A.

Definition

Diabetes mellitus is a group of metabolic diseases characterized by

elevated levels of glucose in the blood (hyperglycemia) resulting from
defects in insulin secretion, insulin action, or both (American Diabetes
Association [ADA], Expert Committee on the Diagnosis and Classification
of Diabetes Mellitus, 2003). Normally a certain amount of glucose
circulates in the blood. The major sources of this glucose are absorption of
ingested food in the gastrointestinal (GI) tract and formation of glucose by
the liver from food substances.

Insulin, a hormone produced by the pancreas, controls the level of glucose

in the blood by regulating the production and storage of glucose. In the
diabetic state, the cells may stop responding to insulin or the pancreas
may stop producing insulin entirely.

Risk Factors

Family history of diabetes (ie, parents or siblings with diabetes)

Obesity (ie, 20% over desired body weight or BMI 27 kg/m2)
Race/ethnicity (eg, African Americans, Hispanic Americans, Native
Americans, Asian Americans, Pacific Islanders)
Age 45 years
Hypertension (140/90 mm Hg)
HDL cholesterol level 35 mg/dL (0.90 mmol/L) and/or triglyceride
level 250 mg/dL (2.8 mmol/L)
History of gestational diabetes or delivery of babies over 9 lbs

Classification

There are several different types of diabetes mellitus; they may differ in
cause, clinical course, and treatment. The major classifications of diabetes
are:

Type 1 diabetes (previously referred to as insulin-dependent diabetes

mellitus)

Type 2 diabetes (previously referred to as non-insulin dependent

diabetes mellitus)

Gestational diabetes mellitus (ADA, Expert Committee on the Diagnosis

and Classification of Diabetes Mellitus, 2003)

TYPE 2 DIABETES

The two main problems related to insulin in type 2 diabetes are insulin
resistance and impaired insulin secretion. Insulin resistance refers to a
decreased tissue sensitivity to insulin. Normally, insulin binds to special
receptors on cell surfaces and initiates a series of reactions involved in
glucose metabolism. In type 2 diabetes, these intracellular reactions are
diminished, thus rendering insulin less effective at stimulating glucose
uptake by the tissues and at regulating glucose release by the liver. The
exact mechanisms that lead to insulin resistance and impaired insulin
secretion in type 2 diabetes are unknown, although genetic factors are
thought to play a role.

Gerontologic Considerations

Elevated blood glucose levels appear to be age-related and occur in both

men and women throughout the world. Elevated blood glucose levels
commonly appear in the fifth decade of life and increase in frequency with
advancing age. When elderly people with overt diabetes are excluded from
the statistics, approximately 10% to 30% of elderly people have age-
related hyperglycemia. What causes age-related changes in carbohydrate
metabolism is unresolved. Possibilities include poor diet, physical
inactivity, a decrease in the lean body mass in which ingested
carbohydrate may be stored, altered insulin secretion, and increase in fat
tissue, which increases insulin resistance.

Chronic Kidney Disease

Chronic renal disease (CRD) is a pathophysiologic process with

multiple etiologies, resulting in the inexorable attrition of nephron number
and function and frequently leading to end-stage renal disease (ESRD). In
turn, ESRD represents a clinical state or condition in which there has been
an irreversible loss of endogenous renal function, of a degree sufficient to
render the patient permanently dependent upon renal replacement therapy
(dialysis or transplantation) in order to avoid life-threatening uremia.

Incidence and Prevalence

The website of the National Kidney and Transplant Institute (NKTI) said
kidney diseases, especially End Stage Renal Disease (ESRD), are the 7th
leading cause of death in the country for the year 2014. One Filipino develops
chronic renal failure every hour, or about 120 Filipinos per million people per
year.

About 1 in 10 people have some degree of CKD. It can develop at any

age and various conditions can lead to CKD. Kidney disease can affect people
of all ages and races. African Americans, Hispanics, American Indians and
people of South Asian origin (those from India, Bangladesh, Sri Lanka or
Pakistan) have a higher risk of CKD. This risk is due in part to high rates of
diabetes and high blood pressure in these communities.

Risk factors
 Diabetes
High blood pressure
Heart disease
Smoking
Obesity
High cholesterol
Being African-American, Native American or Asian-American
Family history of kidney disease
Age 65 or older

Stages of CKD according to Glomerular Filtration Rate

Increased risk of CKD. A GFR of 90 or above is considered normal. Even
with a normal GFR, you may be at increased risk for developing CKD if you
have diabetes, high blood pressure, or a family history of kidney disease. The
risk increases with age: People over 65 are more than twice as likely to develop
CKD as people between the ages of 45 and 65. African Americans also have a
higher risk of developing CKD.
Stage 1: Kidney damage with normal GFR (90 or above). Kidney damage may
be detected before the GFR begins to decline. In this first stage of kidney
disease, the goals of treatment are to slow the progression of CKD and reduce
the risk of heart and blood vessel disease.
Stage 2: Kidney damage with mild decrease in GFR (60 to 89).
Stage 3: Moderate decrease in GFR (30 to 59). When CKD has advanced to
this stage, anemia and bone problems become more common. W
Stage 4: Severe reduction in GFR (15 to 29).
Stage 5: Kidney failure (GFR less than 15). When the kidneys do not work
well enough to maintain life, you will need dialysis or a kidney transplant.

Stages of Chronic Kidney Disease

Stage 1 (Reduced renal reserve) - characterized by a 40% to 75% loss
of nephron function. The patient usually does not have symptoms because
the remaining nephrons are able to carry out the normal functions of the
kidney.
Stage 2 (Renal insufficiency) - occurs when 75% to 90% of nephron
function is lost. At this point, the serum creatinine and blood urea nitrogen
rise, the kidney loses its ability to concentrate urine and anemia develops.
The patient may report polyuria and nocturia.
Stage 3 (End-stage renal disease) - the final stage of chronic renal
failure, occurs when there is less than 10% nephron function remaining.
All of the normal regulatory, excretory, and hormonal functions of the
kidney are severely impaired. ESRD is evidenced by elevated creatinine
 and BUN levels as well as electrolyte imbalances. Once the patient
reaches this point, dialysis is usually indicated. Many of the symptoms of
uremia are reversible with dialysis.

Complications

Potential complications of chronic renal failure that concern the nurse and
that necessitate a collaborative approach to care include the following:

Hyperkalemia due to decreased excretion, metabolic acidosis,

catabolism, and excessive intake (diet, medications, fluids)

Pericarditis, pericardial effusion, and pericardial tamponade due to

retention of uremic waste products and inadequate dialysis

Hypertension due to sodium and water retention and malfunction of the

reninangiotensinaldosterone system

Anemia due to decreased erythropoietin production, decreased RBC life

span, bleeding in the GI tract from irritating toxins, and blood loss during
hemodialysis

Bone disease and metastatic calcifications due to retention of

phosphorus, low serum calcium levels, abnormal vitamin D metabolism,
and elevated aluminum levels.

Gerontologic Considerations

Changes in kidney function with normal aging increase the

susceptibility of elderly patients to kidney dysfunction and renal failure.
Because alterations in renal blood flow, glomerular filtration, and renal
clearance increase the risk for medication-associated changes in renal
function, precautions are indicated with all medications. This is because
of the frequent use of multiple prescription and over-the-counter
medications by elderly patients.
The incidence of systemic diseases, such as atherosclerosis,
hypertension, heart failure, diabetes, and cancer, increases with
advancing age, predisposing older adults to renal disease associated
with these disorders. Therefore, nurses in all settings need to be alert
for signs and symptoms of renal dysfunction in elderly patients.
With age, the kidney is less able to respond to acute fluid and
electrolyte changes. Therefore, acute problems need to be prevented if
possible or recognized and treated quickly to avoid kidney damage.
When the elderly patient must undergo extensive diagnostic tests, or
when new medications (eg, diuretic agents) are added, precautions
must be taken to prevent dehydration, which can compromise marginal
renal function and lead to ARF.
The elderly patient may develop atypical and nonspecific signs and
symptoms of disturbed renal function and fluid and electrolyte
imbalances. Recognition of these problems is further hampered by their
association with preexisting disorders and the misconception that they
are normal changes of aging.
DIABETIC NEPHROPATHY/Diabetic Kidney Disease

Nephropathy, or renal disease secondary to diabetic microvascular

changes in the kidney, is a common complication of diabetes. People with
diabetes account for nearly half of new cases of end stage renal disease
(ESRD) each year. About 20% to 30% of people with type 1 or type 2
diabetes develop nephropathy, but fewer of those with type 2 diabetes
progress to ESRD.

Patients with type 1 diabetes frequently show initial signs of renal

disease after 10 to 15 years, whereas patients with type 2 diabetes
develop renal disease within 10 years of the diagnosis of diabetes. Many
patients with type 2 diabetes have had diabetes for many years before it
was diagnosed and treated. Therefore, they have evidence of nephropathy
at the time of diagnosis.
Soon after the onset of diabetes, and especially if the blood glucose
levels are elevated, the kidneys filtration mechanism is stressed, allowing
blood proteins to leak into the urine. As a result, the pressure in the blood
vessels of the kidney increases.

Uremia

Uremia (uremic syndrome) is a serious complication of chronic kidney

disease and acute kidney injury (also known as acute renal failure). It occurs
when urea and other waste products build up in the body because the kidneys
are unable to eliminate them. These substances can become poisonous (toxic)
to the body if they reach high levels.

Uremic syndrome may affect any part of the body and can cause:

Nausea, vomiting, loss of appetite, and weight loss.

Changes in mental status, such as confusion, reduced awareness,
agitation, psychosis, seizures, and coma.
Abnormal bleeding, such as bleeding spontaneously or profusely from a
very minor injury.
Heart problems, such as an irregular heartbeat, inflammation in the sac
that surrounds the heart (pericarditis), and increased pressure on the
heart.
Shortness of breath from fluid buildup in the space between the lungs
and the chest wall (pleural effusion).

Anemia

Anemia is not a specific disease state but a sign of an underlying disorder.

It is by far the most common hematologic condition. Anemia, a condition in
which the hemoglobin concentration is lower than normal, reflects the
presence of fewer than normal RBCs within the circulation. As a result, the
amount of oxygen delivered to body tissues is also diminished.

Three broad etiologic categories:

Loss of RBCsoccurs with bleeding, potentially from any major source, such
as the gastrointestinal tract, the uterus, the nose, or a wound

Decreased production of RBCscan be caused by a deficiency in cofactors

(including folic acid, vitamin B12, and iron) required for erythropoiesis; RBC
production may also be reduced if the bone marrow is suppressed (eg, by
tumor, medications, toxins) or is inadequately stimulated because of a lack of
erythropoietin (as occurs in chronic renal disease).

Increased destruction of RBCsmay occur because of an overactive RES

(including hypersplenism) or because the bone marrow produces abnormal
RBCs that are then destroyed by the RES (eg, sickle cell anemia).

Symptoms common to many types of anemia include the

following:

Easy fatigue and loss of energy.

Unusually rapid heart beat, particularly with exercise.
Shortness of breath and headache, particularly with exercise.
Difficulty concentrating.
Dizziness.
Pale skin.
Leg cramps.
Insomnia.

Pneumonia

Pneumonia is an inflammation of the lung parenchyma that is caused

by a microbial agent. Pneumonitis is a more general term that describes an
inflammatory process in the lung tissue that may predispose a patient to or
place a patient at risk for microbial invasion.

Community-acquired pneumonia (CAP) occurs either in the community

setting or within the first 48 hours of hospitalization or institutionalization. The
need for hospitalization for CAP depends on the severity of the pneumonia.
The agents that most frequently cause CAP requiring hospitalization are S.
pneumoniae, H. influenzae, Legionella, Pseudomonas aeruginosa, and other
gram negative rods.

Incidence and Prevalence

Pneumonia is the most common cause of death from infectious

diseases in the United States. It is the seventh leading cause of death in the
United States for all ages and both genders, resulting in almost 70,000 deaths
per year. In persons 65 years of age and older, it is the fifth leading cause of
death (National Center for Health Statistics, 2000; Minino & Smith, 2001).

According to the DOH Philippines, Pneumonia was the 4 th leading cause

of mortality last 2010.

Risk Factors
Conditions that produce mucus or bronchial obstruction and interfere
with normal lung drainage (eg, cancer, cigarette smoking, COPD)
Immunosuppressed patients and those with a low neutrophil count
(neutropenic)
Smoking; cigarette smoke disrupts both mucociliary and macrophage
activity
Prolonged immobility and shallow breathing pattern
Depressed cough reflex (due to medications, a debilitated state, or
weak respiratory muscles); aspiration of foreign material into the ungs
during a period of unconsciousness (head injury, anesthesia, depressed
level of consciousness), or abnormal swallowing mechanism
Nothing-by-mouth (NPO) status; placement of nasogastric,orogastric, or
endotracheal tube
Antibiotic therapy (in very ill people, the oropharynx is likely to be
colonized by gram-negative bacteria)
Alcohol intoxication (because alcohol suppresses the bodys reflexes,
may be associated with aspiration, and decreases white cell
mobilization and tracheobronchial ciliary motion)
General anesthetic, sedative, or opioid preparations that promote
respiratory depression, which causes a shallow breathing pattern and
predisposes to the pooling of bronchial secretions and potential
development of pneumonia
Advanced age, because of possible depressed cough and glottis
reflexes and nutritional depletion
Respiratory therapy with improperly cleaned equipment

Clinical Features of patients with CAP according to

risk categories
Low-risk CAP Moderate-risk CAP High-risk CAP
Presence of: Any of the following: Any of the criteria under
Stable vital signs; RR <30 Unstable vital signs: RR moderate- risk CAP
breaths/min PR <125 >30 breaths/min PR >125 category plus
beats/min Temp >36 oC beats/min Temp >40oC or Severe Sepsis and Septic
or <40 oC SBP >90 <36oC SBP <90 shock
DBP >60 mmHg mmHg DBP <60 mmHg

No altered mental state of altered mental state of Need for mechanical

acute onset acute onset ventilation

No suspected aspiration Suspected aspiration

No or stable comorbid Decompensated co-morbid
conditions condition
Chest X-ray: Chest X-ray:
- localized infiltrates multilobar infiltrates
- no evidence of pleural pleural effusion or abscess
effusion, abscess

Preventive Measures

Promote coughing and expectoration of secretions.

Encourage smoking cessation.
Initiate special precautions against infection.
Encourage smoking cessation.
Reposition frequently and promote lung expansion exercises and
coughing. Initiate suctioning and chest physical therapy if indicated.
Promote frequent oral hygiene.
Encourage reduced or moderate alcohol intake (in case of alcohol
stupor, position patient to prevent aspiration).
Promote frequent turning, early ambulation and mobilization, effective
coughing, breathing exercises, and nutritious diet.
Make sure that respiratory equipment is cleaned properly; participate
in continuous quality improvement monitoring with the respiratory care
department.

Gerontologic Considerations

Pneumonia in the elderly patient may occur as a primary problem or as

a complication of a chronic disease process.
Pulmonary infections in the elderly frequently are difficult to treat and
have
a higher mortality rate than in younger patients.
General deterioration, weakness, abdominal symptoms, anorexia,
confusion, tachycardia, and tachypnea may signal the onset of
pneumonia.
The diagnosis of pneumonia may be missed because the classic
symptoms of cough, chest pain, sputum production, and fever may be
absent or masked in the elderly patient. Also, the presence of some
signs may be misleading. Abnormal breath sounds, for example, may
be due to microatelectasis that occurs in the aged as a result of
decreased mobility, decreased lung volumes, and other respiratory
function changes.
Because chronic heart failure is often seen in the elderly, chest x-rays
may be obtained to assist in differentiating it from pneumonia as the
cause of clinical signs and symptoms.
Supportive treatment includes hydration (with caution and frequent
assessment because of the risk of fluid overload in the elderly),
supplemental oxygen therapy, assistance with deep breathing,
coughing, frequent position changes, and early ambulation.
All of these are particularly important in the care of the elderly patient
with pneumonia.
To reduce or prevent serious complications of pneumonia in the elderly,
vaccination against pneumococcal and influenza infections is
recommended.
B. Signs and Symptoms

SIGNS AND SYMPTOMS DATE MANIFESTED

ACCORDING TO TEXTBOOK

Pallor +(June 2016)

Grey-bronze skin color -

Ecchymoses + (2008)

Purpura -

Dry, flaky skin -

Pruritus -

Volume overload -

Hypertension +(2008)

Pitting edema -

Crackles -

Thick, tenacious sputum +(June 8,2016)

Pulmonary effusion +(June 8,2016)

Dyspnea +(June 8,2016)

Tachypnea -

Pleuritic pain -

Fatigue +(2013)

Confusion +(2009)

Depression -

Headache -

Inability to concentrate +(2009)

Peripheral and autonomic -

neruopathy

Tremors -

Restless legs -

Seizures -
Loss of recent memory +(2009)

Perceptual errors in identifying -

persons and/or objects

Odors of anemia on the breath -

Hiccups -

Anorexia +(2009)

Nausea and vomiting -

Malnutrition +(2009)

GI bleeding -

Anemia +(June 11,2016)

Leukocyte and immune system +(June 11,2016)

dysfunction

Platelet dysfunction -

Impotence -

Testicular atrophy -

Loss of libido -

Muscle cramps -

Loss of muscle strength -

Renal osteodystrophy -

Bone pain -

Fractures -

Increased creatinine, BUN +(June 11,2016)

Metabolic acidosis +(June 12,2016)

Hyperkalemia +(June 11,2016)

Uremia +(June 11,2016)

Hypocalcemia +(June 11,2016)

Hyperparathyroidism -

Hyperphosphatemia -

Oliguria +(2013)

Anuria -
D. Management

Medical Management

Diabetes

The main goal of diabetes treatment is to normalize insulin activity and

blood glucose levels to reduce the development of vascular and
neuropathic complications.

There are five components of diabetes management:

Nutritional management

Exercise

Monitoring

Pharmacologic therapy

Education

Chronic Kidney Disease

The goal of management is to maintain kidney function and homeostasis for

as long as possible. All factors that contribute to ESRD and all factors that are
reversible (eg, obstruction) are identified and treated. Management is
accomplished primarily with medications and diet therapy, although dialysis
may also be needed to decrease the level of uremic waste products in the
blood (Fink et al., 2001).

PHARMACOLOGIC THERAPY

Complications can be prevented or delayed by administering

prescribed antihypertensives, erythropoietin (Epogen), iron
supplements, phosphate-binding agents, and calcium supplements.
Antacids. Hyperphosphatemia and hypocalcemia are treated with
aluminum-based antacids that bind dietary phosphorus in the GI tract.
However, concerns about the potential long-term toxicity of aluminum
and the association of high aluminum levels with neurologic symptoms
and osteomalacia have led some physicians to prescribe calcium
carbonate in place of high doses of aluminum-based antacids. This
medication also binds dietary phosphorus in the intestinal tract and
permits the use of smaller doses of antacids. Both calcium carbonate
and phosphorus binding antacids must be administered with food to be
effective. Magnesium-based antacids must be avoided to prevent
magnesium toxicity.
Antihypertensive and Cardiovascular Agents. Hypertension is managed
by intravascular volume control and a variety of antihypertensive
agents. Heart failure and pulmonary edema may also require treatment
with fluid restriction, low-sodium diets, diuretic agents, inotropic agents
 such as digitalis or dobutamine, and dialysis. The metabolic acidosis of
chronic renal failure usually produces no symptoms and requires no
treatment; however, sodium bicarbonate supplements or dialysis may
be needed to correct the acidosis if it causes symptoms (Tonelli et al.,
2001).
Antiseizure Agents. Neurologic abnormalities may occur, so the patient
must be observed for early evidence of slight twitching, headache,
delirium, or seizure activity. If seizures occur, the onset of the seizure is
recorded along with the type, duration, and general effect on the
patient. The physician is notified immediately. Intravenous diazepam
(Valium) or phenytoin (Dilantin) is usually administered to control
seizures. The side rails of the bed should be padded to protect the
patient.
Erythropoietin. Anemia associated with chronic renal failure is treated
with recombinant human erythropoietin (Epogen). Anemic patients
(hematocrit less than 30%) present with nonspecific symptoms, such
as malaise, general fatigability, and decreased activity tolerance.
Epogen therapy is initiated to achieve a hematocrit of 33% to 38%,
which generally alleviates the symptoms of anemia. Epogen is
administered either intravenously or subcutaneously three times a
week. It may take 2 to 6 weeks for the hematocrit to rise; therefore,
Epogen is not indicated for patients who need immediate correction of
severe anemia. Adverse effects seen with Epogen therapy include
hypertension (especially during early stages of treatment), increased
clotting of vascular access sites, seizures, and depletion of body iron
stores (Fink et al., 2001).

Diaebetic Kidney Disease

In addition to achieving and maintaining near-normal blood glucose levels,

management for all patients with diabetes should include careful attention to
the following:

Control of hypertension (the use of angiotensin-converting enzyme [ACE]

inhibitors, such as captopril, because control of hypertension may also
decrease or delay the onset of early proteinuria)

Prevention or vigorous treatment of urinary tract infections

Avoidance of nephrotoxic substances

Adjustment of medications as renal function changes

Low-sodium diet

Low-protein diet

Uremia and Anemia

Treatment for uremia frequently requires hospitalization. It begins with
treating the cause of the kidney injury so that nitrogen waste will not
continue to build up in the blood. Treatment may require dialysis, which
filters the waste out of the blood while the kidneys recover. Fluid therapy,
blood transfusions, and blood pressure medications may also be
administered. Ongoing treatment after the acute symptoms of uremia
have been addressed may include medication, dialysis, or dietary
modification.

Management of anemia is directed toward correcting or controlling the

cause of the anemia; if the anemia is severe, the RBCs that are lost or
destroyed may be replaced with a transfusion of packed RBCs (PRBCs).

Anemia associated with chronic renal failure is treated with recombinant

human eyrthropoietin. Epogen therapy is initiated to achieve a hematocrit
of 33% to 38% which generally alleviates the symptoms of anemia.
Epogen is administered either intravenously or subcutaneously three
times a week. It may take 2 to 6 weeks for the hematocrit to rise.

Pneumonia

The treatment of pneumonia includes administration of the appropriate

antibiotic as determined by the results of the Gram stain.
Recommendations for treatment of outpatients with CAP who have no
cardiopulmonary disease or other modifying factors include a macrolide
(erythromycin, azithromycin [Zithromax], or clarithromycin [Biaxin]),
doxycycline (Vibramycin), or a fluoroquinolone (eg, gatifloxacin
[Tequin], levofloxacin [Levaquin]) with enhanced activity against S.
pneumoniae (Bartlett et al., 2000; American Thoracic Society, 2001).
For those outpatients who have cardiopulmonary disease or other
modifying factors, treatment should include a beta-lactam (oral
cefpodoxime [Vantin], cefuroxime [Zinacef, Ceftin], high-dose
amoxicillin or amoxicillin/clavulanate [Augmentin, Clavulin]) plus a
macrolide or doxycycline. Also, a beta-lactam plus an
antipneumococcal fluoroquinolone can be used (American Thoracic
Society, 2001).
For patients with CAP who are hospitalized and do not have
cardiopulmonary disease or modifying factors, management consists of
intravenous azithromycin (Zithromax) or monotherapy with an
antipneumococcal fluoroquinolone.
For inpatients with cardiopulmonary disease or modifying factors, the
treatment involves an intravenous beta-lactam plus an intravenous or
oral macrolide or doxycycline. An intravenous antipneumococcal
fluoroquinolone may also be used alone (American Thoracic Society,
2001).
For acutely ill patients admitted to the intensive care unit,
management includes an intravenous beta-lactam plus either an
intravenous macrolide or fluoroquinolone.
 If specific pathogens have been identified for the CAP, more specific
agents may be utilized.
If hypoxemia develops, oxygen is administered.
Pulse oximetry or arterial blood gas analysis is performed to determine
the need for oxygen and to evaluate the effectiveness of the therapy.
Nursing Management

Chronic Kidney Disease

The patient with chronic renal failure requires astute nursing care to
avoid the complications of reduced renal function and the stresses and
anxieties of dealing with a life-threatening illness.
Nursing care is directed toward assessing fluid status and identifying
potential sources of imbalance
Implementing a dietary program to ensure proper nutritional intake
within the limits of the treatment regimen.
Promoting positive feelings by encouraging increased self-care and
greater independence.
It is extremely important to provide explanations and information to the
patient and family concerning ESRD, treatment options, and potential
complications. A great deal of emotional support is needed by the
patient and family because of the numerous changes experienced.

Pneumonia

IMPROVING AIRWAY PATENCY

Removing secretions is important because retained secretions interfere

with gas exchange and may slow recovery.
The nurse encourages hydration (2 to 3 L/day) because adequate
hydration thins and loosens pulmonary secretions.
Humidification may be used to loosen secretions and improve
ventilation. A high humidity facemask (using either compressed air or
oxygen) delivers warm, humidified air to the tracheobronchial tree,
helps to liquefy secretions, and relieves tracheobronchial irritation.
Lung expansion maneuvers, such as deep breathing with an incentive
spirometer, may induce a cough.
The nurse encourages the patient to perform an effective, directed
cough, which includes correct positioning, a deep inspiratory
maneuver, glottic closure, contraction of the expiratory muscles
against the closed glottis, sudden glottis opening, and an explosive
expiration.
Chest physiotherapy (percussion and postural drainage) is important in
loosening and mobilizing secretions.
If the patient is too weak to cough ffectively, the nurse may need to
remove the mucus by nasotracheal suctioning.
It may take time for secretions to mobilize and move into the central
airways for expectoration. Thus, it is important for the nurse to monitor
the patient for cough and sputum production after the completion of
chest physiotherapy.
The nurse administers and titrates oxygen therapy as prescribed.
The effectiveness of oxygen therapy is monitored by improvement in
 clinical signs and symptoms, and adequate oxygenation values
measured by pulse oximetry or arterial blood gas analysis.

PROMOTING REST AND CONSERVING ENERGY

The nurse encourages the debilitated patient to rest and avoid

overexertion and possible exacerbation of symptoms.
The patient should assume a comfortable position to promote rest and
breathing (eg, semi-Fowlers) and should change positions frequently to
enhance secretion clearance and ventilation/perfusion in the lungs. It is
important to instruct outpatients not to overexert themselves and to
engage in only moderate activity during the initial phases of treatment.

PROMOTING FLUID INTAKE

The respiratory rate of a patient with pneumonia increases because of

the increased workload imposed by labored breathing and fever. An
increased respiratory rate leads to an increase in insensible fluid loss
during exhalation and can lead to dehydration. Therefore, it is
important to encourage increased fluid intake (at least 2 L/day), unless
contraindicated.

PROMOTING THE PATIENTS KNOWLEDGE

The patient and family are instructed about the cause of pneumonia,
management of symptoms of pneumonia, and the need for follow-up.
The patient also needs information about factors (both patient risk
factors and external factors) that may have contributed to developing
pneumonia and strategies to promote recovery and to prevent
recurrence.
If hospitalized for treatment, the patient is instructed about the
purpose and importance of management strategies that have been
implemented and about the importance of adhering to them during and
after the hospital stay.
Explanations need to be given simply and in language that the patient
can understand.
If possible, written instructions and information should be provided.
Because of the severity of symptoms, the patient may require that
instructions and explanations be repeated several times.

Anemia

Management involves adjustment of heparin to prevent clotting of the

dialysis lines during hemodialysis treatment, frequent monitoring of
hematocrit, and periodic assessment of serum iron and transferrin
levels.

Blood pressure and serum potassium level are monitored to detect

hypertension and rising potassium levels which may occur with therapy
and the increasing RBC mass.
Dialysis

Dialysis is used to remove fluid and uremic waste products from the body
when the kidneys cannot do so. It may also be used to treat patients with
edema that does not respond to treatment, hepatic coma, hyperkalemia,
hypercalcemia, hypertension, and uremia. Methods of therapy include
hemodialysis, continuous renal replacement therapy (CRRT; discussed
later), and various forms of peritoneal dialysis.

The need for dialysis may be acute or chronic.

Acute dialysis is indicated when there is a high and rising level of

serum potassium, fluid overload, or impending pulmonary edema,
increasing acidosis, pericarditis, and severe confusion. It may also
be used to remove certain medications or other toxins (poisoning or
medication overdose) from the blood.

Chronic or maintenance dialysis is indicated in chronic renal failure,

known as end-stage renal disease (ESRD), in the following
instances: the presence of uremic signs and symptoms affecting all
body systems (nausea and vomiting, severe anorexia, increasing
lethargy, mental confusion), hyperkalemia, fluid overload not
responsive to diuretics and fluid restriction, and a general lack of
well-being. An urgent indication for dialysis in patients with chronic
renal failure is pericardial friction rub.

HEMODIALYSIS
Hemodialysis is the most commonly used method of dialysis: more than
300,000 Americans currently receive hemodialysis (Parker, Bliwise & Rye,
2000). It is used for patients who are acutely ill and require short-term
dialysis (days to weeks) and for patients with ESRD who require long-term
or permanent therapy.

A dialyzer (once referred to as an artificial kidney) serves as a synthetic

semipermeable membrane, replacing the renal glomeruli and tubules as
the filter for the impaired kidneys. For patients with chronic renal failure,
hemodialysis prevents death, although it does not cure renal disease and
does not compensate for the loss of endocrine or metabolic activities of
the kidneys.

Principles of Hemodialysis
The objectives of hemodialysis are to extract toxic nitrogenous substances
from the blood and to remove excess water. In hemodialysis, the blood,
laden with toxins and nitrogenous wastes, is diverted from the patient to a
machine, a dialyzer, in which the blood is cleansed and then returned to
the patient.

Diffusion, osmosis, and ultrafiltration are the principles on which

hemodialysis is based. The toxins and wastes in the blood are removed by
diffusionthat is, they move from an area of higher concentration in the
blood to an area of lower concentration in the dialysate. The dialysate is
a solution made up of all the important electrolytes in their ideal
extracellular concentrations.
Equipment: Dialyzers
Most dialyzers, or artificial kidneys, are either flat-plate dialyzers or
hollow-fiber artificial kidneys that contain thousands of tiny cellophane
tubules that act as semipermeable membranes. The blood flows through
the tubules, while a solution (the dialysate) circulates around the tubules.
The exchange of wastes from the blood to the dialysate occurs through the
semipermeable membrane
of the tubules.

Vascular Access
Access to the patients vascular system must be established to allow blood
to be removed, cleansed, and returned to the patients vascular system at
rates between 200 and 800 mL/minute.

Several types of access are available.

SUBCLAVIAN, INTERNAL, JUGULAR, AND FEMORAL CATHETERS

FISTULA

A more permanent access, known as a fistula, is created surgically

(usually in the forearm) by joining (anastomosing) an artery to a vein,
either side to side or end to side. Needles are inserted into the vessel to
obtain blood flow adequate to pass through the dialyzer. The arterial
segment of the fistula is used for arterial flow and the venous segment for
reinfusion of the dialyzed blood. The fistula takes 4 to 6 weeks to mature
before it is ready for use.

Complications of Hemodialysis
Hypotension may occur during the treatment as fluid is removed.
Nausea and vomiting, diaphoresis, tachycardia, and dizziness are common
signs of hypotension.
Painful muscle cramping may occur, usually late in dialysis as fluid and
electrolytes rapidly leave the extracellular space.
Exsanguination may occur if blood lines separate or dialysis needles
accidentally become dislodged.
Dysrhythmias may result from electrolyte and pH changes or from
removal of antiarrhythmic medications during dialysis.
Air embolism is rare but can occur if air enters the vascular system.
Chest pain may occur in patients with anemia or arteriosclerotic heart
disease.
Dialysis disequilibrium results from cerebral fluid shifts. Signs and
symptoms include headache, nausea and vomiting, restlessness,
decreased level of consciousness, and seizures. It is more likely to occur in
acute renal failure or when blood urea nitrogen levels are very high
(exceeding 150 mg/dL).

Nursing Management

MEETING PSYCHOSOCIAL NEEDS

Dialysis alters the lifestyle of the patient and family. The amount of time
required for dialysis and physician visits and being chronically ill can
create conflict, frustration, guilt, and depression. It may be difficult for the
patient, spouse, and family to express anger and negative feelings. The
nurse needs to give the patient and family the opportunity to express
feelings of anger and concern over the limitations that the disease and
treatment impose and over possible financial problems and job insecurity.
If anger is not expressed, it may be directed inward and lead to
depression, despair, and attempts at suicide (suicide is more prevalent in
dialysis patients necessary.

PROMOTING HOME AND COMMUNITY-BASED CARE

Preparing a patient for hemodialysis is challenging. Often the patient does
not fully comprehend the impact of dialysis, and learning needs may go
unrecognized. Good communication between the dialysis staff (in the
hospital and outpatient clinic), unit staff, and home care nurses is
essential for providing sound continuous care.

PERITONEAL DIALYSIS
The goals of peritoneal dialysis are to remove toxic substances and
metabolic wastes and to re-establish normal fluid and electrolyte balance.
Peritoneal dialysis may be the treatment of choice for patients with renal
failure who are unable or unwilling to undergo hemodialysis or renal
transplantation. Patients who are susceptible to the rapid fluid, electrolyte
and metabolic changes that occur during hemodialysis experience fewer
of these problems with the slower rate of peritoneal dialysis. Peritoneal
dialysis can be performed using several different approaches:

Underlying Principles
In peritoneal dialysis, the peritoneum, a serous membrane that covers the
abdominal organs and lines the abdominal wall, serves the semipermeable
membrane. The surface of the peritoneum constitutes a body surface area
of about 22,000 cm2. Sterile dialysate fluid is introduced into the
peritoneal cavity through an abdominal catheter at intervals. Urea and
creatinine, metabolic end products normally excreted by the kidneys, are
cleared from the blood by diffusion and ossmosis as waste products move
from an area of higher concentration (the peritoneal blood supply) to an
area of lower concentration (the peritoneal cavity) across a
semipermeable membrane (the peritoneal membrane).

Urea is cleared at a rate of 15 to 20 mL/min, whereas creatinine is

removed at a slower rate. It usually takes 36 to 48 hours to achieve with
peritoneal dialysis what hemodialysis accomplishes in 6 to 8 hours.
Ultrafiltration (water removal) occurs in peritonealdialysis through an
osmotic gradient created by using a dialysate fluid with a higher glucose
concentration.

Complications of Peritoneal Dialysis

Peritoneal dialysis is not without complications. Most are minor, but
several, if unattended, can have serious consequences.

Peritonitis (inflammation of the peritoneum) is the most common and

most serious complication of peritoneal dialysis. The organism responsible
for peritoneal dialysis-related peritonitis is an important factor in clinical
outcome and the basis of treatment guidelines. There has been a
significant decrease in the rate of cases of peritonitis, from 1.37
episodes/patient-year in 1991 to 0.55 episodes/patient-year in 1998.
Staphylococcus aureus and Staphylococcus epidermidis remain the most
common Gram-positive organisms responsible for peritonitis, although the
rates of each have decreased. Pseudomonas aeruginosa, E. coli, and
Klebsiella species are the most common causes of Gram-negative
peritonitis. Resistance to antibacterial agents (ie, ciprofloxacin, methicillin)
used in their treatment increased dramatically from 1991 to 1998
(Zelenitsky et al., 2000).