The placenta is implanted in the lower uterine segment near or over the internal cervical os. The degree to which the internal cervical os is covered by the placenta has been used to classify four types of placenta previa; total, partial, marginal and low–lying. In total previa the internal os is entirely covered by the placenta. Partial placenta previa implies incomplete coverage of the internal os. Marginal placenta previa indicates that only an edge of the placenta extends to the margin of the internal os. And the last is the low – lying placenta has been used when the placenta is implanted in the lower uterine segment but not reach the os. The more descriptive classification that includes placenta previa is in the third trimester.

The incidence of placenta previa is approximately 0.5% of births. The most important risk factors are previous placenta previa, previous cesarean birth, and suction curettage for miscarriage or induced abortion, possible related to endometrial scarring. The risk also increases with multiple gestations because of the larger placental area, closely spaced pregnancies, advanced maternal age older than 34 years, African or Asian ethnicity, male fetal sex, smoking, cocaine use, multiparity, and tobacco use.

Classification of Placenta Previa:

1. Total Previa- the placenta completely covers the internal cervical os.
2. Partial Previa- the placenta covers a part of the internal cervical os.
3. Marginal Previa- the edge of the placenta lies at the margin of the internal cervical os and may be exposed during dilatation.
4. Low-lying placenta- the placenta is implanted in the lower uterine segment but does not reach to the internal os of the cervix.

Predisposing Factors:

1. Multiparity (80% of affected clients are multiparous)
2. Advanced maternal age (older than 35 years old in 33% of cases
3. Multiple gestation
4. Previous Cesarean birth
5. Uterine Incisions
6. Prior placenta previa ( incidence is 12 times greater in women with previous placenta previa)

Complications for the baby include:

• Problems for the baby, secondary to acute blood loss
• Intrauterine growth retardation due to poor placental perfusion
• Increased incidence of congenital anomalies

Clinical Manifestations:

• Painless vaginal bleeding > occurs after 20 weeks of gestation, bright red in color associated with the stretching and thinning of the lower uterine segment that occurs in third trimester.
• Adequately contract and stop blood flow from open vessels.
• Stop blood flow from open vessels
• Decreasing urinary output

Normal Placenta During Childbirth

Process of placental growth and uterine wall changes during pregnancy

1. The placenta grows with the placental site during pregnancy.
2. During pregnancy and early labor the area of the placental site probably changes little, even during uterine contractions.
3. The semirigid, noncontractile placenta cannot alter its surface area.

Anatomy of the uterine/placental compartment at the time of birth

1. The cotyledons of the maternal surface of the placenta extend into the decidua basalis, which forms a natural cleavage plane between the placenta and the uterine wall.
2. There are interlacing uterine muscle bundles, consisting of tiny myofibrils, around the branches of the uterine arteries that run through the wall of the uterus to the placental area.
3. The placental site is usually located on either the anterior or the posterior uterine wall.
4. The amniotic membranes are adhered to the inner wall of the uterus except where the placenta is located

Anatomy of Female Reproductive System
Physiology of Female Reproductive System
Anatomy and Physiology of Male Reproductive System

Pathophysiology

No specific cause of placenta previa has yet been found but it is hypothesized to be related to abnormal vascularisation of the endometrium caused by scarring or atrophy from previous trauma, surgery, or infection.

In the last trimester of pregnancy the isthmus of the uterus unfolds and forms the lower segment. In a normal pregnancy the placenta does not overlie it, so there is no bleeding. If the placenta does overlie the lower segment, it may shear off and a small section may bleed.

Women with placenta previa often present with painless, bright red vaginal bleeding. This bleeding often starts mildly and may increase as the area of placental separation increases. Praevia should be suspected if there is bleeding after 24 weeks of gestation. Abdominal examination usually finds the uterus non-tender and relaxed. Leopold’s Maneuvers may find the fetus in an oblique or breech position or lying transverse as a result of the abnormal position of the placenta. Praevia can be confirmed with an ultrasound.[3] In parts of the world where ultrasound is unavailable, it is not uncommon to confirm the diagnosis with an examination in the surgical theatre.

The proper timing of an examination in theatre is important. If the woman is not bleeding severely she can be managed non-operatively until the 36th week. By this time the baby’s chance of survival is as good as at full term.

Diagnostic Evaluation:

Placenta previa is diagnosed using transabdominal ultrasound.
-    transabdominal scans with fewer false positive results

Transvaginal ultrasound

• If a woman is bleeding she is usually placed in the labor and birth unit or for cesarean birth because profound hemorrhage can occur during the examination. This type of vaginal examination knows as the double- setup procedure

Ultrasonographic scan

• If ultrasonographic scanning reveals a normally implanted placenta, an examination may be performed to rule out local causes of bleeding and a coagulation profile is obtained to rule out other causes of bleeding management of placenta previa depends of the gestational age and condition of the fetus and the amount and cesarean birth.

Complete blood count (CBC)

• To monitor mother’s blood volume

Fetoscope

• To monitor fetal heart rate and conditions

Medical Management:

• Maternal stabilization and fetal monitoring
• Control of blood loss, blood replacement
• Delivery of viable neonate
• With fetus of less than 36 weeks gestation, careful observation to determine safety of continuing pregnancy or need for preterm delivery
• Hospitalization with complete bed rest until 36 weeks gestation with complete placenta previa
• Possible vaginal delivery with minimal bleeding or rapidly progressing labor

Nursing Interventions:

1. If continuation of the pregnancy is deemed safe for patient and fetus administer magnesium sulfate as ordered for premature labor
2. Obtain blood samples for complete blood count and blood type and cross matching
3. Institute complete bed rest
4. If the patient and placenta previa is experiencing active bleeding, continuously monitor her blood pressure, pulse rate, respiration, central venous pressure, intake and output, and amount of vaginal bleeding as well as the fetal heart rate and rhythm
5. Assist with application of intermittent or continuous electronic fetal monitoring as indicated by maternal and fetal status.
6. Have oxygen readily available for use should fetal distress occur, as indicated by bradycardia, tachycardia, late or available decelerations, pathologic sinusoidal pattern, unstable baseline, or loss of variability.
7. If the patient is Rh-negative and not sensitized, administer Rh (D) immune globulin (RhoGAM) after every bleeding episode.
8. Administer prescribed IV fluids and blood products.
9. Provide information about labor progress and the condition of the fetus.
10. Prepare the patient and her family for a possible caesarian delivery and the birth of a preterm neonate, and provide thorough instructions for postpartum care.
11. If the fetus less than 36 weeks gestation expect to administer an initial dose of betamethasone: explain that additional doses may be given again in 24 hours and possibly for the next 2 weeks to help mature the neonates lungs.
12. Explain that the fetus survival depends on gestational age and amount of maternal blood loss. Request consultation with a neontologist or pediatrician to discuss a treatment plan with the patient and her family.
13. Assure the patient that frequent monitoring and prompt management greatly reduce the risk of neonatal death.
14. Encourage the patient and her family to verbalize their feelings helps them to develop effective coping strategies, and refer them for counseling, if necessary.
15. Anticipate the need for a referral for home care if the patient bleeding ceases and she’s to return home in bed rest.
16. During the postpartum period, monitor the patient for signs of early and late postpartum hemorrhage and shock.
17. Monitor VS for elevated temperature, pulse, and blood pressure, monitor laboratory results for elevated WBC count, differential shift; check for urine tenderness and malodorous vaginal discharge to detect early signs of infection resulting from exposure of placental tissue.
18. Provide or teach perineal hygiene to decrease the risk of ascending infection.
19. Observe for abnormal fetal heart rate patterns such as loss of variability, decelerations tachycardia to identify fetal distress.
20. Position the patient in side lying position and wedge for support to maximize placental perfusion.
21. Assess fetal movement to evaluate for possible fetal hypoxia.
22. Teach woman to monitor fetal movement to evaluate well being
23. Administer oxygen as ordered to increase oxygenation to mother and fetus.

Discharge Plan:

Medication

• Betamethasone (Celestone) is a corticosteroid that acts as an anti-inflammatory and immunosuppressive agent.
• Assess for contraindications of Betamethasone administration. Obtain reports of urine and cervical cultures and fibronectin.

Exercise

• Needs to adequate her time with her child to be certain he or she is all right, and nurse can states hearing fetal heart beat helps to reassure her about baby’s health.
• Attach contraction and fetal heart rate monitoring for continuous evaluation of contractions of fetal response.

Treatment

• Used of drugs
• Catheterization

Health Teaching

• Maintain a bed rest
• Maintain a 8 glasses of water

Ongoing Assessment

• Assess client’s home surrounding to determine whether they are appropriate for bed rest and continuing monitoring at home. Administer oral dose and home monitoring requires professional supervision.

Diet

• She might to begin to neglect her diet or her supplementary vitamins because “It doesn’t matter anymore”.

Spiritual

• Assess anxiety level of client over preterm labor possible feelings.
• Determine whether client wants a support person to be wit her, to the presence of a support person can offer additional comfort to a client.

Possible Nursing Diagnosis for Placenta Previa:

• Risk for Impaired Fetal Gas Exchange r/t Disruption of Placental Implantation
• Fluid Volume Deficit r/t Active Blood Loss Secondary to Disrupted Placental Implantation
• Active Blood Loss (Hemorrhage) r/t Disrupted Placental Implantation
• Fear r/t Threat to Maternal and Fetal Survival Secondary to Excessive Blood Loss
• Activity Intolerance r/t Enforced Bed Rest During Pregnancy Secondary to Potential for Hemorrhage
• Altered Diversional Activity r/t Inability to Engage in Usual Activities Secondary to Enforced Bed Rest and Inactivity During Pregnancy

View Nursing Care Plan – Placenta Previa

References:

• Maternal & Child Nursing Seventh Edition Vol.1 page 413.
• Maternity nursing, Lowdermilk Perry, seventh edition, chapter 23, page 751.
• Maternal Neonatial Nursing Lippincott manual of Nursing Practice
• http://wikipedia.org
• Pregnancy care

Related posts:

1. Placenta Previa
2. Nursing Care Plan – Placenta Previa
3. Nursing Care Plan – Abruptio Placenta

Pregnancy Induced Hypertension (PIH) is a condition in which vasospasms occur during pregnancy in both small and large arteries. Signs of hypertension, proteinuria, and edema develop. It is unique to pregnancy and occurs in 5% to 7% of pregnancies in the united states. Despite years of research, the cause of the disorder is still unknown. Originally it was called toxemia because researchers pictured a toxin of some kind being produced by a women in response to foreign protein of the growing fetus, the toxin leading to the topical symptoms. No such toxins have ever been identified.

A condition separate from chronic hypertension, PIH tends to occur most frequently in women of color or with a multiple pregnancy; primiparas are younger than 20 years of age or older than 40 years, women from low socio economic backgrounds, those who have an underlying disease such as heart disease, diabetes with vessel or renal involvement and essential hypertension.

PIH is classified as gestational hypertension, mild preeclampsia, severe preeclampsia and eclampsia, depending on how far development advances. Gestational hypertension when develops an elevated blood pressure but has no proteinuria or edema. Perinatal mortality is not increased with simple gestational hypertension, so no drug therapy is necessary; and blood pressure returns to normal after birth. Mild preeclampsia when blood pressure rises to 140/90 mmHg or systolic pressure elevated 15 mmHg above pregnancy level; mild edema in upper extremities or face. Severe preeclampsia when blood pressure has risen to 160 mmHg systolic and 110 mmHg diastolic; proteinuria; pulmonary or cardiac involvement; extensive peripheral edema; hepatic dysfunction; theombocytopenia. Eclampsia is the most severe classification of PIH and seizure or coma Accompanied by s/s of preeclampsia. Any woman who falls into one of the high-risk categories for PIH should be observed carefully for symptoms at prenatal visits. She needs instructions about what symptoms to watch for so she can alert her clinician if additional symptoms occur between visits.

Anatomy and Physiology:

When most people hear the term cardiovascular system, they immediately think of the heart. We have all felt our own heart "pound" from time to time, and we tend to get a bit nervous when this happens. The crucial importance of the heart has been recognized for a long time. However, the cardiovascular system is much more than just the heart, and from a scientific and medical standpoint, it is important to understand why this system is so vital to life.

Most simply stated, the major function of the cardiovascular system is transportation. Using blood as the transport vehicle, the system carries oxygen, nutrients, cell wastes, hormones, and many other substances vital for body homeostasis to and from the cells. The force to move the blood around the body is provided by the beating heart. The cardiovascular system can be compared to a muscular pump equipped with one-way valves and a system of large and small plumbing tubes within which the blood travels.

HEART:

The heart is a muscular organ found in all vertebrates that is responsible for pumping blood throughout the blood vessels by repeated, rhythmic contractions.
The heart is enclosed in a double-walled sac called the pericardium. The superficial part of this sac is called the fibrous pericardium. This sac protects the heart, anchors its surrounding structures, and prevents overfilling of the heart with blood. It is located anterior to the vertebral column and posterior to the sternum. The size of the heart is about the size of a fist and has a mass of between 250 grams and 350 grams. The heart is composed of three layers, all of which are rich with blood vessels. The superficial layer, called the visceral layer, the middle layer, called the myocardium, and the third layer which is called the endocardium. The heart has four chambers, two superior atria and two inferior ventricles. The atria are the receiving chambers and the ventricles are the discharging chambers. The pathway of blood through the heart consists of a pulmonary circuit and a systemic circuit. Blood flows through the heart in one direction, from the atrias to the ventricles, and out of the great arteries, or the aorta for example. This is done by four valves which are the tricuspid atrioventicular valve, the mitral atrioventicular valve, the aortic semilunar valve, and the pulmonary semilunar valve.
Systemic circulation is the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. The term is contrasted with pulmonary circulation.

Pulmonary circulation is the portion of the cardiovascular system which carries oxygen-depleted blood away from the heart, to the lungs, and returns oxygenated blood back to the heart. The term is contrasted with systemic circulation. A separate system known as the bronchial circulation supplies blood to the tissue of the larger airways of the lung.

Arteries are blood vessels that carry blood away from the heart. All arteries, with the exception of the pulmonary and umbilical arteries, carry oxygenated blood.

Pulmonary arteries
The pulmonary arteries carry deoxygenated blood that has just returned from the body to the heart towards the lungs, where carbon dioxide is exchanged for oxygen.

Systemic arteries
Systemic arteries can be subdivided into two types – muscular and elastic – according to the relative compositions of elastic and muscle tissue in their tunica media as well as their size and the makeup of the internal and external elastic lamina. The larger arteries (>10mm diameter) are generally elastic and the smaller ones (0.1-10mm) tend to be muscular. Systemic arteries deliver blood to the arterioles, and then to the capillaries, where nutrients and gasses are exchanged.

The Aorta
The aorta is the root systemic artery. It receives blood directly from the left ventricle of the heart via the aortic valve. As the aorta branches, and these arteries branch in turn, they become successively smaller in diameter, down to the arteriole. The arterioles supply capillaries which in turn empty into venules. The very first branches off of the aorta are the coronary arteries, which supply blood to the heart muscle itself. These are followed by the branches off the aortic arch, namely the brachiocephalic artery, the left common carotid and the left subclavian arteries.

Aorta the largest artery in the body, originating from the left ventricle of the heart and extends down to the abdomen, where it branches off into two smaller arteries (the common iliacs). The aorta brings oxygenated blood to all parts of the body in the systemic circulation.

The aorta is usually divided into five segments/sections:

• Ascending aorta—the section between the heart and the arch of aorta
• Arch of aorta—the peak part that looks somewhat like an inverted "U"
• Descending aorta—the section from the arch of aorta to the point where it divides into the common iliac arteries
  o    Thoracic aorta—the half of the descending aorta above the diaphragm
  o    Abdominal aorta—the half of the descending aorta below the diaphragm

Arterioles
Arterioles, the smallest of the true arteries, help regulate blood pressure by the variable contraction of the smooth muscle of their walls, and deliver blood to the capillaries.
Veins are blood vessels that carry blood towards the heart. Most veins carry deoxygenated blood from the tissues back to the lungs; exceptions are the pulmonary and umbilical veins, both of which carry oxygenated blood. Veins differ from arteries in structure and function; for example, arteries are more muscular than veins and they carry blood away from the heart.
Veins are classified in a number of ways, including superficial vs. deep, pulmonary vs. systemic, and large vs. small.

Superficial veins
Superficial veins are those whose course is close to the surface of the body, and have no corresponding arteries.

Deep veins
Deep veins are deeper in the body and have corresponding arteries.

Pulmonary veins
The pulmonary veins are a set of veins that deliver oxygenated blood from the lungs to the heart.

Systemic veins
Systemic veins drain the tissues of the body and deliver deoxygenated blood to the heart.
Atrium sometimes called auricle, refers to a chamber or space. It may be the atrium of the lateral ventricle in the brain or the blood collection chamber of a heart. It has a thin-walled structure that allows blood to return to the heart. There is at least one atrium in animals with a closed circulatory system.

Right atrium is one of four chambers (two atria and two ventricles) in the human heart. It receives deoxygenated blood from the superior and inferior vena cava and the coronary sinus, and pumps it into the right ventricle through the tricuspid valve. Attached to the right atrium is the right auricular appendix.

Left atrium is one of the four chambers in the human heart. It receives oxygenated blood from the pulmonary veins, and pumps it into the left ventricle, via the atrioventricular valve.
Ventricle is a chamber which collects blood from an atrium (another heart chamber that is smaller than a ventricle) and pumps it out of the heart.
Right ventricle is one of four chambers (two atria and two ventricles) in the human heart. It receives deoxygenated blood from the right atrium via the tricuspid valve, and pumps it into the pulmonary artery via the pulmonary valve and pulmonary trunk.

Left ventricle is one of four chambers (two atria and two ventricles) in the human heart. It receives oxygenated blood from the left atrium via the mitral valve, and pumps it into the aorta via the aortic valve.

Pathophysiology of Pregnancy Induced Hypertension (PIH):

Clinical Manifestations:

A.  Mild Preeclampsia

• BP of 140/90
• 1+ to 2+ proteinuria on random
• weight gain of 2 lbs per week on the 2nd trimester and 1 lb per week on the 3rd trimester
• Slight edema in upper extremities and face

B. Severe Preeclampsia

• BP of 160/110
• 3-4+ protenuria on random
• Oliguria (less than 500 ml/24 hrs)
• Cerebral or visual disturbances
• Epigastric pain
• Pulmonary edema
• Peripheral edema
• Hepatic dysfunction

C. Eclampsia is an extension of preeclampsia and is characterized by the client experiencing seizures.

Diagnostic Evaluation:

1. Based on the presenting symptoms. Often the disease process has been developing and affecting the renal and vascular system
2. Frequently a sudden weight gain will occur, of 2 lb. or more in 1 week, or 6 lb. or more within 1 month. This often occurs before the edema is present.

Medical Treatment and Evaluation:

1. Magnesium Sulfate (Pregnancy risk category B)
     muscle relaxant, prevent seizures
     loading dose 4-6g, maintenance dose 1-2g/h IV
     infuse IV dose slowly over 15-30 min.
      •Always administer as a piggy back infusion.
      •Assess PR, urine output, DTR, and clonus every hour.
      •Observe for CNS depression and hypotonia in infant at birth.
2. Hydrazaline (Apresoline) Pregnancy risk category C
     anti hypertensive (peripheral vasodilator) use to decrease hypertension
     5-10mg/IV
     Administer slowly to avoid sudden fall of BP
      •Maintain diastolic pressure over 90 mmHg to ensure adequate placental filling.
3. Diazepam (Valium) Pregnancy risk category D
     halt seizures
     5-10mg/IV
     administer slowly. Dose may be repeated every 10-15 min. (up to 30mg/hr)
      •Observe for respiratory depression for both mother and infant at birth.
4. Calcium Gluconate (Pregnancy risk category C)
     antidote for Magnesium Sulfate
     1g/IV (10 mL of a 10% solution)
     have prepared at bed side when administering Magnesium Sulfate
     administer at 5mL/min.

Complications of PIH:

1. Intrauterine growth restriction (IUGR) – an abnormally restricted symmetric or asymmetric growth of fetus
2. Oligohydramnios – abnormally low volume of amniotic fluid
3. Risk of placental abruption – premature separation of a normally situated placenta from the wall of uterus
4. Risk of preterm delivery (often iatrogenic) – delivery before 37 weeks of gestation
5. Coagulopathy
6. Stillbirth
7. Seizures
8. Coma
9. Renal failure
10. Maternal hepatic damage
11. Hemolysis
12. Elevated liver enzymes levels
13. Low platelet count (HELLP syndrome)

Nursing Interventions:

Discharge Plan:

Exercise

1. encourage patient’s on deep breathing exercises.
2. move extremities when lying.
3. elevate the head part when sleeping, to promote increase peripheral circulation
4. encourage overall passive and active exercises program during pregnancy to prevent need for cesarean birth.
5. exercises like tailor sitting, squatting, kegel exercise, pelvic rocking, and abdominal muscle contraction will promote easy delivery. 

Treatment:

1. use of drugs
2. catheterization
3. obtaining labs. (CBC, platelets count, liver function, BUN and creatinine, and fibrin degregation)

Health Teaching:

1. Encourage patient foe sodium restriction.
2. Encourage to avoid foods rich in oil and fats.
3. Encourage patient to limit her daily activities and exercises.

Ongoing Assessment:

1. Observe carefully for symptoms at prenatal visit.
2. Give instruction about what symptoms to watch for so she can alert her clinician if additional symptoms occur between visits.

Diet:

1. low fats and sodium diet, restriction if possible.
2. high in protein, calcium and iron.
3. Adequate fluid intake

Sex:

1. limit sexual activity
2. sexual intercourse at 2nd trimester should be avoided.

View Nursing Care Plan – Pregnancy Induced Hypertension (PIH)

References:

• Maternal and child health nursing by Adele Pillitteri 5th edition;volume 1 page 426-433;page 329-332
• All-in-one care planning resource page 748; by Pamela L. Swearlngen, RN
• Maternal neonatal nursing;page 30 by Lippincott Williams and Wilkins
• Luckman and Sorensen’s Medical-Surgical Nursing a Physiologic Approach 4th edition Volume 1 page 734
• http://wikipedia.org
• http://nursingcrib.com

Related posts:

1. Nursing Care Plan – Pregnancy Induced Hypertension (PIH; Preeclampsia and Eclampsia)
2. Fetal Circulation
3. Pathophysiology of Congestive Heart Failure

Dementia is an acquired syndrome that causes progressive loss of intellectual abilities, such as memory, as well as aphasia, apraxia, and loss of executive function. Dementing disorders are characterized by gradual onset plus continuing cognitive decline that is not due to other brain disease. Screening tests can identify persons who should be referred for a complete diagnostic workup.

Early diagnosis of dementia is the goal of a diagnostic workup, which is done to exclude potentially reversible causes and initiate therapy as early as possible. Short term memory impairment is usually the first symptom of dementia. Clinical diagnosis of dementia requires (1) loss of an intellectual ability with impairment severe enough to interfere with social or occupational functioning and (2) ruling out delirium. Delirium must be ruled out because cognitive impairment caused by delirium may be reversible.

Mild cognitive impairment is another risk factor for dementia. Persons with mild cognitive impairment have complaints and objective evidence of memory problems, but do not have deficits in activities of daily living or in other cognitive functions and do not meet the diagnostic criteria for dementia. Mild cognitive impairment refers to a transitional state between normal aging and dementia; it is associated with an increased risk of death, greater decline in cognitive abilities, and incident, with annual conversion rate of 8.3% to Alzheimer disease. Elder persons with mild cognitive impairment who are depressed are at greater risk of converting to Alzheimer disease. Dementia may be caused by more than one mechanism, even in the same individual. An autopsy examination is necessary to confirm the diagnosis.

Anatomy and Physiology of the human brain

Pathophysiology of Dementia

Clinical Manifestations:

Dementia

DSM –IV DIAGNOSIS

• Dementia of the Alzheimer’s type
• Vascular dementia
• Dementia due to a general medical condition
• Dementia due to multiple etiologies

DEFINING CHARACTERISTICS

• Slow, insidious onset
• Impaired long and short term memory
• Deterioration of cognitive abilities – judgement, abstract thinking
• Often irreversible if untreated
• Personality changes
• No or slow EEG changes

Diagnostic Evaluation:

Various diagnostic tests may be done to determine the cause. A comprehensive neuropsychiatric evaluation must be completed to make an accurate diagnosis.

1. Basic laboratory examination, including CBC with differential, chemistry panel (including blood urea nitrogen, creatinine, and ammonia), arterial blood gas values, chest x-ray, toxicology screen (comprehensive), thyroid function tests, and serologic tests for syphilis.
2. Additional test may include CT scan, MRI, additional blood chemistries (heavy metals, thiamine, folate, antinuclear antibody, and urinary porphobilinogen), lumbar puncture, PET/ single photon emission computed tomography scans.
3. Complete mental status examination.
4. Comprehensive physical examination.

Treatment:

1. Treatment is generally community focused; the goal of treatment is to maintain the quality of life as long as possible despite the progressive nature of the disease. Effective treatment is based on:
   • Diagnosis of primary illness and concurrent psychiatric disorders.
   • Assessment of auditory and visual impairment
   • Measurement of the degree, nature, and progression of cognitive deficits.
   • Assessment of functional capacity and ability for self care
   • Family and social system assessment.
2. Environmental strategies in order to assist in maintaining the safety and functional abilities of the patient as long as possible.

Pharmacologic Treatment

1. Pharmacologic therapy used for the person with DAT is directed toward the use of anticholinesterase drugs to slow the progression of the disorder by increasing the relative amount of acetylcholine. Available drugs include donepezil (Aricept), galantamine (Reminyl), rivastigmine (Exelon) and tacrine (Cognex). An NMDA-receptor antagonist memantine (Namenda) may be provided in an attempt to improve recognition. Other drugs may be used for behavioral control and symptom reduction.

• Agitation management: neuroleptic drugs
• Psychosis: neuroleptic drugs
• Depression: antidepressants, ECT

Complications:

1. Without accurate diagnosis and treatment, secondary dementias may become permanent.
2. Falls with serious orthopedic or cerebral injuries.
3. Self-inflicted injuries
4. Aggression or violence to self, others, or property.
5. Wandering events, in which the person can get lost and potentially suffer exposure, hypothermia, injury, and even death.
6. Serious depression is demonstrated in caregivers who receive inadequate support.
7. Caregiver stress and burden may result in patient neglect or abuse.

Nursing Interventions:

Improving communication

1. Speak slowly and use short, simple words and phrases.
2. Consistently identify yourself, and address the person by name at each meeting.
3. Focus on one piece of information at a time. Review what has been discussed with patient.
4. If patient has vision or hearing disturbances, have him wear prescription eye glasses and/or hearing device.
5. Keep environment well lit.
6. Use clocks, calendars, and familiar personal effects in the patient’s view.
7. If patient becomes aggressive, shift the topic for a safer, more familiar one.

Promoting Independence in Self-care

1. Assess and monitor patient’s ability to perform activities of daily living.
2. Encourage decision making regarding activities of daily living as much as possible.
3. Monitor food and fluid intake.
4. Weigh patient weekly.
5. Provide food that patient can eat while moving.
6. Sit with the patient during meals and assist by cueing.

Ensuring Safety

1. Discuss restriction of driving when recommended.
2. Assess patient’s home for safety; remove throw rugs, label rooms, and keep the house well lit.
3. Assess community for safety.
4. Alert neighbors about the patient’s wandering behavior.
5. Alert police and have current picture taken
6. Install safety bars in the bathroom.
7. Encourage physical activity during day time

Preventing Violence and Aggression

1. Respond calmly and do not raise your voice.
2. Remove objects that might be used to harm self or others.
3. Identify stressors that increase agitation.
4. Distract patient when an upsetting situation develops.

Related posts:

1. Pathophysiology of Dementia
2. Schizophrenia Case Study
3. Alzheimer’s Disease

The appendix is a small fingerlike appendage about 10 cm (4 in) long, attached to the cecum just below the ileocecal valve. No definite functions can be assigned to it in humans. The appendix fills with food and empties as regularly as does the cecum, of which it is small, so that it is prone to become obstructed and is particularly vulnerable to infection (appendicitis).

Appendicitis is the most common cause of acute inflammation in the right lower quadrant of the abdominal cavity. About 7% of the population will have appendicitis at some time in their lives, males are affected more than females, and teenagers more than adults. It occurs most frequently between the age of 10 and 30.

The disease is more prevalent in countries in which people consume a diet low in fiber and high in refined carbohydrates.

The lower quadrant pain is usually accompanied by a low-grade fever, nausea, and often vomiting. Loss of appetite is common. In up to 50% of presenting cases, local tenderness is elicited at Mc Burney’s point applied located at halfway between the umbilicus and the anterior spine of the Ilium.

Rebound tenderness (ex. Production or intensification of pain when pressure is released) may be present. The extent of tenderness and muscle spasm and the existence of the constipation or diarrhea depend not so much on the severity of the appendiceal infection as on the location of the appendix.

If the appendix curls around behind the cecum, pain and tenderness may be felt in the lumbar region. Rovsing’s sign maybe elicited by palpating the left lower quadrant. If the appendix has ruptured, the pain become more diffuse, abdominal distention develops as a result of paralytic ileus, and the patient condition become worsens.

Constipation can also occur with an acute process such as appendicitis. Laxative administered in the instance may result in perforation of the in flared appendix. In general a laxative should never be given when a person’s has fever, nausea or pain.

Anatomy and Physiology of Digestive System

The mouth, or oral cavity, is the first part of the digestive tract. It is adapted to receive food by ingestion, break it into small particles by mastication, and mix it with saliva. The lips, cheeks, and palate form the boundaries. The oral cavity contains the teeth and tongue and receives the secretions from the salivary glands.

Lips and Cheeks
The lips and cheeks help hold food in the mouth and keep it in place for chewing. They are also used in the formation of words for speech. The lips contain numerous sensory receptors that are useful for judging the temperature and texture of foods.

Palate
The palate is the roof of the oral cavity. It separates the oral cavity from the nasal cavity. The anterior portion, the hard palate, is supported by bone. The posterior portion, the soft palate, is skeletal muscle and connective tissue. Posteriorly, the soft palate ends in a projection called the uvula. During swallowing, the soft palate and uvula move upward to direct food away from the nasal cavity and into the oropharynx.

Tongue
The tongue manipulates food in the mouth and is used in speech. The surface is covered with papillae that provide friction and contain the taste buds.

Teeth
A complete set of deciduous (primary) teeth contains 20 teeth. There are 32 teeth in a complete permanent (secondary) set. The shape of each tooth type corresponds to the way it handles food.

Pharynx
The pharynx is a fibromuscular passageway that connects the nasal and oral cavities to the larynx and esophagus. It serves both the respiratory and digestive systems as a channel for air and food. The upper region, the nasopharynx, is posterior to the nasal cavity. It contains the pharyngeal tonsils, or adenoids, functions as a passageway for air, and has no function in the digestive system. The middle region posterior to the oral cavity is the oropharynx. This is the first region food enters when it is swallowed. The opening from the oral cavity into the oropharynx is called the fauces. Masses of lymphoid tissue, the palatine tonsils, are near the fauces. The lower region, posterior to the larynx, is the laryngopharynx, or hypopharynx. The laryngopharynx opens into both the esophagus and the larynx.

Esophagus
The esophagus is a collapsible muscular tube that serves as a passageway between the pharynx and stomach. As it descends, it is posterior to the trachea and anterior to the vertebral column. It passes through an opening in the diaphragm, called the esophageal hiatus, and then empties into the stomach. The mucosa has glands that secrete mucus to keep the lining moist and well lubricated to ease the passage of food. Upper and lower esophageal sphincters control the movement of food into and out of the esophagus. The lower esophageal sphincter is sometimes called the cardiac sphincter and resides at the esophagogastric junction

Stomach
the stomach, which receives food from the esophagus, is located in the upper left quadrant of the abdomen. The stomach is divided into the fundic, cardiac, body, and pyloric regions. The lesser and greater curvatures are on the right and left sides, respectively, of the stomach.

Small Intestine
The small intestine extends from the pyloric sphincter to the ileocecal valve, where it empties into the large intestine. The small intestine finishes the process of digestion, absorbs the nutrients, and passes the residue on to the large intestine. The liver, gallbladder, and pancreas are accessory organs of the digestive system that are closely associated with the small intestine. The small intestine is divided into the duodenum, jejunum, and ileum. The small intestine follows the general structure of the digestive tract in that the wall has a mucosa with simple columnar epithelium, submucosa, smooth muscle with inner circular and outer longitudinal layers, and serosa. The absorptive surface area of the small intestine is increased by plicae circulares, villi, and microvilli. Exocrine cells in the mucosa of the small intestine secrete mucus, peptidase, sucrase, maltase, lactase, lipase, and enterokinase. Endocrine cells secrete cholecystokinin and secretin. The most important factor for regulating secretions in the small intestine is the presence of chyme. This is largely a local reflex action in response to chemical and mechanical irritation from the chyme and in response to distention of the intestinal wall. This is a direct reflex action, thus the greater the amount of chyme, the greater the secretion.

Large Intestine
The large intestine is larger in diameter than the small intestine. It begins at the ileocecal junction, where the ileum enters the large intestine, and ends at the anus. The large intestine consists of the colon, rectum, and anal canal. The wall of the large intestine has the same types of tissue that are found in other parts of the digestive tract but there are some distinguishing characteristics. The mucosa has a large number of goblet cells but does not have any villi. The longitudinal muscle layer, although present, is incomplete. The longitudinal muscle is limited to three distinct bands, called teniae coli, that run the entire length of the colon. Contraction of the teniae coli exerts pressure on the wall and creates a series of pouches, called haustra, along the colon. Epiploic appendages, pieces of fat-filled connective tissue, are attached to the outer surface of the colon. Unlike the small intestine, the large intestine produces no digestive enzymes. Chemical digestion is completed in the small intestine before the chyme reaches the large intestine. Functions of the large intestine include the absorption of water and electrolytes and the elimination of feces.

Rectum and Anus
The rectum continues from the signoid colon to the anal canal and has a thick muscular layer. It follows the curvature of the sacrum and is firmly attached to it by connective tissue. The rectum and ends about 5 cm below the tip of the coccyx, at the beginning of the anal canal. The last 2 to 3 cm of the digestive tract is the anal canal, which continues from the rectum and opens to the outside at the anus. The mucosa of the rectum is folded to form longitudinal anal columns. The smooth muscle layer is thick and forms the internal anal sphincter at the superior end of the anal canal. This sphincter is under involuntary control. There is an external anal sphincter at the inferior end of the anal canal. This sphincter is composed of skeletal muscle and is under voluntary control.

Clinical Manifestations

1. Generalized or localized abdominal pain in the epigastric or periumbilical areas and upper right abdomen. Within 2 to 12 hours, the pain localizes in the right lower quadrant and intensity increases.
2. Anorexia, moderate malaise, mild fever, nausea and vomiting.
3. Usually constipation occurs ; occasionally diarrhea.
4. Rebound tenderness, involuntary guarding, generalized abdominal rigidity.

Diagnostic Evaluation

1. Physical examination consistent with clinical manifestations.
2. WBC count reveal moderate leukocytosis (10,000 to 16,000/mm3) with shift to the left (increased immature neutrophils).
3. Urinalysis rule out urinary disorders.
4. Abdominal x-ray may visualize shadow consistent with fecalith in appendix; perforation will reveal free air.
5. Abdominal ultrasound or CT scan can visualize appendix and rule out other conditions, such as diverticulitis and crohn’s disease. Focused appendiceal CT can quickly evaluate for appendicitis.

Medications

• Analgesics
• Intravenous fluids replacements
• Analgesics

Treatment

Appendectomy is the effective treatment if peritonitis develops treatment involves.

• GI Intubation
• Parenteral replacement of IV fluids and electrolytes
• Administration of Antibiotics

Surgery is indicated if appendicitis is diagnosed. Antibiotics and IV fluids are administered until surgery is performed analgesics can be administered after the diagnosed is made.

An appendectomy (surgical removal of the appendix) is performed as soon as possible to decrease the risk of perforation. T he appendectomy may be performed under a (general or spinal anesthetics) with a low abdominal incisions or by (laparoscopy) which is recently highly effective method.

Complications

The major complication of appendicitis is perforation of the appendix, which can lead to peritonitis, abscess formation (collection of purulent material), or portal pylephlebitis, which is septic thrombosis of the portal vein caused by vegetative emboli that arise from septic intestines.

Perforation generally occurs 24 hours after the onset of pain symptoms include a fever of 37.7 degree Celsius or 100 degree Fahrenheit or greater, a toxic appearance and continued abdominal pain or tenderness.

Nursing Interventions

1. Monitor frequently for signs and symptoms of worsening condition, indicating perforation, abscess, or peritonitis (increasing severity of pain, tenderness, rigidity, distention, absent bowel sounds, fever, malaise, and tachycardia).
2. Notify health care provider immediately if pain suddenly ceases, this indicates perforation, which is a medical emergency.
3. Assist patient to position of comfort such as semi-fowlers with knees are flexed.
4. Restrict activity that may aggravate pain, such as coughing and ambulation.
5. Apply ice bag to abdomen for comfort.
6. Avoid indiscriminate palpation of the abdomen to avoid increasing the patients discomfort.
7. Promptly prepare patient for surgery once diagnosis is established.
8. Explain signs and symptoms of postoperative complications to report-elevated temperature, nausea and vomiting, or abdominal distention; these may indicate infection.
9. Instruct patient on turning, coughing, or deep breathing, use of incentive spirometer, and ambulation. Discuss purpose and continued importance of these maneuvers during recovery period.
10. Teach incisional care and avoidance of heavy lifting or driving until advised by the surgeon.
11. Advise avoidance of enemas or harsh laxatives; increased fluids and stool softeners may be used for postoperative constipation.

Discharge Planning

M     Antibiotics for infection
        Analgesic agent (morphine) can be given for pain after the surgery

E     Within 12 hrs of surgery you may get up and move around.
       You can usually return to normal activities in 2-3 weeks after laparoscopic surgery.

T     Pretreatment of foods with lactase preparations (e.g. lactacid drops) before ingestion can reduce symptoms.
       Ingestion of lactase enzyme tablets with the first bite of food can reduce symptoms.

H     To care wound perform dressing changes and irrigations as prescribe avoid taking laxative or applying heat to abdomen when abdominal pain of unknown cause is experienced.
       Reinforce need for follow-up appointment with the surgeon
       Call your physician for increased pain at the incision site

O     Document bowel sounds and the passing of flatus or bowel movements (these are signs of the return of peristalsis)
       Watch for surgical complications such as continuing pain or fever, which indicate an abscess or wound dehiscence
       Stitches removed between fifth and seventh day (usually in physicians office)

D    Liquid or soft diet until the infection subsides
      Soft diet is low in fiber and easily breaks down in the gastrointestinal tract

Pathophysiology of Appendicitis
Nursing Care Plan – Appendicitis

References:

Medical and Surgical Nursing by Brunner and Suddarth’s
Medical Surgical Nursing by Josie Quiambao Udan
Manuals of Nursing Practice by Lippincott
Mosby’s Medical Surgical Nursing

Related posts:

1. Appendicitis
2. Amoebiasis/Amebiasis (Amoebic Dysentery) Case Study
3. Pathophysiology of Appendicitis

INTRODUCTION:

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible. This newest definition COPD, provided by the Global Initiative for Chrnonic Obstructive Lung Disease (GOLD), is a broad description that better explains this disorder and its signs and symptoms (GOLD, World Health Organization [WHO] & National Heart, Lung and Blood Institute [NHLBI], 2004). Although previous definitions have include emphysema and chronic bronchitis under the umbrella classification of COPD, this was often confusing because most patient with COPD present with over lapping signs and symptoms of these two distinct disease processes.

COPD may include diseases that cause airflow obstruction (e.g., Emphysema, chronic bronchitis) or any combination of these disorders. Other diseases as cystic fibrosis, bronchiectasis, and asthma that were previously classified as types of chronic obstructive lung disease are now classified as chronic pulmonary disorders. However, asthma is now considered as a separate disorder and is classified as an abnormal airway condition characterized primarily by reversible inflammation. COPD can co-exist with asthma. Both of these diseases have the same major symptoms; however, symptoms are generally more variable in asthma than in COPD.

Currently, COPD is the fourth leading cause of mortality and the 12^th leading cause of disability. However, by the year 2020 it is estimated that COPD will be the third leading cause of death and the firth leading cause of disability (Sin, McAlister, Man. Et al., 2003). People with COPD commonly become symptomatic during the middle adult years, and the incidence of the disease increases with age.

ANATOMY AND PHYSIOLOGY:

The respiratory system consists of all the organs involved in breathing. These include the nose, pharynx, larynx, trachea, bronchi and lungs. The respiratory system does two very important things: it brings oxygen into our bodies, which we need for our cells to live and function properly; and it helps us get rid of carbon dioxide, which is a waste product of cellular function. The nose, pharynx, larynx, trachea and bronchi all work like a system of pipes through which the air is funneled down into our lungs. There, in very small air sacs called alveoli, oxygen is brought into the bloodstream and carbon dioxide is pushed from the blood out into the air. When something goes wrong with part of the respiratory system, such as an infection like pneumonia, chronic obstructive pulmonary diseases, it makes it harder for us to get the oxygen we need and to get rid of the waste product carbon dioxide. Common respiratory symptoms include breathlessness, cough, and chest pain.

The Upper Airway and Trachea

When you breathe in, air enters your body through your nose or mouth. From there, it travels down your throat through the larynx (or voicebox) and into the trachea (or windpipe) before entering your lungs. All these structures act to funnel fresh air down from the outside world into your body. The upper airway is important because it must always stay open for you to be able to breathe. It also helps to moisten and warm the air before it reaches your lungs.

The Lungs

Structure

The lungs are paired, cone-shaped organs which take up most of the space in our chests, along with the heart. Their role is to take oxygen into the body, which we need for our cells to live and function properly, and to help us get rid of carbon dioxide, which is a waste product. We each have two lungs, a left lung and a right lung. These are divided up into ‘lobes’, or big sections of tissue separated by ‘fissures’ or dividers. The right lung has three lobes but the left lung has only two, because the heart takes up some of the space in the left side of our chest. The lungs can also be divided up into even smaller portions, called ‘bronchopulmonary segments’.

These are pyramidal-shaped areas which are also separated from each other by membranes. There are about 10 of them in each lung. Each segment receives its own blood supply and air supply.

COPD VERSUS HEALTHY LUNG

How they work

Air enters your lungs through a system of pipes called the bronchi. These pipes start from the bottom of the trachea as the left and right bronchi and branch many times throughout the lungs, until they eventually form little thin-walled air sacs or bubbles, known as the alveoli. The alveoli are where the important work of gas exchange takes place between the air and your blood. Covering each alveolus is a whole network of little blood vessel called capillaries, which are very small branches of the pulmonary arteries. It is important that the air in the alveoli and the blood in the capillaries are very close together, so that oxygen and carbon dioxide can move (or diffuse) between them. So, when you breathe in, air comes down the trachea and through the bronchi into the alveoli. This fresh air has lots of oxygen in it, and some of this oxygen will travel across the walls of the alveoli into your bloodstream. Traveling in the opposite direction is carbon dioxide, which crosses from the blood in the capillaries into the air in the alveoli and is then breathed out. In this way, you bring in to your body the oxygen that you need to live, and get rid of the waste product carbon dioxide.

Blood Supply

The lungs are very vascular organs, meaning they receive a very large blood supply. This is because the pulmonary arteries, which supply the lungs, come directly from the right side of your heart. They carry blood which is low in oxygen and high in carbon dioxide into your lungs so that the carbon dioxide can be blown off, and more oxygen can be absorbed into the bloodstream. The newly oxygen-rich blood then travels back through the paired pulmonary veins into the left side of your heart. From there, it is pumped all around your body to supply oxygen to cells and organs.

The Work of Breathing

The Pleurae

The lungs are covered by smooth membranes that we call pleurae. The pleurae have two layers, a ‘visceral’ layer which sticks closely to the outside surface of your lungs, and a ‘parietal’ layer which lines the inside of your chest wall (ribcage). The pleurae are important because they help you breathe in and out smoothly, without any friction. They also make sure that when your ribcage expands on breathing in, your lungs expand as well to fill the extra space.

The Diaphragm and Intercostal Muscles

When you breathe in (inspiration), your muscles need to work to fill your lungs with air. The diaphragm, a large, sheet-like muscle which stretches across your chest under the ribcage, does much of this work. At rest, it is shaped like a dome curving up into your chest. When you breathe in, the diaphragm contracts and flattens out, expanding the space in your chest and drawing air into your lungs. Other muscles, including the muscles between your ribs (the intercostal muscles) also help by moving your ribcage in and out. Breathing out (expiration) does not normally require your muscles to work. This is because your lungs are very elastic, and when your muscles relax at the end of inspiration your lungs simply recoil back into their resting position, pushing the air out as they go.

The Respiratory System and Ageing

The normal process of ageing is associated with a number of changes in both the structure and function of the respiratory system. These include:

• Enlargement of the alveoli. The air spaces get bigger and lose their elasticity, meaning that there is less area for gases to be exchanged across. This change is sometimes referred to as ’senile emphysema’.
• The compliance (or springiness) of the chest wall decreases, so that it takes more effort to breathe in and out.
• The strength of the respiratory muscles (the diaphragm and intercostal muscles) decreases. This change is closely connected to the general health of the person.

All of these changes mean that an older person might have more difficulty coping with increased stress on their respiratory system, such as with an infection like pneumonia, than a younger person would.

PREDISPOSING FACTORS

Risk factors for COPD include environmental exposures and host factors. The most important risk factor for COPD is cigarette smoking. Other risk factors are pipe, cigar, and other types of tobacco smoking. In addition, passive smoking contributes to respiratory symptoms and COPD. Smoking depresses the activity of scavenger cells and affects the respiratory tract’s ciliary cleansing mechanism, which keeps breathing passages free of inhaled irritants, bacteria, and other foreign matter. When smoking damages this cleansing mechanism, airflow is obstructed and air becomes trapped behind the obstruction. The alveoli greatly distend, diminished lung capacity. Smoking also irritates the goblet cells and mucus glands, causing an increased accumulation of mucus, which in turn produces more irritation, infection, and damage to the lung. In addition, carbon monoxide (a by product of smoking) combines with hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently.

A host risk factor for COPD is a deficiency of alpha antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury. This deficiency predisposes young people to rapid development of lobular emphysema, even if they do not smoke. Genetically susceptible people are sensitive to environmental factors (eg. Smoking, air pollution, infectious agents, allergens) and eventually developed chronic obstructive symptoms. Carriers of this genetic defect must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease.

PATHOPHYSIOLOGY

In COPD, the airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. The inflammatory response occurs throughout the airways, parenchyma, and pulmonary vasculature. Because of the chronic inflammation and the body’s attempts to repair it, narrowing occurs in the small peripheral airways. Over time, this injury-and-repair process causes scar tissue formation and narrowing of the airway lumen. Airflow obstruction may also be caused by parenchymal destruction, as is seen with emphysema, a disease of the alveoli or gas exchange units.

In addition to inflammation, processes related to imbalances of proteinases and antiproteinases in the lung may be responsible for airflow limitation. When activated by chronic inflammation, proteiness and other substances may be released, damaging the parenchyma of the lung. The parenchymal changes may occur as a consequence of inflammation or environmental or genetic factors (eg. Alpha1-antitrypsin deficiency).

Early in the course of COPD, the inflammatory response causes pulmonary vasculature changes that are characterized by thickening of the vessel wall. These changes may result from exposure to cigarette smoke, use of tobacco products, and the release of inflammatory medicators.

CHRONIC BRONCHITIS

Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. In the airways of the lung, the hallmark of chronic bronchitris is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.

Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as “blue bloaters” because of the bluish color of the skin and lips (cyanosis) seen in them. The hypoxia and fluid retention leads to them being called “Blue Bloaters.”

ACUTE BRONCHITIS

PHYSICAL MANIFESTATIONS

One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: “My breathing requires effort”, “I feel out of breath”, or “I can not get enough air in”. People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly present. Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness. People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.

There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are:

• tachypnea, a rapid breathing rate
• wheezing sounds or crackles in the lungs heard through a stethoscope
• breathing out taking a longer time than breathing in
• enlargement of the chest, particularly the front-to-back distance (hyperinflation)
• active use of muscles in the neck to help with breathing
• breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).

EMPHYSEMA

Emphysema is a chronic obstructive pulmonary disease (COPD, as it is otherwise known, formerly termed a chronic obstructive lung disease). It is often caused by exposure to toxic chemicals, including long-term exposure to tobacco smoke. Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli, owing to the action of alpha 1 antitrypsin deficiency. This causes the small airways to collapse during forced exhalation, as alveolar collapsibility has decreased. As a result, airflow is impeded and air becomes trapped in the lungs, in the same way as other obstructive lung diseases. Symptoms include shortness of breath on exertion, and an expanded chest. However, the constriction of air passages isn’t always immediately deadly, and treatment is available.

PHYSICAL MANIFESTATIONS

Signs of emphysema include pursed-lipped breathing, central cyanosis and finger clubbing. The chest has hyper resonant percussion notes, particularly just above the liver, and a difficult to palpate apex beat, both due to hyperinflation. There may be decreased breath sounds and audible expiratory wheeze. In advanced disease, there are signs of fluid overload such as pitting peripheral edema. The face has a ruddy complexion if there is a secondary polycythemia. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist.

DIAGNOSTIC EVALUATION

1. PFTs demonstrative airflow obstruction – reduced forced vital capacity (FVC), FEV1, FEV1 to FVC ration; increased residual volume to total lung capacity (TLC) ratio, possibly increased TLC.
2. ABG levels- decreased PaO2, pH, and increased CO2.
3. Chest X-ray – in late stages, hyperinflation, flattened diaphragm, increased rettrosternal space, decreased vascular markings, possible bullae.
4. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema.

TREATMENT

The goals of COPD treatment are 1) to prevent further deterioration in lung function, 2) to alleviate symptoms, 3) to improve performance of daily activities and quality of life. The treatment strategies include 1) quitting cigarette smoking, 2) taking medications to dilate airways (bronchodilators) and decrease airway inflammation, 3) vaccinating against flu influenza and pneumonia and 4) regular oxygen supplementation and 5) pulmonary rehabilitation.

Quitting cigarette smoking

The most important treatment for COPD is quitting cigarette smoking. Patients who continue to smoke have a more rapid deterioration in lung function when compared to others who quit. Aging itself can cause a very slow decline in lung function. In susceptible individuals, cigarette smoking can result in a much more dramatic loss of lung function. It is important to note that when one stops smoking the decline in lung function eventually reverts to that of a non-smoker.

Nicotine in cigarettes is addictive, and, therefore, cessation of smoking can cause symptoms of nicotine withdrawal including anxiety, irritability, anger, depression, fatigue, difficulty concentrating or sleeping, and intense craving for cigarettes. Patients likely to develop withdrawal symptoms typically smoke more than 20 cigarettes a day, need to smoke shortly after waking up in the morning, and have difficulty refraining from smoking in non-smoking areas. However, some 25% of smokers can stop smoking without developing these symptoms. Even in those smokers who develop symptoms of withdrawal, the symptoms will decrease after several weeks of abstinence.

Bronchodilators

Treating airway obstruction in COPD with bronchodilators is similar but not identical to treating bronchospasm in asthma. Bronchodilators are medications that relax the muscles surrounding the small airways thereby opening the airways. Bronchodilators can be inhaled, taken orally or administered intravenously. Inhaled bronchodilators are popular because they go directly to the airways where they work. As compared with bronchodilators given orally, less medication reaches the rest of the body, and, therefore, there are fewer side effects.

Metered dose inhalers (MDIs) are used to deliver bronchodilators. An MDI is a pressurized canister containing a medication that is released when the canister is compressed. A standard amount of medication is released with each compression of the MDI. To maximize the delivery of the medications to the airways, the patient has to learn to coordinate inhalation with each compression. Incorrect use of the MDI can lead to deposition of much of the medication on the tongue and the back of the throat instead of on the airways.

To decrease the deposition of medications on the throat and increase the amount reaching the airways, spacers can be helpful. Spacers are tube-like chambers attached to the outlet of the MDI canister. Spacer devices can hold the released medications long enough for patients to inhale them slowly and deeply into the lungs. Proper use of spacer devices can greatly increase the proportion of medication reaching the airways.

Oxygen Therapy

Other treatments

• Pulmonary rehabilitation has become a cornerstone in the management of moderate to severe COPD. Pulmonary rehabilitation is a program of education regarding lung function and dysfunction, proper breathing techniques (diaphragmatic breathing, pursed lip breathing), and proper use of respiratory equipment and medications. An essential ingredient in this program is the use of increasing physical exercise to overcome the reduced physical capacity that usually has developed over time. In addition, occupational and physical therapy are used to teach optimal and efficient body mechanics.
• Lung volume reduction surgery (LVRS) has received much fanfare in the lay press. LVRS is a surgical procedure used to treat some patients with COPD. The premise behind this surgery is that the over-inflated, poorly-functioning upper parts of the lung compress and impair function of the better-functioning lung elsewhere. Thus, if the over-inflated portions of lung are removed surgically, the compressed lung may expand and function better. In addition, the diaphragm and the chest cavity achieve more optimal positioning following the surgery, and this improves breathing further. The best criteria for choosing patients for LVRS are still uncertain. A national study was completed in 2003. Patients primarily with emphysema at the top of their lungs, whose exercise tolerance was low even after pulmonary rehabilitation, seemed to do the best with this procedure. On average, lung function and exercise capacity among surviving surgical patients improved significantly following LVRS, but after two years returned to about the same levels as before the procedure. Patients with forced expiratory volume in FEVI of less than 20% of predicted and either diffuse disease on the CAT scan or lower than 20% diffusing capacity or elevated carbon dioxide levels had higher mortality. The role of LVRS is at present is very limited.

PHARMACOLOGIC INTERVENTIONS

• Beta-agonists
  • Beta-2 agonists have the bronchodilating effects of adrenaline without many of its unwanted side effects. Beta-2 agonists can be administered by MDI inhalers or orally. They are called “agonists” because they activate the beta-2 receptor on the muscles surrounding the airways. Activation of beta-2 receptors relaxes the muscles surrounding the airways and opens the airways. Dilating airways helps to relieve the symptoms of dyspnea (shortness of breath). Beta-2 agonists have been shown to relieve dyspnea in many COPD patients, even among those without demonstrable reversibility in airway obstruction. The action of beta-2 agonists starts within minutes after inhalation and lasts for about 4 hours. Because of their quick onset of action, beta-2 agonists are especially helpful for patients who are acutely short of breath. Because of their short duration of action, these medications should be used for symptoms as they develop rather than as maintenance. Evidence suggests that when these drugs are used routinely, their effectiveness is diminished. These are referred to as rescue inhalers. Examples of beta-2 agonists include albuterol (Ventolin, Proventil), metaproterenol (Alupent), pirbuterol (Maxair), terbutaline (Brethaire), and isoetharine (Bronkosol). Levalbuterol (Xopenex) is a recently approved Beta-2 agonist.
  • In contrast, Beta-2 agonists with a slower onset of action but a longer period of activity, such as salmeterol xinafoate (Serevent) and formoterol fumarate (Foradil) may be used routinely as maintenance medications. These drugs last twelve hours and should be taken twice daily and no more. Along with some of these inhalers to be mentioned, these are often referred to as maintenance inhalers.
  • Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast heart rate, and low blood potassium.
• Anti-cholinergic Agents
  • Acetylcholine is a chemical released by nerves that attaches to receptors on the muscles surrounding the airway causing the muscles to contract and the airways to narrow. Anti-cholinergic drugs such as ipratropium bromide (Atrovent) dilate airways by blocking the receptors for acetylcholine on the muscles of the airways and preventing them from narrowing. Ipratropium bromide (Atrovent) usually is administered via a MDI. In patients with COPD, ipratropium has been shown to alleviate dyspnea, improve exercise tolerance and improve FEV1. Ipratropium has a slower onset of action but longer duration of action than the shorter-acting beta-2 agonists. Ipratropium usually is well tolerated with minimal side effects even when used in higher doses. Tiotropium (SPIRIVA) is a long acting and more powerful version of Ipratropium and has been shown to be more effective.
  • In comparing ipratropium with beta-2 agonists in the treatment of patients with COPD, studies suggest that ipratropium may be more effective in dilating airways and improving symptoms with fewer side effects. Ipratropium is especially suitable for use by elderly patients who may have difficulty with fast heart rate and tremor from the beta-2 agonists. In patients who respond poorly to either beta-2 agonists or ipratropium alone, a combination of the two drugs sometimes results in a better response than to either drug alone without additional side effects.
• Methylxanthines
  • Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl, Theo-24) and aminophylline are examples of methylxanthines. Methylxanthines are administered orally or intravenously. Long acting theophylline preparations can be given orally once or twice a day. Theophylline, like a beta agonist, relaxes the muscles surrounding the airways but also prevents mast cells around the airways from releasing bronchoconstricting chemicals such as histamine. Theophylline also can act as a mild diuretic and increase urination. Theophylline also may increase the force of contraction of the heart and lower pressure in the pulmonary arteries. Thus, theophylline can help patients with COPD who have heart failure and pulmonary hypertension. Patients who have difficulty using inhaled bronchodilators but no difficulty taking oral medications find theophylline particularly useful.
  • The disadvantage of methylxanthines is their side effects. Dosage and blood levels of theophylline or aminophylline have to be closely monitored. Excessively high levels in the blood can lead to nausea, vomiting, heart rhythm problems, and even seizures. In patients with heart failure or cirrhosis, dosages of methylxanthines are lowered to avoid high blood levels. Interactions with other medications, such as cimetidine (Tagamet), calcium channel blockers (Procardia), quinolones (Cipro), and allopurinol (Zyloprim) also can alter blood levels of methylxanthines.
• Corticosteroids
  • When airway inflammation (which causes swelling) contributes to airflow obstruction, anti-inflammatory medications (more specifically, corticosteroids) may be beneficial. Examples of corticosteroids include Prednisone and Prednisolone. Twenty to thirty percent of patients with COPD show improvement in lung function when given corticosteroids by mouth. Unfortunately, high doses of oral corticosteroids over prolonged periods can have serious side effects, including osteoporosis, bone fractures, diabetes mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia, emotional changes, and weight gain. Therefore, many doctors use oral corticosteroids as the treatment of last resort. When oral corticosteroids are used, they are prescribed at the lowest possible doses for the shortest period of time to minimize side effects. When it is necessary to use long term oral steroids, medications are often prescribed to help reduce the development of the above side effects.
  • Corticosteroids also can be inhaled. Inhaled corticosteroids have many fewer side effects than long term oral corticosteroids. Examples of inhaled corticosteroids include beclomethasone dipropionate (Beclovent, Beconase, Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), fluticasone (Flovent), budesonide (Pulmicort), mometasone furoate (Asmanex) and flunisolide (Aerobid). Inhaled corticosteroids have been useful in treating patients with asthma, but in patients with COPD, it is not clear whether inhaled corticosteroid have the same benefit as oral corticosteroids. Nevertheless, doctors are less concerned about using inhaled corticosteroids because of their safety. The side effects of inhaled corticosteroids include hoarseness, loss of voice, and oral yeast infections. A spacing device placed between the mouth and the MDI can improve medication delivery and reduce the side effects on the mouth and throat. Rinsing out the mouth after use of a steroid inhaler also can decrease these side effects.
• Treatment of Alpha-1 antitrypsin deficiency
  • Emphysema can develop at a very young age in some patients with severe alpha-1 antitrypsin deficiency (AAT). Replacement of the missing or inactive AAT by injection can help prevent progression of the associated emphysema. This therapy is of no benefit in other types of COPD.

COMPLICATIONS

1. Respiratory failure
2. Pneumonia, overwhelming respiratory infection
3. Right-sided heart failure, dysrhythmias
4. Depression
5. Skeletal muscle dysfunction

NURSING INTERVENTIONS

Monitoring

1. Monitor for adverse effects of bronchodilators – tremulousness, tachycardia, cardiac arrhythmias, central nervous system stimulation, hypertension.
2. Monitor condition after administration of aerosol bronchodilators to assess for improved aeration, reduced adventitious sounds, reduced dyspnea.
3. Monitor serum theophylline level, as ordered, to ensure therapeutic level and prevent toxicity.
4. Monitor oxygen saturation at rest and with activity.

Supportive Care

1. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually reduces pulmonary irritation, sputum production, and cough. Keep the patient’s room as dust-free as possible.
2. Use postural drainage positions to help clear secretions responsible for airway obstructions.
3. Teach controlled coughing.
4. Encourage high level of fluid intake ( 8 to 10 glasses; 2 to 2.5 liters daily) within level of cardiac reserve.
5. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Add moisture (humidifier, vaporizer) to indoor air.
6. Avoid dairy products if these increases sputum production.
7. Encourage the patient to assume comfortable position to decrease dyspnea.
8. Instruct and supervise patient’s breathing retraining exercises.
9. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and depth of respiration and improve respiratory muscle coordination.
10. Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.
11. Maintain the patient’s nutritional status.
12. Reemphasize the importance of graded exercise and physical conditioning programs.
13. Encourage use of portable oxygen system for ambulation for patients with hypoxemia and marked disability.
14. Train the patient in energy conservation technique.
15. Assess the patient for reactive-behaviors such as anger, depression and acceptance.

Education and health maintenance

1. Review with the patient the objectives of treatment and nursing management.
2. Advise the patient to avoid respiratory irritants. Suggest that high efficiency particulate air filter may have some benefit.
3. Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial obstruction and sputum obstruction.
4. Warn patient to avoid persons with respiratory infections, and to avoid crowds and areas with poor ventilation.
5. Teach the patient how to recognize and report evidence of respiratory infection promptly such as chest pain, changes in character of sputum (amount, color and consistency), increasing difficulty in raising sputum, increasing coughing and wheezing, increasing of shortness of breath.

UNDERSTANDING COPD (VIDEO)

NURSING CARE PLAN – BRONCHITIS

Sources:

http://wikipedia.org

http://www.virtualmedicalcentre.com/

http://medicine.net

Medical and Surgical Nursing by Brunner and Suddarth’s

Medical Surgical Nursing by Josie Quiambao Udan

Manuals of Nursing Practice by Lippincott

Mosby’s Medical Surgical Nursing

Related posts:

1. Nursing Care Plan Chronic Obstructive Pulmonary Disease (COPD)
2. Pathophysiology of Chronic Bronchitis (COPD)
3. Pulmonary Tuberculosis (PTB) Case Study

Introduction

Leukemias are cancers of the blood-forming tissues. White blood cells may be produced in excessive amounts and are unable to work properly which weakens the immune system.

The blood is made up of fluid called plasma and three types of cells and each type has special functions. White blood cells (also called WBCs or leukocytes) help the body fight infections and other diseases. Red blood cells (also called RBCs or erythrocytes) carry oxygen from the lungs to the body’s tissues and take carbon dioxide from the tissues back to the lungs. The red blood cells give blood its color. Platelets (also called thrombocytes) help form blood clots that control bleeding.

Blood cells are formed in the bone marrow, the soft, spongy center of bones. New (immature) blood cells are called blasts. Some blasts stay in the marrow to mature. Some travel to other parts of the body to mature.

Normally, blood cells are produced in an orderly, controlled way, as the body needs them. This process helps keep us healthy. When leukemia develops, the body produces large numbers of abnormal blood cells. In most types of leukemia, the abnormal cells are white blood cells. The leukemia cells usually look different from normal blood cells, and they do not function properly.

In both men and women, leukemia incidence is highest among whites and lowest among Chinese, Japanese, and Koreans. The incidence in men is about 50% higher than in women for all racial/ethnic groups except Vietnamese, among whom the male rates are only slightly higher. Ethnic differences in the incidence rates are small in the youngest adult age group (30-54 years), but become more evident in each of the older age groups. It is found that childhood leukemia rates are highest among Filipinos, followed by white Hispanics, non-Hispanic whites and blacks.

Anatomy and physiology

Blood

Blood is one of the connective tissues. As a connective tissue, it consists of cells and cell fragments (formed elements) suspended in an intercellular matrix (plasma). Blood is the only liquid tissue in the body that measures about 5 liters in the adult human and accounts for 8 percent of the body weight.

The body consists of metabolically active cells that need a continuous supply of nutrients and oxygen. Metabolic waste products need to be removed from the cells to maintain a stable cellular environment. Blood is the primary transport medium that is responsible for meeting these cellular demands.

Blood cells are formed in the bone marrow, the soft, spongy center of bones. New (immature) blood cells are called blasts. Some blasts stay in the marrow to mature. Some travel to other parts of the body to mature.

The activities of the blood may be categorized as transportation, regulation, and protection.

These functional categories overlap and interact as the blood carries out its role in providing suitable conditions for celluar functions.

The transport functions include:

• carrying oxygen and nutrients to the cells.
• transporting carbon dioxide and nitrogenous wastes from the tissues to the lungs and kidneys where these wastes can be removed from the body.
• Carrying hormones from the endocrine glands to the target tissues.

The regulation functions include:

• Helping regulate body temperature by removing heat from active areas, such as skeletal muscles, and transporting it to other regions or to the skin where it can be dissipated.
• Playing a significant role in fluid and electrolyte balance because the salts and plasma proteins contribute to the osmotic pressure.
• Functioning in pH regulation through the action of buffers in the blood.

The protection functions include:

• Preventing fluid loss through hemorrhage when blood vessels are damaged due to its clotting mechanisms.
• Helping (phagocytic white-blood cells) to protect the body against microorganisms that cause disease by engulfing and destroying the agent.
• Protecting (antibodies in the plasma) protect against disease by their reactions with offending agents.

Composition of blood

When a sample of blood is spun in a centrifuge, the cells and cell fragments are separated from the liquid intercellular matrix. Because the formed elements are heavier than the liquid matrix, they are packed in the bottom of the tube by the centrifugal force. The light yellow colored liquid on the top is the plasma, which accounts for about 55 percent of the blood volume and red blood cells is called the hematocrit,or packed cell volume (PCV). The white blood cells and platelets form a thin white layer, called the “buffy coat,” between plasma and red blood cells.

Plasma

The watery fluid portion of blood (90 percent water) in which the corpuscular elements are suspended. It transports nutrients as well as wastes throughout the body. Various compounds, including proteins, electrolytes, carbohydrates, minerals, and fats, are dissolved in it.

Formed Elements

The formed elements are cells and cell fragments suspended in the plasma. The three classes of formed elements are the erythrocytes (red blood cells), leukocytes (white blood cells), and the thrombocytes (platelets).

Erythrocytes (red blood cells)

Erythrocytes, or red blood cells, are the most numerous of the formed elements. Erythrocytes are tiny biconcave disks, thin in the middle and thicker around the periphery. The shape provides a combination of flexibility for moving through tiny capillaries with a maximum surface area for the diffusion of gases. The primary function of erythrocytes is to transport oxygen and, to a lesser extent, carbon dioxide.

Leukocytes (white blood cells)

Leukocytes or white blood cells are generally larger than erythrocytes, but they are fewer in number. Even though they are considered to be blood cells, leukocytes do most of their work in the tissues. They use the blood as a transport medium. Some are phagocytic, others produce antibodies, some secrete histamine and, heparin, and others neutralize histamine. Leukocytes are able to move through the capillary walls into the tissue spaces, a process called diapedesis.In the tissue spaces they provide a defense against organisms that cause disease and either promote or inhibit inflammatory responses.

There are two main groups of leukocytes in the blood. The cells that develop granules in the cytoplasm are called granulocytes and those that do not have granules are called agranulocytes. Neutrophils, eosinophils, and basophils are granulocytes. Monocytes and lymphocytes are agranulocytes.

Neutrophils, the most numerous leukocytes, are phagocytic and have light-colored granules. Eosinophils have granules and help counteract the effects of histamine. Basophils secrete histomine and heparin and have blue granules. In the tissues, they are called mastcells. Lymphocytes are agranulocytes that have a special role in immune processes. Some attack bacteria directly; others produce antibodies.

Thrombocytes (platelets)

Thrombocytes, or platelets, are not complete cells, but are small fragments of very large cells called megakaryocytes. Megakaryocytes develop from hemocytoblasts in the red bone marrow. Thrombocytes become sticky and clump together to form platelet plugs that close breaks and tears in blood vessels. They also initiate the formation of blood clots.

Blood Cell Lineage:

The production of formed elements, or blood cells, is called hemopoiesis. Before birth, hemopoiesis occurs primarily in the liver and spleen, but some cells develop in the thymus, lymph nodes, and red bone marrow. After birth, most production is limited to red bone marrow in specific regions, but some white blood cells are produced in lymphoid tissue.

All types of formed elements develop from a single cell type – stem cell (pleuripotential cells or hemocytoblasts). Seven different cell lines, each controlled by a specific growth factor, develop from the hemocytoblast. When a stem cell divides, one of the “daughters” remains a stem cell and the other becomes a precursor cell, either a lymphoid cell or a myeloid cell. These cells continue to mature into various blood cells.

A leukemia can develop at any point in cell differentiation. The illustration below shows the development of the formed elements of the blood.

Blood-related cancers, or leukemias, have been shown to arise from a rare subset of cells that escape normal regulation and drive the formation and growth of the tumor. The finding that these so-called cancer stem cells, or leukemic stem cells (LSC), can be purified away from the other cells in the tumor allows their precise analysis to identify candidate molecules and regulatory pathways that play a role in progression, maintenance, and spreading of leukemias. The analyses of the other, numerically dominant, cells in the tumor, while also interesting, do not directly interrogate these key properties of malignancies. Mouse models of human myeloproliferative disorder and acute myelogenous leukemia have highlighted the remarkable conservation of disease mechanisms between both species. They can now be used to identify the LSC for each type of human leukemia and understand how they escape normal regulation and become malignant. Given the clinical importance of LSC identification, the insights gained through these approaches will quickly translate into clinical applications and lead to improved treatments for human leukemias.

Predisposing factors

The exact cause of leukemia is unknown, although many genetic and environmental factors are involved in its development. The basic mechanism involves damage to genes controlling cell growth. This damage then changes cells from a normal to a malignant (cancer) state. Analysis of bone marrow of a client with acute leukemias shows abnormal chromosomes about 50% of the time. Possible risk factors for the development of leukemia include ionizing radiation, exposure to chemicals and drugs, bone marrow hypoplasia (reduced production of blood cells), genetic factors, immunologic factors, environmental factors, and the interaction of theses factors.

Ionizing radiation exposures such as radiation therapy for cancer treatment or environmental irradiation increase the risk for leukemia development, particularly acute myelogenous leukemia (AML).

Certain chemicals and drugs have been linked to the development of leukemia because of their ability to damage DNA. Previous treatment for cancer that included melphaplan, cyclosphamide, doxorubicin, and etoposide poses risks for leukemia development about 5 to 8 years after treatment.

Bone marrow hypoplasia can increase leukemia risk by reducing or changing bone marrow cell production. Disorders that have marrow hypoplasia and may lead to leukemia development include Fanconi’s anemia, paroxysmal nocturnal  hemoglobinuria, and myelodysplastic syndromes.

Genetic factors influence leukemia development. There is an increased incidence of the disease among clients with hereditary conditions such as Down syndrome, blooms syndrome, Klinefelter syndrome, and Fanconi’s anemia. Identical sibling’s of client with leukemia have a higher rate of leukemia than does general population.

Immunologic factors, especially immune deficiencies, may promote the development of leukemia. Leukemia among immunodeficient people may be a result of immune surveilance failure, or the same mechanisms that cause the immune deficiency may also trigger cancer in the white blood cells population.

Interaction of many host and environmental factors may result in leukemia. Because each person tolerates the interaction of these factors differently, it is difficult to determine the origin of any specific leukemia.

Pathophysiology

Leukemia is a type of cancer with uncontrolled production of immature white blood cells (usually blast cells) in the bone marrow. As a result, the bone marrow becomes overcrowded with immature, nonfunctional calls and production of normal blood cell is greatly decreased. Leukemia may be acute, with sudden onset ans short duration, or chronic with a slow onset and symptoms that persist for a period of years.

Leukemias are classified by cell type. Abnormal leukemic cells coming from lymphoid pathways are lymphocytic or lymphoblastic. Leukemias in which the abnormal cells come from the myeloid pathways are myelocytic or lymphoblastic. Several subtype exist for each of these diseases, which are classified according to the degree of maturity of the abnormal cell and the specific cell type involved.

With leukemia, cancer occurs in the stem cells or early precursor leukocyte cell, causing excessive growth of a specific type of leukocyte. These cells are abnormal and their excessive production in the bone marrow stops normal bone marrow production of red blood cells, platelets, and mature leukocytes. Anemia, thrombocytopenia, and leukopenia result. The number of immature, abnormal white blood cells in the blood is greatly elevated. Leukemic cells can also be found in the spleen, liver, liver nodes and central nervous system. Without treatment, the client dies of infection or hemorrhage. For clients with acute leukemia, theae changes occur rapidly and, without intervention, progress to death. Chronic leukemia may be present for years before changes appear.

Physical Manifestations

Leukemias affects all blood cells, and blood influences the health and function of all organs and systems, thus many body areas and system cells may be affected. The following manifestations occur with the acute luekemias. Some of this findings may also be present in the client with chronic leukemia in the blast phase.

Integumantary Manifestations:

• Ecchymoses
• Petechiae
• Open infected lesions
• Pallor of the conjunctiva, nail beds, palmar creases, and around the mouth.

Gastrointestinal Manifestations:

• Bleeding gums
• Anorexia
• Weight loss
• Enlarged liver and spleen

Renal Manifestations:

• Hematuria

Cardiovascular Manifestations:

• Tachycardia at basal activity levels.
• Orthostatic hypotension
• Palpitations

Respiratory Manifestations:

• Dyspnea on exertion.

Neurologic Manifestations:

• Fatigue
• Headache
• Fever

Musculoskeletal Manifestations:

• Bone pain
• Joint swelling and pain.

Diagnostic Evaluation

1. CBC and blood smear – peripheral WBC count varies widely from 1,000 to 100,000/mm3 and may include significant numbers of abnormal immature (blast) cells, anemia may be profound; platelet count may be abnormal and coagulopathies may exist.
2. Bone marrow aspiration and biopsy – cells also studied for chromosomal abnormalities (cytogenetics) and immunologic markers to classify type of leukemia further.
3. Lymph node biopsy – to detect the spread.
4. Lumbar puncture and examination of cerebrospinal fluid for leukemic cells (especially ALL).

Treatment

To eradicate leukemic cells and allow restoration of normal hematopoiesis.

1. High-dose chemotherapy given as an induction course to obtain a remission (disappearance of abnormal cells in bone marrow and blood) and then in cycles as consolidation or maintenance therapy to prevent recurrence of disease.
2. Leukapheresis (or exchange transfusion to infants) may be used when abnormally high numbers of white cells are present to reduce the risk of leukostasis and tumor burden before chemotherapy.
3. Radiation particularly of central nervous system (CNS) in ALL.
4. Autologous or allogeneic bone marrow or stem cell transplantation.

Complications

1. Leukostasis; in setting of high numbers (greater than 50,000/mm3) of circulating leukemic cells (blasts), blood vessel walls are infiltrated and weakened, with high risk of rupture and bleeding, including intracranial hemorrhage.
2. Disseminated intravascular coagulation(DIC).
3. Tumor lysis syndrome: rapid destruction of large numbers of malignant cells leads to alteration in electrolytes (hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia).
4. May lead to renal failure and other complications.
5. Infection, bleeding, and organ damage.

Pharmacologic Interventions

Acute leukemia

Different types of leukemia are best treated with different kinds of medicine.

• Acute lymphoblastic leukemia (ALL) drugs include prednisone, vincristine, daunorubicin, L-asparaginase or pegaspargase, methotrexate, and cyclophosphamide. Imatinib (Gleevec) is sometimes used to treat ALL. Dasatinib (Sprycel) is a newer drug for treating some ALL that has not improved with other drugs.
• Acute myelogenous leukemia (AML) drugs include daunorubicin, idarubicin, cytosine arabinoside, and mitoxantrone.¹⁰ Gemtuzumab (Mylotarg) may be given to people whose AML has relapsed. It helps your body destroy cancer cells.
• Acute promyelocytic leukemia (APL) drugs include all-trans-retinoic acid (ATRA) and chemotherapy with arsenic trioxide, idarubicin, or daunorubicin. ATRA helps control the risk of life-threatening bleeding from disseminated intravascular coagulation (DIC). Later treatment can include ATRA with or without methotrexate and 6-mercaptopurine. Or if a first round of ATRA and chemotherapy does not work, arsenic trioxide may be used.¹⁰
• To treat leukemia in the brain or prevent it from spreading to the brain and central nervous system, methotrexate and cytarabine/cytosine arabinoside are injected into the spinal canal. This is called intrathecal chemotherapy.

Supportive treatments during cancer treatment include:

• Antibiotics and immunoglobulins help to prevent or fight infections. This is important when you do not have enough normal white blood cells to fight infections on your own.
• Transfusions of red blood cells and platelets.
• Epoetin and hematopoietic stimulants help your body make new blood cells.
• Allopurinol to prevent kidney problems and gout.
• Saline or steroid eyedrops for relief during treatment with cytarabine/cytosine arabinoside.

Chronic leukemia

• Chemotherapy for chronic leukemia can involve a single drug or a combination of drugs. For example, you may be given a combination of cyclophosphamide, vincristine, and prednisone. Other drug choices include fludarabine, chlorambucil, hydroxyurea (hydroxycarbamide), cytarabine, busulfan, rituximab, and alemtuzumab.
• Allopurinol may be given to prevent kidney problems and gout.
• Dasatinib (Sprycel) blocks the growth of cancer cells. It can be used for CML that has not been helped by imatinib or other drugs.
• Imatinib (Gleevec) blocks the growth of cancer cells. It is often given to people who have chronic myelogenous leukemia (CML).
• Immune globulin (IG) helps prevent infections. It is sometimes used for people with chronic lymphocytic leukemia (CLL), because CLL weakens the immune system.
• Interferon alfa helps your immune system fight disease and may keep cancer cells from growing. It is often given to people who have CML.

Medication for nausea and vomiting

Nausea and vomiting are common side effects of chemotherapy. These side effects usually are temporary and go away when treatment is stopped. Your doctor will prescribe drugs to help relieve nausea. These may include:

• Aprepitant (Emend), which is used in combination with ondansetron and dexamethasone as part of a 3-day program.
• Dimenhydrinate, such as Dramamine.
• Metoclopramide, such as Reglan and Octamide.
• Phenothiazines, such as Compazine and Phenergan.
• Serotonin antagonists, such as ondansetron (Zofran), granisetron (Kytril), or dolasetron (Anzemet). These drugs work best when they are combined with corticosteroids such as dexamethasone (Hexadrol).

Nursing Interventions

Preventing infection:

• Frequently monitor the client for pneumonia, pharyngitis, esophagitis, perianal cellulitis, urinary tract infection, and cellulitis, which are common in leukemia and which  carry significant morbidity and mortality.
• Monitor for fever, flushed appearance, chills, tachycardia; appearance of white patches in the mouth; redness, swelling, heat or pain in the eyes, ears, throat, skin, joints, abdomen, rectal and perineal areas; cough, changes in sputum; skin rash.
• Check results of granulocyte counts. Concentrations less than 500/mm3 put the patient at serious risk for infection.
• Avoid invasive procedures and trauma to skin or mucous membrane to prevent entry of microorganisms.
• Use the following rectal precautions to prevent infections: Avoid diarrhea and constipation, which can irritate the rectal mucosa, avoid the use of rectal thermometers, and keep perineal are clean.
• Care for the patient in private room with strict handwashing practice.
• Encourage and assist patient with personal hygiene, bathing, and oral care.
• Obtain cultures and administer antimicrobials promptly as directed.

Preventing and Managing bleeding:

• Watch for signs of minor bleeding, such as petechiae, ecchymosis, conjunctival hemorrhage, epistaxis, bleeding gums, bleeding at puncture sites, vaginal spotting, heavy menses.
• Be alert for signs of serious bleeding, such as headache with change in responsiveness, blurred vision, hemoptysis, hematemesis, melena, hypotension, tachycardia, dizziness.
• Test all urine, stool, emesis for gross and occult blood.
• Monitor platelet counts daily.
• Administer blood components as directed.
• Keep patient on bed rest during bleeding episodes.

Patient Education and Health Maintenance:

• Teach signs and symptoms of infection and advise whom to notify.
• Encourage adequate nutrition to prevent emaciation from chemotherapy.
• Teach avoidance of constipation with increased fluid and fiber, and good perineal care.
• Teach bleeding precautions.
• Encourage regular dental visits to detect and treat dental infections and disease.

Related posts:

1. Pathophysiology of Leukemia
2. Nursing Care Plan – Leukemia
3. Liver Cirrhosis Case Study