fluctuations: Both extreme heat and cold can constrict blood vessels and lead to blockage.
    • High Altitude: The thinner air at high altitudes can lead to oxygen deprivation, increasing the likelihood of sickling.
    • Hypoxia: Low oxygen levels in the blood, from any cause, can trigger sickling.
    • Acidosis: Increased acidity in the blood can also contribute to sickling.

    Lifestyle and Emotional Factors:

    • Strenuous Physical Exercise: Intense physical activity can increase the body’s demand for oxygen and contribute to sickling.
    • Extreme Fatigue: Prolonged exhaustion weakens the body’s ability to fight off crises.
    • Extreme Exertion: Similar to intense exercise, any extreme physical effort can trigger a crisis.
    • Emotional Stress: Stress hormones can constrict blood vessels and increase the likelihood of sickling.

    Other Contributing Factors:

    • Pregnancy: The increased blood volume and hormonal changes during pregnancy can make women more susceptible to crises.
    • Asthma: The inflammatory response in asthma can trigger sickle cell crises.
    • Anxiety: Similar to stress, anxiety can constrict blood vessels and increase the risk of a crisis.
    • Dehydration.
    • Infection.
    • Trauma.
    • Strainous Physical exercises.
    • Extreme fatigue.
    • Extreme exertion
    • Severe cold that constricts peripheral vessels
    • Fever Excessive exercise
    • Hypoxia.
    • Acidosis.
    • Extreme temperature
    • High attitude
    • Emotional stress
    • Pregnancy
    • Asthma
    • Anxiety
    • Abrupt changes in temperature
    Diagnosis and Investigations sickle (2) (1)

    Diagnosis and Investigations:

    • Family history: A strong family history of sickle cell disease is a big indicator.
    • Full blood count and peripheral film: The blood test may show leukocytosis (increased white blood cell count) due to bacterial infection and reveal the presence of sickle cells.
    • Haemoglobin estimation: Will reveals a low haemoglobin level (6-8 g/dL) with a high reticulocyte count (10-20%), indicating the body’s attempt to compensate for the loss of red blood cells.
    • Sickling test: This simple test, done by finger or heel prick, observes a drop of blood under a microscope after removing oxygen. Sickle-shaped cells are indicative of the disease. However, it doesn’t distinguish between the trait and the disease or other sickle haemoglobin opathies.
    • Haemoglobin electrophoresis: This more definitive test involves separating different types of haemoglobin through an electric current. It identifies the presence and amount of HbS (sickle haemoglobin), providing a definitive diagnosis for both the trait and the disease.
    • Sickledex test: A rapid screening test for detecting the presence of HbS in the blood.
    • Peripheral blood smear: Examines a blood sample under a microscope to identify sickle cells and reticulocytes.
    • Urinalysis: Analyzes urine for signs of kidney damage.
    • Liver and renal function tests: Assess the function of the liver and kidneys.
    • Chest radiography: Used to diagnose Acute Chest Syndrome.
    • Abdominal ultrasound: Can help detect problems in the abdomen, such as a mesenteric crisis (blockage of blood vessels in the intestines).
    • Sickling test (emergency screening): Can be performed before surgery to identify individuals with sickle cell disease.
    Differential Diagnosis
    • Acute anaemia
    • Carotid-Cavernous Fistula (CCF)
    • haemoglobin  C Disease
    • Hemolytic Anaemia
    • Osteomyelitis in Emergency Medicine
    • Pulmonary Embolism (PE)
    • Rheumatoid Arthritis Hand Imaging
    • Septic Arthritis

    Management of Sickle Cell Disease.

    Management is according to the type of crisis .

    Aims of Management

    • Avoiding pain episodes.
    • Relieving symptoms.
    • Preventing complications.
    1. Acute painful attacks require supportive therapy with intravenous fluids, oxygen, antibiotics and adequate analgesia.
    2. Crises can be extremely painful and usually require narcotic analgesia. Morphine is the drug of choice. Milder pain can sometimes be relieved by codeine, paracetamol and NSAIDs.
    3. Oxygen Therapy: Supplementary oxygen is provided to address hypoxia and alleviate symptoms.
    4. Prophylaxis is with penicillin twice daily, up to 5 years of age due to the immature immune system that makes them more prone to early childhood illnesses is recommended and vaccination with polyvalent pneumococcal and Haemophilus influenzae type B vaccine .
    5. Hydration: Drinking plenty of fluids is essential to prevent dehydration and improve blood flow.
    6. Blood Transfusions: Regular transfusions are used to increase haemoglobin levels and reduce the frequency of crises. Transfusions should be given for heart failure, strokes, acute chest syndrome, acute splenic sequestration and aplastic crises.
    7. Anaemia Transfusions should only be given for clear indications.
    8. Patients with steady state anaemia, those having minor surgery or having painful episodes without complications should not be transfused.
    9. Transfusion and splenectomy may be life-saving for young children with splenic sequestration. A full compatibility screen should always be performed.
    10. Folic acid 5 mg daily for life is recommended.
    11. Hydroxycarbamide (hydroxyurea)starting dose 20 mg/kg is the first drug which has been widely used as therapy for sickle cell anaemia. It acts by increasing Hb F concentrations but the reduction in neutrophils may also help. Hydroxycarbamide has been shown in trials to reduce the episodes of pain, the acute chest syndrome and the need for blood transfusions.
    12. Malaria prevention: Since they are more vulnerable to malaria, because the most common cause of painful crises in malaria countries is infection with malaria. It has therefore been recommended that people with sickle-cell disease living in malarial countries should receive anti-malarial chemoprophylaxis monthly for life i.e sulfadoxine pyrimethamine.
    13. Pain management
    14. Home management
    • Paracetamol 1 g every 8 hours
    • Child: 10-15 mg/kg 6-8 hourly
    • And/or ibuprofen Child: 5-10 mg/kg 8 hourly.
    • Adults 400-600 mg 6-8 hourly.
    • And/or diclofenac 50 mg 8 hourly
    • Children only >9 years and >35 kg: 2 mg/kg in 3 divided doses.
    • If pain not controlled, add:
    • Codeine 30-60 mg every 6 hours (only in patients >12 years).
    • Or tramadol 50-100 mg every 6-8 hours (only in  patients >12 years)
    • Or Oral morphine at 0.2-0.4 mg/kg every 4 hours and re-assess pain level.
    • If pain still not controlled, refer to hospital

    • At the hospital; 

    • Morphine oral: Child and Adult: 0.3-0.6 mg/kg per dose and re-assess

    • Morphine Intravenously.

    • Child: 0.1-0.2 mg/kg per dose

    • Adult: 5-10 mg dose and re-assess

    • Use of laxative: bisacodyl 2.5 mg to 5 mg orally to prevent constipation due to morphine intake.

    Cure

    • The only therapy approved by the FDA that may be able to cure SCD is a bone marrow or stem cell transplant.
    • Bone marrow or stem cell transplants are very risky and can have serious side effects, including death. For the transplant to work, the bone marrow must be a close match. Usually, the best donor is a brother or sister.

     Lifestyle Modifications:

    • Regular Exercise: Moderate exercise, when tolerated, can improve cardiovascular health and reduce the risk of complications.
    • Stress Management: Techniques like relaxation, meditation, and yoga can help manage stress levels and reduce the risk of crises.
    • Healthy Diet: A nutritious diet rich in fruits, vegetables, and whole grains can support overall health.
    • Avoidance of Extreme Temperatures: Extreme heat and cold can trigger crises.
    • Altitude Management: Individuals should avoid high altitudes to minimize the risk of hypoxia.

    Surgery:

    • Bone Marrow Transplant: This is a potential cure, but it is a high-risk procedure with limited availability.
    • Other Surgical Interventions: Surgical procedures may be necessary to correct bone deformities or treat complications like leg ulcers.

    Support and Counseling:

    • Genetic Counselling: Provides information about the inheritance of sickle cell disease and family planning options.
    • Psychosocial Support: Provides emotional and practical support to help individuals cope with the challenges of living with sickle cell disease.
    • Patient Education: Empowers individuals to manage their condition effectively by providing information on symptoms, triggers, and treatment options.

    Prevention of Sickle cell crisis.

    1. Hydration:

    • Drink plenty of water: Staying well-hydrated is crucial for maintaining adequate blood flow and preventing sickling.
    • Carry a water bottle and sip water regularly throughout the day.
    • Avoid dehydration, especially during exercise, hot weather, or travel.

    2. Temperature Management:

    • Avoid extreme temperatures: Both excessive heat and cold can trigger sickle cell crises.
    • Stay in air-conditioned environments during hot weather.
    • Dress in layers to adjust to temperature changes.
    • Be aware of the risk of hypothermia during cold weather.

    3. Altitude Management:

    • Avoid high altitudes: Low oxygen levels at high altitudes can worsen sickle cell symptoms.

    4. Oxygen Management:

    • Avoid situations with low oxygen levels: Avoid intense physical exertion, especially in hot, humid, or high-altitude environments.
    • Use proper breathing techniques during exercise.

    5. Infection Prevention:

    • Vaccination: Receive all recommended vaccinations, including the pneumococcal vaccine, to protect against infections.
    • Wash your hands frequently with soap and water.
    • Use hand sanitizer when soap and water are unavailable.
    • Avoid close contact with sick individuals.
    • Practice safe food handling and preparation to prevent foodborne illness.

    6. Routine Medical Care:

    • Yearly visits to an eye doctor: Regular eye exams are crucial to monitor for signs of retinopathy, a serious complication of sickle cell disease.
    • Regular checkups with a haematologist: Follow your doctor’s recommendations for regular blood tests and monitoring.
    • Early intervention: Seek medical attention promptly for any unusual symptoms or signs of a sickle cell crisis.

    7. Stress Management:

    • Practice stress-reducing techniques: Stress can trigger sickle cell crises.
    • Engage in activities you enjoy, like meditation, yoga, or spending time in nature.
    • Seek counselling or therapy if you’re struggling to manage stress.

    8. Lifestyle Modifications:

    • Maintain a healthy weight: Obesity can worsen sickle cell symptoms.
    • Eat a balanced diet rich in fruits, vegetables, and whole grains.
    • Avoid smoking and excessive alcohol consumption.
    • Get regular exercise, but consult your doctor about safe levels.

    9. Advocacy and Support:

    • Join a sickle cell support group: Connect with other individuals living with sickle cell disease and share experiences and resources.
    Nursing Diagnosis
    1. Acute pain related to tissue hypoxia due to agglutination of sickled cells within blood vessels evidenced by patient verbalization.
    2. Risk for infection related to lowered immunity.
    3. Impaired Gas Exchange related to decreased oxygen-carrying capacity of the blood, reduced RBC life span/premature destruction, abnormal RBC structure; sensitivity to low oxygen tension (strenuous exercise, increase in altitude) as evidenced by difficulty in breathing.
    4. Ineffective Tissue Perfusion related to vaso-occlusive nature of sickling as evidenced by changes in vital signs: diminished peripheral pulses/capillary refill, general pallor or decreased mentation, restlessness.
    5. Risk for Deficient Fluid Volume related to increased fluid needs, e.g., hypermetabolic state/fever, inflammatory processes.
    6. Acute Pain related to Intravascular sickling with localized stasis, occlusion, and infarction/necrosis as evidenced by  generalized pain, described as throbbing,  or severe ; affecting peripheral extremities, bones, joints, back, abdomen, or head (headaches)
    7. Risk for Impaired Skin Integrity related to impaired circulation (venous stasis and vaso-occlusion)

    Prevention Of Sickle Cell Disease

    • Genetic counselling is important to prevent passing on the trait or disease to children for those wanting to have them.
    • Premarital counselling is encouraged. Early recognition/screening of children with low Hb.

    Complications of Sickle Cell anaemia

    1. Stroke. Issues in circulation will result to blockages, therefore predisposing the patient to develop thrombolytic strokes
    2. Acute chest syndrome. This is characterized by chest pain, fever and difficulty breathing requiring emergency medical treatment
    3. Pulmonary hypertension. This type of anaemia can cause build-up of unnecessary lung pressure due to problems with circulation as a result of erythrocyte clumping
    4. Organ damage. Due to the chronic inability of the red blood cells to provide essential oxygen for normal organ function, patients with sickle cell anaemia may develop organ failure, which can be fatal.
    5. Blindness. One of the potential complications of having abnormal red blood cells circulating in the body is damage to smaller blood vessels, particularly the eye. This in turn will cause eye damage and eventually blindness.
    6. Leg ulcers. Poor wound healing and rampant skin breakdown can be observed for patients suffering from sickle cell anaemia.
    7. Gallstones. The build of bilirubin caused by the metabolism of the abnormal erythrocytes will result to gall stones that will block the flow of bile.
    8. Priapism. This is a condition wherein men with Sickle cell anaemia will present with painful and long-lasting erections due to the blockages of the tiny blood vessels of the penis.
    9. Pregnancy complications. Sickle cell anaemia increases the risk of high blood pressure and the presence of clots that will interfere with the normal development of the fetus.

    NURSING CARE PLAN FOR A PATIENT WITH SICKLE CELL CRISIS

    Assessment

    Diagnosis

    Goals/Expected Outcomes

    Intervention

    Rationale

    Evaluation

    Cyanosis, breathlessness at a rate of 28 breaths/min, restlessness, and SpO2 of 80%.

    Impaired gaseous exchange related to increased viscosity of blood evidenced by cyanosis, breathlessness, restlessness, and SpO2 of 80%.

    – Establish adequate gaseous exchange within 2 hours.

    – Improve SpO2 by 10% within the first 30 minutes.

    – Establish a normal breathing pattern without assisted respiration within 1 hour.

    – Restore normal skin color in 30 minutes.

    – Establish an intravenous line and administer fluids (normal saline 500 mL every 6 hours for 24 hours).

    – Encourage fluid intake by mouth.

    – Start a fluid input and output chart.

    – Assess the need for more fluids after 24 hours.

    – Take vital signs every 30 minutes for 2 hours, paying attention to breathing and SpO2, then adjust according to findings.

    – Administer oxygen 3 L/min for 1 hour using a face mask.

    – Establishing IV access and administering fluids help to reduce blood viscosity and improve circulation.

    – Encouraging oral fluid intake promotes hydration.

    – Fluid balance chart helps to monitor fluid status.

    – Regular assessment ensures timely adjustments in fluid therapy.

    – Oxygen therapy increases oxygen saturation in the blood.

    – Patient is resting.

    – Normal breathing pattern restored, rate 20 breaths/min.

    – SpO2 improved to 98% on room air.

    – Normal skin colour restored, lips look pink.

    Patient verbalizing throbbing pain in the legs and joints, rating score of 8 on the pain scale.

    Acute pain related to intravascular sickling with localized stasis evidenced by patient verbalizing throbbing pain in the legs and joints.

    – Relieve pain within 4 hours.

    – Improve venous patency

    –  Improve circulatory flow.

    – Administer analgesia (pethidine 50 mg single dose, then tramadol 50 mg every 8 hours for 3 days as prescribed and document).

    – Continue intravenous fluids as above and monitor pain hourly.

    – Analgesics provide comfort and relieve restlessness.

    – IV fluids maintain normal circulatory flow.

    – Patient reports pain relief after 4 hours, score 2 on the pain scale.

    Reduced haemoglobin  levels of 5 g/L according to laboratory results, swelling of the lower limbs and joints.

    Altered tissue perfusion related to decreased red blood cells as evidenced by reduced haemoglobin levels of 5 g/L, swelling of the lower limbs and joints.

    – Restore normal tissue perfusion within 24 hours.

    – Establish normal tissue perfusion.

    – Transfuse with units of packed cells 5 mL/kg/h as prescribed.

    – Continue with fluid balance chart.

    – Apply a warm compress to the affected areas.

    – Elevate the affected limbs.

    – Blood transfusion increases haemoglobin levels.

    – Fluid balance chart monitors fluid status.

    – Warm compresses promote vasodilation and circulation to hypoxic areas.

    – Elevation reduces swelling and promotes venous return.

    – Increased haemoglobin  levels of 7 g/dL as seen in post-transfusion lab report.

    – Swelling has subsided, and the patient is able to move the limb.

    Fever, hypermetabolic state, dehydration symptoms (dry mucous membranes, poor skin turgor).

    Risk for fluid volume deficit related to increased fluid needs due to hypermetabolic state or fever.

    – Maintain adequate hydration.

    – Prevent fluid volume deficit.

    – Monitor vital signs and fluid status regularly.

    – Encourage oral fluid intake and administer IV fluids as needed.

    – Educate the patient on the importance of fluid intake.

    – Regular monitoring detects early signs of fluid deficit.

    – Ensuring adequate hydration prevents complications.

    – Fluid balance is maintained, and signs of dehydration are absent.

    Presence of venous stasis, vaso-occlusion, decreased mobility, and risk of skin breakdown.

    Risk for impaired skin integrity related to impaired circulation due to venous stasis and vaso-occlusion, and decreased mobility.

    – Prevent skin breakdown.

    – Maintain skin integrity.

    – Assess skin regularly for signs of breakdown.

    – Reposition the patient every 2 hours.

    – Provide skin care and keep the skin clean and dry.

    – Use pressure-relieving devices as needed.

    – Regular assessment and repositioning prevent pressure ulcers.

    – Good skin care promotes skin integrity.

    – Skin remains intact without signs of breakdown.

     

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