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Nurses
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Diseases
Second Edition

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STAFF
Executive Publisher
Judith A. Schilling McCann, RN, MSN
Editorial Director
H. Nancy Holmes
Clinical Director
Joan M. Robinson, RN, MSN
Art Director
Elaine Kasmer
Editorial Project Manager
Ann E. Houska
Clinical Project Manager
Janet Rader Clark, RN, BSN
Editor
Kimberly A.J. Bilotta
Clinical Editors
Collette Bishop Hendler, RN, BS, MS, CCRN;
Anita Lockhart, RN, MSN; Dorothy P. Terry, RN
Copy Editors
Leslie Dworkin, Jeannine Fielding, Linda Hager
Designer
Joseph John Clark
Digital Composition Services
Diane Paluba (manager), Joyce Rossi Biletz,
Donald G. Knauss, Donna S. Morris
Associate Manufacturing Manager
Beth J. Welsh
Editorial Assistants
Karen J. Kirk, Jeri OShea, Linda K. Ruhf
Indexer
Dianne Schneider

The clinical treatments described and recommended in


this publication are based on research and consultation
with nursing, medical, and legal authorities. To the best
of our knowledge, these procedures reflect currently
accepted practice. Nevertheless, they cant be considered
absolute and universal recommendations. For individual
applications, all recommendations must be considered in
light of the patients clinical condition and, before
administration of new or infrequently used drugs, in light
of the latest package-insert information. The authors and
publisher disclaim any responsibility for any adverse
effects resulting from the suggested procedures, from any
undetected errors, or from the readers misunderstanding
of the text.
2009 by Lippincott Williams & Wilkins. All rights
reserved. This book is protected by copyright. No part of
it may be reproduced, stored in a retrieval system, or
transmitted, in any form or by any meanselectronic,
mechanical, photocopy, recording, or otherwise
without prior written permission of the publisher, except
for brief quotations embodied in critical articles and
reviews and testing and evaluation materials provided by
the publisher to instructors whose schools have adopted
its accompanying textbook. Printed in China. For
information, write Lippincott Williams & Wilkins, 323
Norristown Road, Suite 200, Ambler, PA 19002-2756.
NQCD2010408
Library of Congress Cataloging-in-Publication Data
Nurses quick check. Diseases. 2nd ed.
p. ; cm.
Includes bibliographical references and index.
1. DiseasesHandbooks, manuals, etc. 2. Nursing
Handbooks, manuals, etc. I. Lippincott Williams & Wilkins.
[DNLM: 1. DiseaseHandbooks. 2. Nursing Care
Handbooks. 3. TherapeuticsHandbooks.
WY 49 N9742 2008]
RT65.N78 2008
616dc22
ISBN-13: 978-0-7817-8940-0 (alk. paper)
ISBN-10: 0-7817-8940-0 (alk. paper) 2007049036

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Contents
Contributors and consultants vii

Diseases (in alphabetical order)

Less common diseases 922


Selected references

933

Web resources 935


Index 937

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Contributors
and consultants
Beverly Anderson, RN, MSN, MOT

Kendra S. Seiler, RN, MSN

Associate Professor
Malcolm X College
Chicago

Nursing Instructor
Rio Hondo College
Whittier, Calif.

Elizabeth A. Archer, RN, EdD

LaDelle Smothers, RN, BSN, MS

Associate Professor
Baptist College of Health Sciences
Memphis

RN Consultant (traveling)
Britthaven, Inc.
Kinston, N.C.

Julie A. Calvery, RN, MS

Rita M. Wick, RN, BSN

Instructor
University of Arkansas
Fort Smith

Education Specialist
Berkshire Health Systems
Pittsfield, Mass.

Kim Cooper, RN, MSN


Nursing Department Chair
Ivy Tech Community College
Terre Haute, Ind.

Lillian Craig, RN, MSN, FNP-C


Adjunct Faculty
Oklahoma Panhandle State University
Goodwell

Shelley Yerger Hawkins, APRN-BC, DSN, FNP, GNP,


FAANP

Post Doctoral Fellow


University of North Carolina
Chapel Hill

Elizaveta House, RN, BSN


Procurement Coordinator
LifeChoice Donor Services, Inc.
Windsor, Conn.

Angela R. Irvin, RN, MSN, ARNP, NP-C


Nurse Practitioner
University of Louisville (Ky.) Family & Geriatric Medicine

Vanessa Kramasz, RN, MSN, FNP


Lead Faculty & Nurse Practitioner
Gateway Technical College
Burlington, Wis.

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Diseases
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Abortion, spontaneous
Overview
Description

H Also known as miscarriage


H Expelled products of conception from the uterus be-

fore fetal viability (see Types of spontaneous abortion)

Pathophysiology
H Abortion may result from fetal, placental, or maternal

factors.
Fetal factors
H Fetal factors usually cause abortion to occur between
9 and 12 weeks gestation.
H Spontaneous abortion may result from defective embryologic development.
H Faulty implantation of a fertilized ovum may cause
the ovum to be rejected.
H Abortion may also result from failure of the endometrium to accept the fertilized ovum.
Placental factors
H Placental factors usually cause abortion to occur
around 14 weeks gestation when the placenta takes
over the hormone production necessary to maintain
pregnancy. These factors include:
premature separation of a normally implanted
placenta
abnormal placental implantation
abnormal platelet function.
Maternal factors
H Maternal factors usually cause abortion to occur
between 11 and 19 weeks gestation.

Causes
Spontaneous abortion
H Fetal factors
H Placental factors
H Maternal infection
H Severe malnutrition
H Abnormalities of the reproductive organs
H Thyroid gland dysfunction
H Lowered estriol secretion
H Diabetes mellitus
H Trauma
H Surgery that necessitates manipulation of the pelvic
organs
H Blood group incompatibility and Rh isoimmunization
H Illicit drug use
H Environmental toxins
H Incompetent cervix

Incidence
H Percentage of all pregnancies that end in miscar-

riage: up to 15%
H First pregnancies that end in miscarriage: about 30%
H Miscarriages that occur during the first trimester: at

least 75%

Abortion, spontaneous

Common characteristics
H Pink discharge for several days before cramping
H Scant brown discharge for several weeks before

cramping
H Abdominal cramps
H Vaginal bleeding

Complications
H Infection
H Hemorrhage
H Anemia
H Coagulation defects
H Disseminated intravascular coagulation
H Psychological issues of loss and failure

Assessment
History
H Pink discharge for several days or scant brown dis-

charge for several weeks before onset of cramps and


increased vaginal bleeding
H Cramps that appear for a few hours, intensify, then
occur more frequently
H Continued cramps and bleeding if any uterine contents remain (cramps and bleeding may subside if
entire contents expelled)

Physical findings
H Vaginal bleeding
H Cervical dilation
H Passage of nonviable products of conception

Test results
Laboratory
H Serum human chorionic gonadotropin levels are
decreased, suggesting spontaneous abortion.
H Cytologic analysis shows evidence of products of
conception.
H Serum hemoglobin level and hematocrit are decreased due to blood loss.
Imaging
H Presence or absence of fetal heart tones or empty
amniotic sac is revealed by ultrasound examination.

Treatment
General
H Accurate evaluation of uterine contents before plan-

ning treatment
H Progression of spontaneous abortion unpreventable,

except in cases caused by an incompetent cervix


H Hospitalization to control severe hemorrhage
H Possible bed rest

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Medications
H Transfusion with packed red blood cells or whole

blood (severe bleeding)


H I.V. oxytocin (stimulates uterine contractions)
H Rho(D) immune globulin for an Rh-negative female

with a negative indirect Coombs test

Surgery
H Dilatation and curettage or dilatation and evacuation,

if remnants remain in the uterus


H Surgical reinforcement of the cervix (cerclage) to

prevent abortion

Nursing considerations
Key outcomes
The patient will:
H exhibit no signs and symptoms of infection
H communicate feelings about the current situation
H express feelings of having greater control over the
current situation
H use available support systems, such as family and
friends, to aid in coping.

Nursing interventions
H Do not allow bathroom privileges because the pa-

tient may expel uterine contents without knowing it.


H Inspect bedpan contents carefully for intrauterine

material.
H Save all sanitary pads for evaluation.
H Give prescribed drugs.
H Provide perineal care.
H Provide emotional support and counseling.
H Encourage expression of feelings.
H Help the patient develop effective coping strategies.

Monitoring
H Amount, color, and odor of vaginal bleeding
H Vital signs
H Intake and output

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H vaginal bleeding or spotting
H bleeding that lasts longer than 8 days or excessive
bleeding
H importance of reporting signs of bright red blood
immediately
H signs of infection, such as fever and foul-smelling
vaginal discharge
H gradual increase of daily activities
H schedule for returning to work (normally within 1
to 4 weeks)
H abstinence from intercourse for 1 to 2 weeks
H prevention of spontaneous abortion

Types of spontaneous abortion


Depending on clinical findings, a spontaneous abortion
(miscarriage) may be threatened or inevitable, incomplete
or complete, or missed, habitual, or septic. Heres how the
seven types compare.

Threatened abortion
Bloody vaginal discharge occurs during the first half of
pregnancy. About 20% of pregnant women have vaginal
spotting or actual bleeding early in pregnancy; of these,
about 50% abort.

Inevitable abortion
The membranes rupture and the cervix dilates. As labor
continues, the uterus expels the products of conception.

Incomplete abortion
The uterus retains part or all of the placenta. Before 10
weeks gestation, the fetus and placenta are usually expelled together; after the 10th week, theyre expelled separately. Because part of the placenta may adhere to the
uterine wall, bleeding continues. Hemorrhage is possible
because the uterus doesnt contract and seal the large
vessels that feed the placenta.

Complete abortion
The uterus passes all the products of conception. Minimal
bleeding usually accompanies complete abortion because
the uterus contracts and compresses the maternal blood
vessels that feed the placenta.

Missed abortion
The uterus retains the products of conception for 2
months or more after the death of the fetus. Uterine
growth ceases; uterine size may even seem to decrease.
Prolonged retention of the dead products of conception
may cause coagulation defects such as disseminated intravascular coagulation.

Habitual abortion
Spontaneous loss of three or more consecutive pregnancies constitutes habitual abortion.

Septic abortion
Infection accompanies abortion. This may occur with
spontaneous abortion, but usually results from an illegal
abortion or from the presence of an intrauterine device.

H contraceptive information
H avoidance of tampons for 1 to 2 weeks
H follow-up examination.

Discharge planning
H Refer the patient for professional counseling, if

indicated.

Abortion, spontaneous

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Abruptio placentae
Overview
Description

H Disseminated intravascular coagulation (DIC)


H Maternal death
H Fetal death

Assessment

H Premature separation of the placenta from the uter-

History

ine wall
H Usually occurs after 20 weeks gestation, most commonly during the third trimester
H Common cause of bleeding during the second half of
pregnancy
H Fetal prognosis depending on gestational age and
amount of blood lost
H Good maternal prognosis if hemorrhage can be controlled
H Classified according to degree of placental separation
and severity of maternal and fetal symptoms (see Degrees of placental separation in abruptio placentae)
H Also called placental abruption

Mild abruptio placentae (marginal


separation)
H Mild to moderate vaginal bleeding
H Vague lower abdominal discomfort
H Mild to moderate abdominal tenderness
Moderate abruptio placentae (about 50%
placental separation)
H Continuous abdominal pain
H Moderate dark red vaginal bleeding
H Severe or abrupt onset of symptoms
Severe abruptio placentae (70% placental
separation)
H Abrupt onset of agonizing, unremitting uterine pain
H Moderate vaginal bleeding

Pathophysiology

Physical findings

H Spontaneous rupture of blood vessels at the placental

Mild abruptio placentae


H Fetal monitoring possibly indicating uterine irritability
H Strong and regular fetal heart tones
Moderate abruptio placentae
H Vital signs possibly indicating impending shock
H Tender uterus remaining firm between contractions
H Barely audible or irregular and bradycardic fetal
heart tones
H Labor that usually starts within 2 hours and proceeds
rapidly
Severe abruptio placentae
H Vital signs that indicate rapidly progressive shock
H Absence of fetal heart tones
H Tender uterus with boardlike rigidity
H Possible increased uterine size in severe concealed
abruptions

bed may be due to lack of resiliency or to abnormal


changes in uterine vasculature.
H State may be complicated by hypertension or by an
enlarged uterus that cant contract sufficiently to seal
off the torn vessels.
H Bleeding continues unchecked, possibly shearing off
the placenta partially or completely.

Causes
H Exact cause unknown
H Traumatic injury
H Amniocentesis
H Chronic or gestational hypertension
H Multiparity
H Short umbilical cord
H Dietary deficiency
H Smoking
H Advanced maternal age
H Pressure on the vena cava from an enlarged uterus
H Diabetes mellitus

Test results

Common characteristics

Laboratory
H Serum hemoglobin level and platelet counts are decreased.
H Progression of abruptio placentae and detection of
DIC is shown by fibrin split products.
Imaging
H Pelvic examination under double setup (preparations
for an emergency cesarean delivery) and ultrasonography may rule out placenta previa.

H Vaginal bleeding
H Abdominal discomfort
H Abdominal tenderness

Treatment

Complications

General

H Hemorrhage
H Shock
H Renal failure

H Blood loss evaluated and controlled


H Viable infant delivered
H Coagulation disorders prevented

Incidence
H Most common in multigravida women older than

age 35, women with gestational hypertension, and


women who use cocaine

Abruptio placentae

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Degrees of placental separation in abruptio placentae


Mild separation

Moderate separation

Severe separation

Internal bleeding between the placenta


and uterine wall characterizes mild
separation.

In moderate separation, external hemorrhage occurs through the vagina.

External hemorrhage is also characteristic in severe separation.

H For severe placental separation with no signs of fetal

life, vaginal delivery unless contraindicated by uncontrolled hemorrhage or other complications

ALERT
Because of possible fetal blood loss through the placenta, a pediatric team should be ready at delivery
to assess and treat the neonate for shock, blood
loss, and hypoxia.

ALERT
Complications of abruptio placentae require
prompt appropriate treatment. With a complication such as DIC, the patient needs immediate intervention with platelets and whole blood, as ordered, to prevent exsanguination.
H Nothing to eat or drink until delivery of the fetus
H Bed rest until delivery of the fetus

H Obtain blood samples for hemoglobin level and

hematocrit, coagulation studies, and type and crossmatching, as ordered.


H Provide emotional support during labor.
H Provide information of progress and condition of
fetus during labor.
H Encourage verbalization of feelings.
H Help develop effective coping strategies.
H Administer I.V. fluids and blood products.

Monitoring
H Maternal vital signs
H Central venous pressure
H Intake and output
H Vaginal bleeding
H Fetal heart rate (electronically)
H Progression of labor

Patient teaching

Nursing considerations

Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of placental abruption
H possibility of an emergency cesarean delivery
H possibility of the delivery of a premature neonate
H changes to expect in the postpartum period
H possibility of neonatal death
H factors affecting survival of the neonate
H importance of frequent monitoring and prompt
management to reduce the risk of death.

Key outcomes

Discharge planning

The patient will:


H maintain stable vital signs
H maintain balanced fluid volume
H express feelings of increased comfort
H communicate feelings about the situation
H use available support systems to aid in coping.

H Refer the patient for professional counseling, if

Medications
H I.V. fluid infusion (by large-bore catheter) as

ordered

Surgery
H Cesarean delivery if the fetus is in distress

indicated.

Nursing interventions
H Insert an indwelling urinary catheter.

Abruptio placentae

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Accelerationdeceleration injuries

Physical findings

Overview

H Neck muscle asymmetry


H Reduced neck mobility
H Gait disturbances
H Rigidity or numbness in the arms
H Tenderness at the exact location of the injury
H Decreased active and passive range of motion

Description

Test results

H Injury resulting from sharp hyperextension and flex-

Imaging
H Full cervical spine X-rays rule out cervical fracture.

ion of the neck that damages muscles, ligaments,


disks, and nerve tissue
H Excellent prognosis; symptoms usually subside with
symptomatic treatment
H Also called whiplash

Pathophysiology
H Unexpected force causes the head to jerk back and

then forward.
H The neck bones snap out of position, causing injury.
H Irritated nerves can interfere with blood flow and

transmission of nerve impulses.


H Pinched nerves can affect certain body part functions.

Causes

Treatment
General
H Soft cervical collar (see Applying a cervical collar)
H Ice packs
H Physical therapy
H Limited activity during the first 72 hours after the in-

jury
H Limited neck movement
H Limited strenuous activities, such as lifting and con-

tact sports, until full recovery has been established


(which may take more than 2 years)

H Motor vehicle accident


H Sports accident
H Fall
H Assault, including shaking a child

Medications

Risk factors

H Corticosteroids

H Absence of head restraint in automobile


H Osteoporosis
H Driving under the influence of alcohol or drugs

Surgery

Incidence
H 1,000,000 cases each year in the United States
H Average age of patient with acceleration-deceleration

injury: the late 40s

Common characteristics
H Nuchal rigidity
H Neck muscle asymmetry

Complications
H Temporomandibular disorder

H Oral analgesics, such as acetaminophen, non-

steroidal anti-inflammatory drugs, and opioids


H Muscle relaxants, such as baclofen, carisoprodol,

and cyclobenzaprine

H Surgical stabilization possible in severe cervical

acceleration-deceleration injuries

Nursing considerations
Key outcomes
The patient will:
H identify factors that intensify pain
H modify behavior to limit movement and avoid extended injury
H develop effective coping mechanisms
H attain the highest degree of mobility possible
H state feelings and fears about the injury.

Assessment

Nursing interventions

History

H Provide protection of the spine during all care.


H Give prescribed drugs.
H Apply a soft cervical collar.

H Mechanism of injury
H Pain initially minimal, but increases 12 to 72 hours

after the accident


H Dizziness
H Headache
H Back pain
H Shoulder pain
H Vision disturbances
H Tinnitus

Acceleration-deceleration injuries

Monitoring
H Pain control
H Response to medications
H Complications
H Neurologic status

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Applying a cervical collar


Cervical collars are used to support an injured or weakened cervical spine and to maintain alignment during
healing.The soft cervical collar, made of spongy foam,
provides gentler support and reminds the patient to avoid
cervical spine motion.

Patient teaching
Be sure to cover:
H activity restrictions
H proper application of soft cervical collar
H medication administration, dosage, and possible
adverse effects
H instructions regarding driving and the use of alcohol
while taking opioids.

Acceleration-deceleration injuries

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Acne vulgaris
Overview
Description
H Inflammatory disorder of the sebaceous gland con-

tiguous with a hair follicle (pilosebaceous follicle)


H Possibly developing in distinctive pilosebaceous units

(sebaceous follicles)
H Acne lesions: inflammatory (pustules, papules, and

nodules) and noninflammatory (closed and open


comedones) lesions
H Good prognosis with treatment

Pathophysiology
H Acne begins with sebum accumulation that obstructs

the pilosebaceous unit.


H The mass of accumulated keratinous sebaceous ma-

terial and bacteria within the pilosebaceous follicle


causes inflammation when its exposed to the dermis
with rupture of a follicle.
H The Propionibacterium acnes bacteria produce
substances that promote inflammation.
H In noninflammatory acne, the comedones are open,
called blackheads, or closed, called whiteheads; accumulated material causes distention of the follicle
and thinning of follicular canal walls.
H Inflammatory acne develops in closed comedones
when the follicular wall ruptures, expelling sebum
into the surrounding dermis and initiating inflammation.
H Pustules form when the inflammation is close to the
surface; papules and cystic nodules can develop
when the inflammation is deeper, causing mild to
severe scarring.

Causes
H Exact cause unknown
H Follicular hyperkeratinization
H Excessive sebum production
H Proliferation of P. acnes
H Hormonal dysfunction

Causes of acne flare-ups


H Menstrual cycle
H Stress
H Trauma
H Tropical climates
H Rubbing from tight clothing
H Environmental exposure to coal tar derivatives, certain chemicals, cosmetics, or hair pomades
H Hormonal contraceptives containing norethindrone
and norgestrel; testosterone
H Anabolic agents
H Corticotropin, gonadotropins, corticosteroids (prolonged use)
H Iodine- or bromine-containing drugs
H Trimethadione
H Phenytoin
H Isoniazid
8

Acne vulgaris

H Lithium
H Halothane

Incidence
H Affects nearly 75% of adolescents, although lesions

can appear as young as age 8


H Affects males more commonly and more severely
H Occurs in females at an earlier age and tends to

affect them for a longer time, sometimes into adulthood


H Tends to be familial

Common characteristics
H Pustules, papules, nodules
H Closed and open comedones
H Follicles located primarily on face and upper parts of

chest and back

Complications
H Deep cystic process
H Gross inflammation
H Abscess formation
H Secondary bacterial infection
H Acne scars

Assessment
History
H Presence of one or more predisposing factors
H Seasonal or monthly eruption patterns
H Pain and tenderness around area of infected follicle

Physical findings
H Acne lesions, typically located on the face, neck,

shoulders, chest, and upper back


H Red, swollen area around the infected follicle
H Acne plugs that appear as closed or open comedones
H Oily and thickened skin
H Visible scars

Test results
Laboratory
H Culture and sensitivity of pustules or abscesses shows
causative organism of secondary bacterial infection.

Treatment
General
H Treatment of causative factors
H Well-balanced diet
H Regular exercise

Medications
H Topical

Antibiotics, including erythromycin, clindamycin,


and sodium sulfacetamide
Keratolytics, including benzoyl peroxide, azelaic
acid, and salicylic acid

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Retinoids, including adapalene, tretinoin, and


tazarotene
H Systemic
Antibiotics, such as tetracycline, erythromycin, and
clindamycin
Diuretics such as spironolactone
Oral hormonal contraceptives
Retinoids, including isotretinoin

Surgery
H Comedo extraction
H Intralesional steroids such as triamcinolone
H Cryosurgery
H Dermabrasion

Special populations
Tetracycline is contraindicated during pregnancy
and childhood because it may cause permanent
discoloration of teeth (in children younger than
age 8), enamel defects, and bone growth retardation. Erythromycin is an alternative for these patients.

H Sensitivity reactions
H GI disturbances
H Liver dysfunction
H Response to treatment
H Skin and mucous membranes

Patient teaching
Be sure to cover:
H the disorder and treatment
H medications and possible adverse reactions
H when to notify the physician
H signs and symptoms of infection
H causative factors associated with acne flare-up
H well-balanced diet
H adequate rest
H stress management.

ALERT
Because oral tretinoin is known to cause birth defects, the manufacturer, with Food and Drug Administration approval, recommends pregnancy
testing before dispensing, dispensing only a 30-day
supply, repeat pregnancy testing throughout the
treatment period, effective contraception during
treatment, and informed consent of the patient or
parents regarding the danger of the drug.

Nursing considerations
Key outcomes
The patient will:
H exhibit improved or healed wounds or lesions
H demonstrate the recommended skin care regimen
H verbalize feelings about body image
H verbalize understanding of the condition and treatment.

Nursing interventions
H Give prescribed drugs.
H Assist the patient in identifying and eliminating pre-

disposing factors.
H Encourage good personal hygiene and the use of oil-

free skin care products.


H Discourage picking or squeezing the lesions.
H Encourage the patient to verbalize his feelings.
H Encourage patient to develop interests that support a

positive self-image and de-emphasize appearance.

Monitoring
H Liver function studies, serum triglyceride levels, and

pregnancy testing with tretinoin use


H Complications

Acne vulgaris

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Acquired
immunodeficiency
syndrome and human
immunodeficiency virus

Assessment

Overview

Physical findings

Description

H Persistent generalized adenopathy


H Nonspecific symptoms (weight loss, fatigue, night

H Human immunodeficiency virus (HIV) type 1; retro-

virus causing acquired immunodeficiency syndrome


(AIDS)
H Causes patients to become susceptible to opportunistic infections, unusual cancers, and other abnormalities
H Marked by progressive failure of the immune system
H Transmitted by contact with infected blood or body
fluids and associated with identifiable high-risk behaviors

Pathophysiology
H HIV strikes helper T cells bearing the CD4 antigen.
H The antigen serves as a receptor for the retrovirus

and lets it enter the cell.


H After invading a cell, HIV replicates, leading to cell
death, or becomes latent.
H HIV infection leads to profound pathology, either
directly, through destruction of CD4+ cells, other
immune cells, and neuroglial cells, or indirectly,
through the secondary effects of CD4+ T-cell dysfunction and resultant immunosuppression.

History
H Mononucleosis-like syndrome after high-risk expo-

sure and inoculation; then may remain asymptomatic


for years
H Laboratory evidence of seroconversion only sign in
latent stage

sweats, fevers)
H Neurologic symptoms resulting from HIV encepha-

lopathy
H Opportunistic infection or cancer (Kaposis sarco-

ma)

Special populations
Children show a higher incidence of bacterial
infections.

Test results
Laboratory
H CD4+ T-cell count of at least 200 cells/ml confirms
HIV infection.
H Screening test enzyme-linked immunosorbent assay
and confirmatory test (Western blot) detect the presence of HIV antibodies, which indicate HIV infection.

Treatment

Causes

General

H Infection with HIV, a retrovirus

H Variety of therapeutic options for opportunistic infec-

Risk factors
H I.V. drug users who share needles or syringes
H Unprotected sexual intercourse
H Placental transmission
H History of sexually transmitted disease
H Homosexual lifestyle
H Contact with infected blood

Incidence
H Average time between exposure to the virus and diag-

nosis of AIDS: 8 to 10 years, but can be shorter and


longer

Common characteristics
H May produce no symptoms for years
H Flulike symptoms

Complications
H Repeated opportunistic infections
H Neoplasms
H Premalignant diseases
H Organ-specific syndrome

10

tions (the leading cause of morbidity and mortality in


patients infected with HIV)
H Disease-specific therapy for a variety of neoplastic
and premalignant diseases and organ-specific syndromes
H Symptom management (fatigue and anemia)
H Well-balanced diet
H Regular exercise, as tolerated, with adequate rest
periods

Medications
H Immunomodulatory agents
H Anti-infectives, as appropriate
H Antineoplastics
H Highly active antiretroviral therapy (HAART)

Primary therapy
H Protease inhibitors, such as ritonavir, amprenavir,
and nelfinavir
H Nucleoside reverse transcriptase inhibitors, such as
zidovudine and lamivudine
H Nonnucleoside reverse transcriptase inhibitors, such
as delavirdine and nevirapine

Acquired immunodeficiency syndrome and human immunodeficiency virus

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Preventing HIV transmission


H Use precautions in all situations that risk exposure to
blood, body fluids, and secretions. Diligently practicing
standard precautions can prevent the inadvertent
transmission of human immunodeficiency virus (HIV),
hepatitis B, and other infectious diseases that are
transmitted by similar routes.
H Teach the patient, his family, sexual partners, and friends
about disease transmission and prevention of extending
the disease to others.
H Tell the patient not to donate blood, blood products,
organs, tissue, or sperm.
H If the patient uses I.V. drugs, caution him not to share
needles.

Nursing considerations
Key outcomes
The patient will:
H achieve management of symptoms of illness
H demonstrate use of protective measures, including
conservation of energy, maintenance of wellbalanced diet, and getting adequate rest
H follow safer sex practices
H use available support systems to help with coping
H express feelings about changes in sexual identity and
social response to disease
H develop no complications of illness
H comply with the treatment regimen.

Nursing interventions

H Inform the patient that high-risk sexual practices for HIV


transmission are those that exchange body fluids, such
as vaginal or anal intercourse without a condom.
H Discuss safer sexual practices, such as hugging, petting,
mutual masturbation, and protected sexual intercourse.
Abstinence is the most effective method to prevent
transmission.
H Advise the female patient of childbearing age to avoid
pregnancy. Explain that an infant may become infected
before birth, during delivery, or during breast-feeding.

Patient teaching
Be sure to cover:
H medication regimens
H importance of informing potential sexual partners,
caregivers, and health care workers of HIV infection
(see Preventing HIV transmission)
H signs of impending infection and the importance of
seeking immediate medical attention
H symptoms of AIDS dementia and its stages and
progression.

Discharge planning
H Refer the patient to a local support group.
H Refer the patient to hospice care, as indicated.

H Help the patient cope with an altered body image, the

emotional burden of serious illness, and the threat of


death.
H Avoid glycerin swabs for mucous membranes. Use
normal saline or bicarbonate mouthwash for daily
oral rinsing.
H Ensure adequate fluid intake during episodes of
diarrhea.
H Provide meticulous skin care, especially in the debilitated patient.
H Encourage the patient to maintain as much physical
activity as he can tolerate. Make sure his schedule
includes time for exercise and rest.

Monitoring
H Fever, noting any pattern
H Skin integrity
H Signs of illness, such as cough, sore throat, and

diarrhea
H Swollen, tender lymph nodes
H Laboratory values
H Calorie intake
H Progression of lesions in Kaposis sarcoma
H Opportunistic infections or signs of disease

progression
H Compliance with medication regimen

Acquired immunodeficiency syndrome and human immunodeficiency virus

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Acute poststreptococcal
glomerulonephritis

Assessment
History
H Untreated respiratory streptococcal infection 1 to

Overview
Description
H Renal disease in which the glomeruli become

inflamed

3 weeks before
H Decreased urination
H Smoky or coffee-colored urine
H Fatigue
H Dyspnea and orthopnea

H Usually associated with a postinfectious state, com-

Physical findings

monly a streptococcal infection of the respiratory


tract or, less commonly, a skin infection such as
impetigo
H Up to 95% recovery in children and 70% in adults
H Possible chronic renal failure within months in elderly patients
H Relatively common
H Also called acute glomerulonephritis

H Oliguria
H Mild to moderate periorbital edema
H Mild to severe hypertension
H Bibasilar crackles (with heart failure)

Pathophysiology
H Antigen-antibody complexes are produced in re-

sponse to group A beta-hemolytic streptococcus


infection.
H Entrapment and collection of antigen-antibody complexes occurs in the glomerular capillary membranes.
H Inflammatory damage results, impeding glomerular
function.
H Immune complement may further damage the glomerular membrane.
H Damaged and inflamed glomeruli lose the ability to
be selectively permeable.
H Red blood cells (RBCs) and proteins then filter
through as the glomerular filtration rate decreases.
H Uremic poisoning may result.

Causes
H Untreated group A beta-hemolytic streptococcus in-

fection, especially of the respiratory tract

Risk factors
H Streptococcal infection
H Impetigo

Incidence
H Occurs most commonly in boys ages 3 to 7; can oc-

cur at any age

Common characteristics

Test results
Laboratory
H Electrolyte imbalances are evident.
H Blood urea nitrogen (BUN) and creatinine levels are
elevated.
H Serum protein levels are decreased.
H The presence of RBCs, white blood cells, mixed cell
casts, and protein in the urine indicates renal failure.
H Fibrin-degradation products and C3 protein levels
are high.

Special populations
Proteinuria in an elderly patient usually isnt as
pronounced.
H Antistreptolysin-O titers (in 80% of patients), strep-

tozyme, and anti-DNase B titers are elevated; serum


complement levels, which verify recent streptococcal
infection, are low.
H Group A beta-hemolytic streptococci is revealed by
throat culture.
Imaging
H Kidney-ureter-bladder radiography reveals bilateral
kidney enlargement.
Diagnostic procedures
H Renal biopsy or assessment of renal tissue confirms
diagnosis.

Treatment
General
H Correction of electrolyte imbalances (possible dialy-

H Oliguria
H Fluid overload
H Periorbital edema

H Fluid restriction
H High-calorie, low-protein, low-sodium, low-

Complications

H Bed rest

H Progressive deterioration of renal function

sis)
potassium diet

Medications
H Antibiotics if appropriate
H Loop diuretics, such as metolazone and furosemide

12

Acute poststreptococcal glomerulonephritis

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Nursing considerations
Key outcomes
The patient will:
H avoid or minimize complications
H maintain fluid balance
H maintain urine specific gravity within the designated
limits
H report increased comfort
H identify risk factors that exacerbate the condition and
modify lifestyle accordingly.

Nursing interventions
H Give prescribed drugs.
H Encourage verbalization.
H Provide support.

Monitoring
H Vital signs
H Electrolyte values and serum creatinine and BUN

levels
H Urine creatinine clearance test results
H Intake and output
H Daily weight

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of follow-up examinations to monitor
renal function
H medication administration, dosage, and possible
adverse effects.

Discharge planning
H Refer the patient to appropriate resources for infor-

mation and support.

Acute poststreptococcal glomerulonephritis

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Acute pyelonephritis
Overview
Description
H Inflammation of the kidney occurring mainly in the

interstitial tissue and renal pelvis and occasionally in


the renal tubules
H Affecting one or both kidneys
H Good prognosis; extensive permanent damage rarely
occurs
H Also called acute infective tubulointerstitial
nephritis

Pathophysiology
H Infection spreads from the bladder to the ureters to

the kidneys, commonly through vesicoureteral reflux.


H Vesicoureteral reflux may result from congenital

weakness at the junction of the ureter and bladder.


H Bacteria refluxed to intrarenal tissues may create

colonies of infection within 24 to 48 hours.


H Female anatomy allows for higher incidence of
infection.

Causes
H Bacterial infection of the kidneys

Risk factors
H Renal procedures that involve instrumentation such

as cystoscopy
H Hematogenic infection such as septicemia
H Sexually active women
H Pregnant women
H Neurogenic bladder
H Obstructive disease
H Renal diseases

Incidence

Assessment
History
H Pain over one or both kidneys
H Urinary urgency and frequency
H Burning during urination
H Dysuria, nocturia, hematuria
H Anorexia, vomiting, diarrhea
H Fatigue
H Symptoms that develop rapidly over a few hours or a

few days

Physical findings
H Pain on flank palpation
H Cloudy urine
H Ammonia-like or fishy odor to urine
H Fever of 102 F (38.9 C) or higher
H Shaking chills

Test results
Laboratory
H Urinalysis and culture and sensitivity testing reveal
pyuria, significant bacteriuria, low specific gravity
and osmolality, slightly alkaline urine pH, or proteinuria, glycosuria, and ketonuria (less frequent).
H White blood cell count, neutrophil count, and erythrocyte sedimentation rate are elevated.
Imaging
H Kidney-ureter-bladder radiography reveals calculi,
tumors, or cysts in the kidneys or urinary tract.
H Excretory urography shows asymmetrical kidneys,
possibly indicating a high frequency of infection.

Treatment
General
H Identification and correction of predisposing factors

to infection, such as obstruction or calculi

H More common in females than in males


H Community-acquired cases in 15 per 100,000

H Short courses of therapy for uncomplicated infec-

annually
H Hospital-acquired cases in 7 per 10,000 annually

H Increased fluid intake

Common characteristics

H Antibiotics, as appropriate
H Urinary analgesics such as phenazopyridine

H Pain over one or both kidneys


H Urinary urgency and frequency
H Dysuria
H Nocturia

tions

Medications

Nursing considerations

Complications

Key outcomes

H Renal calculi
H Renal failure
H Renal abscess
H Multisystem infection
H Septic shock
H Chronic pyelonephritis

The patient will:


H maintain fluid balance
H maintain urine specific gravity within the designated
limits
H identify risk factors that exacerbate decreased tissue
perfusion and modify lifestyle appropriately
H report increased comfort.

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Acute pyelonephritis

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Nursing interventions
H Give prescribed drugs.

Monitoring
H Vital signs
H Intake and output
H Characteristics of urine
H Pattern of urination
H Daily weight
H Renal function studies

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H avoidance of bacterial contamination by following hygienic toileting practices (wiping the perineum from
front to back after bowel movements for women)
H proper technique for collecting a clean-catch urine
specimen
H medication administration, dosage, and possible
adverse effects
H routine checkup with a history of urinary tract
infections
H signs and symptoms of recurrent infection.

Acute pyelonephritis

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Life-threatening disorder

Incidence
H Patients with three concurrent causes: 85% probabil-

ity of developing ARDS

Acute respiratory
distress syndrome

Common characteristics

Overview

Complications

Description
H Severe form of alveolar injury or acute lung injury
H A form of pulmonary edema; may be difficult to

H Shortness of breath
H Dry cough with thick, frothy sputum
H Bloody, sticky secretions

H Metabolic acidosis
H Respiratory acidosis
H Cardiac arrest
H Multiple organ dysfunction syndrome

recognize
H Hallmark sign: hypoxemia despite increased supple-

mental oxygen
H A four-stage syndrome; can rapidly progress to intractable and fatal hypoxemia
H Little or no permanent lung damage in patients who
recover
H May coexist with disseminated intravascular coagulation (DIC)
H Also known as ARDS, adult respiratory distress syndrome and shock, stiff, white, wet, or Da Nang
lung

Pathophysiology
H Increased permeability of the alveolocapillary mem-

branes allows fluid to accumulate in the lung interstitium, alveolar spaces, and small airways, causing the
lung to stiffen.
H Ventilation is impaired, reducing oxygenation of pulmonary capillary blood.
H Elevated capillary pressure increases interstitial and
alveolar edema.
H Alveolar closing pressure then exceeds pulmonary
pressures.
H Closure and collapse of the alveoli occurs.

Causes
H Indirect or direct lung trauma (most common)
H Anaphylaxis
H Aspiration of gastric contents
H Diffuse pneumonia (especially viral)
H Drug overdose
H Idiosyncratic drug reaction
H Inhalation of noxious gases
H Near-drowning
H Oxygen toxicity
H Coronary artery bypass grafting
H Hemodialysis
H Leukemia
H Acute miliary tuberculosis
H Pancreatitis
H Thrombotic thrombocytopenic purpura
H Uremia
H Venous air embolism

16

Acute respiratory distress syndrome

Assessment
History
H Causative factor (one or more)
H Dyspnea, especially on exertion

Physical findings
Stage I
H Shortness of breath, especially on exertion
H Normal to increased respiratory and pulse rates
H Diminished breath sounds
Stage II
H Respiratory distress
H Use of accessory muscles for respiration
H Pallor, anxiety, and restlessness
H Dry cough with thick, frothy sputum
H Bloody, sticky secretions
H Cool, clammy skin
H Tachycardia and tachypnea
H Elevated blood pressure
H Basilar crackles
Stage III
H Respiratory rate greater than 30 breaths/minute
H Tachycardia with arrhythmias
H Labile blood pressure
H Productive cough
H Pale, cyanotic skin
H Crackles and rhonchi possible
Stage IV
H Acute respiratory failure with severe hypoxia
H Deteriorating mental status (may become comatose)
H Pale, cyanotic skin
H Lack of spontaneous respirations
H Bradycardia with arrhythmias
H Hypotension
H Metabolic and respiratory acidosis

Test results
Laboratory
H Arterial blood gas (ABG) analysis initially shows a
reduced partial pressure of arterial oxygen (PaO2)
(less than 60 mm Hg) and a decreased partial pressure of arterial carbon dioxide (PaCO2) (less than
35 mm Hg).

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H ABG analysis later shows increased PaCO2 (more than

45 mm Hg) and decreased bicarbonate levels (less


than 22 mEq/L) and decreased PaO2 despite oxygen
therapy.
H Gram stain and sputum culture and sensitivity show
infectious organism.
H Blood cultures reveal infectious organisms.
H Toxicology tests show drug ingestion in overdose.
H Serum amylase levels are increased in pancreatitis.
Imaging
H Chest X-rays may show early bilateral infiltrates; in
later stages, a ground-glass appearance and, eventually, whiteouts of both lung fields.
Diagnostic procedures
H Pulmonary artery catheterization may show a pulmonary artery wedge pressure of 12 to 18 mm Hg.

Treatment
General
H Treatment of the underlying cause
H Correction of electrolyte and acid-base imbalances

For mechanical ventilation


H Target low tidal volumes; use of increased respiratory
rates
H Target plateau pressures less than or equal to
40 cm H2O
H Positive end-expiratory pressure (PEEP) as necessary
H Fluid restriction
H Tube feedings or parenteral nutrition
H Bed rest

Medications
H Humidified oxygen
H Bronchodilators, such as albuterol and theophylline
H Diuretics, such as furosemide and torsemide

Nursing interventions
H Give prescribed drugs.
H Maintain a patent airway.
H Perform tracheal suctioning, as necessary.
H Ensure adequate humidification.
H Reposition the patient often.
H Consider prone positioning for alveolar recruitment.
H Administer tube feedings or parenteral nutrition, as

ordered.
H Allow periods of uninterrupted sleep.
H Perform passive range-of-motion exercises.
H Provide meticulous skin care.
H Reposition the endotracheal (ET) tube per facility

policy.
H Provide emotional support.
H Provide alternative communication means.

Monitoring
H Vital signs and pulse oximetry
H Hemodynamics
H Intake and output
H Respiratory status (breath sounds, ABG results)
H Mechanical ventilator settings
H Sputum characteristics
H Level of consciousness
H Daily weight
H Laboratory studies
H Response to treatment
H Complications, such as cardiac arrhythmias, DIC, GI

bleeding, infection, malnutrition, or pneumothorax


H Nutritional status

ALERT
Because PEEP may lower cardiac output, check for
hypotension, tachycardia, and decreased urine
output. To maintain PEEP, suction only as needed.

For mechanical ventilation


H Sedatives
H Opioids
H Neuromuscular blockers
H Short course of high-dose corticosteroids if fatty
emboli or chemical injury
H Sodium bicarbonate if severe metabolic acidosis
H Fluids and vasopressors if hypotensive
H Antimicrobials, as appropriate, for nonviral infection

If the patient requires mechanical


ventilation
H Ventilator settings
H Cuff pressure
H Complications of mechanical ventilation
H ET tube position and patency
H Signs and symptoms of stress ulcer

Surgery

Patient teaching

H Possible tracheostomy

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain a patent airway
H use effective coping strategies
H maintain skin integrity
H report feelings of increased comfort.

Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H complications, such as GI bleeding, infection, and
malnutrition
H recovery time.

Discharge planning
H Refer the patient to a pulmonary rehabilitation

program, if indicated.

Acute respiratory distress syndrome

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Life-threatening disorder

Acute respiratory
failure
Overview
Description
H Inadequate ventilation resulting from the inability of

the lungs to adequately maintain arterial oxygenation


or eliminate carbon dioxide

Pathophysiology
H If respiratory failure is primarily hypercapnic, its the

result of inadequate alveolar ventilation.

H Metabolic alkalosis
H Respiratory and cardiac arrest

Assessment
History
Precipitating events
H Infection
H Accumulated pulmonary secretions secondary to
cough suppression
H Trauma
H MI
H Heart failure
H Pulmonary emboli
H Exposure to irritants (smoke or fumes)
H Myxedema
H Metabolic acidosis

H If respiratory failure is primarily hypoxemic, its the

Physical findings

result of inadequate exchange of oxygen between the


alveoli and capillaries.
H Many people have a combined hypercapnic and
hypoxemic respiratory failure.

H Cyanosis of the oral mucosa, lips, and nail beds


H Yawning and use of accessory muscles
H Pursed-lip breathing
H Nasal flaring
H Ashen skin
H Rapid breathing
H Cold, clammy skin
H Asymmetrical chest movement
H Decreased tactile fremitus over an obstructed

Causes
H Any condition that increases the work of breathing

and decreases the respiratory drive of patients with


chronic obstructive pulmonary disease
H Respiratory tract infection
H Bronchospasm
H Accumulated secretions secondary to cough suppression
H Ventilatory failure
H Gas exchange failure
H Central nervous system depression
H Myocardial infarction (MI)
H Heart failure
H Pulmonary emboli
H Airway irritants
H Endocrine or metabolic disorders
H Thoracic abnormalities

Incidence
H Occurs in patients with hypercapnia and hypoxemia
H Occurs in patients who have an acute deterioration in

arterial blood gas (ABG) values

Common characteristics
H Rapid breathing
H Restlessness
H Anxiety
H Depression
H Lethargy
H Agitation
H Confusion

Complications
H Tissue hypoxia
H Chronic respiratory acidosis

18

Acute respiratory failure

bronchi or pleural effusion


H Increased tactile fremitus over consolidated lung

tissue
H Hyperresonance
H Diminished or absent breath sounds
H Wheezes (in asthma)
H Rhonchi (in bronchitis)
H Crackles (in pulmonary edema)

Test results
Laboratory
H ABG analysis reveals hypercapnia and hypoxemia.
H Serum white blood cell count is increased in bacterial infections.
H Serum hemoglobin level and hematocrit show decreased oxygen-carrying capacity.
H Serum electrolyte results reveal hypokalemia and
hypochloremia.
H Blood cultures, Gram stain, and sputum cultures
show the pathogen. (See Identifying respiratory
failure.)
Imaging
H Chest X-rays may show underlying pulmonary diseases or conditions, such as emphysema, atelectasis,
lesions, pneumothorax, infiltrates, and effusions.
Diagnostic procedures
H Electrocardiography may show arrhythmias, cor pulmonale, and myocardial ischemia.
H Pulse oximetry may show decreased arterial oxygen
saturation.

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H Pulmonary artery catheterization may show pulmo-

nary or cardiovascular causes of acute respiratory


failure.

Treatment
General
H Mechanical ventilation with an endotracheal (ET) or

a tracheostomy tube

Identifying respiratory failure


Use these measurements to identify respiratory failure:
H vital capacity less than 15 cc/kg
H tidal volume less than 3 cc/kg
H negative inspiratory force less than 25 cm H2O
H respiratory rate more than twice the normal rate
H diminished partial pressure of arterial oxygen despite
increased fraction of inspired oxygen
H elevated partial pressure of arterial carbon dioxide with
pH lower than 7.25.

H High-frequency ventilation, if the patient doesnt

respond to conventional mechanical ventilation


H Fluid restriction with heart failure
H Activity as tolerated

Medications
H Cautious oxygen therapy to increase partial pressure

of arterial oxygen
H Antacids
H Histamine-receptor antagonists, such as cimetidine

and ranitidine
H Antibiotics, as appropriate
H Bronchodilators, such as albuterol and theophylline
H Corticosteroids
H Positive inotropics, such as digoxin and milrinone
H Vasopressors, such as dopamine and dobutamine
H Diuretics, such as furosemide and torsemide

Surgery
H Possible tracheostomy

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate ventilation
H use a support system to assist with coping
H maintain skin integrity
H express feelings of increased comfort
H modify lifestyle to minimize the risk of decreased
tissue perfusion.

Nursing interventions
H Give prescribed drugs.
H Orient the patient frequently.
H Administer oxygen, as ordered.
H Maintain a patent airway.
H Encourage pursed-lip breathing.
H Encourage the use of an incentive spirometer.
H Reposition the patient every 1 to 2 hours.
H Help clear the patients secretions with postural

drainage and chest physiotherapy.


H Assist with or perform oral hygiene.
H Position the patient for comfort and optimal gas

exchange.
H Maintain normothermia.
H Schedule care to provide frequent rest periods.

If the patient requires mechanical


ventilation
H Obtain blood samples for ABG analysis, as ordered.
H Suction the trachea after hyperoxygenation, as
needed.
H Provide humidification.
H Secure the ET tube per facility policy.
H Prevent infection.
H Prevent tracheal erosion.
H Maintain skin integrity.
H Provide alternative communication means.
H Provide sedation, as necessary.

Monitoring
H Vital signs and pulse oximetry
H Intake and output
H Laboratory studies
H Daily weight
H Cardiac rate and rhythm
H Respiratory status (breath sounds and ABG results)
H Chest X-ray results
H Complications
H Sputum quality, consistency, and color
H Signs and symptoms of infection

If the patient requires mechanical


ventilation
H Ventilator settings
H Cuff pressures
H Complications of mechanical ventilation
H ET tube position and patency
H Signs and symptoms of stress ulcers

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H smoking cessation, if appropriate
H communication techniques, if intubated
H signs and symptoms of respiratory infection.

Discharge planning
H Refer the patient to a smoking-cessation program, if

applicable.

Acute respiratory failure

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Acute tubular necrosis

Physical findings

Overview

H Evidence of bleeding abnormalities, such as petechi-

H Acute tubular necrosis usually in advanced stage

when diagnosis made

Description
H Injury to the nephrons tubular segment resulting

from ischemic or nephrotoxic injury and causing


renal failure and uremic syndrome
H Also known as acute tubulointerstitial nephritis

Pathophysiology
H In ischemic injury, circulatory collapse, severe hy-

potension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, and
reactions to transfusions may cause disruption of
blood flow to the kidneys.
H Nephrotoxic injury may follow ingestion of certain
chemical agents, such as contrast medium or antibiotics, or result from a hypersensitive reaction of the
kidneys.

Causes
H Diseased tubular epithelium
H Obstructed urine flow
H Ischemic injury to glomerular epithelial cells or vas-

cular endothelium

Incidence
H Accounts for about 75% of acute renal failure cases
H Most common cause of acute renal failure in critical-

ly ill patients

Common characteristics
H Decreased urine output
H Hyperkalemia
H Uremic syndrome with oliguria or, rarely, anuria

Complications
H Heart failure
H Uremic pericarditis
H Pulmonary edema
H Uremic lung
H Anemia
H Anorexia, intractable vomiting
H Poor wound healing due to debilitation

ALERT
Fever and chills may signal the onset of an infection, the leading cause of death in acute tubular
necrosis.

Assessment
History
H Ischemic or nephrotoxic injury
H Low urine output (less than 400 ml/24 hours)
H Fever and chills

20

Acute tubular necrosis

ae and ecchymosis
H Dry, pruritic skin
H Dry mucous membranes
H Uremic breath
H Cardiac arrhythmia, if hyperkalemic
H Muscle weakness

Test results
Laboratory
H Urinary sediment contains red blood cells (RBCs)
and casts.
H Urine specific gravity is low (1.010).
H Urine osmolality is low (less than 400 mOsm/kg).
H Urine sodium level is high(40 to 60 mEq/L).
H Potassium, blood urea nitrogen, and serum creatinine levels are elevated.
H Complete blood count shows decreased RBC count,
hemoglobin level, and hematocrit.
H Metabolic acidosis is evident from blood gas and
electrolyte study results.
Diagnostic procedures
H Electrocardiography may show arrhythmias and, with
hyperkalemia, a widening QRS complex, disappearing P waves, and tall, peaked T waves.

Treatment
General
Acute phase
H Vigorous supportive measures until normal kidney
function resumes
Long-term management
H Daily replacement of projected and calculated fluid
loss (including insensible loss)
H Peritoneal dialysis or hemodialysis if the patient is
catabolic or if hyperkalemia and fluid volume overload arent controlled by other measures
H Fluid restriction
H Low-sodium, low-potassium diet
H Rest periods when fatigued

Medications
H Diuretics
H Transfusion of packed RBCs
H Epoetin alfa
H Antibiotics, as appropriate
H Emergency I.V. administration of 50% glucose, regu-

lar insulin, and sodium bicarbonate (with hyperkalemia)


H Sodium polystyrene sulfonate with sorbitol by mouth
or enema (with hyperkalemia)

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Nursing considerations
Key outcomes
The patient will:
H maintain fluid balance
H maintain hemodynamic stability
H maintain urine specific gravity within the designated
limits
H have improved kidney function.

Nursing interventions
H Give prescribed drugs and blood products.
H Restrict foods containing high sodium and potassium

levels.
H Use aseptic technique, particularly when handling

catheters.
H Perform passive range-of-motion exercises.
H Provide good skin care.

Monitoring
H Intake and output
H Vital signs
H Laboratory studies
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of infection and when to report them to the
physician
H dietary restrictions
H how to set goals that are realistic for the patients
prognosis.

Discharge planning
H Refer the patient to appropriate supportive services

or social service.

Acute tubular necrosis

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Adrenal hypofunction
Overview
Description
H Primary adrenal hypofunction or insufficiency (Addi-

sons disease) originating within the adrenal gland


and characterized by the decreased secretion of mineralocorticoids, glucocorticoids, and androgens
H Secondary adrenal hypofunction due to a disorder
outside the gland such as impaired pituitary secretion of corticotropin; characterized by decreased glucocorticoid secretion
H Adrenal crisis (addisonian crisis), a critical deficiency of mineralocorticoids and glucocorticoids generally following acute stress, sepsis, trauma, surgery, or
the omission of steroid therapy in patients who have
chronic adrenal insufficiency; adrenal crisis, a medical emergency that needs immediate, vigorous treatment

Pathophysiology
H Dysfunction of the adrenal gland results from the

partial or complete destruction of the adrenal cortex.


H It manifests as a clinical syndrome in which the

symptoms are associated with deficient production of


the adrenocortical hormones cortisol, aldosterone,
and androgen.
H High levels of corticotropin and corticotropinreleasing hormone are produced.
H Addisons disease involves all zones of the cortex,
causing deficiencies of the adrenocortical secretions,
glucocorticoids, androgens, and mineralocorticoids.
H Cortisol deficiency causes decreased liver gluconeogenesis (the formation of glucose from molecules
that arent carbohydrates); resulting low blood glucose levels can become dangerously low in patients
who take insulin routinely.
H An aldosterone deficiency causes increased renal
sodium loss and enhances potassium reabsorption.
H Hypotension then develops due to sodium excretion.
H Angiotensin II production increases due to the low
plasma volume and decreased arteriolar pressure.
H Androgen deficiency may decrease hair growth in
axillary and pubic areas (less noticeable in men)
as well as on the extremities of women.

Causes
Primary hypofunction
H Autoimmune process in which circulating antibodies
react specifically against the adrenal tissue
H Tuberculosis (once the chief cause, now responsible
for less than 20% of adult cases)
H Bilateral adrenalectomy
H Hemorrhage into the adrenal gland
H Neoplasms
H Infections (histoplasmosis, cytomegalovirus)

22

Adrenal hypofunction

H Family history of autoimmune disease (may predis-

pose the patient to Addisons disease and other


endocrinopathies)
Secondary hypofunction
H Hypopituitarism
H Abrupt withdrawal of long-term corticosteroid
therapy
H Removal of a corticotropin-secreting tumor
Adrenal crisis
H Exhausted body stores of glucocorticoids in a patient
with adrenal hypofunction after trauma, surgery, or
other physiologic stress

Incidence
Primary hypofunction
H Relatively uncommon
H Can occur at any age and in both sexes
Autoimmune Addisons disease
H Most common in white females (genetic predisposition likely)
H More common in patients with a familial predisposition to autoimmune endocrine diseases

Special populations
Most people with Addisons disease are diagnosed
in their 20s to 40s.

Common characteristics
Primary hypofunction
H Conspicuous bronze color of the skin
H Darkening of scars, areas of vitiligo (absence of pigmentation), and increased pigmentation of the mucous membranes, especially the buccal mucosa
H Decreased tolerance for even minor stress
H Fasting hypoglycemia
H Craving for salty food
Secondary hypofunction
H Similar to primary hypofunction, but without hyperpigmentation
Addisonian crisis
H Profound weakness and fatigue
H Nausea, vomiting, and dehydration
H Hypotension
H High fever followed by hypothermia (occasionally)

Complications
H Hyperpyrexia
H Psychotic reactions
H Deficient or excessive steroid treatment
H Shock
H Profound hypoglycemia
H Ultimate vascular collapse, renal shutdown, coma,

and death (if untreated)

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Assessment

Nursing considerations

History

Key outcomes

H Synthetic steroid use, adrenal surgery, or recent

The patient will:


H maintain stable vital signs
H maintain an adequate fluid balance
H remain free from signs and symptoms of infection
H develop adequate coping skills.

infection
H Muscle weakness
H Fatigue
H Weight loss
H Craving for salty food
H Decreased tolerance for stress
H GI disturbances
H Dehydration
H Amenorrhea (in females)
H Impotence (in males)

Physical findings
H Poor coordination
H Decreased axillary and pubic hair (in females)
H Bronze coloration of the skin, darkening of scars
H Areas of vitiligo
H Increased pigmentation of mucous membranes
H Weak, irregular pulse
H Hypotension

Test results
Laboratory
H Rapid corticotropin stimulation test: low corticotropin level indicates a secondary disorder; elevated
level indicates a primary disorder.
H Plasma cortisol level is decreased (less than 10
mcg/dl in the morning; less in the evening).
H Serum sodium and fasting blood glucose levels are
decreased.
H Serum potassium, calcium, and blood urea nitrogen
levels are increased.
H Hematocrit is elevated and lymphocyte and eosinophil counts are increased.
Imaging
H Chest X-ray shows small heart.
H Computed tomography scan of the abdomen shows
adrenal calcification (if the cause is infectious).

Treatment
General
H I.V. fluids
H Periods of rest
H Small, frequent, high-protein meals

Medications
H Lifelong corticosteroid replacement, usually with

cortisone or hydrocortisone
H Oral fludrocortisone
H Hydrocortisone
H I.V. saline and glucose solutions (for adrenal crisis)

Nursing interventions
H Until onset of mineralocorticoid effect, encourage

fluids to replace excessive fluid loss.


H Arrange for a diet that maintains sodium and potassi-

um balances; if the patient is anorexic, suggest six


small meals per day to increase caloric intake.
H Observe for cushingoid signs such as fluid retention
around the eyes and face.
H Check for petechiae.
H If the patient receives glucocorticoids alone, observe
for orthostatic hypotension or electrolyte abnormalities.

Monitoring
H Vital signs
H Signs of shock (decreased level of consciousness and

urine output)
H Hyperkalemia before treatment; hypokalemia after

treatment
H Cardiac rhythm
H Blood glucose levels
H Daily weight
H Intake and output

Patient teaching
Be sure to cover:
H lifelong steroid therapy requirement
H symptoms of steroid overdose (swelling, weight gain)
and steroid underdose (lethargy, weakness)
H risk for developing diabetes
H dosage may need to be increased during times of
stress or illness (when the patient has a cold, for
example)
H infection, injury, or profuse sweating in hot weather
may precipitate adrenal crisis
H importance of carrying a medical identification card
that states the patient is on steroid therapy (name of
the drug and its dosage should be included on the
card)
H how to give a hydrocortisone injection and to keep
an emergency kit containing hydrocortisone in a prepared syringe available for use in times of stress
H stress-management techniques.

Discharge planning
H Refer the patient to the National Adrenal Diseases

Foundation for support and information.

Adrenal hypofunction

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Adrenogenital
syndrome
Overview
Description
H A group of disorders resulting from hyperplasia of

the adrenal cortex


H May be inherited (congenital adrenal hyperplasia

[CAH]) or acquired, usually as a result of an adrenal


tumor (adrenal virilism)
H May cause fatal adrenal crisis in neonates (salt-losing
CAH)

Pathophysiology
H Deficiencies occur in the enzymes needed for adre-

nocortical secretion of cortisol and, possibly, aldosterone.


H Compensatory secretion of corticotropin produces
varying degrees of adrenal hyperplasia.
Simple virilizing CAH
H Deficiency of the enzyme 21-hydroxylase results in
underproduction of cortisol.
H This cortisol deficiency stimulates increased secretion of corticotropin, producing large amounts of
cortisol precursors and androgens that dont require
21-hydroxylase for synthesis.
Salt-losing CAH
H 21-hydroxylase is almost completely absent.
H Corticotropin secretion increases, causing excessive
production of cortisol precursors, including saltwasting compounds.
H Plasma cortisol and aldosterone levels both dependent on 21-hydroxylase fall precipitously and,
in combination with the excessive production of saltwasting compounds, precipitate acute adrenal crisis.
H Corticotropin hypersecretion stimulates adrenal androgens and produces masculinization.

Causes
H Transmitted as an autosomal recessive trait

Incidence
H Acquired adrenal virilism: rare and affects twice as

many females as males

Special populations
CAH is the most prevalent adrenal disorder in infants and children; simple virilizing CAH and saltlosing CAH are the most common forms.

Common characteristics
Simple virilizing CAH
H Ambiguous genitalia but normal genital tract and gonads (Female neonates may present with labioscrotal

24

Adrenogenital syndrome

fusion and an enlarged clitoris with a urethral opening at its base.)


Salt-losing CAH
FEMALES
H More complete virilization than the simple form
H Results in development of male external genitalia

without testes
MALES
H No external genital abnormalities
H Difficult immediate neonatal diagnosis; commonly

delayed until the infant develops severe systemic


symptoms

Complications
H Hypertension
H Hyperkalemic infertility
H Adrenal tumor
H Adrenal crisis
H Altered growth, external genitalia, and sexual

maturity
Salt-losing CAH
H Cardiovascular collapse
H Cardiac arrest

Assessment
History
Simple virilizing CAH
H Failure to begin menstruation
H Frequent erections at an early age
Salt-losing CAH
H Apathy, failure to eat, and diarrhea (in infants)
H Symptoms of adrenal crisis in the first week of life
(vomiting, dehydration from hyponatremia, hyperkalemia)

Physical findings
H In CAH, pseudohermaphroditism in females or pre-

cocious puberty in both sexes


Salt-losing CAH
H Signs of progressive virilization at an early age: early
appearance of pubic and axillary hair, deep voice,
acne, facial hair
H Small testes
H Possible greater height than other children of the
same age

Test results
Laboratory
H Plasma 17-ketosteroid (17-KS) levels , which can be
suppressed by administering oral dexamethasone,
are elevated.
H Urine levels of hormone metabolites, particularly
pregnanetriol, are elevated.
H Plasma 17-hydroxyprogesterone level is elevated.
H Urine levels of 17-hydroxycorticosteroids are normal
or decreased.
H Plasma aldosterone and cortisol levels are decreased.
H Serum DHEA sulfate levels are high.

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Special populations
Adrenal hypofunction or adrenal crisis in the first
week of life suggests salt-losing CAH. Hyperkalemia, hyponatremia, and hypochloremia with excessive urinary 17-KS and pregnanetriol and decreased urinary aldosterone levels confirm it.

Diagnostic procedures
H Gonadal biopsy and chromosomal studies confirm
hermaphrodism.
Other
H Sex chromatin and karyotype studies determine the
genetic sex of patients with ambiguous external genitalia.
H X-ray evaluates accelerated bone aging.

Treatment
General
H Well-balanced diet
H No activity restriction

Medications
Simple virilizing CAH
H Daily administration of cortisone or hydrocortisone
Salt-losing CAH with patient in adrenal crisis
H Immediate I.V. sodium chloride and glucose infusion
H Desoxycorticosterone I.M. and hydrocortisone I.V.
H Maintenance includes mineralocorticoid (desoxycorticosterone, fludrocortisone, or both) and glucocorticoid (cortisone or hydrocortisone) replacement

Monitoring
H Body weight
H Blood pressure
H Serum electrolyte levels
H Edema, weakness, and hypertension for the patient

receiving desoxycorticosterone or fludrocortisone

Patient teaching
Be sure to cover:
H possible adverse effects (cushingoid symptoms) of
long-term therapy (lifelong maintenance therapy with
hydrocortisone, cortisone, or the mineralocorticoid
fludrocortisone is essential)
H importance of not withdrawing therapeutic drugs
suddenly because potentially fatal adrenal hypofunction will result
H need to report stress and infection, which require increased steroid dosages
H importance of carrying a medical identification card
that states the patient is on steroid therapy (name of
the drug and its dosage should be included on the
card)
H risk of developing diabetes due to long-term
cortisone therapy.

Discharge planning
H Refer the patient for psychological counseling to help

accept this disorder.

Surgery
H Reconstructive surgery based on the determined sex

and external genitalia

Nursing considerations
Key outcomes
The patient will:
H maintain stable vital signs
H maintain adequate fluid balance
H have normal laboratory test results
H express understanding of the disorder and treatment
modality, as will his family.

Nursing interventions
H Maintain I.V. access, infuse fluids, and give steroids,

as ordered.
H Watch for cyanosis, hypotension, tachycardia, tachyp-

nea, and signs of shock.


H Minimize external stressors.
H If a child is receiving maintenance therapy with

steroid injections, rotate I.M. injection sites to


prevent atrophy; tell the parents to do the same.

Adrenogenital syndrome

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Age-related macular
degeneration

Causes

Overview

H Smoking
H Age
H Race
H High blood pressure
H Vascular disease
H High intake of saturated fat and cholesterol
H Farsightedness
H Exposure to sunlight

Description
H Deterioration of the macular portion of the retina,

which is responsible for detailed vision


H May be atrophic, also called involutional or dry
H May be exudative, also called hemorrhagic or wet
H No cure for atrophic form
H Commonly affects both eyes
H Also known as AMD

Pathophysiology
H Pathologic changes occur primarily in the retinal pig-

ment epithelium, Bruchs membrane, and choriocapillaries in the macular region that result from the
hardening and obstruction of retinal arteries.
H Formation of new blood vessels in the macular area
obscures central vision.
H Vision loss occurs as the retinal pigment epithelium
detaches and becomes atrophic.
H Exudative macular degeneration develops as new
blood vessels in the choroid project through abnormalities in Bruchs membrane, invading the potential
space underneath the retinal pigment epithelium.
H The vessels leak, and fluid in the retinal pigment epithelium increases, resulting in blurry vision.

H Unknown
H Genetic in origin

Risk factors

Incidence
H Affects as many as 15 million Americans
H Leading cause of vision loss in people older than age

60 in the United States


H Irreversible central vision loss in at least 10% of

elderly people
H Atrophic form in about 85% of patients
H More common in whites, but affects all races

Common characteristics
H Decreased central vision, for near and distance (see

How AMD affects central vision)


H Progressive worsening
H Blind spots

Complications
H Blindness
H Nystagmus

How AMD affects central vision


Central vision occurs in the macula and involves the ability
to perceive sharp, detailed images. At the center of the macula is the fovea containing the highest concentration of
rods and cones and the most light-sensitive portion of
the macula.
Light entering the cornea and lens are focused on the
fovea. If any part of the macula deteriorates, the eye must

Lens

Visual
axis

Cornea
Iris
Macula
Fovea
Optic nerve

26

Age-related macular degeneration

rely on the less-sensitive, outer portion of the retina, which


is responsible for peripheral vision.
With age-related macular degeneration (AMD), grayness,
haziness, or a blind spot may appear in the area of central
vision. Words may be blurred on a page; straight lines may
appear to have kinks in them; colors may seem dimmer.

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Assessment
History
H Blank spot seen in the center of a page (scotoma)

while reading

Monitoring
H Visual acuity
H Environment (for safety purposes)

Patient teaching

H Central vision that blurs intermittently and has graduH Straight lines appearing distorted
H Letters appearing fragmented

Be sure to cover:
H ways to modify the home environment for safety
H effects on peripheral vision.

Physical findings

Discharge planning

H Tiny yellowish spots (drusen) beneath retina

H Refer the patient to the American Foundation for

Test results

the Blind or Associated Services for the Blind, as


indicated.
H Refer the patient to a local support group.

ally worsened

Diagnostic procedures
H Indirect ophthalmoscopy may show changes in the
macular region of the fundus.
H Fluorescein angiography may show leaking vessels in
subretinal neovascular net.
H Amsler grid test may detect visual distortion.

Treatment
General
H Laser treatment, if leaking blood vessels have devel-

oped away from the fovea


H Diet high in vitamins A, C, and E; beta-carotene; and

zinc
H Activity restrictions based on visual acuity

Medications
H Copper and zinc supplements
H Lutein, vitamins C and E, and beta-carotene

Surgery
H In exudative form, argon laser photocoagulation

(may slow the progression of severe visual loss)

Nursing considerations
Key outcomes
The patient will:
H express feelings and concerns over diminishing eyesight
H sustain no harm or injury
H verbalize understanding of the condition and treatment
H maintain optimal visual function or adapt as necessary.

Nursing interventions
H Help the patient obtain optical aids such as magni-

fiers.
H Offer the patient emotional support.
H Encourage expression of fears and concerns.

Age-related macular degeneration

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Alcoholism
Overview
Description
H Chronic disorder of uncontrolled intake of alcoholic

beverages
H Interferes with physical and mental health, social and

familial relationships, and occupational responsibilities

Pathophysiology
H Alcohol is soluble in water and lipids and permeates

all body tissues.


H Liver metabolizes 90% of alcohol absorbed and is the

most severely affected organ; hepatic steatosis followed by hepatic fibrosis is evident days after heavy
drinking.
H Laennecs cirrhosis may develop after inflammatory
response (alcoholic hepatitis) or in absence of inflammation, as a consequence of direct activation of
lipocytes (Ito cells).
H Lactic acidosis and excess uric acid is promoted; gluconeogenesis, B-oxidation of fatty acids, and the
Krebs cycle are opposed; and hypoglycemia and hyperlipidemia develop.
H Toxicity of cells occurs through reduction of mitochondrial oxygenation utilization, depletion of deoxyribonucleic acid, and other actions.

Causes
H Biological factors
H Psychological factors
H Sociocultural factors

Risk factors
H Male gender
H Low socioeconomic status
H Family history
H Depression
H Anxiety
H History of other substance abuse disorders

Incidence
H Affects all social and economic groups
H 10% of the population accounts for 50% of all alco-

hol consumed
H About 13% of all adults older than age 18 have suf-

fered from alcohol abuse or dependence


H Males are two to five times more likely to abuse alco-

hol than females


H Occurs at all stages of the life cycle, beginning as
early as elementary school age
H Prevalent in 20% of adult hospital inpatients

Special populations
Prevalence of drinking is highest between ages 21
and 34, but current statistics show that up to 19%

28

Alcoholism

of 12- to 17-year-olds have serious drinking problems. Research also suggests that alcoholism affects
2% to 10% of adults older than age 60.

Common characteristics
H Hide or deny addiction
H May temporarily manage to maintain a functional

lifestyle

Complications
H Cardiomyopathy
H Pneumonia
H Cirrhosis
H Esophageal varices
H Pancreatitis
H Alcoholic dementia
H Wernickes encephalopathy
H Seizure disorder
H Depression
H Multiple substance abuse
H Hypoglycemia
H Leg and foot ulcers
H Suicide and homicide
H Death

Assessment
History
H Need for daily or episodic alcohol use for adequate

function
H Inability to discontinue or reduce alcohol intake
H Episodes of anesthesia or amnesia during intoxica-

tion
H Episodes of violence during intoxication
H Interference with social and familial relationships

and occupational responsibilities


H Malaise, dyspepsia, mood swings or depression, and

an increased incidence of infection


H Secretive behavior

Physical findings
H Poor personal hygiene
H Unusually high tolerance for sedatives and opioids
H Signs of nutritional deficiency
H Signs of injury
H Withdrawal signs and symptoms
H Major motor seizures

DSM-IV-TR criteria
A diagnosis is confirmed when the patient meets at least
three of these signs and symptoms:
H more alcohol ingested than intended
H persistent desire or efforts to diminish alcohol use
H excessive time spent obtaining alcohol
H frequent intoxication or withdrawal symptoms
H impairment of social, occupational, or recreational
activities

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H continued alcohol consumption despite knowledge

of a social, psychological, or physical problem thats


caused or exacerbated by alcohol use
H marked tolerance
H characteristic withdrawal symptoms
H alcohol used to relieve or avoid withdrawal symptoms
H persistent symptoms for at least 1 month or recurrence over a longer time.

Test results
Laboratory
H Blood alcohol tests show levels of at least 0.10%
weight/volume (200 mg/dl).
H Serum electrolyte levels are abnormal.
H Serum ammonia levels are increased.
H Serum amylase levels are increased.
H Urine toxicology may show abuses of other drugs.
H Liver function study results are abnormal.

Other
H CAGE screening test: two affirmative responses make

patient 7 times more likely to be alcohol dependent.

Nursing considerations
Key outcomes
The patient (or family) will:
H report feeling safe in hospital environment
H join gradually in self-care and the decision-making
process
H engage in appropriate social interaction with others
H demonstrate a decrease in negative self-evaluation
verbally and behaviorally
H identify support systems to assist them and participate in mobilizing these systems.

Nursing interventions
H Institute seizure precautions.
H Give prescribed drugs.
H Orient the patient to reality.
H Maintain a calm environment, minimizing noise and

shadows.
H Avoid restraints, unless necessary for protection.
H Use a nonthreatening approach.

H Alcohol disorders identification test (AUDIT): score

Monitoring

greater than 8 indicates alcohol dependency.


H Michigan alcohol screening test (MAST): score
greater than 5 indicates alcohol dependency.

H Mental status
H Vital signs
H Safety measures
H Nutritional and hydration status
H Intake and output

Treatment
General
Immediate
H Support for respiration
H Prevention of aspiration of vomitus
H Replacement of fluids
H Administration of I.V. glucose
H Correction of hypothermia or acidosis
H Treatment of trauma, infection, or GI bleeding
Long-term
H Total abstinence
H Detoxification, rehabilitation, and aftercare program
H Supportive counseling
H Individual, group, or family psychotherapy
H Ongoing support groups
H Well-balanced diet
H Safety precautions, including preventing aspiration
of vomitus
H Seizure precautions

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H alcohol abstinence
H plan for relapse
H medication administration, dosage, and possible
adverse effects
H effects of disorder on significant others.

Discharge planning
H Refer the patient to a rehabilitation program.
H Refer the patient to social services.
H Refer the patient to support services.
H Refer the patient to personal and family counseling.

Medications
H Anticonvulsants
H Antiemetics
H Antidiarrheals
H Tranquilizers, particularly benzodiazepines
H Naltrexone
H Antipsychotics
H Daily oral disulfiram
H Vitamin supplements

Alcoholism

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Allergic purpura
Overview
Description
H An acute or chronic vascular inflammation affecting

the skin, joints, and GI and genitourinary (GU)


tracts, in association with allergy symptoms
H Purpura associated with other conditions such as
erythema nodosum
H A nonthrombocytopenic purpura
H Known as Henoch-Schnlein syndrome or anaphylactoid purpura when it primarily affects the GI tract
and is accompanied by joint pain

Pathophysiology
H An autoimmune reaction triggered by a bacterial in-

fection is directed against vascular walls.


H Inflammation of the veins and capillaries disrupts the

vascular wall, resulting in loss of red blood cells and


bleeding and leakage into the skin and mucous
membranes.

Causes
H Bacterial infection (particularly streptococcal infec-

tion)
H Allergic reactions to some drugs and vaccines, insect

bites, and foods (such as wheat, eggs, milk, and


chocolate)

Henoch-Schnlein syndrome
H Transient or severe colic
H Tenesmus (spasmodic contraction of the anal
sphincter)
H GI bleeding
H Rheumatoid pains and periarticular effusions, usually
affecting the legs and feet

Complications
H Renal disease (renal failure and acute glomeru-

lonephritis)
H Hypertension

Assessment
History
H Bacterial infection or exposure to allergen
H Moderate and irregular fever
H Headache
H Anorexia
H Pruritus and paresthesia in areas of lesions

Physical findings
H Characteristic lesions that usually appear in symmet-

rical patterns on the arms, legs, and buttocks


H In children, urticarial skin lesions that expand and

become hemorrhagic
H Possibly scattered petechiae on the legs, buttocks,

and perineum
H Localized edema of the hands, feet, or scalp

Incidence

Test results

H Affects more males than females


H Most prevalent in children ages 3 to 7

Laboratory
H Results of tests for blood in the urine and stool may
be positive.
H Increased blood urea nitrogen and creatinine levels
may indicate renal involvement.

Common characteristics
H Skin lesions that are purple, macular, ecchymotic,

and of varying size and are caused by vascular leakage into the skin and mucous membranes (see Identifying purpuric lesions)

Identifying purpuric lesions


Lesions of allergic purpura, such as those pictured on the
foot and leg below, characteristically vary in size.

ALERT
No laboratory test clearly identifies allergic purpura (although white blood cell count and erythrocyte
sedimentation rate are elevated).

Imaging
H Small-bowel X-rays may reveal areas of transient
edema.

Treatment
General
H Symptomatic

Medications
H Steroids
H Analgesics

30

Allergic purpura

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Nursing considerations
Key outcomes
The patient will:
H express feelings of comfort and relief of pain
H exhibit improved or healed lesions
H identify precipitating factors with appropriate skin
care regimen.

Nursing interventions
H Encourage maintenance of an elimination diet to

help identify specific allergenic foods.


H Provide analgesics, as needed.
H Provide passive range-of-motion exercises, if appro-

priate.
H Provide emotional support and reassurance, espe-

cially if the patient is temporarily disfigured by florid


skin lesions.

Monitoring
H Condition and number of skin lesions
H Level of pain
H GI and GU complications

Patient teaching
Be sure to cover:
H need for the patient to immediately report recurrence of symptoms (most common about 6 weeks
after initial symptoms)
H importance of returning for follow-up urinalysis as
scheduled.

Allergic purpura

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Allergic rhinitis
Overview
Description
H An immune response of the upper airways triggered

by inhaled airborne allergens


H Seasonal allergic rhinitis: an immunoglobulin (Ig) E-

mediated type I hypersensitivity response to an environmental antigen (allergen) in a genetically susceptible person
H Perennial rhinitis: inhaled allergens provoke antigen
responses that produce signs and symptoms
year-round

Pathophysiology
H The bodys immune system overresponds to common

Perennial allergic rhinitis


H Chronic and extensive nasal obstruction or stuffiness

Physical findings
Seasonal allergic rhinitis
H Pale, cyanotic, edematous nasal mucosa
H Red and edematous eyelids and conjunctivae
H Excessive lacrimation
Perennial allergic rhinitis
H Nasal polyps
H Dark circles under the eyes (allergic shiners)

Test results
Laboratory
H Sputum and nasal secretions show a high number of
eosinophils.
H IgE levels are normal or elevated, possibly linked to
seasonal overproduction of interleukin-4 and -5
(involved in the allergic inflammatory process).

allergens in the nose.


H Antibodies attach to mast cells, which release several

chemicals, including histamine, which cause dilation


of blood vessels, skin redness, and swollen membranes in the nose.

Causes
Seasonal allergic rhinitis
H Tree pollens (in spring)
H Grass and weed pollens (in summer)
H Weed pollens (in fall)
H Mold spores (occasionally, in summer and fall)
Perennial allergic rhinitis
H House dust and dust mites
H Molds
H Animal dander
H Tobacco smoke
H Processed materials or industrial chemicals

Incidence
H Affects more than 20 million Americans
H Can affect anyone at any age
H Most prevalent in young children and adolescents

Common characteristics
H Swollen nasal membranes

Complications

Treatment
General
H Elimination of environmental antigens, if possible
H Increased fluid intake to loosen secretions
H Restriction of activities in areas of allergen exposure

Medications
H Antihistamines, such as cetirizine, diphenhydramine,

and loratadine
H Intranasal corticosteroids, such as budesonide and

triamcinolone
H Leukotriene receptor antagonists such as mon-

telukast
H Nasal decongestants, such as oxymetazoline and

pseudoephedrine
Long-term management
H Immunotherapy or desensitization with injections of
allergen extracts administered before or during the
allergy season or perennially

Nursing considerations
Key outcomes

H Secondary sinus and middle ear infections


H Nasal polyps

The patient (or family) will:


H maintain current health status
H verbalize feelings and concerns
H express feelings of increased comfort.

Assessment

Nursing interventions

History
Seasonal allergic rhinitis
H Paroxysmal sneezing, profuse watery rhinorrhea
H Nasal obstruction or congestion
H Pruritus of the nose and eyes
H Headache or sinus pain
H Itchy throat, malaise, and fever

32

Allergic rhinitis

H Implement measures to relieve signs and symptoms

and increase the patients comfort.


H Encourage increased fluid intake to loosen secre-

tions.
H Elevate the head of the bed and provide humidifica-

tion to ease breathing.

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ALERT
Before giving a desensitization injection, assess the
patients symptoms. After giving the injection, observe him for 30 minutes to detect adverse reactions, including anaphylaxis and severe localized
erythema. Make sure epinephrine and emergency
resuscitation equipment are available.

Monitoring
H Compliance with the prescribed drug regimen
H Changes in control of signs and symptoms
H Indications of drug misuse

Patient teaching
Be sure to cover:
H importance of calling the physician if the patient experiences a delayed reaction to the desensitizing injections
H reduction of environmental exposure to airborne allergens
H skin protectant applications
H possible lifestyle changes, such as relocation to a
pollen-free area either seasonally or year-round, in
severe and resistant allergic rhinitis
H medication administration, dosage, and possible
adverse effects.

Allergic rhinitis

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Alopecia
Overview
Description
H More commonly known as hair loss, typically occurs

on the scalp; less common and conspicuous elsewhere on the body


H Can be irreversible because scarring alopecia usually
destroys hair follicle
H Nonscarring form (noncicatricial alopecia): hair
generally regrows
H Most common form of nonscarring alopecia known
as male-pattern alopecia or androcentric alopecia
H Telogen effluvium: a diffuse alopecia in which numerous hair follicles simultaneously change from the
growing anagen phase to the resting telogen phase of
the hair growth cycle
H Alopecia areata (idiopathic form): a generally reversible and self-limiting disorder most prevalent in
young and middle-aged adults of both sexes
H Time of onset, degree of baldness, speed with which
it spreads, and pattern of hair loss dependent on genetic predisposition
H Poor prognosis for regrowth with hair loss that persists for more than 1 year

Pathophysiology
H In male-pattern alopecia, a genetically predisposed

response to androgens causes transformation of the


androgen-sensitive follicles into vellus follicles; normal hair is shed and replaced by fine, light, short
hair.
H In female-pattern alopecia, theres usually an elevation in serum adrenal androgen dehydroepiandrosterone sulfate.

Causes
Nonscarring alopecia
H Genetic predisposition
H Androgen response
H Aging
H Radiation
H Chemotherapy
H Drugs (see Cancer drugs that cause alopecia)
H Bacterial and fungal infections
H Psoriasis
H Seborrhea
H Endocrine disorders
H Excess vitamin A
Scarring alopecia
H Physical or chemical trauma
H Radiation
H Chemotherapy
H Chronic tension on a hair shaft
H Destructive skin tumors
H Granulomas
H Lupus erythematosus
H Scleroderma
34

Alopecia

H Follicular lichen planus


H Severe bacterial or viral infections

Incidence
H Affects males more than females
H Occurs most commonly in males older than age 50

in male-pattern alopecia
H Rises with increasing age in male-pattern alopecia
H Occurs to some degree in 37% of postmenopausal

women

Common characteristics
H Hair loss

Complications
H Impaired self-image

Assessment
History
Male-pattern alopecia
H Presence of predisposing factors
H Family history of hair loss
H Gradual onset of hair loss
H Typically describes hairline as receding and his
crown becoming bald
Female-pattern alopecia
H Typically describes a widening of her part and increasing visibility of her front scalp or crown
Telogen effluvium
H Loss of about 400 hairs per day, which is four to five
times greater than the normal daily hair loss
Alopecia areata
H Sudden loss of hair

Physical findings
H Small patches of visible scalp or entire scalp visible

(alopecia totalis); may involve the entire body


(alopecia universalis)
H Generally, normal scalp appearance
H Exclamation point hairs (loose hairs with dark,
rough, brushlike tips on narrow, less pigmented
shafts) at the periphery of new patches
H Regrowth initially as fine, white, downy hair; replaced by normal hair

Test results
Laboratory
H Direct microscopic examination shows structural
abnormalities or signs of infection.
Diagnostic procedures
TELOGEN EFFLUVIUM
H Pluck or pull test reveals positive results if more than

four hairs come out.


H Woods lamp examination shows presence of fungal

infection.
H Trichogram shows abnormal ratio of anagen to

telogen hairs.
H Scalp biopsy shows hair phase and the extent of

structural damage.

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Cancer drugs that cause alopecia


Certain cancer drugs can cause hair loss ranging from sporadic thinning to complete baldness. Some drugs damage hair follicles and cause hair roots to atrophy.

Mild alopecia

H bleomycin
H carmustine
H fluorouracil
H hydroxyurea
H melphalan

Moderate alopecia

Severe alopecia

H busulfan
H etoposide
H floxuridine
H methotrexate
H mitomycin

Treatment
General
H Identification and treatment of underlying cause
H Cosmetic interventions, such as hairpieces, weaving,

or bonding

H cyclophosphamide
H daunorubicin
H doxorubicin
H vinblastine
H vincristine

H For the patient undergoing radiation therapy or

chemotherapy with drugs that cause alopecia, suggest selecting a hair replacement before treatment.
H Encourage the patient to express his feelings. Help
him develop interests that contribute to a positive
self-image.

H Occlusive dressing that promotes normal hair growth

Monitoring

by protecting the site of hair loss (in trichotillomania)


H Cold cap application and scalp tourniquet that reduce the blood supply to the scalp and thereby preserve more hair structure

H Complications
H Response to treatment

Medications
H Topical application of minoxidil
H Oral finasteride

ALERT
Finasteride is contraindicated in women of childbearing age.
H Corticosteroids
H Photochemotherapy with methoxsalen and ultraviolet

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H familial link in male-pattern alopecia
H well-balanced diet with adequate protein
H avoidance of excess vitamin A
H myths concerning commercial preparations
H signs and symptoms of skin infection
H possibility that hair may grow back in a different color or type, such as curly or straight.

light
H Dermatomucosal agents
H Antibiotics
H Antifungal agents

Surgery
H Surgical redistribution of hair follicles by auto-

grafting
H Hair transplantation and tunnel grafting

Nursing considerations
Key outcomes
The patient will:
H express concerns about his condition or treatment
H avoid complications
H verbalize feelings about changed body image.

Nursing interventions
H Give prescribed drugs.
H Reassure the patient with female-pattern alopecia

that hair thinning doesnt lead to total baldness. Suggest that she wear a wig or hairpiece.

Alopecia

35

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Alzheimers disease

H Pneumonia and other infections


H Malnutrition and dehydration

Overview

Assessment

Description

History

H Degenerative disorder of the cerebral cortex (espe-

H History obtained from a family member or caregiver


H Insidious onset
H Initial changes almost imperceptible
H Forgetfulness and subtle memory loss
H Recent memory loss
H Difficulty learning and remembering new information
H General deterioration in personal hygiene
H Inability to concentrate
H Tendency to perform repetitive actions and experi-

cially the frontal lobe), which accounts for more


than 50% of all cases of dementia
H Poor prognosis
H No cure or definitive treatment

Pathophysiology
H Alzheimers disease is a genetic abnormality on chro-

mosome 21.
H Brain damage is caused by a genetic substance (amy-

loid).
H There are three distinguishing features of brain tissue: neuro-fibrillary tangles, neuritic plaques, and
granulovascular degeneration.

Causes
H Unknown

Risk factors
Neurochemical
H Deficiencies of the neurotransmitters
Environmental
H Aluminum and manganese
H Trauma
H Genetic abnormality on chromosome 21
H Slow-growing central nervous system viruses

Incidence
H Severe form in patients older than age 65
H May affect 5 million Americans
H Affects 13% or 1 in 8 people older than age 65 and

nearly 50% of those older than age 85

ence restlessness
H Negative personality changes (irritability, depression,

paranoia, hostility)
H Nocturnal awakening
H Disorientation
H Suspicious and fearful of imaginary people and situa-

tions
H Misperceives own environment
H Misidentifies objects and people
H Complains of stolen or misplaced objects
H Emotions may be described as labile
H Mood swings, sudden angry outbursts, and sleep dis-

turbances

Physical findings
H Impaired sense of smell (usually an early symptom)
H Impaired stereognosis
H Gait disorders
H Tremors
H Positive snout reflex
H Organic brain disease in adults
H Urinary or fecal incontinence
H Seizures

Common characteristics

Test results

H Gradual loss of recent and remote memory


H Loss of sense of smell
H Flattening of affect and personality
H Difficulty with learning new information
H Deterioration in personal hygiene
H Inability to concentrate
H Increasing difficulty with abstraction and judgment
H Impaired communication
H Loss of coordination
H Inability to write or speak
H Nocturnal awakenings
H Signs of anxiety
H Loss of eye contact and fearful look
H Acute confusion, agitation, obsessive-compulsive

H Diagnosed by exclusion; tests are performed to rule

behavior

Complications
H Injury from violent behavior, wandering, or unsuper-

vised activity

36

Alzheimers disease

out other diseases.


H Positive diagnosis is made on autopsy.

Imaging
H Position-emission tomography reveals metabolic
activity of the cerebral cortex.
H Computed tomography scan shows excessive and
progressive brain atrophy.
H Magnetic resonance imaging rules out intracranial
lesions.
H Cerebral blood flow studies reveal abnormalities in
blood flow to the brain.
Diagnostic procedures
H Cerebrospinal fluid analysis shows chronic neurologic infection.
H EEG evaluates the brains electrical activity and may
show slowing of the brain waves in late stages of the
disease.

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Other
H Neuropsychologic tests may show impaired cognitive
ability and reasoning.

Treatment
General
H Behavioral interventions (patient-centered or care-

Monitoring
H Response to medications
H Fluid intake and nutrition status
H Environment (for safety purposes)

Patient teaching

Medications

Be sure to cover:
H the disease process
H exercise regimen
H importance of cutting food and providing finger
foods, if indicated
H use of plates with rim guards, built-up utensils, and
cups with lids
H independence.

H Psychostimulators
H Antidepressants, such as paroxetine, sertraline, and

Discharge planning

giver training) focused on managing cognitive and


behavioral changes
H Well-balanced diet (may need to be monitored)
H Safe activities as tolerated (may need to be
monitored)

fluoxetine
H Anxiolytics, such as alprazolam and diazepam
H Antipsychotics, such as haloperidol, risperidone, and
quetiapine
H Anticonvulsants, such as valproic acid, gabapentin,
and lamotrigine
H Anti-inflammatories (experimental)
H Anticholinesterase agents, such as donepezil, rivastigmine, and galantamine
H Vitamin E (experimental)
H N-methyl-D-aspartate receptor antagonists such as
memantine

H Refer the patient to the Alzheimers Association.


H Refer the patient to a local support group.
H Refer the patient to social services for additional sup-

port.

Nursing considerations
Key outcomes
The patient will:
H perform activities of daily living
H maintain daily calorie requirements
H remain free from signs and symptoms of infection
H perform self-care needs
H use support systems and develop adequate coping
behaviors.

Nursing interventions
H Provide an effective communication system.
H Use soft tones and a slow, calm manner when speak-

ing to the patient.


H Allow the patient sufficient time to answer questions.
H Protect the patient from injury.
H Provide rest periods.
H Provide an exercise program.
H Encourage independence.
H Offer frequent toileting.
H Assist with hygiene and dressing.
H Give prescribed drugs.
H Provide familiar objects to help with orientation and

behavior control.

Alzheimers disease

37

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Amebiasis
Overview
Description
H An acute or chronic protozoal infection caused by

Entamoeba histolytica
H Produces varying degrees of illness, from no symp-

toms to mild diarrhea to fulminant dysentery


H Extraintestinal type: may induce hepatic abscess and

infections of the lungs, pleural cavity, pericardium,


peritoneum and, rarely, the brain
H Also known as amebic dysentery

Pathophysiology
H E. histolytica exists in two forms, as a cyst (which

can survive outside the body) and a trophozoite


(which cant survive outside the body).
H The ingested cysts pass through the intestine, where
digestive secretions break them down and liberate
the motile trophozoites within.
H The trophozoites multiply and either invade and ulcerate the mucosa of the large intestine or simply
feed on intestinal bacteria.
H As the trophozoites are carried slowly toward the
rectum, theyre encysted and then excreted in feces.

Causes
H Ingestion of feces-contaminated food or water

Incidence
H Occurs worldwide: most common in the tropics, sub-

tropics, and other areas with poor sanitation and


health practices
H In the United States: overall incidence between 1%
and 3% but may be higher among homosexuals and
institutionalized people, in whom fecal-oral contamination is more common and in immigrants from developing countries

Common characteristics
H The clinical effects of amebiasis varying with the

severity of the infestation


Acute amebic dysentery
H Sudden high temperature of 104 to 105 F (40 to
40.6 C)
H Profuse, bloody, mucoid diarrhea with tenesmus
Chronic amebic dysentery
H Intermittent diarrhea that lasts for 1 to 4 weeks and
recurs several times per year
Amebic granuloma
H Blood and mucus in the stool
H Partial or complete bowel obstruction

Complications
H Subacute appendicitis
H Perforation of the intestinal wall with spread to the

liver, lungs, pleural cavity, peritoneum, and brain.

38

Amebiasis

Assessment
History
Acute amebic dysentery
H Fever, chills
H Abdominal cramping
H Profuse, bloody, mucoid diarrhea
Chronic amebic dysentery
H Multiple (4 to 18) foul-smelling mucus- and bloodtinged stools daily
H Mild fever
H Vague abdominal cramps
H Possible weight loss

Physical findings
Acute amebic dysentery
H Diffuse abdominal tenderness
Chronic amebic dysentery
H Tenderness over the cecum and ascending colon
H Hepatomegaly (occasionally)

Test results
Laboratory
H Stool or aspirates from abscesses, ulcers, or tissue
show E. histolytica.
H Indirect hemagglutination test with current or previous infection is positive.
H Complement fixation is positive (usually only during
active disease).
Imaging
H Barium studies rule out nonamebic causes of diarrhea, such as polyps and cancer.
Diagnostic procedures
H Sigmoidoscopy detects rectosigmoid ulceration.

Treatment
General
H Small, frequent meals
H Increased fluid intake
H Frequent rest periods
H Avoidance of enemas

Medications
H Metronidazole
H Emetine hydrochloride
H Iodoquinol (diiodohydroxyquin)
H Chloroquine
H Tetracycline (in combination with emetine hydro-

chloride, metronidazole, or paromomycin)

Surgery
H Exploratory surgery hazardous; can lead to peritoni-

tis, perforation, and pericecal abscess

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Nursing considerations
Key outcomes
The patient will:
H maintain or improve weight
H maintain skin integrity
H return to a normal elimination pattern
H express feelings of increased comfort and relief from
pain.

Nursing interventions
H Encourage adequate fluid intake.
H Give prescribed drugs.
H Apply perirectal protective cream to prevent excoria-

tion and skin breakdown.

Monitoring
H Vital signs, especially temperature
H Fluid and electrolyte balance
H Daily weight
H Frequency, amount, and character of stools
H Skin integrity

Patient teaching
Be sure to cover:
H need for avoiding alcohol ingestion when taking
metronidazole, which can cause nausea, vomiting,
and headache
H importance of returning for follow-up appointments
H advising family and sexual partners to seek medical
attention for amebiasis
H how to handle infectious material and perform
proper hand washing
H safer sex practices
H boiling untreated or contaminated water when traveling to endemic areas.

Amebiasis

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Amenorrhea
Overview
Description
H The abnormal absence or suppression of menstrua-

tion
H Primary amenorrhea: the absence of menarche in an

adolescent (age 16 and older)


H Secondary amenorrhea: the failure of menstruation
for at least 3 months after the normal onset of
menarche

Pathophysiology
Primary amenorrhea
H The hypothalamic-pituitary-ovarian axis is dysfunctional.
H Anatomic defects of the central nervous system cause
the ovary not to receive the hormonal signals that
normally initiate the development of secondary sex
characteristics and the beginning of menstruation.
Secondary amenorrhea
H The endometrium is sufficiently scarred and no functional endometrium exists.

Causes
H Pregnancy
H Hormonal abnormalities
H Lack of ovarian response to gonadotropins
H Constant presence of progesterone or other en-

docrine abnormalities
H Absence of a uterus
H Endometrial damage
H Ovarian, adrenal, or pituitary tumors
H Emotional disorders
H Malnutrition and intense exercise

Incidence
H Primary amenorrhea: 0.3% of women
H Secondary amenorrhea: 5% of women

Common characteristics
H Absence of menstruation
H Vasomotor flushes, vaginal atrophy, hirsutism (ab-

normal hairiness), and acne (secondary amenorrhea)

Complications
H Infertility
H Endometrial adenocarcinoma
H Estrogen deficiency syndrome
H Osteoporosis

Assessment
History
H Failure to menstruate in females age 16 and older

40

Amenorrhea

H Absence of menstruation for 3 months in a previously

established menstrual pattern


H Change in menstrual pattern
H Dependent on cause: may include headaches, hot

flashes, nausea, weight gain or loss, emotional upset,


trauma, extreme exercise, prolonged use of hormonal contraceptives

Physical findings
H Based on cause of amenorrhea: may include hir-

sutism, acne, abdominal mass, signs of malnutrition

Test results
Laboratory
H Pregnancy test is positive (when pregnancy is the
cause).
H Pituitary gonadotropin levels are either elevated or
low.
H Thyroid levels are abnormal.
H Serum progesterone levels are abnormal.
H Serum androgen levels are abnormal.
H Urine 17-ketosteroid levels are elevated with excessive androgen secretions.
H Plasma follicle-stimulating hormone (FSH) level is
greater than 50 International Units/L, depending on
the laboratory; this suggests primary ovarian failure.
H FSH level is either normal or low; this suggests possible hypothalamic or pituitary abnormality, depending
on the clinical situation.
Imaging
H X-rays identify ovarian, adrenal, and pituitary tumors.
Diagnostic procedures
H Microscopic examination shows ferning of cervical
mucus (an estrogen effect).
H Vaginal cytologic examination and endometrial biopsy evaluate hormone levels.
Other
H Pelvic examination reveals anatomic abnormalities.

Treatment
General
H Based on cause
H Well-balanced diet
H Moderate exercise routine

Medications
H Progestational agents (to stimulate menstruation)
H Calcium supplement (if cause is hypoestrogenism)
H Clomiphene citrate (may induce ovulation in women

with amenorrhea caused by gonadotropin deficiency,


polycystic ovary syndrome, or excessive weight loss
or gain)
H FSH and human menopausal gonadotropins for
women with pituitary disease

Surgery
H Removal of tumor or obstruction

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Nursing considerations
Key outcomes
The patient will:
H maintain adequate nutrition
H express understanding of disorder
H communicate feelings about the situation.

Nursing interventions
H Provide reassurance and emotional support.
H Give prescribed drugs.

Monitoring
H Signs and symptoms
H Intake and output
H Laboratory test results

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to keep an accurate record of menstrual cycles
to aid early detection of recurrent amenorrhea.

Discharge planning
H Refer the patient for psychological counseling, if

appropriate.

Amenorrhea

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Amyotrophic lateral
sclerosis
Overview
Description
H Most common motor neuron disease of muscular

atrophy
H Chronic, progressive, and debilitating disease thats

invariably fatal
H Also known as Lou Gehrig disease

Pathophysiology
H An excitatory neurotransmitter accumulates to toxic

levels.
H Motor units no longer innervate.
H Progressive degeneration of axons cause loss of

myelin.
H Progressive degeneration of upper and lower motor

neurons occurs.
H Progressive degeneration of motor nuclei in the cere-

bral cortex and corticospinal tracts occurs.

Causes
H Exact cause unknown
H 10% of patients inherit as an autosomal dominant

trait
H Virus that creates metabolic disturbances in motor

neurons
H Immune complexes such as those formed in autoim-

mune disorders
Precipitating factors that cause acute
deterioration
H Severe stress such as myocardial infarction
H Traumatic injury
H Viral infections
H Physical exhaustion

Incidence
H Three times more common in males than in females
H Affects people ages 40 to 70

Common characteristics
H Muscle weakness
H Atrophy
H Fasciculations

Complications
H Respiratory tract infections
H Complications of physical immobility

Assessment
History
H Mental function intact
H Family history of amyotrophic lateral sclerosis (ALS)
H Asymmetrical weakness first noticed in one limb

42

Amyotrophic lateral sclerosis

H Easy fatigue and easy cramping in the affected mus-

cles

Physical findings
H Location of the affected motor neurons
H Severity of the disease
H Fasciculations in the affected muscles
H Progressive weakness in muscles of the arms, legs,

and trunk
H Brisk and overactive stretch reflexes
H Difficulty talking, chewing, swallowing, and breathing
H Shortness of breath and occasional drooling

Test results
Laboratory
H Cerebrospinal fluid analysis shows increased protein
levels.
Imaging
H Computed tomography scan rules out other disorders.
Diagnostic procedures
H Muscle biopsy discloses atrophic fibers.
Other
H EEG rules out other disorders.
H Electromyography shows the electrical abnormalities
of involved muscles.
H Nerve conduction studies appear normal.

Treatment
General
H Rehabilitative measures
H May need tube feedings
H Activity as tolerated

Medications
H Muscle relaxants or antispasmodics such as dantro-

lene and baclofen


H I.V. or intrathecal administration of thyrotropin-

releasing hormone
H Riluzole to slow progression

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway and adequate ventilation
H maintain joint mobility and range of motion (ROM)
H maintain daily calorie requirements
H seek support systems and exhibit adequate coping
behaviors
H remain free from infection.

Nursing interventions
H Provide emotional and psychological support.
H Promote independence.
H Turn and reposition the patient frequently.
H Give prescribed drugs.
H Provide airway and respiratory management.

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Modifying the home for a patient with ALS


To help the patient with amyotrophic lateral sclerosis (ALS)
live safely at home, follow these guidelines:
H Explain basic safety precautions, such as keeping stairs
and pathways free from clutter; using nonskid mats in
the bathroom and in place of loose throw rugs; keeping
stairs well lit; installing handrails in stairwells and the
shower, tub, and toilet areas; and removing electrical and
telephone cords from traffic areas.
H Discuss the need for rearranging the furniture, moving
items in or out of the patients care area, and obtaining a
hospital bed, a commode, or oxygen equipment.

H Recommend devices to ease the patients and caregivers


work, such as extra pillows or a wedge pillow to help the
patient sit up, a draw sheet to help him move up in bed,
a lap tray for eating, or a bell for calling the caregiver.
H Help the patient adjust to changes in the environment.
Encourage independence.
H Advise the patient to keep a suction machine handy to
reduce the fear of choking due to secretion accumulation
and dysphagia. Teach him how to suction himself when
necessary.

H Promote nutrition.
H Maintain aspiration precautions.

Monitoring
H Muscle weakness
H Respiratory status
H Speech
H Swallowing ability
H Skin integrity
H Nutritional status
H Environment (for safety purposes)
H Response to treatment
H Complications
H Signs and symptoms of infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H swallowing therapy regimen
H medications and adverse effects
H skin care
H ROM exercises
H deep-breathing and coughing exercises
H safety in the home. (See Modifying the home for a
patient with ALS.)

Discharge planning
H Refer the patient to a local ALS support group.
H Refer the patient to hospice, as appropriate.

Amyotrophic lateral sclerosis

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Life-threatening disorder

Anaphylaxis
Overview
Description

H A lump in the patients throat caused by angioedema


H Dyspnea and complaints of chest tightness

Physical findings
H Hives
H Hoarseness or stridor, wheezing
H Severe abdominal cramps, nausea, diarrhea
H Urinary urgency and incontinence
H Dizziness, drowsiness, headache, restlessness, and

seizures

H Dramatic, acute atopic reaction to an allergen


H Marked by sudden onset of rapidly progressive ur-

H Hypotension, shock; sometimes, angina and cardiac

ticaria and respiratory distress


H More severe the sooner signs and symptoms appear
after exposure to the antigen
H Vascular collapse, leading to systemic shock and,
possibly, death from severe reaction

H Angioedema

Pathophysiology
H After initial exposure to an antigen, the immune sys-

tem produces specific immunoglobulin (Ig) antibodies in the lymph nodes. Helper T cells enhance the
process.
H The antibodies (IgE) then bind to membrane receptors located on mast cells and basophils.
H After the body re-encounters the antigen, the IgE antibodies, or cross-linked IgE receptors, recognize the
antigen as foreign; this activates the release of power
chemical mediators.
H IgG or IgM enters into the reaction and activates the
release of complement factors.

Causes
H Systemic exposure to sensitizing drugs, foods, insect

venom, or other specific antigens

Incidence
H Most common anaphylaxis-causing antigen is peni-

cillin, which induces a reaction in 1 to 4 of every


10,000 patients treated

Common characteristics
H Apprehension and anxiety
H Dyspnea
H Hoarseness
H Angioedema

Complications
H Respiratory obstruction
H Systemic vascular collapse
H Death

Assessment
History
H Immediately after exposure, complaints of a feeling

of impending doom or fright and exhibiting apprehension, restlessness, cyanosis, cool and clammy
skin, erythema, edema, tachypnea, weakness, sweating, sneezing, dyspnea, nasal pruritus, and urticaria

44

Anaphylaxis

arrhythmias

Test results
H No tests are required to identify anaphylaxis. The pa-

tients history and signs and symptoms establish the


diagnosis.
Laboratory
H Skin testing may help identify a specific allergen.

Treatment
General
H Patent airway (establish and maintain)
H Cardiopulmonary resuscitation, if cardiac arrest oc-

curs
H Nothing by mouth, until stable
H Bed rest, until stable

Medications
H Immediate injection of epinephrine 1:1,000 aque-

ous solution, 0.1 to 0.5 ml subcutaneously or I.V.


H Corticosteroids
H Diphenhydramine I.V.
H Volume expander infusions, as needed
H Vasopressors, such as norepinephrine and dopamine
H Aminophylline I.V.
H Antihistamines

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate ventilation
H express feelings of increased comfort and decreased
pain
H maintain normal cardiac output and normal heart
rate
H identify causative allergen.

Nursing interventions
H Provide supplemental oxygen and prepare to assist

with insertion of an endotracheal tube, if necessary.


H Insert a peripheral I.V. line
H Administer medications as prescribed.
H Continually reassure the patient, and explain all tests

and treatments.

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H If the patient undergoes skin or scratch testing, mon-

itor for signs of a serious allergic reaction. Keep


emergency resuscitation equipment readily available.

ALERT
If a patient must receive a drug to which hes allergic, prevent a severe reaction by making sure he
receives careful desensitization with gradually increasing doses of the antigen or with advance administration of corticosteroids. Closely monitor the
patient during testing and have resuscitation
equipment and epinephrine readily available.

Monitoring
H Vital signs
H Adverse reactions from radiographic contrast media
H Respiratory status
H Serious allergic response after skin or scratch testing
H Neurologic status
H Response to treatment
H Complications
H Degree of edema

Patient teaching
Be sure to cover:
H risk for delayed symptoms and importance of reporting them immediately
H avoidance of exposure to known allergens
H importance of carrying and becoming familiar with
an anaphylaxis kit and learning to use it before the
need arises
H need for medical identification jewelry to identify allergy.

Anaphylaxis

45

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Anemia, aplastic
Overview

H Bibasilar crackles, tachycardia, and a gallop murmur


H Fever, oral and rectal ulcers, and sore throat
H Nausea
H Decreased hair and skin quality
H Petechial rash

Description

Test results

H Potentially fatal marrow failure syndrome resulting

Laboratory
H RBC count is 1 million/mm3 or less, usually with normochromic and normocytic cells; absolute reticulocyte count is very low.
H Serum iron levels are elevated (unless bleeding
occurs), but total iron-binding capacity is normal or
slightly reduced.
H Serum platelet and white blood cell counts are decreased.
Diagnostic procedures
H Bone marrow biopsies performed at several sites
may yield a dry tap or show severely hypocellular or
aplastic marrow, with a varying amount of fat, fibrous
tissue, or gelatinous replacement; absence of tagged
iron and megakaryocytes; and depression of erythroid elements.

from injury to or destruction of stem cells in bone


marrow or the bone marrow matrix
H Causes pancytopenia (anemia, leukopenia, thrombocytopenia) and bone marrow hypoplasia

Pathophysiology
H Aplastic anemia usually develops when damaged or

destroyed stem cells inhibit red blood cell (RBC)


production.
H Less commonly, this disease develops when damaged
bone marrow microvasculature creates an unfavorable environment for cell growth and maturation.

Causes
H Result of adverse drug reaction
H Immunologic factors; severe disease, especially hep-

atitis; viral infection, especially in children; and preleukemic and neoplastic infiltration of bone marrow
H Congenital hypoplastic anemia, also known as
Diamond-Blackfan anemia, which develops
between ages 2 and 3 months and Fanconis
syndrome, between birth and age 10
H May be idiopathic

Treatment
General
H Elimination of identifiable cause
H Vigorous supportive measures, such as packed

H Pallor and ecchymoses

RBCs, platelets, and experimental histocompatibility


antigen-matched leukocyte transfusions
H Respiratory support with oxygen
H Prevention of infection ranging from frequent hand
washing to filtered airflow
H Well-balanced diet
H Neutropenic precautions, if appropriate

Complications

Medications

H Hemorrhage
H Infection
H Heart failure

H Antibiotics
H Marrow-stimulating agents, such as erythropoietin,

Incidence
H More common in children and young adults

Common characteristics

Assessment
History
H Fatigue
H Weakness
H Weight loss
H Dizziness
H Syncope
H Bruising
H Nosebleeds
H Shortness of breath

Physical findings
H Pallor, ecchymosis, petechiae, or retinal hemorrhage
H Alterations in level of consciousness, weakness, fa-

tigue

46

Anemia, aplastic

and colony-stimulating factors, such as filgrastim and


sargramostim
H Immunosuppressants
Corticosteroids such as methylprednisolone
Antithymocyte globulin
Cyclosporine

Surgery
H Bone marrow transplantation (for severe aplasia and

patients who need constant RBC transfusions)

Nursing considerations
Key outcomes
The patient will:
H state the need to increase activity level gradually
H maintain vital signs within prescribed limits during
activity

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H maintain normal cardiac output


H exhibit adequate ventilation
H express feelings of increased comfort and decreased

pain.

Nursing interventions
H Help the patient to prevent or manage hemorrhage,

infection, adverse effects of drug therapy, and blood


transfusion reaction.
H If the patients platelet count is low (less than
20,000/mm3), prevent hemorrhage by avoiding I.M.
injections, and suggesting the use of an electric razor
and a soft toothbrush. Apply pressure to venipuncture sites until bleeding stops.
H Follow neutropenic precautions.
H Make sure throat, urine, nasal, stool, and blood cultures are done regularly and correctly to check for
infection.
H Schedule frequent rest periods.
H Administer oxygen therapy.
H Ensure a comfortable environmental temperature.
H If blood transfusions are necessary, administer according to facility policy and assess for transfusion
reactions.

Monitoring
H Blood studies in patients receiving anemia-inducing

drugs
H Early detection of bleeding

Patient teaching
Be sure to cover:
H avoidance of contact with potential sources of infection, such as crowds, soil, and standing water that
can harbor organisms
H the disorder and its treatment
H prescribed drugs and possible adverse reactions and
when to report them
H normal lifestyle with appropriate restrictions until remission occurs (for the patient who doesnt require
hospitalization).

Discharge planning
H Refer the patient to the Aplastic Anemia Foundation

of America for additional information, assistance,


and support.

Anemia, aplastic

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Anemia, folic acid


(folate) deficiency

H Palpitations
H Weakness and light-headedness
H Numbness or tingling in hands and feet

Overview

H Generalized pallor and jaundice


H Weight loss
H Wasted or malnourished appearance
H Possible reddened lips with fissures (cheilosis)
H Red, swollen, smooth, shiny, and tender tongue

Description
H A common, slowly progressive megaloblastic anemia
H Caused by a deficiency of the vitamin folate

Pathophysiology
H When folic acid stores in the body are low or diet is

deficient in folic acid, the bone marrow produces


large red blood cells or megaloblasts resulting in
anemia.

Causes
H Alcohol abuse
H Poor diet
H Impaired absorption from small intestine
H Bacteria competing for available folic acid
H Excessive cooking of foods, which destroys the avail-

able nutrient
H Limited storage capacity in infants
H Prolonged drug therapy with such drugs as anticon-

vulsants, estrogens, and methotrexate


H Increased folic acid requirements during pregnancy,

rapid growth periods in infancy, childhood and adolescence, and in patients with neoplastic diseases or
some skin diseases such as exfoliative dermatitis

Physical findings

(glossitis)
H Reduced sense of taste
H Tachycardia

Test results
Laboratory
H Folic acid deficiency anemia and pernicious anemia
can be distinguished by the Schilling test and a therapeutic trial of vitamin B12 injections.
H Blood studies show macrocythemia, decreased reticulocyte count, increased mean corpuscular volume,
abnormal platelets, and serum folate levels less than
4 mg/ml.

Treatment
General
H Elimination of contributing causes
H Well-balanced diet high in folic acid (see Foods high

in folic acid)
H Frequent rest periods during activity, as needed

Incidence

Medications

H Most prevalent in infants, adolescents, pregnant and

H Folic acid supplements


H Vitamin supplementation (should begin at least 3

lactating women, alcoholics, elderly people, and people with malignant or intestinal diseases

Common characteristics
H Progressive fatigue
H Systemic signs of anemia

Complications
H Pregnant women deficient in folic acid have an in-

creased risk for giving birth to a neonate with a neural tube defect.

Assessment
History
H Severe, progressive fatigue, the hallmark of

folic acid deficiency


H Diarrhea
H Nausea
H Anorexia
H Headaches
H Forgetfulness
H Irritability
H Chest pain
H Shortness of breath

48

Anemia, folic acid (folate) deficiency

months before conception in women trying to become pregnant)


H Blood transfusions in severe cases

Nursing considerations
Key outcomes
The patient will:
H state the need to increase activity level gradually
H maintain vital signs within prescribed limits during
activity
H remain hemodynamically stable
H have normal bowel movements
H experience no further weight loss.

Nursing interventions
H Plan activities, rest periods, and necessary diagnostic

tests to conserve energy.


H Advise the patient to report signs and symptoms of

decreased perfusion to vital organs (dyspnea, chest


pain, dizziness).
H If the patient has glossitis, emphasize the importance
of good oral hygiene.

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Foods high in folic acid


The body needs folic acid to develop healthy red blood cells
and synthesize deoxyribonucleic acid. Although body stores
are comparatively small (about 70 mg), this vitamin is plentiful in most well-balanced diets. But because folic acid is
water-soluble and heat-labile, its easily destroyed by cooking. Also, about 20% of folic acid intake is excreted unabsorbed. Daily folic acid intake less than 50 mcg/day usually
induces folic acid deficiency within 4 months. Heres a list of
foods high in folic acid.

Food

mcg/100 g

Asparagus spears
Beef liver
Broccoli spears
Collards (cooked)
Mushrooms
Oatmeal
Peanut butter
Red beans
Wheat germ

109
294
54
102
24
33
57
180
305

H Ask the dietitian to give the patient nonirritating

foods because a sore mouth and tongue make eating


painful. If these symptoms make talking difficult,
supply a pad and pencil or some other aid to facilitate communication.
H To ensure accurate Schilling test results, make sure
that all urine excreted over a 24-hour period is collected and that the specimens remain uncontaminated by bacteria.
H Provide a well-balanced diet, including foods high in
folate, such as dark green leafy vegetables, organ
meats, eggs, milk, oranges, bananas, dry beans, and
whole-grain breads.

Monitoring
H Vital signs
H Fluid and electrolyte balance

Patient teaching
Be sure to cover:
H importance of a well-balanced diet high in folic acid
H use of commercially prepared formulas for mothers
who arent breast-feeding
H daily folic acid requirements and the need to keep
taking the supplements even when he begins to feel
better
H importance of guarding against infections and reporting signs of infection promptly.

Anemia, folic acid (folate) deficiency

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Anemia, iron deficiency

Common characteristics

Overview

Complications

Description
H Decreased total iron body content diminishing ery-

thropoiesis
H Produces smaller (microcytic) cells with less color

H Fatigue
H Systemic signs of anemia

H Infection
H Pneumonia
H Overreplacement of oral or I.M. iron supplements,

which can affect the liver, heart, pituitary glands, and


joints

on staining (hypochromia)

Special populations

Pathophysiology
H Body stores of iron, including plasma iron, decrease.
H Transferrin, which binds with and transports iron,

also decreases.

In a child, iron deficiency anemia can cause pica,


which may lead to eating lead-based paint resulting in lead poisoning.

H Insufficient body stores of iron lead to a depleted red

blood cell mass and to a decreased hemoglobin concentration.


H Anemic state results in decreased oxygen-carrying
capacity of the blood. (See Iron absorption and
storage.)

Causes
H Inadequate dietary intake of iron
H Iron malabsorption
H Blood loss secondary to drug-induced GI bleeding or

Assessment
History
H Can persist for years without signs and symptoms
H Fatigue
H Inability to concentrate
H Headache, shortness of breath (especially on exer-

tion)

due to heavy menses, hemorrhage from trauma, GI


ulcers, malignant tumors, and varices
H Pregnancy
H Intravascular hemolysis-induced hemoglobinuria or
paroxysmal nocturnal hemoglobinuria
H Mechanical erythrocyte trauma caused by a prosthetic heart valve or vena cava filter
H Can be related to lead poisoning in children

H Increased frequency of infections


H Pica, an uncontrollable urge to eat strange things,

Incidence

Physical findings

H Common worldwide
H Affects 10% to 30% of the adult population of the

H Red, swollen, smooth, shiny, and tender tongue

United States
H Most prevalent among premenopausal women, infants, children, adolescents, alcoholics, and elderly
people

H Corners of the mouth may be eroded, tender, and

Iron absorption and storage


Found in abundance throughout the body, iron is needed
for erythropoiesis. Two-thirds of total-body iron is found
in hemoglobin; the other third, mostly in the reticuloendothelial system (liver, spleen, and bone marrow), with
small amounts in muscle, serum, and body cells.
Adequate iron in the diet and recirculation of iron released from disintegrating red blood cells maintain iron
supplies. The duodenum and upper part of the small intestine absorb dietary iron. Such absorption depends on gastric acid content, the amount of reducing substances
(ascorbic acid, for example) present in the alimentary
canal, and amount of iron intake. If iron intake is deficient,
the body gradually depletes its iron stores, causing decreased hemoglobin levels and, eventually, signs and
symptoms of iron deficiency anemia.

50

Anemia, iron deficiency

such as clay, starch, ice and, in children, lead


H Menorrhagia
H Dysphagia
H Vasomotor disturbances
H Numbness and tingling of the extremities
H Neuralgic pain

(glossitis)
swollen (angular stomatitis)
H Spoon-shaped, brittle nails
H Tachycardia

Test results
Laboratory
H Serum hemoglobin levels are decreased (males, less
than 12 g/dl; females, less than 10 g/dl) or, in severe
anemia, decreased mean corpuscular hemoglobin
level.
H Serum hematocrit is decreased (males, less than
47 ml/dl; females, less than 42 ml/dl).
H Serum iron levels are decreased with high binding
capacity.
H Serum ferritin levels are decreased.
H Serum red blood cell (RBC) count is decreased with
microcytic and hypochromic cells (in early stages,
RBC count may be normal, except in infants and children).

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Diagnostic procedures
H Bone marrow studies reveal depleted or absent iron
stores (done by staining) as well as normoblastic
hyperplasia.
H GI studies, such as guaiac stool tests, barium swallow
and enema, endoscopy, and sigmoidoscopy, rule out
or confirm the diagnosis of bleeding causing the iron
deficiency.

Recognizing iron overdose


Excessive iron replacement may produce signs and symptoms, such as diarrhea, fever, severe stomach pain, nausea, and vomiting.
When these signs and symptoms occur, notify the
physician and give prescribed treatment, which may include chelation therapy, vigorous I.V. fluid replacement,
gastric lavage, whole-bowel irrigation, and supplemental
oxygen.

Treatment
General

Monitoring

H Determination of underlying cause


H Nutritious, nonirritating foods
H Planned rest periods during activity

H Vital signs
H Compliance with prescribed iron supplement therapy
H Iron replacement overdose (see Recognizing iron

Medications
H Oral preparation of iron or a combination of iron

and ascorbic acid


H I.M. iron in rare cases
H Total-dose I.V. infusions of supplemental iron for

pregnant and elderly patients with severe disease

Nursing considerations
Key outcomes
The patient will:
H maintain weight without further loss
H maintain vital signs within prescribed limits during
activity
H express feelings of increased energy
H express feelings of increased comfort and decreased
pain.

Nursing interventions
H Note the patients signs or symptoms of decreased

overdose)

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dangers of lead poisoning, especially if the patient
reports pica
H importance of continuing therapy, even after the patient begins to feel better
H absorption interference with milk or antacid of iron
supplementation
H increased absorption with vitamin C
H avoidance of staining teeth by drinking liquid supplemental iron through a straw
H when to report adverse effects of iron therapy
H basics of a nutritionally balanced diet
H importance of avoiding infection and when to report
signs of infection
H need for regular checkups
H compliance with prescribed treatment.

perfusion to vital organs.


H Provide oxygen therapy, as necessary.
H Assess the familys dietary habits for iron intake, not-

ing the influence of childhood eating patterns, cultural food preferences, and family income on adequate
nutrition.
H Ask the dietitian to give the patient nonirritating
foods.
H Give prescribed analgesics for headache and other
discomfort.
H Evaluate the patients drug history. Certain drugs,
such as pancreatic enzymes and vitamin E, can interfere with iron metabolism and absorption; aspirin,
steroids, and other drugs can cause GI bleeding.
H Provide frequent rest periods.
H If the patient receives iron I.V., monitor the infusion
rate carefully and observe for an allergic reaction.
H Use the Z-track injection method when administering
iron I.M. to prevent skin discoloration, scarring, and
irritating iron deposits in the skin.
H Provide good nutrition and meticulous care of I.V.
sites.

Anemia, iron deficiency

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Anemia, pernicious
Overview
Description
H Deficiency of vitamin B12 causing serious neurologic,

psychological, gastric, and intestinal abnormalities

H Characterized by decreased gastric production of hy-

drochloric acid and deficiency of intrinsic factor, essential for vitamin B12 absorption
H Also known as Addisons anemia

Pathophysiology
H An inherited autoimmune response may cause gastric

mucosal atrophy and resultant decreased hydrochloric acid and intrinsic factor production, a substance
normally secreted by the parietal cells of the gastric
mucosa.
H Intrinsic factor deficiency impairs vitamin B12 absorption.
H Vitamin B12 deficiency inhibits the growth of all
cells, particularly red blood cells (RBCs), leading to
insufficient and deformed RBCs with poor oxygencarrying capacity.

Causes
H Genetic predisposition
H Secondary pernicious anemia results from partial

removal of the stomach


H Chronic gastric inflammation

Incidence

Assessment
History
H Characteristic triad of symptoms: weakness; a beefy

red, sore tongue; and numbness and tingling in the


extremities
H GI disturbance: nausea, vomiting, anorexia, weight
loss, flatulence, diarrhea, and constipation
H Peripheral numbness and paresthesia
H Light-headedness
H Headache
H Diplopia and blurred vision
H Loss of taste
H Tinnitus

Physical findings
H Smooth, beefy red, painful tongue
H Slightly jaundiced sclera and pale to bright yellow

skin
H Tachycardia
H Systolic murmur
H Enlarged liver and spleen
H Weakness in the extremities
H Disturbed position sense
H Lack of coordination
H Impaired fine finger movement
H Loss of bowel and bladder control
H Impotence (in males)
H Irritable, depressed, delirious, and ataxic
H Memory loss
H Positive Babinskis and Rombergs signs
H Optic muscle atrophy

H In the United States, most common in New England

Test results

and the Great Lakes region because of ethnic concentration


H Common in Northern Europeans of fair complexion
H Rare in children, Blacks, and Asians
H Onset typically between ages 50 and 60; incidence
increases with advancing age

Laboratory
H Hemoglobin level is decreased.
H RBC count is decreased.
H Mean corpuscular volume is increased (less than
120 mm3); mean corpuscular hemoglobin concentration is also increased.
H White blood cell and platelet counts may be decreased, and the platelets are large and malformed.
H Serum vitamin B12 tests may show levels less than
0.1 mcg/ml.
H Serum lactate dehydrogenase levels are elevated.
Diagnostic procedures
H Bone marrow studies reveal erythroid hyperplasia
with increased numbers of megaloblasts but few normally developing RBCs.
H Gastric analysis shows an absence of free hydrochloric acid after histamine or pentagastrin injection.
H The Schilling test may reveal a urinary excretion of
less than 3% in the first 24 hours in patients with
pernicious anemia; may reveal normal excretion of
vitamin B12 when repeated with intrinsic factor
added.

Common characteristics
H Weakness
H Beefy red, sore tongue
H Systemic signs of anemia

Complications
H Heart failure with severe anemia
H Myocardial ischemia
H Paralysis
H Psychotic behavior
H Loss of sphincter control of bowel and bladder
H Peptic ulcer disease

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Anemia, pernicious

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Treatment
General
H Based on underlying cause
H Well-balanced diet, including foods high in vitamin

B12

Dietary sources of vitamin B12


The following foods are good sources of vitamin B12:
H Meat, especially organ meats
H Poultry, fresh fish, and seafood
H Eggs
H Dairy products
H Fortified cereals and flours

H Sodium and fluid restriction for heart failure


H If anemia causes extreme fatigue, bed rest until

hemoglobin level increases

Medications
H Early I.M. vitamin B12 replacement
H Maintenance levels (monthly) of vitamin B12 doses,

after the patients condition improves

H observance of and when to report confusion and irri-

tability
H prevention of pernicious anemia, by taking vitamin

B12 supplements, in patients who have had extensive


gastric resections or who follow strict vegetarian
diets.

Nursing considerations
Key outcomes
The patient will:
H state his understanding of the need to increase activity level gradually
H modify lifestyle to minimize risk for decreased tissue
perfusion
H maintain normal hemoglobin level and hematocrit
H maintain normal coagulation profile.

Nursing interventions
H If the patient has severe anemia, plan activities, rest

periods, and necessary diagnostic tests to conserve


his energy.
H To ensure accurate Schilling test results, make sure
that all urine excreted over a 24-hour period is collected.
H Provide a well-balanced diet, including foods high in
vitamin B12. (See Dietary sources of vitamin B12.)
H Institute safety precautions to prevent falls.

Monitoring
H Vital signs
H Mental and neurologic status
H Environment (for safety purposes)

Patient teaching
Be sure to cover:
H protection against infections and when to report
signs of infection
H when to report signs and symptoms of decreased
perfusion to vital organs and symptoms of neuropathy
H avoidance of irritating foods
H avoidance of exposure to extreme heat or cold on the
extremities
H continuation of vitamin B12 replacement even after
symptoms subside
H proper injection techniques

Anemia, pernicious

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Anemia, sickle cell


Overview
Description
H Congenital hemolytic disease that results from a de-

fective hemoglobin (Hb) molecule, HbS, that causes


red blood cells (RBCs) to become sickle-shaped
H Impaired circulation caused by sickle cells resulting
in chronic ill health (fatigue, dyspnea on exertion,
swollen joints), periodic crises, long-term complications, and premature death
H No cure

Pathophysiology
H The abnormal HbS found in the patients RBCs be-

comes insoluble whenever hypoxia occurs.


H The RBCs become rigid, rough, and elongated, form-

ing a crescent or sickle shape.


H Sickling can produce hemolysis (cell destruction).
H The altered cells accumulate in capillaries and small-

er blood vessels, making the blood more viscous.


H Normal circulation is impaired, causing pain, tissue

infarctions, and swelling.

Causes
H Homozygous inheritance of the HbS-producing gene

(defective Hb gene from each parent)

Incidence
H Most common in tropical Africans and in people of

African descent
H Abnormal gene about 1 in 10 blacks (if two such

carriers have offspring, each child has a 1-in-4


chance of developing the disease)
H Found in one in every 500 blacks in the United States
H Also occurs in Puerto Rico, Turkey, India, the Middle
East, and the Mediterranean area

Common characteristics
H Chronic fatigue
H Intense pain due to vascular occlusion in a sickling

episode
H Frequent bacterial infections due to involvement of

spleen
H Systemic signs of anemia

Complications
H Chronic obstructive pulmonary disease
H Heart failure
H Retinopathy
H Nephropathy

54

Anemia, sickle cell

Assessment
History
H Signs and symptoms usually dont develop until after

age 6 months
H Chronic fatigue
H Unexplained dyspnea or dyspnea on exertion
H Joint swelling
H Aching bones
H Chest pain
H Ischemic leg ulcers
H Increased susceptibility to infection
H Pulmonary infarctions and cardiomegaly

Physical findings
H Jaundice or pallor
H May appear small in stature for age
H Delayed growth and puberty
H Spiderlike body build (narrow shoulders and hips,

long extremities, curved spine, and barrel chest) in


adult
H Tachycardia
H Hepatomegaly and, in children, splenomegaly
H Systolic and diastolic murmurs
H Sleepiness with difficulty awakening
H Hematuria
H Pale lips, tongue, palms, and nail beds
H Body temperature greater than 104 F (40 C) or a
temperature of 100 F (37.8 C) that persists for 2
or more days
In painful crisis
H Most common crisis and the hallmark of the disease,
usually appears periodically after age 5, characterized by severe abdominal, thoracic, muscle, or bone
pain and, possibly, increased jaundice, dark urine,
and a low-grade fever
In aplastic crisis
H Pallor, lethargy, sleepiness, dyspnea, possible coma,
markedly decreased bone marrow activity, and RBC
hemolysis
In acute sequestration crisis
H Occurs in infants between ages 8 months and 2
years, causes lethargy and pallor and, if untreated,
progresses to hypovolemic shock and death
In hemolytic crisis
H Liver congestion and hepatomegaly

Test results
Laboratory
H Stained blood smear shows sickle cells and Hb electrophoresis shows HbS. (Electrophoresis should be
done on umbilical cord blood samples at birth to
provide sickle cell disease screening for all neonates
at risk.)
H RBC counts and erythrocyte sedimentation rate are
decreased; white blood cell and platelet counts are
elevated; and serum iron levels are increased.
H RBC survival is decreased and reticulocytosis is present; Hb levels are normal or low.

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Imaging
H A lateral chest X-ray detects the characteristic Lincoln log deformity. (This spinal abnormality develops in many adults and some adolescents with sickle
cell anemia, leaving the vertebrae resembling logs
that form the corner of a cabin.)
Diagnostic procedures
H Ophthalmoscopic examination reveals corkscrew or
comma-shaped vessels in the conjunctivae.

Treatment
General
H Avoidance of extreme temperatures
H Avoidance of stress
H Well-balanced diet
H Adequate amounts of folic acidrich foods
H Adequate fluid intake
H Bed rest during crises
H Activity as tolerated

Medications
H Vaccines, such as polyvalent pneumococcal vaccine

and Haemophilus influenzae B vaccine


H Anti-infectives, as appropriate
H Analgesics
H Iron supplements
H Transfusion of packed RBCs, if Hb level decreases
suddenly or if condition deteriorates rapidly
H Sedation and administration of analgesics, blood
transfusion, oxygen therapy, and large amounts of
oral or I.V. fluids, in an acute sequestration crisis

Nursing considerations
Key outcomes
The patient will:
H demonstrate age-appropriate skills and behaviors to
the extent possible
H exhibit adequate ventilation
H maintain collateral circulation
H maintain balanced fluid volume where input will
equal output
H express feelings of increased comfort and decreased
pain
H maintain normal peripheral pulses
H maintain normal skin color and temperature.

Nursing interventions
H Encourage the patient to talk about his fears and

concerns.
H If a male patient develops sudden, painful priapism,
reassure him that such episodes are common and
have no permanent harmful effects.
H Make sure that the patient receives adequate
amounts of folic acidrich foods such as green,
leafy vegetables.
H Encourage adequate fluid intake.

H Apply warm compresses, warmed thermal blankets,

and warming pads or mattresses to painful areas of


the patients body, unless he has neuropathy.
H Administer analgesics and antipyretics, as needed.
H When cultures demonstrate the presence of infection,
administer prescribed antibiotics.
H Administer prescribed prophylactic antibiotics.
H Use strict sterile technique when performing treatments.
H Encourage bed rest with the head of the bed elevated
to decrease tissue oxygen demand.
H Administer oxygen, as needed.
H Administer blood transfusions.
H If the patient requires general anesthesia for surgery,
help ensure that he receives adequate ventilation to
prevent hypoxic crisis.

Monitoring
H Vital signs
H Intake and output
H Complete blood count and other laboratory study

results

Patient teaching
Be sure to cover:
H avoidance of tight clothing that restricts circulation
H conditions that provoke hypoxia, such as strenuous
exercise, vasoconstricting medications, cold temperatures, unpressurized aircraft, and high altitude
H importance of normal childhood immunizations,
meticulous wound care, good oral hygiene, regular
dental checkups, and a balanced diet as safeguards
against infection
H need for prompt treatment of infection
H need to increase fluid intake to prevent dehydration,
which can cause increased blood viscosity
H symptoms of vaso-occlusive crisis
H need for hospitalization in a vaso-occlusive crisis in
which I.V. fluids, parenteral analgesics, oxygen therapy, and blood transfusions may be necessary
H need to inform all health care providers that the patient has this disease before undergoing any treatment, especially major surgery
H pregnancy and the disease
H balanced diet, including folic acid supplements during pregnancy.

Discharge planning
H Refer parents of children with sickle cell anemia for

genetic counseling to answer their questions about


the risk to future offspring.
H Refer other family members for genetic counseling to
determine if theyre heterozygote carriers.
H If necessary, refer the patient for psychological counseling to help him cope.
H Refer women with sickle cell anemia for birth control counseling.

Anemia, sickle cell

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Anemia, sideroblastic
Overview
Description

Physical findings
H Pale skin and oral mucous membranes
H Slight jaundice
H Petechiae or bruises
H Enlarged lymph nodes
H Hepatosplenomegaly

H A group of heterogenous disorders with a common

Test results

defect that causes failure to use iron in hemoglobin


synthesis despite the availability of adequate iron
stores
H Can be acquired or hereditary; the acquired form, in
turn, can be primary or secondary

Laboratory
H Red blood cell (RBC) indices that are revealed by
microscopic examination of blood show erythrocytes
to be hypochromic or normochromic and slightly
macrocytic; RBC precursors may be megaloblastic,
with anisocytosis (abnormal variation in RBC size)
and poikilocytosis (abnormal variation in RBC
shape).
H Vitamin B12 and folic acid levels are normal unless
combined anemias are present.
H Serum reticulocyte count is low because young cells
die in the marrow.
Diagnostic procedures
H Ringed sideroblasts on microscopic examination of
bone marrow aspirate stained with Prussian blue dye
confirms the diagnosis. (See Ringed sideroblast.)

Pathophysiology
H Normoblasts fail to use iron to synthesize hemoglo-

bin.
H Iron is deposited in the mitochondria of normo-

blasts, rather than in the hemoglobin molecules.


H Iron toxicity can cause organ damage.

Causes
H Hereditary; may be due to a rare genetic defect on

the X chromosome
H Acquired form may be secondary to ingestion of or

exposure to toxins, such as alcohol and lead, or to


drugs such as isoniazid and chloramphenicol
H Complication of neoplastic and inflammatory diseases, such as lymphoma, rheumatoid arthritis, lupus
erythematosus, multiple myeloma, tuberculosis, and
severe infections
H Primary acquired form cause unknown

Incidence
H Most prevalent in young males
H Appears to be transmitted by X-linked inheritance; fe-

males are carriers and usually show no signs of this


disorder
H Primary acquired form most common in elderly people but occasionally found in young people

Common characteristics
H Anorexia and fatigue
H Systemic signs of anemia

Complications

Treatment
General
H Underlying cause determines the course of treatment

(for example, in acquired secondary form, the causative drug or toxin is removed)
H Nutritious diet
H Frequent rest periods
H Chelation therapy to decrease iron overload from
repeated transfusions

Medications
In hereditary sideroblastic anemia
H High doses of pyridoxine
In primary acquired anemia
H Transfusion or high doses of androgens
In chronic iron overload
H Deferoxamine

H Severe cardiac, hepatic, splenic, and pancreatic

Nursing considerations

disease
H Acute myelogenous leukemia

Key outcomes

Assessment
History
H Anorexia
H Fatigue
H Weakness
H Dizziness
H Dyspnea

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Anemia, sideroblastic

The patient will:


H express feelings of increased energy
H maintain skin integrity
H not develop infection
H show improvement or healing in his lesions or
wounds
H express feelings of increased comfort and decreased
pain.

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Nursing interventions
H Provide frequent rest periods. Plan activities and di-

agnostic tests so the patient can rest in between.


H Institute safety measures to prevent falls.
H Give prescribed drugs.
H Provide comfort measures; have the patient perform

Ringed sideroblast
Electron microscopy shows large iron deposits in the mitochondria that surround the nucleus, forming the characteristic ringed sideroblast.

relaxation techniques to facilitate coping.


H Administer blood transfusions. Notify the physician if

signs of a transfusion reaction occur.


H If the patient has jaundice or pruritus, provide metic-

ulous skin care.


H Ask about possible exposure to lead in the home

(especially for children) or on the job.

Monitoring
H Vital signs
H Complications
H Response to treatment
H Signs and symptoms of neuropathy
H Signs and symptoms of decreased perfusion

Patient teaching
Be sure to cover:
H prescribed treatment and possible complications
H importance of continuing prescribed therapy, even
after the patient begins to feel better
H precautions for parents about house paint and not allowing children to eat paint chips because of the possibility of lead
H recognition of and when to report adrenergic adverse effects, if androgens are used as part of the
treatment
H recognition of and when to report signs and symptoms of heart failure
H need for proper hygiene and other measures to
guard against infections and when to report signs
and symptoms of infection.

Discharge planning
H Identify patients who abuse alcohol and refer them

for appropriate therapy.

Anemia, sideroblastic

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Aneurysm,
abdominal aortic

H Lower back pain unaffected by movement


H Gastric or abdominal fullness
H Sudden onset of severe abdominal pain or lumbar

pain with radiation to flank and groin


H May note a pulsating mass in the periumbilical area:

Overview
Description
H Abnormal dilation in the arterial wall of the aorta,

commonly between the renal arteries and iliac


branches
H Can be fusiform (spindle-shaped), saccular (pouchlike), or dissecting

Pathophysiology
H Focal weakness in the tunica media layer of the aorta

due to degenerative changes allows the tunica intima


and tunica adventitia layers to stretch outward.
H Blood pressure within the aorta progressively weakens vessel walls and enlarges the aneurysm.

Causes
H Arteriosclerosis or atherosclerosis (95%)
H Trauma
H Syphilis; other infections

Risk factors
H Hypertension
H Smoking
H Hypercholesterolemia
H Obesity

Incidence
H Seven times more common in hypertensive males

than in females
H Most common in whites ages 50 to 80

Common characteristics
H Located in the infrarenal aorta (98%)
H Most develop at bifurcations in the vessels

Complications
H Hemorrhage
H Shock
H Dissection

dont palpate
Ruptured aneurysm
H Into the peritoneal cavity, severe, persistent abdominal and back pain
H Into the duodenum, GI bleeding with massive hematemesis and melena
H Mottled skin; poor distal perfusion
H Absent peripheral pulses distally
H Decreased level of consciousness
H Diaphoresis
H Hypotension
H Tachycardia
H Oliguria
H Distended abdomen
H Ecchymosis or hematoma in the abdominal, flank, or
groin area
H Paraplegia if aneurysm rupture reduces blood flow to
the spine
H Systolic bruit over the aorta
H Tenderness over affected area

Test results
Imaging
H Abdominal ultrasonography or echocardiography
determines the size, shape, and location of the
aneurysm.
H Anteroposterior and lateral abdominal X-rays detect
aortic calcification, which outlines the mass, at least
75% of the time.
H Computed tomography scan can visualize the aneurysms effect on nearby organs.
H Aortography shows the condition of vessels proximal
and distal to the aneurysm and the extent of the
aeurysm; aneurysm diameter may be underestimated
because it shows only the flow channel and not the
surrounding clot.

Treatment
General
H Delayed surgery if aneurysm is small and produces

Assessment
History
H Asymptomatic until the aneurysm enlarges and com-

presses surrounding tissue


H Syncope when aneurysm ruptures
H Asymptomatic when clot forms and bleeding stops or

abdominal pain when bleeding continues into the


peritoneum

Physical findings
Intact aneurysm
H Gnawing, generalized, steady abdominal pain
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Aneurysm, abdominal aortic

no symptoms
H Careful control of hypertension
H Fluid and blood replacement
H Weight reduction, if appropriate
H Low-fat diet
H Activity as tolerated

Medications
H Beta-adrenergic blockers such as metoprolol
H Antihypertensives
H Analgesics
H Antibiotics, as appropriate

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Endovascular grafting for repair of AAA


Endovascular grafting is a minimally invasive procedure for the patient who
requires repair of an abdominal aortic aneurysm (AAA). Endovascular
grafting reinforces the walls of the aorta to prevent rupture and expansion
of the size of the aneurysm.
The procedure is performed with fluoroscopic guidance, whereby a delivery catheter with an attached compressed graft is inserted through a
small incision into the femoral or iliac artery over a guidewire. The delivery
catheter is advanced into the aorta, where its positioned across the
aneurysm. A balloon on the catheter expands the graft and affixes it to the
vessel wall. The procedure usually takes 2 to 3 hours to perform. Patients
are instructed to walk the first day after surgery and are discharged from
the hospital in 1 to 3 days.

Surgery
H Endovascular grafting or resection of large aneu-

rysms or those that produce symptoms (see Endovascular grafting for repair of AAA)
H Bypass procedures for poor perfusion distal to
aneurysm
H Repair of ruptured aneurysm with a graft replacement

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain hemodynamic stability
H maintain palpable pulses distal to the aneurysm site
H maintain adequate urine output (output equivalent to
intake)
H express feelings of increased comfort and decreased
pain.

Nursing interventions
In a nonacute situation
H Allow the patient to express his fears and concerns
and identify effective coping strategies.
H Offer the patient and his family psychological support.
H Give prescribed drugs.
In an acute situation
H Insert an I.V. line with at least a 14G needle to facilitate blood replacement.
H Obtain blood samples for laboratory tests as ordered.
H Give prescribed drugs.

ALERT
Be alert for signs of rupture, which may be immediately fatal. If rupture does occur, surgery needs to
be immediate. Medical antishock trousers may be
used while transporting the patient to surgery.

After surgery
H Assess peripheral pulses for graft failure or occlusion.

H Watch for signs of bleeding retroperitoneally from

the graft site.


H Maintain blood pressure in prescribed range with

fluids and medications.

ALERT
Assess the patient for severe back pain, which can
indicate that the graft is tearing.
H Have the patient cough, or suction the endotracheal

tube, as needed.
H Provide frequent turning, and assist with ambulation

as soon as the patient is able.

Monitoring
H Cardiac rhythm and hemodynamics
H Vital signs, intake and output hourly, neurologic sta-

tus, and pulse oximetry


H Respirations and breath sounds at least every hour
H Arterial blood gas values as ordered
H Daily weight
H Fluid status
H Nasogastric intubation for patency, amount, and type

of drainage
H Laboratory studies
H Abdominal dressings
H Wound site for infection

Patient teaching
Be sure to cover:
H surgical procedure and expected postoperative care
H importance of taking all medications as prescribed
and carrying a list of medications at all times, in case
of an emergency
H physical activity restrictions until medically cleared
by the physician
H need for regular examination and ultrasound checks
to monitor progression of the aneurysm, if surgery
wasnt performed.

Aneurysm, abdominal aortic

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Aneurysm,
femoral and popliteal
Overview
Description
H Progressive atherosclerotic changes occurring in the

walls (medial layer) of the femoral and popliteal


arteries resulting in a dilation or outpouching (see
Arteries of the leg)
H May be fusiform (spindle-shaped) or saccular
(pouchlike)
H Usually progressive, eventually ending in thrombosis,
embolization, and gangrene

Pathophysiology
H Atherosclerotic plaque formation or loss of elastin

and collagen in the vessel wall causes localized outpouching or dilation of a weakened arterial wall.

Causes
H Atherosclerosis
H Congenital weakness in the arterial wall (rare)
H Trauma (blunt or penetrating)
H Bacterial infection
H Peripheral vascular reconstructive surgery (which

causes suture line or false aneurysms, whereby a


blood clot forms a second lumen)

Incidence
H Most common in males older than age 50

Common characteristics
H Pain
H Edema and venous distention
H Symptoms of severe ischemia in the leg or foot

Complications
H Gangrene

Assessment
History
H Pain in affected extremity

Physical findings
H Loss of pulse and color, coldness in the affected leg

or foot
H Distal petechial hemorrhages (from aneurysmal emboli)
H Pulsating mass above or below the inguinal ligament
H Firm, nonpulsating mass above or below the inguinal
ligament when thrombosis has occurred

Test results
Diagnostic procedures
H Arteriography or ultrasonography reveals aneurysm.
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Aneurysm, femoral and popliteal

Treatment
General
H Nothing by mouth before surgery
H Limited movement of the affected extremity

Medications
H Analgesics
H Antibiotics (before surgery), as appropriate
H Anticoagulants, such as warfarin and heparin

Surgery
H Surgical bypass and reconstruction of the artery, usu-

ally with an autogenous saphenous vein graft replacement


H Leg amputation if arterial occlusion causes severe
ischemia and gangrene

Nursing considerations
Key outcomes
The patient will:
H maintain pulses and adequate circulation to damaged
aneurysm site
H express feelings of increased comfort and decreased
pain
H carry out activities of daily living without excess fatigue or exhaustion.

Nursing interventions
Before corrective surgery
H Evaluate the patients circulatory status, noting the location and quality of peripheral pulses in the affected
arm or leg.
H Administer a prophylactic antibiotic or anticoagulant,
as needed.
H Discuss expected postoperative procedures with the
patient, and review the surgical procedure.
After arterial surgery
H Correlate condition of extremity with preoperative
circulatory assessment. Mark the sites on the patients skin where pulses are palpable, to facilitate repeated checks.
H Help the patient walk soon after surgery, to prevent
venostasis and thrombus formation.

Monitoring
H Neurovascular condition of affected extremity (pulse,

temperature, sensation, color)


H Vital signs
H Pain control

Patient teaching
Be sure to cover:
H importance of immediately informing the physician
of any recurrence of symptoms

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Arteries of the leg


Front view

Back view
Abdominal
aorta
Common
iliac artery
Internal
iliac artery
External
iliac artery

Deep femoral
artery

Deep femoral
artery

Superficial
femoral artery

Superficial
femoral artery

Popliteal artery
Popliteal artery

Anterior tibial
artery

Anterior
tibial artery

Posterior tibial
artery

Dorsalis pedis
Medial plantar
artery

Lateral plantar
artery

H how to apply antiembolism stockings (Warn the pa-

tient against wearing constrictive clothing.)


H measures to prevent bleeding (if an anticoagulant is
prescribed) such as using an electric razor
H importance of reporting signs of bleeding immediately (bleeding gums, easy bruising, or black, tarry
stools)

H importance of follow-up blood studies to monitor an-

ticoagulant therapy.

Aneurysm, femoral and popliteal

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Life-threatening disorder

Aneurysm, intracranial
Overview
Description

Assessment
History
H Headache
H Intermittent nausea
H Seizure
H Photophobia
H Blurred vision

H Weakness in the wall of a cerebral artery that causes

Physical findings

localized dilation
H Most common form is the berry aneurysm, a saclike
outpouching in a cerebral artery
H Usually occurs at an arterial junction in the Circle of
Willis, the circular anastomosis forming the major
cerebral arteries at the base of the brain
H Commonly ruptures and causes subarachnoid hemorrhage

Typically, the severity of a ruptured intracranial


aneurysm is graded according to the patients signs and
symptoms. (See Determining severity of an intracranial aneurysm rupture.)
H Nuchal rigidity
H Back and leg pain
H Fever
H Restlessness
H Irritability
H Hemiparesis
H Hemisensory defects
H Dysphagia
H Visual defects (diplopia, ptosis, dilated pupil, and inability to rotate the eye caused by compression on
the oculomotor nerve if aneurysm is near the internal
carotid artery)

Pathophysiology
H Blood flow exerts pressure against a congenitally

weak arterial wall, stretching it like an overblown


balloon and making it likely to rupture.
H Such a rupture is followed by a subarachnoid hemorrhage, in which blood spills into the space normally
occupied by cerebrospinal fluid.
H Blood spills into brain tissue, where a clot can cause
potentially fatal increased intracranial pressure and
brain tissue damage.

Causes
H Congenital defect
H Degenerative process
H Combination of congenital defect and degenerative

process
H Trauma

Incidence
H Slightly higher in females than in males, especially

those in their late 40s or early- to mid-50s

Test results
Imaging
H Computed tomography scan reveals subarachnoid or
ventricular bleeding with blood in subarachnoid
space and displaced midline structures.
H Magnetic resonance imaging shows a cerebral blood
flow void.
H Skull X-rays may reveal calcified wall of the aneurysm
and areas of bone erosion.
Diagnostic procedures
H Cerebral angiography reveals altered cerebral blood
flow, vessel lumen dilation, and differences in arterial
filling.

H May occur at any age in either sex

Common characteristics

Treatment

H Headache
H Nuchal rigidity
H Stiff back and legs

General

With rupture
H Sudden severe headache
H Altered level of consciousness (LOC)

H Avoidance of coffee, other stimulants, and aspirin

Complications
H Neurologic deficits
H Recurrent bleeding
H Vasospasm
H Death

H Bed rest in a quiet, darkened room with minimal

stimulation

Medications
H Analgesics
H Antihypertensive agents
H Sedatives
H Calcium channel blockers, such as nicardipine and

diltiazem for vasodilation


H Corticosteroids
H Anticonvulsants
H Aminocaproic acid to control bleeding

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Determining severity of an intracranial aneurysm rupture


The severity of symptoms varies from patient to patient, depending on the site and amount of bleeding. Five grades
characterize a ruptured cerebral aneurysm:
H Grade I: minimal bleeding The patient is alert with no
neurologic deficit; he may have a slight headache and
nuchal rigidity.
H Grade II: mild bleeding The patient is alert, with a mild
to severe headache and nuchal rigidity; he may have
third-nerve palsy.

Surgery

H Grade III: moderate bleeding The patient is confused


or drowsy, with nuchal rigidity and, possibly, a mild focal
deficit.
H Grade IV: severe bleeding The patient is stuporous,
with nuchal rigidity and, possibly, mild to severe
hemiparesis.
H Grade V: moribund (usually fatal) If the rupture is
nonfatal, the patient is in a deep coma or decerebrate.

Patient teaching

H Surgical repair by clipping, ligation, or wrapping

(before or after rupture)

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain or improve LOC
H maintain hemodynamic stability.

Be sure to cover:
H the disorder, diagnosis, and treatment
H how to recognize signs of rebleeding.

Discharge planning
H Refer the patient to a visiting nurse or a rehabilita-

tion center when necessary.

Nursing interventions
H Establish and maintain a patent airway.
H Position the patient to promote pulmonary drainage

and prevent upper airway obstruction.


H Impose aneurysm precautions (bed rest in a quiet,

darkened room, keeping the head of the bed flat or


less than 30 degrees, as ordered; limited visitation;
avoidance of strenuous physical activity and straining
with bowel movements; and restricted fluid intake).
H Assist with active range-of-motion (ROM) exercises;
if the patient is paralyzed, perform regular passive
ROM exercises.
H If the patient has facial weakness, assess the gag reflex and assist him during meals, placing food in the
unaffected side of his mouth. If he cant swallow, insert a nasogastric tube, as ordered, and administer
tube feedings.
H If the patient cant speak, establish a simple means of
communication or use cards or a notepad. Encourage his family to speak to him in a normal tone, even
if he doesnt seem to respond.
H Provide emotional support, and include the patients
family in his care as much as possible. Encourage
family members to adopt a realistic attitude, but
dont discourage hope.

Monitoring
H Vital signs
H Neurologic status
H Arterial blood gas levels
H Intake and output

Aneurysm, intracranial

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Aneurysm, thoracic
aortic
Overview
Description

H Dyspnea
H Cyanosis
H Leg weakness
H Transient paralysis
H Abrupt onset of intermittent neurologic deficits
H Abrupt loss of radial and femoral pulses and right

and left carotid pulses


H Increasing area of flatness over the heart, suggesting

Incidence

cardiac tamponade and hemopericardium


In dissecting ascending aneurysm
H Pain with a boring, tearing, or ripping sensation in
the thorax or the right anterior chest; may extend to
the neck, shoulders, lower back, and abdomen
H Pain most intense at onset
H Murmur of aortic insufficiency, a diastolic murmur
H Pericardial friction rub (if hemopericardium present)
H Blood pressure may be normal or significantly elevated, with a large difference in systolic blood pressure
between the right and left arms
In dissecting descending aneurysm
H Sharp, tearing pain located between the shoulder
blades that usually radiates to the chest
H Carotid and radial pulses present and equal
bilaterally
H Systolic blood pressure equal
H May detect bilateral crackles and rhonchi if pulmonary edema present
In dissecting transverse aneurysm
H Sharp, boring, and tearing pain that radiates to the
shoulders
H Hoarseness
H Dyspnea
H Throat pain
H Dysphagia
H Dry cough

H Ascending thoracic aorta most common site


H Occurs predominantly in males younger than age 60

Test results

H Abnormal widening of the ascending, transverse, or

descending part of the thoracic aorta


H May be saccular (outpouching), fusiform (spindle-

shaped), or dissecting

Pathophysiology
H Thoracic aortic aneurysm is caused by a circumfer-

ential or transverse tear of the aortic wall intima,


usually within the medial layer.
H This occurs in about 60% of patients; its usually an
emergency with poor prognosis.

Causes
H Atherosclerosis
H Blunt chest trauma
H Bacterial infections, usually at an atherosclerotic

plaque
H Coarctation of the aorta
H Syphilis infection
H Rheumatic vasculitis
H Marfan syndrome

Risk factors
H Cigarette smoking
H Hypertension

who have coexisting hypertension


H Descending thoracic aortic aneurysms most common

in younger patients who have had chest trauma

Common characteristics
H Asymptomatic until dissection

Complications
H Cardiac tamponade
H Dissection

Assessment
History
H Without signs and symptoms until aneurysm expands

and begins to dissect


H Sudden pain and possibly syncope

Physical findings
H Pallor
H Diaphoresis

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Aneurysm, thoracic aortic

Laboratory
H Hemoglobin levels are normal or decreased due to
blood loss caused by a leaking aneurysm.
Imaging
H Posteroanterior and oblique chest X-rays show
widening of the aorta and mediastinum.
H Aortography shows lumen of the aneurysm and its
size and location.
H Magnetic resonance imaging and computed tomography scan help confirm and locate the presence of
aortic dissection.
Diagnostic procedures
H Electrocardiography helps rule out the presence of
myocardial infarction.
H Echocardiography may help identify dissecting
aneurysm of the aortic root.
H Transesophageal echocardiography can be used to
measure the aneurysm in the ascending and descending aorta.

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Treatment
General
H I.V. fluids and whole blood transfusions, if needed
H Weight reduction, if appropriate
H Low-fat diet
H No activity restrictions unless surgery

Medications
H Antihypertensives
H Analgesics
H Antibiotics, as appropriate

Surgery
H Surgical resection with a Dacron or Teflon graft

replacement

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output and hemodynamic
stability
H maintain adequate ventilation
H express feelings of increased comfort and decreased
pain
H show no signs or symptoms of infection
H maintain adequate fluid volume.

ALERT
After surgical repair, monitor for signs that resemble those of the initial dissecting aneurysm, suggesting a tear at the graft site.

Patient teaching
Be sure to cover:
H the diagnosis
H procedure and expected postoperative care, if
surgery is scheduled
H compliance with antihypertensive therapy, including
the need for such drugs and the expected adverse
effects
H monitoring of blood pressure
H when to call the physician if the patient has any sharp
pain in the chest or back of the neck.

Discharge planning
H Refer the patient to a smoking-cessation program, if

indicated.

Nursing interventions
H In a nonemergency situation, allow the patient to ex-

press his fears and concerns and identify and use effective coping strategies.
H Offer the patient and his family psychological support.
H Give prescribed analgesics to relieve pain.
After repair of thoracic aneurysm
H Maintain blood pressure in prescribed range with
fluids and medications.
H Give prescribed analgesics.
H After stabilization of vital signs, encourage and assist
the patient in turning, coughing, and deep breathing.
H Help the patient walk as soon as hes able.
H Assist the patient with range-of-motion exercises.

Monitoring
H Vital signs and hemodynamics
H Chest tube drainage
H Heart and lung sounds
H Laboratory results
H Distal pulses
H Level of consciousness and pain
H Signs of infection
H I.V. therapy and intake and output

Aneurysm, thoracic aortic

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Aneurysm, ventricular
Overview
Description
H An outpouching, almost always of the left ventricle,

that produces ventricular wall dysfunction


H May develop within days to weeks after myocardial

infarction (MI) or may be delayed for years

Pathophysiology
H When MI destroys a large muscular section of the left

ventricle, necrosis reduces the ventricular wall to a


thin sheath of fibrous tissue.
H Under intracardiac pressure, the thin sheath stretches and forms a separate noncontractile sac (aneurysm).
H Abnormal muscle wall movement accompanies ventricular aneurysm.
H During systolic ejection, the abnormal muscle wall
movements cause the remaining normally functioning myocardial fibers to increase the force of contraction to maintain stroke volume and cardiac
output.
H At the same time, a portion of the stroke volume is
lost to passive distention of the noncontractile sac.

Causes
H MI

Incidence
H Occurs in about 20% of patients after MI

Common characteristics
H Occurs after MI

Complications
H Ventricular arrhythmias
H Cerebral embolization
H Heart failure

H Double, diffuse, or displaced apical impulse


H Gallop rhythm
H Crackles and rhonchi

Test results
Imaging
H Two-dimensional echocardiography demonstrates
abnormal motion in the left ventricular wall.
H Left ventriculography reveals left ventricular enlargement, with an area of akinesia or dyskinesia (during
cineangiography) and diminished cardiac function.
H Chest X-rays may disclose an abnormal bulge distorting the hearts contour if the aneurysm is large;
X-rays may be normal if the aneurysm is small.
H Noninvasive nuclear cardiology scan may indicate the
site of infarction and suggest the area of aneurysm.
Diagnostic procedures
H Electrocardiography may show persistent ST-T wave
elevations.

Treatment
General
H Depends on the size of the aneurysm and the pres-

ence of complications
H May require only routine medical examination to fol-

low the patients condition


H May require aggressive measures, such as cardiover-

sion, defibrillation, and endotracheal intubation


H Weight reduction, if appropriate
H Low-fat diet
H No activity restrictions, unless surgery

Medications
H Antiarrhythmics, such as lidocaine and procainamide
H Cardiac glycosides such as digoxin
H Diuretics, such as furosemide and torsemide
H Fluid and electrolyte replacement
H Analgesics
H Antihypertensives, as appropriate
H Nitrates
H Anticoagulants, such as heparin and warfarin

Assessment

Surgery

History

H Embolectomy
H Aneurysmectomy with myocardial revascularization

H Previous MI
H Dyspnea
H Fatigue

Nursing considerations

Physical findings

Key outcomes

H Edema
H Visible or palpable systolic precordial bulge
H Distended jugular veins, if heart failure is present
H Irregular peripheral pulse rhythm
H Arrhythmias such as premature ventricular contrac-

The patient will:


H maintain adequate cardiac output
H maintain hemodynamic stability
H maintain adequate fluid balance
H express feelings of increased energy and decreased
fatigue
H express feelings of decreased anxiety.

tions
H Pulsus alternans

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Nursing interventions
H Give prescribed drugs.
H Prepare for surgery, if indicated.

ALERT
Be alert for sudden changes in sensorium that may
indicate cerebral embolization and for any signs
that suggest renal failure or MI.
H Provide psychological support for the patient and his

family.

Monitoring
Heart failure
H Vital signs and heart sounds
H Cardiac rhythm, especially for ventricular arrhythmias
H Intake and output; and fluid and electrolyte balance
H Blood urea nitrogen and serum creatinine levels
After surgery
H Pulmonary artery catheter pressures
H Signs and symptoms of infection
H Type and amount of chest tube drainage

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H expected postoperative care, if the patient is scheduled to undergo resection
H monitoring pulse irregularity and rate changes.

Discharge planning
H Refer family or caregiver to a community-based car-

diopulmonary resuscitation training program.


H Refer the patient to a weight-reduction program, if

indicated.
H Refer the patient to a smoking-cessation program, if

indicated.

Aneurysm, ventricular

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Ankylosing spondylitis
Overview
Description
H Rheumatoid disease primarily affecting sacroiliac,

apophyseal, and costocervical joints and adjacent ligamentous or tendinous attachments to bone
H Usually occurs as a primary disorder; may occur secondary to Reiters syndrome, psoriatic arthritis, or
inflammatory bowel disease
H Also called rheumatoid spondylitis or MarieStrmpell disease

Pathophysiology
H Disease begins in the sacroiliac; gradually progresses

to the lumbar, thoracic, and cervical spine.


H Bone and cartilage deterioration leads to fibrous

tissue formation and eventual fusion of the spine


or peripheral joints.

Causes
H Unknown
H Familial tendency
H Initial inflammation may result from immune system

activation by bacterial infection

Incidence
H Affects males two to three times more commonly

than females
H Well-recognized in males but commonly overlooked

or missed in females
H More peripheral joint involvement in females

Common characteristics
H Symptoms can unpredictably remit, exacerbate, or

arrest at any stage

Complications
H Atlantoaxial subluxation of cervical vertebrae
H Deposits of amyloid material in the kidneys, which

may lead to renal impairment or failure

Detecting ankylosing spondylitis


in women
Ankylosing spondylitis seldom occurs in women, which is
why if a womans symptoms include pelvic pain diagnosticians typically overlook ankylosing spondylitis and suspect pelvic imflammatory disease. However, its important
to assess a female patient with apparent pelvic disease
carefully especially if culture results identify no apparent cause of her discomfort. Otherwise, misdiagnosis can
lead to unwarranted invasive tests and treatments and
cause the patient needless anxiety related to contracting a
sexually transmitted disease. Asking the patient if theres a
family history of ankylosing spondylitis and the performance of a thorough health and social history is advisable.

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Ankylosing spondylitis

Assessment
History
H Intermittent lower back pain most severe in the

morning or after inactivity and relieved by exercise


H Mild fatigue, fever, anorexia, and weight loss
H May describe pain in shoulders, hips, knees, and an-

kles
H Pain over the symphysis pubis, which may lead to its

being mistaken for pelvic inflammatory disease (see


Detecting ankylosing spondylitis in women)

Physical findings
H Stiffness or limited motion of the lumbar spine
H Pain and limited chest expansion
H Kyphosis
H Iritis
H Warmth, swelling, or tenderness of affected joints
H Sausage shape to small joints such as toes
H Aortic murmur caused by insufficiency
H Cardiomegaly
H Upper lobe pulmonary fibrosis, which mimics tuber-

culosis, that may reduce vital capacity to 70% or less


of predicted volume

Test results
H Diagnosis of primary ankylosing spondylitis requires

meeting established criteria. (See Diagnosing primary ankylosing spondylitis.)


Laboratory
H HLA antigen typing test shows serum findings that include HLA-B27 in about 95% of patients with primary
ankylosing spondylitis and up to 80% of patients with
secondary disease.
H Serum rheumatoid factor tests show the absence of
rheumatoid factor, which helps rule out rheumatoid
arthritis, which has similar symptoms.
H Serum alkaline phosphate and creatine kinase tests
show slightly elevated erythrocyte sedimentation rate,
serum alkaline phosphate levels, and creatine kinase
levels in active disease.
H Serum immunoglobulin (Ig) profile shows elevated
serum IgA levels.
Imaging
H X-ray studies define characteristic changes, such as
bilateral sacroiliac involvement (the hallmark of the
disease); blurring of the joints bony margins in early
disease; patchy sclerosis with superficial bony erosions; eventual squaring of vertebral bodies; and
bamboo spine with complete ankylosis.

Treatment
General
H Good posture; stretching and deep-breathing

exercises
H Braces and lightweight supports, if appropriate
H Heat, warm showers, baths, and ice

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H Nerve stimulation
H Nutritious diet
H Encourage activity as tolerated

Medications
H Nonsteroidal anti-inflammatory drugs such as

ibuprofen
H Sulfasaline
H Methotrexate
H Corticosteroids
H Tumor-necrosis-factor alpha inhibitors

Surgery
H Hip replacement surgery with severe hip involvement
H Spinal wedge osteotomy with severe spinal involve-

ment

Diagnosing primary ankylosing


spondylitis
For a reliable diagnosis, the patient must meet:
H criterion 7 and any one of criteria 1 through 5, or
H any five of criteria 1 through 6 if he doesnt have
criterion 7.

Seven criteria
1. Axial skeleton stiffness for at least 3 months thats
relieved by exercise
2. Lumbar pain that persists at rest
3. Thoracic cage pain of at least 3 months duration that
persists at rest
4. Past or current iritis
5. Decreased lumbar range of motion
6. Decreased chest expansion (age-related)
7. Bilateral, symmetrical sacroiliitis demonstrated by
radiographic studies

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H express feelings of increased energy
H recognize limitations imposed by illness and express
feelings about these limitations
H identify factors that increase the risk for injury.

Nursing interventions
H Keep in mind the patients limited range of motion

(ROM) when planning self-care tasks and activities.


H Offer support and reassurance.
H Give prescribed analgesics.
H Apply heat locally and massage, as indicated.
H Have the patient perform active ROM exercises.
H Pace periods of exercise and rest to help the patient
achieve comfortable energy levels and lung oxygenation.
H If treatment includes surgery, ensure proper body
alignment and positioning.
H Involve other caregivers, such as a social worker, visiting nurse, and dietitian.

H avoidance of prolonged walking, standing, sitting, or

driving
H regular stretching and deep-breathing exercises;

swimming on a regular basis, if possible


H measurement of patients height every 3 to 4 months

to detect kyphosis
H nutrition and weight maintenance.

Discharge planning
H Refer the patient to physical therapy, as needed.
H Refer the patient to the Spondylitis Association of

America or the Arthritis Foundation for additional


support and information.

Monitoring
H Mobility and comfort level
H Respiratory status
H Heart sounds

Patient teaching
Be sure to cover:
H avoidance of physical activity that places stress on the
back such as lifting heavy objects
H importance of standing upright; sitting upright in a
high, straight-back chair; and avoiding leaning over a
desk
H importance of sleeping in a prone position on a hard
mattress and avoiding using pillows under the neck
or knees

Ankylosing spondylitis

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Anorexia nervosa

H Limits or restricts food intake; eats small portions

Overview

Complications

Description
H Psychological disorder of self-imposed starvation re-

sulting from a distorted body image and an intense


and irrational fear of gaining weight
H Actual loss of appetite, which is rare
H May occur simultaneously with bulimia nervosa

Pathophysiology
H Decreased calorie intake depletes body fat and pro-

tein stores.
H Estrogen deficiency occurs (in females) due to lack

of lipid substrate for synthesis, causing amenorrhea.


H Testosterone levels fluctuate (in males), and de-

creased erectile function and sperm count occurs.


H Ketoacidosis occurs from increased use of fat as en-

(see Criteria for hospitalizing a patient with


anorexia nervosa)
H Suicide
H Electrolyte imbalances
H Malnutrition
H Dehydration
H Esophageal erosion, ulcers, tears, and bleeding
H Tooth and gum erosion and dental caries
H Decreased left ventricular muscle mass and chamber

size
H Decreased cardiac output
H Hypotension
H Electrocardiogram (ECG) changes
H Heart failure
H Increased susceptibility to infection
H Amenorrhea
H Anemia
H Death

ergy fuel.

Causes

Assessment

H Exact cause unknown


H Social attitudes that equate slimness with beauty
H Subconscious effort to exert personal control over

History

H Low self-esteem
H Compulsive personality
H High achievement goals

H 15% or greater weight loss for no organic reason


H Morbid fear of being fat
H Compulsion to be thin
H Angry disposition
H Tendency to minimize weight loss
H Ritualistic
H Amenorrhea
H Infertility
H Loss of libido
H Fatigue
H Sleep alterations
H Intolerance to cold
H Constipation or diarrhea

Incidence

Physical findings

H 5% to 10% of the population; more than 90% of

H Hypotension
H Bradycardia
H Emaciated appearance
H Skeletal muscle atrophy
H Loss of fatty tissue
H Atrophy of breast tissue
H Blotchy or sallow skin
H Lanugo on the face and body
H Dryness or loss of scalp hair
H Calluses of the knuckles
H Abrasions and scars on the dorsum of the hand
H Dental caries
H Oral or pharyngeal abrasions
H Painless salivary gland enlargement
H Bowel distention
H Slowed reflexes

life or to protect oneself from dealing with issues


surrounding sexuality
H Elaborate food preparation and eating rituals
H Achievement pressure
H Dependence and independence issues
H Stress caused by multiple responsibilities
H History of sexual abuse

Risk factors

those affected are females

Special populations
Anorexia nervosa occurs primarily in adolescents
and young adults but may also affect older females
and, occasionally, males.

Common characteristics
H Preoccupation with body size
H Tendency to describe self as fat
H Dissatisfaction with a particular aspect of physical

appearance
H Compulsive exercising
H Self-induced vomiting
H Laxative or diuretic abuse

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Anorexia nervosa

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DSM-IV-TR criteria
These criteria must be documented:
H Refusal to maintain or achieve normal weight for age
and height
H Intense fear of gaining weight or becoming fat, even
though underweight
H Disturbance in perception of body weight, size, or
shape
H Absence of at least three consecutive menstrual cycles when otherwise expected to occur (in females)

Test results
Laboratory
H Hemoglobin level, platelet count, and white blood
cell count are decreased.
H Bleeding time is prolonged.
H Erythrocyte sedimentation rate is decreased.
H Serum creatinine, blood urea nitrogen, uric acid,
cholesterol, total protein, albumin, sodium, potassium, chloride, calcium, and fasting blood glucose
levels are decreased.
H Alanine aminotransferase and aspartate aminotransferase levels are elevated in severe starvation states.
H Serum amylase levels are elevated.
H In females, serum luteinizing hormone and folliclestimulating hormone levels are decreased.
H Triiodothyronine levels are decreased.
H Urinalysis shows dilute urine.
Diagnostic procedures
H ECG may show nonspecific ST interval, T-wave
changes, and prolonged PR interval; ventricular
arrhythmias may also be present.

Treatment
General
H Behavior modification
H Curtailed activity for cardiac arrhythmias
H Group, family, or individual psychotherapy
H Balanced diet with a normal eating pattern
H Parenteral nutrition, if necessary
H Gradual increase in physical activity when weight

gain and stabilization occur

Criteria for hospitalizing a patient


with anorexia nervosa
A patient with anorexia nervosa can be successfully treated on an outpatient basis. However, if the patient displays
any of the signs listed here, hospitalization is mandatory:
H rapid weight loss equal to 15% or more of normal body
mass
H persistent bradycardia (50 beats/minute or less)
H hypotension with a systolic reading less than or equal
to 90 mm Hg
H hypothermia (core body temperature less than or equal
to 97 F (36.1 C)
H presence of medical complications, suicidal ideation
H persistent sabotage or disruption of outpatient
treatment resolute denial of condition and the need
for treatment.

Nursing interventions
H Support the patients efforts to achieve target weight.
H Negotiate an adequate food intake with the patient.
H Supervise the patient one-on-one during meals and

for 1 hour afterward.

Monitoring
H Vital signs
H Intake and output
H Electrolyte and complete blood count levels
H Weight on a regular schedule
H Activity for compulsive exercise

ALERT
Monitor the patient for 1 hour after meals to ensure no self-induced vomiting.

Patient teaching
Be sure to cover:
H nutrition
H importance of keeping a food journal
H avoidance of discussions about food between the
patient and her family.

Medications

Discharge planning

H Vitamin and mineral supplements


H Electrolyte replacement
H Serotonin reuptake inhibitors, such as citalopram,

H Refer the patient to support services.

fluoxetine, and sertraline, after weight gain is established

Nursing considerations
Key outcomes
The patient will:
H acknowledge change in body image
H express positive feelings about self
H achieve and maintain expected body weight
H achieve expected state of wellness.

Anorexia nervosa

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Life-threatening disorder

Anthrax

Incidence
H Occurs worldwide
H Most common in developing countries
H Most common in domestic herbivores, including

sheep, cattle, horses, and goats, and wild herbivores


H Estimates of 20,000 to 100,000 cases per year (Ap-

Overview
Description

proximately 95% of human anthrax are the cutaneous form; about 5% are the inhalation form; GI anthrax is rare.)

H An acute bacterial infection occurring most com-

Common characteristics

monly in herbivorous animals; the natural resistance


of humans to anthrax greater than that of these
animals
H Also known as a potential agent for use in bioterrorism and biological warfare; classified as a Category A
biological disease
H Three forms of anthrax in humans, depending on the
mode of transmission: cutaneous, inhalation (woolsorters disease), and GI
H Cutaneous anthrax: the most common form
H Without treatment, mortality rate from cutaneous anthrax, 20%; mortality rate less than 1% with treatment
H Even with treatment, inhalation anthrax usually fatal
H With treatment, death in 25% to 60% of cases of GI
anthrax
H No screening test for anthrax

H History of exposure to B. anthracis spores


H Clinical manifestation will depend on the form of

Pathophysiology
H Bacillus anthracis is an encapsulated, aerobic,

chain-forming, gram-positive rod that forms oval


spores; spores are hardy and can survive for years
under adverse conditions.
H B. anthracis, an extracellular pathogen, evades
phagocytosis, invades the bloodstream, and multiplies rapidly.
H In cutaneous anthrax, spores enter the body through
abraded or broken skin or by biting flies; the spores
germinate within hours, the vegetative cells multiply,
and anthrax toxin is produced.
H In inhalation anthrax, spores are deposited directly
into the alveoli and phagocytized by macrophages;
some are carried to and germinate in mediastinal
nodes. This may result in overwhelming bacteremia,
hemorrhagic mediastinitis, and secondary pneumonia.
H In GI anthrax, primary infection can occur in the intestine by organisms that survive passage through the
stomach; acute inflammation of the intestinal tract
results.

Causes
H Bacterial infection with B. anthracis

Risk factors
H Laboratory and industrial workers at risk for occupa-

tional exposure

72

Anthrax

anthrax

Complications
H Septicemia
H Hemorrhagic mediastinitis
H Pneumonia
H Respiratory failure
H Hemorrhagic thoracic lymphadenitis
H Meningitis
H Death

Assessment
History
Cutaneous anthrax
H Painless ulcer
H Mild or no constitutional symptoms
Inhalation anthrax
H Initial prodromal flulike symptoms:
Malaise; dry cough
Mild fever; chills
Headache; myalgia
Severe respiratory distress
Chest pain
GI anthrax
H Nausea; vomiting
H Decreased appetite
H Fever
H Abdominal pain
H Vomiting blood
H Severe bloody diarrhea

Physical findings
Cutaneous anthrax
H Initially, a small, papular, pruritic lesion that resembles an insect bite
H Lesion that develops into a vesicle in 1 to 2 days
H Lesion that finally becomes a small, painless ulcer
with a necrotic center, surrounded by nonpitting
edema
H Smaller secondary vesicles that may surround some
lesions
H Lesions that are generally located on exposed areas
of the skin
H Painful, regional, nonspecific lymphadenitis

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Inhalational anthrax
H Increasing fever
H Dyspnea, stridor
H Hypoxia; cyanosis
H Hypotension; shock
GI anthrax
H Fever
H Rapidly developing ascites

Test results
Laboratory
H Gram stain, direct fluorescent antibody staining, and
culture show presence of B. anthracis.
H Blood cultures show presence of B. anthracis.
H Cerebrospinal fluid analysis reveals presence of
B. anthracis.
H Complete blood count shows polymorphonuclear
leukocytosis in severe disease.
H Serum antibody tests reveal the presence of the
specific antibody to B. anthracis.
Imaging
H Chest X-ray show symmetrical mediastinal widening
in hemorrhagic mediastinitis.

Treatment
General

H Encourage verbalization of fears and concerns.


H Provide adequate hydration.
H Provide a well-balanced diet.
H Assist the patient in the development of effective cop-

ing mechanisms.
H Provide adequate rest periods.

Monitoring
H Vital signs
H Intake and output
H Respiratory status
H Neurologic status
H Cardiovascular status
H Skin lesions
H GI status
H Complications
H Response to treatment
H Progression of infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H anthrax prevention.

H Treatment initiated as soon as exposure to anthrax is

suspected (essential to preventing anthrax infection;


may also help prevent death)
H No dietary restrictions
H Adequate fluid intake
H Physical activity as tolerated

Medications
H Antibiotics, such as ciprofloxacin, doxycycline, and

amoxicillin
H Oxygen, as needed

Surgery
H May be necessary for complications such as hemor-

rhagic mediastinitis

Nursing considerations
Key outcomes
The patient will:
H maintain adequate nutrition and hydration
H verbalize feelings of fear and anxiety
H demonstrate effective coping mechanisms
H maintain tissue perfusion and cellular oxygenation
H maintain effective ventilation.

Nursing interventions
H Give prescribed drugs.
H Maintain patent airway and adequate ventilation.
H Report any case of anthrax in either livestock or hu-

mans to the local board of health.


H Maintain standard precautions.

Anthrax

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Aortic insufficiency
Overview
Description
H A heart condition in which blood flows back into the

left ventricle, causing excess fluid volume


H Also called aortic regurgitation

Pathophysiology
H Blood flows back into the left ventricle during dias-

tole, causing increased left ventricular diastolic pressure.


H This results in volume overload, dilation and, eventually, hypertrophy of the left ventricle.
H Excess fluid volume also eventually results in increased left atrial pressure and increased pulmonary
vascular pressure.

Causes
H Rheumatic fever
H Primary disease of the aortic valve leaflets, the wall

or the aortic root, or both


H Hypertension
H Infective endocarditis
H Trauma
H Idiopathic valve calcification
H Aortic dissection
H Aortic aneurysm
H Connective tissue diseases

Incidence
H Occurs most commonly in males
H When associated with mitral valve disease: more

common in females

Common characteristics
H Typically asymptomatic until the fourth or fifth

decade of life
H Orthopnea
H Paroxysmal nocturnal dyspnea
H Exertional dyspnea

Complications
H Left-sided heart failure
H Pulmonary edema
H Myocardial ischemia

Assessment
History
H Exertional dyspnea, orthopnea, paroxysmal noctur-

nal dyspnea
H Sensation of a forceful heartbeat, especially in supine
position
H Angina, especially nocturnal
H Fatigue

74

Aortic insufficiency

H Palpitations, head pounding


H Symptoms of heart failure, in late stages

Physical findings
H Corrigans pulse
H Pulsus bisferiens
H Pulsating nail beds and Quinckes sign
H Wide pulse pressure
H Diffuse, hyperdynamic apical impulse, displaced lat-

erally and inferiorly


H Systolic thrill at base or suprasternal notch
H S3 gallop with increased left ventricular end-diastolic

pressure

H High frequency, blowing early-peaking, diastolic de-

crescendo murmur best heard with the patient sitting


leaning forward and in deep fixed expiration (see
Identifying the murmur of aortic insufficiency)
H Austin Flint murmur
H Head bobbing with each heartbeat
H Tachycardia, peripheral vasoconstriction, and pulmonary edema if severe aortic insufficiency

Test results
Imaging
H Chest X-rays may show left ventricular enlargement
and pulmonary vein congestion.
H Echocardiography may show left ventricular enlargement, increased motion of the septum and posterior
wall, thickening of valve cusps, prolapse of the valve,
flail leaflet, vegetations, or dilation of the aortic root.
Diagnostic procedures
H Electrocardiography shows sinus tachycardia, left
axis deviation, left ventricular hypertrophy, and left
atrial hypertrophy in severe disease.
H Cardiac catheterization shows presence and degree
of aortic insufficiency, left ventricular dilation and
function, and coexisting coronary artery disease.

Treatment
General
H Periodic noninvasive monitoring of aortic insufficien-

cy and left ventricular function with echocardiogram


H Medical control of hypertension
H Low-sodium diet
H Planned periodic rest periods to avoid fatigue

Medications
H Cardiac glycosides such as digoxin
H Diuretics, such as furosemide and torsemide
H Vasodilators such as nitrates
H Antihypertensives
H Antiarrhythmics, such as amiodarone and

propafenone
H Infective endocarditis prophylaxis, as appropriate
H Anticoagulants such as warfarin
H Antiplatelets, such as clopidogrel and ticlopidine

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ALERT
Avoid using beta-adrenergic blockers due to their
negative inotropic effects.

Identifying the murmur of aortic


insufficiency
A high-pitched, blowing decrescendo murmur that radiates from the aortic valve area to the left sternal border
characterizes aortic insufficiency.

Surgery
H Valve replacement

SYSTOLE
S1

DIASTOLE
S2

SYSTOLE
S1

S2

Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without excess fatigue or decreased energy
H maintain cardiac output, demonstrate hemodynamic
stability, and not develop arrhythmias
H maintain adequate fluid balance
H maintain adequate ventilation.

Nursing interventions
H Give prescribed drugs.
H If the patient needs bed rest, stress its importance;

provide a bedside commode.


H Alternate periods of activity and rest.
H Allow the patient to express his concerns about the

effects of activity restrictions on his responsibilities


and routines.
H Keep the patients legs elevated while he sits in a
chair.
H Place the patient in an upright position, if necessary,
and administer oxygen.
H Keep the patient on a low-sodium diet. Consult a dietitian.
H Following surgery, watch for hypotension, arrhythmias, and thrombus formation.

Monitoring

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H periodic rest periods in the patients daily routine
H leg elevation whenever the patient sits
H dietary restrictions
H signs and symptoms of heart failure
H importance of consistent follow-up care
H monitoring of pulse rate and rhythm
H blood pressure control.

Discharge planning
H Refer the patient to an outpatient cardiac rehabilita-

tion program, if indicated.


H Refer the patient to a smoking-cessation program, if

indicated.
H Refer the patient to a weight-reduction program, if

indicated.

H Signs and symptoms of heart failure


H Pulmonary edema
H Adverse reactions to drug therapy
H Complications

After surgery
H Vital signs and cardiac rhythm
H Heart sounds
H Chest tube drainage
H Neurologic status
H Arterial blood gas levels
H Intake and output; daily weight
H Blood chemistry studies, prothrombin time, and
International Normalized Ratio values
H Chest X-ray results
H Pulmonary artery catheter pressures

Aortic insufficiency

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Aortic stenosis
Overview
Description
H Narrowing of the aortic valve that affects blood flow

in the heart
H Classified as either acquired or rheumatic

Pathophysiology
H Stenosis of the aortic valve results in impedance to

forward blood flow.


H The left ventricle requires greater pressure to open

the aortic valve.


H Added workload increases myocardial oxygen demands.
H Diminished cardiac output reduces coronary artery
blood flow.
H Left ventricular hypertrophy and failure result.

Causes
H Idiopathic fibrosis and calcification
H Congenital aortic bicuspid valve
H Rheumatic fever
H Atherosclerosis

Risk factors
H Diabetes mellitus
H Hypercholesterolemia

Incidence
H Possibly asymptomatic until ages 50 to 70, even

though stenosis present since childhood


H About 80% of patients: male

Common characteristics
H Long latent period
H Classic triad of angina pectoris, syncope, and

dyspnea

Complications
H Left-sided heart failure
H Right-sided heart failure
H Infective endocarditis
H Cardiac arrhythmias, especially atrial fibrillation
H Sudden death
H Left ventricular hypertrophy

Physical findings
H Small, sustained arterial pulses that rise slowly
H Distinct lag between carotid artery pulse and apical

pulse
H Orthopnea
H Prominent jugular vein a waves
H Peripheral edema
H Diminished carotid pulses with delayed upstroke
H Apex of the heart may be displaced inferiorly and lat-

erally
H Suprasternal thrill

Special populations
An early systolic ejection murmur may be present
in children and adolescents who have noncalcified
valves. The murmur is low-pitched, rough, and
rasping and is loudest at the base in the second intercostal space.
H Split S2 develops as stenosis becomes more severe
H Prominent S4
H Harsh, rasping, mid- to late-peaking systolic murmur

thats best heard at the base and commonly radiates


to carotids and apex (see Identifying the murmur
of aortic stenosis)

Test results
Imaging
H Chest X-ray shows valvular calcification, left ventricular enlargement, pulmonary vein congestion and, in
later stages, left atrial, pulmonary artery, right atrial,
and right ventricular enlargement.
H Echocardiography shows decreased valve area, increased gradient, and increased left ventricular wall
thickness.
Diagnostic procedures
H Cardiac catheterization shows increased pressure
gradient across the aortic valve, increased left ventricular pressures, and presence of coronary artery
disease.
H Electrocardiography may show left ventricular hypertrophy, atrial fibrillation, or other arrhythmia.

Treatment
General
H Periodic noninvasive evaluation of the severity of

valve narrowing

Assessment
History
H May be asymptomatic
H Dyspnea on exertion
H Angina
H Exertional syncope
H Fatigue
H Palpitations
H Paroxysmal nocturnal dyspnea

76

Aortic stenosis

H Lifelong treatment and management of congenital

aortic stenosis
H Low-sodium, low-fat, low-cholesterol diet
H Planned rest periods

Medications
H Cardiac glycosides such as digoxin
H Antibiotic infective endocarditis prophylaxis
H Anticoagulants, such as warfarin
H Antiplatelets such as clopidogrel and ticlopidine

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ALERT
The use of diuretics and vasodilators may lead to
hypotension and inadequate stroke volume.

Surgery
H In adults, valve replacement after they become symp-

Identifying the murmur of aortic stenosis


A low-pitched, harsh crescendo-decrescendo murmur that
radiates from the aortic valve area to the carotid artery
characterizes aortic stenosis.
SYSTOLE
S1

DIASTOLE
S2

SYSTOLE
S1

S2

tomatic with hemodynamic evidence of severe obstruction


H Percutaneous balloon aortic valvuloplasty
H In children without calcified valves, simple commissurotomy under direct visualization
H Ross procedure in patients younger than age 5

Nursing considerations
Key outcomes
The patient will:
H perform activities of daily living without excess fatigue or exhaustion
H avoid complications
H maintain cardiac output
H demonstrate hemodynamic stability
H maintain balanced fluid status
H maintain joint mobility and range of motion
H develop and demonstrate adequate coping skills.

Nursing interventions
H Give prescribed drugs.
H Maintain a low-sodium diet. Consult with a dietitian.
H If the patient requires bed rest, stress its importance.

Provide a bedside commode.


H Alternate periods of activity and rest.
H Allow the patient to voice concerns about the effects
of activity restrictions.
H Keep the patients legs elevated while he sits in a
chair.
H Place the patient in an upright position, and administer oxygen, as needed.
H Allow the patient to express his fears and concerns.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H periodic rest in the patients daily routine
H leg elevation whenever the patient sits
H dietary and fluid restrictions
H importance of consistent follow-up care
H signs and symptoms of heart failure
H infective endocarditis prophylaxis
H pulse rate and rhythm
H monitoring for atrial fibrillation and other arrhythmias.

Discharge planning
H Refer the patient to a weight-reduction program, if

indicated.
H Refer the patient to a smoking-cessation program, if

indicated.

Monitoring
H Vital signs
H Intake and output
H Signs and symptoms of heart failure
H Signs and symptoms of progressive aortic stenosis
H Daily weight
H Arrhythmias
H Respiratory status
H Prothrombin time and International Normalized

Ratio
If the patient has surgery
H Signs and symptoms of thrombus formation
H Hemodynamics
H Arterial blood gas results
H Blood chemistry results
H Chest X-ray results

Aortic stenosis

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Appendicitis
Overview
Description
H Inflammation of the vermiform appendix
H Most common major abdominal surgical disease
H Fatal if left untreated; gangrene and perforation de-

velop within 36 hours

Pathophysiology
H Mucosal ulceration triggers inflammation, which

temporarily obstructs the appendix.


H Obstruction causes mucus outflow, increasing pres-

sure in the distended appendix; the appendix then


contracts.
H Bacteria multiply and inflammation and pressure increase, restricting blood flow and causing thrombus
and abdominal pain.

Causes
H Foreign body
H Neoplasm
H Mucosal ulceration
H Fecal mass
H Stricture
H Barium ingestion
H Viral infection

Risk factors

H Anorexia
H Nausea, vomiting

Physical findings
H Low-grade fever, tachycardia
H Adjusts posture to decrease pain
H Guarding
H Normoactive bowel sounds, with possible constipa-

tion or diarrhea
H Rebound tenderness and spasm of the abdominal

muscles
H Rovsings sign (pain in right lower quadrant that oc-

curs with palpation of left lower quadrant)


H Psoas sign (abdominal pain that occurs when the pa-

tient flexes his hip with pressure applied to his knee)


H Obturator sign (abdominal pain that occurs when the

hip is rotated)
H Absent abdominal tenderness or flank tenderness

with retrocele or pelvic appendix

Test results
Laboratory
H White blood cell count is moderately elevated, with
an increased numbers of immature cells.
Imaging
H Abdominal or transvaginal ultrasound shows appendiceal inflammation.
H Barium enema reveals nonfilling appendix.
H Abdominal computed tomography scan demonstrates
suspected perforation or abscess.

H Adolescent male

Treatment

Incidence

General

H Can occur at any age; however, the majority of cases

H Delaying surgery until antibiotic therapy has been ini-

occur between ages 11 and 20


H Affects both sexes; however, between puberty and age
25, more prevalent in men

H Nothing by mouth until after surgery, then gradual re-

Common characteristics

H Early postoperative ambulation


H Incentive spirometry

H Abdominal pain
H Anorexia
H Vomiting

Medications

Complications
H Wound infection
H Intra-abdominal infection
H Fecal fistula
H Intestinal obstruction
H Incisional hernia
H Peritonitis (most common)
H Death

Assessment
History
H Abdominal pain thats initially generalized, then lo-

calizes in the right lower abdomen (McBurneys


point)

78

Appendicitis

tiated, if an abscess suspected


turn to regular diet

H I.V. fluids
H Analgesics
H Antibiotics preoperatively and if peritonitis develops

Surgery
H Appendectomy

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H avoid complications
H exhibit no signs of infection
H maintain calorie requirement
H maintain normal fluid volume.

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Nursing interventions
H Maintain nothing-by-mouth status until surgery is

performed.
H Administer I.V. fluids
H Avoid administering analgesics until the diagnosis is

confirmed.
H Avoid administering cathartics or enemas that may

rupture the appendix.


H Place the patient in Fowlers position to decrease

pain.
H Give prescribed drugs.

ALERT
Never apply heat to the right lower abdomen; this
can cause the appendix to rupture.

Monitoring
After surgery
H Vital signs
H Intake and output
H Pain control
H Bowel sounds, passing of flatus, or bowel movements
H Wound healing

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative teaching
H possible complications
H appropriate wound care
H medication administration, dosage, and possible
adverse reactions
H postoperative activity limitations.

Appendicitis

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Arterial occlusive
disease
Overview
Description
H An obstruction or narrowing of the lumen of the aor-

ta and its major branches


H May affect arteries, including the carotid, vertebral,

innominate, subclavian, femoral, iliac, renal, mesenteric, and celiac


H Prognosis dependent on location of the occlusion
and development of collateral circulation that counteracts reduced blood flow

Pathophysiology
H Narrowing of vessel leads to interrupted blood flow,

usually to the legs and feet.


H During times of increased activity or exercise, blood

flow to surrounding muscles cant meet the metabolic demand.


H This results in pain in affected areas.

Causes
H Atherosclerosis
H Immune arteritis
H Embolism
H Thrombosis
H Thromboangiitis obliterans
H Raynauds disease
H Fibromuscular disease
H Atheromatous debris (plaques)
H Indwelling arterial catheter
H Direct blunt or penetrating trauma

Risk factors
H Smoking
H Hypertension
H Dyslipidemia
H Diabetes mellitus
H Advanced age

Incidence
H More common in males than in females
H Usually occurs in people older than age 50
H Higher incidence in patients with diabetes
H Arteries in the legs more commonly affected

Common characteristics
H Intermittent claudication
H Decreased temperature in arms and legs
H Numbness or paresthesia

Complications
H Severe ischemia
H Skin ulceration
H Gangrene
H Limb loss

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Arterial occlusive disease

Assessment
History
H One or more risk factors
H Family history of vascular disease
H Intermittent claudication
H Rest pain
H Poor healing wounds or ulcers
H Impotence
H Dizziness or near syncope
H Transient ischemic attack symptoms

Physical findings
H Trophic changes of involved arm or leg
H Diminished or absent pulses in arm or leg
H Presence of ischemic ulcers
H Pallor with elevation of arm or leg
H Dependent rubor
H Arterial bruit
H Hypertension
H Pain
H Pulselessness distal to the occlusion
H Paralysis and paresthesia occurring in the affected

arm or leg
H Cool extremities

Test results
Imaging
H Arteriography shows type, location, and degree of
obstruction, and the establishment of collateral circulation.
H Ultrasonography and plethysmography show decreased blood flow distal to the occlusion.
H Doppler ultrasonography shows a relatively
low-pitched sound and a monophasic waveform.
H EEG and computed tomography scan may show the
presence of brain lesions.
Other
H Segmental limb pressures and pulse volume measurements show the location and extent of the occlusion.
H Ophthalmodynamometry shows the degree of obstruction in the internal carotid artery.
H Electrocardiography may show presence of cardiovascular disease.

Treatment
General
H Smoking cessation
H Hypertension, diabetes, and dyslipidemia control
H Foot and leg care
H Weight control
H Low-fat, low-cholesterol, high-fiber diet
H Regular walking program

Medications
H Antiplatelets, such as clopidogrel and ticlopidine
H Lipid-lowering agents

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H Hypoglycemics
H Antihypertensives
H Thrombolytics, such as alteplase and streptokinase
H Anticoagulants, such as warfarin and heparin
H Niacin or vitamin B complex

Surgery
H Embolectomy
H Endarterectomy
H Atherectomy
H Laser angioplasty
H Endovascular stent placement
H Percutaneous transluminal angioplasty
H Laser surgery
H Patch grafting
H Bypass graft
H Lumbar sympathectomy
H Amputation
H Bowel resection

Nursing considerations
Key outcomes
The patient will:
H report increased comfort and decreased pain
H maintain palpable pulses and collateral circulation
H maintain skin integrity
H maintain joint mobility and range of motion
H develop no signs or symptoms of infection.

Nursing interventions
For chronic arterial occlusive disease
H Use preventive measures, such as minimal pressure
mattresses, heel protectors, a foot cradle, or a footboard.
H Avoid using restrictive clothing such as antiembolism
stockings.
H Give prescribed drugs.
H Allow the patient to express fears and concerns.
For preoperative care during an acute episode
H Assess the patients circulatory status.
H Give prescribed analgesics.
H Give prescribed heparin or thrombolytics.
H Wrap the patients affected foot in soft cotton batting,
and reposition it frequently to prevent pressure on
any one area.
H Strictly avoid elevating or applying heat to the affected leg.
For postoperative care
H Watch the patient closely for signs of hemorrhage.
H In mesenteric artery occlusion, connect a nasogastric
tube to low intermittent suction.
H Give prescribed analgesics.
H Assist with early ambulation, but dont allow the patient to sit for an extended period.
H If amputation has occurred, check the stump carefully for drainage, and note and record its color and
amount and the time.
H Elevate the stump as ordered.

Monitoring
H Signs and symptoms of fluid or electrolyte imbalance

or renal failure
H Signs and symptoms of stroke
H Vital signs
H Intake and output
H Distal pulses
H Neurologic status
H Bowel sounds
H Prothrombin time and International Normalized

Ratio

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H dietary restrictions
H regular exercise program
H foot care
H signs and symptoms of graft occlusion
H signs and symptoms of arterial insufficiency and
occlusion
H avoidance of wearing constrictive clothing, crossing
legs, or wearing garters
H risk factor modification
H avoidance of temperature extremes.

Discharge planning
H Refer the patient to a physical and occupational ther-

apist, as indicated.
H Refer the patient to a podiatrist for foot care, as

needed.
H Refer the patient to an endocrinologist for glucose

control, as indicated.
H Refer the patient to a smoking-cessation program,

as indicated.

Arterial occlusive disease

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Arteriovenous
malformations

H Symptoms of intracranial (intracerebral, subarach-

noid, or subdural) hemorrhage, including sudden


severe headache, seizures, confusion, lethargy, and
meningeal irritation
H Hydrocephalus

Overview

Complications

Description

H Aneurysm development and subsequent rupture


H Hemorrhage (intracerebral, subarachnoid, or sub-

H Tangled masses of thin-walled, dilated blood vessels

between arteries and veins that dont connect by capillaries


H Common in the brain, primarily in the posterior portion of the cerebral hemispheres
H Adequate perfusion of brain tissue prevented due to
abnormal channels between arterial and venous system mixing oxygenated and unoxygenated blood
H Range in size from a few millimeters to large malformations extending from the cerebral cortex to the
ventricles
H Commonly more than one arteriovenous malformation (AVM) present

Pathophysiology

dural, depending on the location of the AVM)


H Hydrocephalus

Assessment
History
H Chronic headache
H Seizures
H Change in mental status

Physical findings
H Systolic carotid bruit
H Neurologic deficits

H Typical structural characteristics of the blood vessels

Test results

arent present.
H Vessels of an AVM are very thin. (One or more arteries feed into the AVM, causing it to appear dilated
and torturous.)
H Typically, high-pressured arterial flow moves into the
venous system through the connecting channels to
increase venous pressure, engorging and dilating the
venous structures.
H If the AVM is large enough, the shunting can deprive
the surrounding tissue of adequate blood flow.
H Thin-walled vessels may ooze small amounts of blood
or actually rupture, causing hemorrhage into the
brain or subarachnoid space.

Diagnostic procedures
H Cerebral arteriogram confirms the presence of AVMs
and evaluates blood flow.
H Doppler ultrasonography of cerebrovascular system
indicates abnormal, turbulent blood flow.

Treatment
General
H Support measures, including aneurysm precautions

to prevent possible rupture

Causes

H Nothing by mouth, if scheduled for surgery


H Limited activity
H Quiet atmosphere

H Congenital (hereditary)
H Penetrating injuries such as trauma

Medications

Incidence
H Males and females equally affected
H AVMs possibly familial
H Most AVMs present at birth; however, typically asymp-

tomatic until ages 10 to 20

Common characteristics
H Chronic mild headache and confusion
H Seizures
H Systolic bruit over carotid artery, mastoid process, or

orbit
H Focal neurologic deficits (depending on the location

of the AVM) resulting from compression and diminished perfusion

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Arteriovenous malformations

H I.V. fluid
H Analgesics
H Sedatives
H Stool softener

Surgery
H Block dissection, laser, or ligation to repair the com-

municating channels and remove the feeding vessels


H Embolization or radiation therapy, if surgery isnt

possible, to close the communicating channels and


feeder vessels and thus reduce the blood flow to the
AVM

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Nursing considerations
Key outcomes
The patient will:
H maintain stable vital signs
H maintain stable neurologic status
H express an understanding of the disorder and treatment.

Nursing interventions
H Control hypertension and seizure activity.
H Maintain a quiet atmosphere and provide relaxation

techniques.
H If the AVM has ruptured, work to control elevated in-

tracranial pressure and intracranial hemorrhage.

Monitoring
H Vital signs
H Neurologic status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of reporting signs of intracranial bleeding immediately (sudden severe headache, vision
changes, decreased movement in extremities, change
in level of consciousness).

Discharge planning
H Refer the patient to social service for support ser-

vices if neurologic deficits have occurred due to a


ruptured AVM.

Arteriovenous malformations

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Asbestosis
Overview
Description
H Lung disease characterized by diffuse interstitial pul-

monary fibrosis resulting from prolonged exposure


to airborne asbestos particles
H May develop many years (about 15 to 20) after regular exposure to asbestos ceases
H Pleural plaques and mesotheliomas of the pleura and
the peritoneum formed by exposure
H A form of pneumoconiosis
H Also known as mesothelioma

Pathophysiology
H Inhaled asbestos fibers travel down the airway and

penetrate respiratory bronchioles and alveolar walls.


H Mucus production and goblet cells are stimulated to

protect the airway and aid in expectoration.


H Fibers become encased in a brown, iron-rich, pro-

teinlike sheath, called asbestosis bodies.


H Chronic irritation by the fibers continues, causing

edema of the airways.


H Fibrosis develops in response to the chronic irrita-

tion.

Causes
H Prolonged inhalation of asbestos fibers from indus-

tries, such as mining and milling, construction, fireproofing, and textile


H Production of paints, plastics, and brake and clutch
linings
H Exposure to fibrous dust shaken off workers clothing
H Exposure to fibrous dust or waste piles from nearby
asbestos plants

Incidence

Assessment
History
H Exposure to asbestos fibers
H Exertional or rest dyspnea
H Cough
H Chest pain
H Recurrent respiratory tract infections

Physical findings
H Tachypnea
H Clubbing of the fingers
H Characteristic dry crackles in the lung bases

Test results
Laboratory
H Arterial blood gas (ABG) analysis shows decreased
partial pressures of arterial oxygen and carbon dioxide.
Imaging
H Chest X-rays may show fine, irregular, and linear diffuse infiltrates; a honeycomb or ground-glass appearance to lungs; and pleural thickening and pleural calcification, bilateral obliteration of costophrenic
angles, and an enlarged heart with shaggy border.
Other
H Pulmonary function tests may show decreased vital
capacity, forced vital capacity (FVC), and total lung
capacity; decreased or normal forced expiratory volume in 1 second (FEV1) a normal ratio of FEV1 to
FVC; and reduced diffusing capacity for carbon
monoxide.

Treatment
General
H Controlled coughing and postural drainage with

chest percussion and vibration

H Commonly occurring between ages 40 and 75


H Affects males more commonly than females

H At least 3 qt (3 L) of fluids daily


H High-calorie, high-protein, low-sodium diet
H Activity as tolerated

Common characteristics

Medications

H Exposure to asbestos fibers


H Exertional or rest dyspnea
H Dry cough
H Chest pain
H Recurrent respiratory tract infections

H Inhaled mucolytics such as acetylcysteine


H Supplemental oxygen
H Diuretics, such as furosemide and torsemide
H Cardiac glycosides such as digoxin
H Antibiotics, as appropriate

Complications

Surgery

H Pulmonary fibrosis
H Respiratory failure
H Pulmonary hypertension
H Cor pulmonale

H Lung transplantation, in severe cases

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Asbestosis

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Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain adequate caloric intake
H express understanding of the illness
H identify measures to prevent or reduce fatigue.

Nursing interventions
H Give prescribed drugs and provide oxygen therapy.
H Provide supportive care.
H Provide chest physiotherapy.
H Provide high-calorie, high-protein, low-sodium foods

in small, frequent meals.


H Encourage oral fluid intake.
H Provide frequent rest periods.

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Respiratory status (breath sounds, ABG results)
H Sputum production
H Mentation
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H transtracheal catheter care, if applicable
H prevention of infection
H signs and symptoms of infection
H influenza and pneumococcus immunizations
H home oxygen therapy, if required
H importance of follow-up care
H chest physiotherapy
H high-calorie, high-protein, low-sodium diet
H adequate oral fluid intake
H energy conservation techniques.

Discharge planning
H Refer the patient to a smoking-cessation program, if

indicated.

Asbestosis

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Ascariasis
Overview
Description
H Intestinal infection caused by the parasitic worm As-

caris lumbricoides, a large roundworm resembling


an earthworm
H Never passes directly from person to person
H Also known as roundworm infection

Pathophysiology
H After ingestion, A. lumbricoides ova hatch and re-

lease larvae, which penetrate the intestinal wall and


reach the lungs through the bloodstream.
H After about 10 days in pulmonary capillaries and
alveoli, the larvae migrate to the bronchioles,
bronchi, trachea, and epiglottis.
H From the epiglottis, the larvae are swallowed and
return to the intestine to mature into worms.

Causes
H Ingestion of food, drink, or soil contaminated with

A. lumbricoides ova

Incidence
H Occurs worldwide but most common in tropical ar-

eas with poor sanitation and in Asia, where farmers


use human stool as fertilizer
H In the United States, more prevalent in the South,
particularly among younger children

Common characteristics
H Stomach discomfort
H Vomiting

Test results
Laboratory
H Microscopic studies show ova in the stool, or adult
worm is observed in emesis.
H Complete blood count: shows eosinophilia
Imaging
H Abdominal X-rays show whirlpool pattern of intraluminal worms. (Intestinal obstruction may be noted.)
H Chest X-rays show characteristic bronchovascular
markings infiltrates, patchy areas of pneumonitis,
and widening of hilar shadows (if migrated to lungs).

Treatment
General
H Nasogastric (NG) suctioning (with intestinal obstruc-

tion)
H Nothing by mouth until stable
H Rest as needed

Medications
H I.V. fluids
H Mebendazole and albendazole
H Anthelmintic therapy (pyrantel or piperazine) (avoid

use if intestinal obstruction is present)

ALERT
Piperazine is contraindicated in patients with
seizure disorder and may cause stomach upset,
dizziness, and urticaria. Pyrantel produces red
stool and vomitus and may cause stomach upset,
headache, dizziness, and rash. Albendazole and
mebendazole may cause abdominal pain and diarrhea.

Complications

Surgery

H Intestinal obstruction
H Pneumonitis

H Intestinal surgery to relieve obstruction, if necessary

Assessment
History
H Stomach discomfort or pain
H Nausea and vomiting
H Recent travel to endemic area
H Restlessness
H Disturbed sleep

Physical findings
H Abdominal tenderness
H Dehydration
H Crackles, wheezing, and tachypnea (if migrated to

the lungs)

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Ascariasis

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid balance
H regain normal intestinal function
H express understanding of proper sanitation of food
and hands.

Nursing interventions
H Isolation is unnecessary; proper disposal of stool and

soiled linen, using standard precautions, should be


adequate.
H If the patient is receiving NG suctioning, provide
good mouth care.

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Monitoring
H Vital signs
H Intake and output
H Appearance of stools (for worms)

Patient teaching
Be sure to cover:
H proper hand washing, especially before eating and
after defecating
H bathing and changing underwear and bed linens
daily
H adverse effects of medications prescribed for the
patient.

Discharge planning
H Refer the patient to social services if living conditions

are questionable regarding cleanliness.

Ascariasis

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Life-threatening disorder

Aspergillosis

H Organ transplants
H TB or another cavitary lung disease (in asper-

gilloma)

Incidence
H Aspergillus: found worldwide, commonly in ferment-

Overview
Description
H An opportunistic, sometimes life-threatening infec-

tion, growth, or allergic response caused by fungi of


the genus Aspergillus, usually A. fumigatus, A.
flavus, or A. niger, occurring in:
Aspergilloma: produces a fungus ball in the lungs
(called a mycetoma)
Allergic aspergillosis: a hypersensitive asthmatic
reaction to Aspergillus antigens
Aspergillosis endophthalmitis: an infection of the
anterior and posterior chambers of the eye that
can lead to blindness
Invasive aspergillosis: an acute infection that produces septicemia, thrombosis, and infarction of
virtually any organ, especially the heart, lungs,
brain, and kidneys
H Variable prognosis according to each form (aspergilloma possibly causing fatal hemoptysis)

Pathophysiology
H Conidia (asexual spores) travel into the alveoli via in-

halation or, in aspergillosis endophthalmitis, through


a wound or other tissue injury.
H Pulmonary macrophages may be able to kill the conidia.
H The alternative complement pathway is activated, resulting in recruitment of neutrophils and monocytes.
H The disease may be accompanied by hyphal invasion
of the blood vessels in the involved tissues.
H In aspergilloma, colonization of the bronchial tree
with Aspergillus produces plugs and atelectasis and
forms a tangled ball of hyphae (fungal filaments),
fibrin, and exudate in a cavity left by a previous illness such as tuberculosis (TB).

Causes
H Contact with Aspergillus, commonly found growing

on dry leaves, stored grain, compost piles, or decaying vegetation

Risk factors
H Excessive or prolonged use of antibiotics, glucocorti-

coids, or other immunosuppressants


H Radiation therapy
H Acquired immunodeficiency syndrome
H Hodgkins disease
H Leukemia
H Azotemia
H Alcoholism
H Sarcoidosis
H Bronchitis and bronchiectasis

88

Aspergillosis

ing compost piles and damp hay

Common characteristics
Aspergilloma
H May produce no symptoms
H Mimics TB, causing a productive cough and purulent
or blood-tinged sputum, dyspnea, empyema, and
lung abscesses
Allergic aspergillosis
H Wheezing
H Dyspnea
H Cough with some sputum production
H Pleural pain
H Fever
Aspergillosis endophthalmitis
H Usually appears 2 to 3 weeks after an eye injury or
surgery
H Clouded vision
H Eye pain
H Reddened conjunctivae
Invasive aspergillosis
H Thrombosis
H Infarctions
H Sepsis

Complications
H Infection of the ear (otomycosis), cornea (mycotic

keratitis), or prosthetic heart valve (endocarditis)


H Pneumonia (especially in those receiving an im-

munosuppressant such as an antineoplastic drug or


high-dose steroid therapy)
H Sinusitis
H Brain abscesses
H Life-threatening hemoptysis
H Septicemia

Assessment
History
Aspergilloma and allergic aspergillosis
H Immunosuppression
H Dyspnea
H Cough with sputum production
Aspergillosis endophthalmitis
H Eye pain
H Vision changes
H Recent eye injury or surgery
Invasive aspergillosis
H History based on infected organ

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Physical findings

Nursing interventions

Aspergilloma and allergic aspergillosis


H Diminished breath sounds
H Adventitious breath sounds
H Cough with sputum production
Aspergillosis endophthalmitis
H Reddened conjunctivae
H Blurred vision
Invasive aspergillosis
H Findings based on infected organ

H Perform chest physiotherapy every 2 hours.


H Encourage coughing and deep breathing every hour.

Test results
Laboratory
ASPERGILLOMA
H Serum is positive for anti-Aspergillus antibodies.
ALLERGIC ASPERGILLOSIS
H Sputum culture reveals hyphae that grow Aspergillus

Monitoring
H Vital signs
H Sputum production, amount, color, and character

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H adverse effects of medications.

and eosinophils.
H Serum is positive for immunoglobulin (Ig) E and IgG

anti-Aspergillus antibodies.
ASPERGILLOSIS ENDOPHTHALMITIS
H Eye culture or exudate shows Aspergillus.

Diagnostic procedures
INVASIVE ASPERGILLOSIS
H Bronchoscopy and open lung biopsy are performed

to obtain a tissue sample that confirms diagnosis.


Imaging
ASPERGILLOMA
H Chest X-ray shows a round to oval mass with a radi-

olucent crescent over the upper portion of the mass


(Monods sign).

Treatment
General
H Supportive therapy

Medications
Allergic aspergillosis
H Desensitization
H Steroids
Aspergillosis endophthalmitis
H Amphotericin B
Invasive aspergillosis
H Antifungal therapy

Surgery
Aspergilloma
H Local excision of the lesion
H Lobectomy

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain stable vital signs
H express understanding of the disorder and treatment.

Aspergillosis

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Life-threatening disorder

Asphyxia
Overview
Description

H Altered respiratory rate


H Little or no air movement
H Intercostal rib retractions
H Pale skin
H Cyanosis in mucous membranes, lips, and nail beds
H Erythema and petechiae on the upper chest (trauma)
H Cherry-red mucous membranes (carbon monoxide

poisoning)
H Decreased or absent breath sounds

H A condition of insufficient oxygen and accumulating

Test results

carbon dioxide in the blood and tissues


H Leads to cardiopulmonary arrest; fatal without
prompt treatment

Laboratory
H Decreased partial pressure of arterial oxygen (less
than 60 mm Hg) and increased partial pressure of
arterial carbon dioxide (more than 50 mm Hg) are
indicated by arterial blood gas (ABG) analysis.
H Toxicology tests show drugs, chemicals, or abnormal
hemoglobin level.
Imaging
H Chest X-rays may detect a foreign body, pulmonary
edema, or atelectasis.
H Pulmonary function tests may indicate respiratory
muscle weakness.
H Bronchoscopy can locate foreign body.

Pathophysiology
H An interference with respiration causes insufficient

oxygen intake and hypoxemia.


H Carbon dioxide accumulates due to the lack of gas

exchange in the lungs.


H This leads to inadequate tissue perfusion and cell

death.

Causes
H Opioid abuse
H Respiratory muscle paralysis
H Airway obstruction
H Aspiration
H Pulmonary edema
H Near drowning
H Tumor
H Strangulation
H Trauma to airway
H Carbon monoxide poisoning
H Smoke inhalation

Incidence
H Can occur at any age

Common characteristics

Treatment
General
H Establish airway and ventilation
H Treat the underlying cause
H Nothing by mouth until able to protect airway
H Activity based on outcome of interventions

Medications
H Oxygen
H Narcan (if caused by opioid abuse)

Surgery
H Tumor removal

H Altered respirations
H Changes in level of consciousness
H Cardiac arrest

Nursing considerations

Complications

Key outcomes

H Neurologic damage
H Death

The patient will:


H maintain a patent airway
H maintain adequate ventilation
H maintain acceptable cardiac output
H demonstrate knowledge of safety measures to prevent
suffocation.

Assessment
History
H Cause of the asphyxia possibly apparent
H Causes of signs and symptoms varying

Physical findings
H Anxiousness or agitation
H Confusion
H Dyspnea
H Prominent neck muscles
H Wheezing and stridor

90

Asphyxia

Nursing interventions
H Perform abdominal thrust, if obstruction is present.
H Maintain patent airway.
H Begin cardiopulmonary resuscitation, if necessary.
H Insert a nasogastric tube or an Ewald tube for lavage

(for opioid abuse).


H Give prescribed drugs.
H Reassure the patient and his family.
H Ensure I.V. access.

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Monitoring
H ABG levels, pulse oximetry
H Respiratory status
H Cardiac status
H Vital signs
H Neurologic status

Patient teaching
Be sure to cover:
H cause of asphyxia (with patient and family members,
discuss measures to prevent recurrence, if appropriate)
H safety measures if the victim is a child.

Discharge planning
H Refer the patient to the proper authorities, if criminal

intent was involved.


H Refer the patient to resource and support services, if

appropriate.

Asphyxia

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Life-threatening disorder

Asthma

H Psychological stress
H Cold air
H Exercise

Incidence
H Can occur at any age; about 50% of all patients with

Overview
Description
H A chronic reactive airway disorder involving episod-

ic, reversible airway obstruction resulting from bronchospasms, increased mucus secretions, and mucosal edema
H Signs and symptoms that range from mild wheezing
and dyspnea to life-threatening respiratory failure
H Signs and symptoms of bronchial airway obstruction
that may persist between acute episodes

Pathophysiology
H Tracheal and bronchial linings overreact to various

stimuli, causing episodic smooth-muscle spasms that


severely constrict the airways.
H Mucosal edema and thickened secretions further
block the airways.
H Immunoglobulin (Ig) E antibodies, attached to
histamine-containing mast cells and receptors on cell
membranes, initiate intrinsic asthma attacks.
H When exposed to an antigen such as pollen, the IgE
antibody combines with the antigen. On subsequent
exposure to the antigen, mast cells degranulate and
release mediators.
H The mediators cause the bronchoconstriction and
edema of an asthma attack.
H During an asthma attack, expiratory airflow decreases, trapping gas in the airways causing alveolar hyperinflation.
H Atelectasis may develop in some lung regions.
H The increased airway resistance initiates labored
breathing.

Causes
H Sensitivity to specific external allergens or from in-

ternal, nonallergenic factors


Extrinsic causes
H Pollen
H Animal dander
H House dust or mold
H Kapok or feather pillows
H Food additives containing sulfites and any other sensitizing substance
Intrinsic causes
H Emotional stress
H Genetic factors
Bronchoconstriction
H Hereditary predisposition
H Sensitivity to allergens or irritants such as pollutants
H Viral infections
H Drugs, such as aspirin, beta-adrenergic blockers,
and nonsteroidal anti-inflammatory drugs
H Tartrazine

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Asthma

asthma are younger than age 10; affects twice as


many boys as girls
H In about one-third of patients, onset between ages 10
and 30
H In about one-third of patients, two or more patients
in same immediate family
H Coexistence of intrinsic and extrinsic causes in many
patients

Common characteristics
H Wheezing
H Shortness of breath, feelings of suffocation
H Tightness in chest
H Extrinsic asthma in children; commonly accompa-

nied by other manifestations of atopy

Complications
H Status asthmaticus
H Respiratory failure
H Death

Assessment
History
H Often preceded by severe respiratory tract infections,

especially in adults
H Irritants, emotional stress, fatigue, endocrine

changes, temperature and humidity variations, and


exposure to noxious fumes possibly aggravating intrinsic asthma attacks
H An asthma attack possibly beginning dramatically,
with simultaneous onset of severe, multiple symptoms, or insidiously, with gradually increasing respiratory distress
H Exposure to a particular allergen then followed by a
sudden onset of dyspnea and wheezing and by tightness in the chest also accompanied by a cough that
produces thick, clear, or yellow sputum

Physical findings
H Visibly dyspneic
H Ability to speak only a few words before pausing for

breath
H Use of accessory respiratory muscles
H Diaphoresis
H Increased anteroposterior thoracic diameter
H Hyperresonance
H Tachycardia; tachypnea; mild systolic hypertension
H Inspiratory and expiratory wheezes
H Prolonged expiratory phase of respiration
H Diminished breath sounds
H Cyanosis, confusion, and lethargy indicating the onset

of life-threatening status asthmaticus and respiratory


failure

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Test results
Laboratory
H Arterial blood gas (ABG) analysis reveals hypoxemia.
H Serum IgE levels are increased due to an allergic reaction.
H Complete blood count with differential shows increased eosinophil count.
Imaging
H Chest X-rays may show hyperinflation with areas of
focal atelectasis.
Diagnostic procedures
H Pulmonary function tests (PFTs) may show decreased
peak flows and forced expiratory volume in 1 second, low-normal or decreased vital capacity, and increased total lung and residual capacities.
H Skin testing may identify specific allergens.
H Bronchial challenge testing shows the clinical significance of allergens identified by skin testing.
Other
H Pulse oximetry measurements may show decreased
oxygen saturation.

H use effective coping strategies


H report feelings of comfort
H maintain skin integrity.

Nursing interventions
H Give prescribed drugs.
H Place the patient in high Fowlers position.
H Encourage pursed-lip and diaphragmatic breathing.
H Administer prescribed humidified oxygen.
H Adjust oxygen according to the patients vital signs

and ABG values.


H Assist with intubation and mechanical ventilation, if

appropriate.
H Perform postural drainage and chest percussion, if

tolerated.
H Suction an intubated patient, as needed.
H Treat the patients dehydration with I.V. or oral fluids

as tolerated.
H Anticipate bronchoscopy or bronchial lavage.
H Keep the room temperature comfortable.
H Advise the patient to use an air conditioner or a fan

in hot, humid weather.

Treatment
General
H Identification and avoidance of precipitating factors
H Desensitization to specific antigens
H Establishment and maintenance of patent airway
H Fluid replacement
H Activity as tolerated

Medications
H Bronchodilators, such as albuterol, pirbuterol, sal-

Monitoring
H Vital signs
H Intake and output
H Response to treatment
H Signs and symptoms of theophylline toxicity
H Breath sounds
H ABG results
H PFT results
H Pulse oximetry
H Complications of corticosteroids
H Level of anxiety

meterol, and theophylline


H Corticosteroids
H Histamine antagonists, such as cetirizine and diphen-

hydramine
H Leukotriene antagonists, such as montelukast, zafirlukast, and zileuton
H Anti-inflammatories, such as cromolyn and nedocromil
H Low-flow oxygen
H Antibiotics, as appropriate

ALERT
The patient with increasingly severe asthma that
doesnt respond to drug therapy is usually admitted
for treatment with corticosteroids, epinephrine,
and sympathomimetic aerosol sprays. He may require endotracheal intubation and mechanical
ventilation.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H avoidance of known allergens and irritants
H metered-dose inhaler or dry powder inhaler use
H pursed-lip and diaphragmatic breathing
H use of peak flow meter
H effective coughing techniques
H maintaining adequate hydration.

Discharge planning
H Refer the patient to a local asthma support group.

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain a patent airway

Asthma

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Atelectasis
Overview
Description
H Incomplete expansion of alveolar clusters or lung

segments leading to partial or complete lung collapse


H May be chronic or acute
H Good prognosis with prompt removal of any airway

obstruction, relief of hypoxia, and re-expansion of


the collapsed lung

Pathophysiology
H Due to incomplete expansion, certain regions of the

lung are removed from gas exchange.


H Unoxygenated blood passes unchanged through these

regions and produces hypoxia.


H Alveolar surfactant causes increased surface tension,

permitting complete alveolar deflation.

Causes
H Bronchial occlusion
H Bronchiectasis
H Cystic fibrosis
H Bed rest in a supine position
H General anesthesia
H Pleural effusion
H Pulmonary embolism
H Sarcoidosis
H Bronchogenic carcinoma
H Inflammatory lung disease
H Idiopathic respiratory distress syndrome of the

neonate
H Oxygen toxicity
H Pulmonary edema
H External compression

Incidence

Assessment
History
H Recent abdominal or other major surgery
H Prolonged immobility
H Mechanical ventilation
H CNS depression
H Smoking
H COPD
H Rib fractures, tight chest dressings

Physical findings
H Decreased chest wall movement
H Cyanosis
H Diaphoresis
H Substernal or intercostal retractions
H Anxiety
H Decreased fremitus
H Mediastinal shift to the affected side
H Dullness or flatness over lung fields
H End-inspiration crackles
H Decreased (or absent) breath sounds
H Tachycardia

Test results
Laboratory
H Arterial blood gas analysis shows hypoxia.
Imaging
H Chest X-rays show characteristic horizontal lines in
the lower lung zones and characteristic dense shadows.
Diagnostic procedures
H Bronchoscopy may show an obstructing neoplasm,
foreign body, or pneumonia.
H Pulse oximetry shows decreased oxygen saturation.

Treatment

H Common in patients after upper abdominal or tho-

General

racic surgery
H More common in patients with prolonged immobility,
on mechanical ventilation, or with central nervous
system (CNS) depression
H Increased predisposition in patients who smoke and
those with chronic obstructive pulmonary disease
(COPD)

H Incentive spirometry
H Chest percussion
H Postural drainage
H Frequent coughing and deep-breathing exercises
H Bronchoscopy if above measures fail
H Humidity
H Intermittent positive-pressure breathing therapy
H Radiation possibly required for obstructing neoplasm
H Diet based on patients condition as tolerated
H Increased fluids
H Activity as tolerated; discourage bed rest

Common characteristics
H Shortness of breath
H Chest pain
H Anxiety

Complications
H Hypoxemia
H Acute respiratory failure
H Pneumonia

Medications
H Bronchodilators, such as albuterol, pirbuterol, and

salmeterol
H Analgesics after surgery

Surgery
H May be required if obstructing neoplasm present

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Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate ventilation
H report feelings of increased comfort
H use support systems to assist with anxiety and fear.

Nursing interventions
H Give prescribed drugs and provide oxygen therapy.
H Encourage coughing and deep breathing.
H Reposition the patient often.
H Encourage and assist with ambulation as soon as

possible.
H Help the patient use an incentive spirometer.
H Humidify inspired air.
H Encourage adequate fluid intake.
H Loosen secretions with postural drainage and chest

percussion.
H Provide suctioning, as needed.
H Offer the patient reassurance and emotional support.

Monitoring
H Vital signs
H Intake and output
H Pulse oximetry
H Respiratory status (breath sounds, arterial blood gas

results)

Patient teaching
Be sure to cover:
H use of incentive spirometer
H postural drainage and percussion
H coughing and deep-breathing exercises
H importance of splinting incisions
H energy-conservation techniques
H stress-reduction strategies
H importance of mobilization.

Discharge planning
H Refer the patient to a smoking-cessation program, if

indicated.
H Refer the patient to a weight-reduction program, if

indicated.

Atelectasis

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Atopic dermatitis
Overview
Description
H A chronic skin disorder characterized by superficial

skin inflammation and intense itching

Pathophysiology
H The allergic mechanism of hypersensitivity results in

a release of inflammatory mediators through sensitized antibodies of the immunoglobulin (Ig) E class.
H Histamine and other cytokines induce acute inflammation.
H Abnormally dry skin and a decreased threshold for
itching set up the itch-scratch-itch cycle, which
eventually causes lesions (excoriations, lichenification).

Causes

Incidence
H May appear at any age but typically begins during in-

fancy or early childhood (may then subside spontaneously, followed by exacerbations in late childhood,
adolescence, or early adulthood)
H Affects less than 1% of the population

Common characteristics
H Erythematous, weeping lesions, usually located in ar-

eas of flexion and extension, such as the neck, antecubital fossa, popliteal folds, and behind the ears
In children with atopic dermatitis
H Pink pigmentation and swelling of the upper eyelid
and a double fold under the lower lid (Morgans line
or Dennies sign)

Complications
H Scarring
H Severe viral infections
H Bacterial and fungal skin infections
H Ocular disorders
H Allergic contact dermatitis

H The exact etiology of atopic dermatitis unknown;

however, genetic predisposition likely


H Possible contributing factors:

Food allergy
Infection
Chemical irritants
Extremes of temperature and humidity
Psychological stress or strong emotions

Special populations
About 10% of juvenile cases of atopic dermatitis
are caused by allergic reactions to certain foods,
especially eggs, peanuts, milk, and wheat.

Assessment
History
H Atopy, such as asthma, hay fever, or urticaria (or

similar family history)(see Factors contributing to


atopy)
H Exposure to allergen
H Pruritus

Physical findings
H Erythematous, weeping lesions (see Signs of atopic

dermatitis)
H Pink pigmentation and swelling of the upper eyelid

and a double fold under the lower lid

Factors contributing to atopy


H Changes associated with industrialization, such as
exposure to new chemicals like diesel fumes, have
proven to increase the antigenicity of common pollens.
H Increased exposure to antigens, such as dust mites (in
wall-to-wall carpets), especially at an early age,
contributes to a predisposition to developing allergies.
H Dietary changes, such as increased fat intake and an
earlier weaning from human breast milk, may be
contributing factors.
H Vaccination may cause a shift in T-cell function away
from the normal helper T cell (Th1) response to the
Th2 allergic response by limiting early bacterial and
viral infections.
H Lack of exposure to intestinal parasites may contribute
to a similar shift in T-cell functioning.
H Frequent use of antibiotics, especially in early
childhood, may decrease normal intestinal flora and
further contribute to the shift.

Test results
Laboratory
H Complete blood count shows eosinophilia.
H Serum IgE levels are elevated.
Other
H Skin testing shows specific allergen.

Treatment
General
H Meticulous skin care
H Environmental control of offending allergens
H Nonirritating topical lubricants

Medications
H Corticosteroids
H Antipruritics such as hydroxyzine
H Antihistamines, such as diphenhydramine and fexofe-

nadine
H Antibiotics if secondary infection develops

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Nursing considerations
Key outcomes
The patient will:
H express relief from itching and pain
H demonstrate improved skin condition
H remain free from infection.

Nursing interventions
H Offer support to help the patient and his family cope

with this chronic disorder.


H Dissuade the patient from scratching during urticaria

Signs of atopic dermatitis


This illustration shows the typical lesions involved in
atopic dermatitis.

Edema, crusting,
and scaling

Erythematous
areas on dry
skin

to help prevent infection.


H Apply prescribed topical medications.
H Give prescribed drugs.

Monitoring
H Compliance with drug therapy
H Treatment of lesions
H Nutritional status

Patient teaching
Be sure to cover:
H when and how to apply topical corticosteroids
H importance of regular personal hygiene using only
water with little soap
H signs and symptoms of secondary infection
H avoidance of laundry additives, such as fragrances
and dyes
H avoidance of allergens.

Atopic dermatitis

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Complications

Atrial fibrillation

H Transient ischemic attack


H Stroke
H Heart failure
H Thromboembolism

Overview
Description
H Rhythm disturbance of the atria
H Characterized by an irregularly irregular cardiac rate

and rhythm (see Recognizing atrial fibrillation)

Pathophysiology
H Rapid discharges from numerous ectopic foci in the

atria occur.
H This leads to erratic and uncoordinated atrial

rhythm.

Assessment
History
H Palpitations
H Fatigue
H Dyspnea
H Chest pain
H Syncope

Physical findings

Causes
H Hypertension
H Myocardial infarction (MI)
H Pulmonary embolism
H Heart failure
H Cardiomyopathy
H Hypersympathetic state associated with acute alcohol

ingestion
H Pericarditis
H Hyperthyroidism
H Valvular disease
H Cardiothoracic surgery
H Atrial fibrosis

Incidence
H Seen more commonly in patients older than age 70
H Males affected more than females

Common characteristics
H Cardiac rhythm: irregularly irregular

H Irregular pulse
H Possible tachycardia
H Hypotension
H Signs of heart failure
H Respiratory distress

Test results
Laboratory
H Cardiac enzymes show myocardial damage (with MI).
H Thyroid function studies reveal hyperthyroidism.
H Complete blood count checks for anemia, if the patient has a history of recent blood loss.
Imaging
H Chest X-ray may determine if pulmonary edema is
present.
H Echocardiogram or transesophageal echocardiography may help identify valvular disease, left ventricular
dysfunction, or atrial clots.
Diagnostic procedures
H Electrocardiography may indicate irregular rhythm.
H Holter monitor may diagnose paroxysmal atrial fibrillation.

Recognizing atrial fibrillation


The following rhythm strip shows atrial fibrillation.

H Rhythm: Irregular
H Rate: Atrial indiscernible;
ventricular 130 beats/minute

98

Atrial fibrillation

H P wave: Absent; replaced by fine


fibrillatory waves
H PR interval: Indiscernible
H QRS complex: 0.08 second

H T wave: Indiscernible
H QT interval: Unmeasurable
H Other: None

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Treatment
General

Discharge planning
H Refer the patient to programs such as Coumadin

Clinic to monitor anticoagulant therapy.

H Possible electrical cardioversion


H Atrial fibrillation suppression pacemaker
H Ablation
H Surgical maze procedure
H Low-fat, low-sodium diet
H Fluid restriction, if indicated
H Planned rest periods, as needed

Medications
H Calcium channel blockers, such as cardizem and am-

lodipine
H Beta-adrenergic blockers, such as metoprolol and

atenolol
H Antiarrhythmics, such as amiodarone, propafenone,

and sotalol
H Cardiac glycosides such as digoxin
H Anticoagulants such as warfarin

Nursing considerations
Key outcomes
The patient will:
H report ways to reduce activity intolerance
H identify effective coping mechanisms to manage
anxiety
H discuss the causes of fatigue
H verbalize understanding of medication regimen.

Nursing interventions
H Give prescribed drugs.
H Encourage the patient and his family to talk about

feelings and concerns.


H Plan rest periods.

Monitoring
H Vital signs at rest and after physical activity
H Signs and symptoms of embolism
H Intake and output
H Daily weight
H Abnormal bleeding
H Prothrombin time and International Normalized

Ratio

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H instructions on how to monitor pulse
H anticoagulation precautions
H abnormal bleeding
H signs and symptoms of embolic events.

Atrial fibrillation

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Atrial septal defect


Overview
Description
H An acyanotic congenital heart defect featuring an

opening between the left and right atria that allows


blood to flow from left to right, resulting in ineffective pumping of the heart, thus increasing the risk of
heart failure
H Three types:
Ostium secundum defect, the most common type:
occurs in the region of the fossa ovalis and, occasionally, extends inferiorly, close to the vena cava
Sinus venosus defect: occurs in the superiorposterior portion of the atrial septum, sometimes
extending into the vena cava, and almost always
associated with abnormal drainage of pulmonary
veins into the right atrium
Ostium primum defect: occurs in the inferior portion of the septum primum and usually associated
with atrioventricular valve abnormalities (cleft mitral valve) and conduction defects

Pathophysiology
H Blood shunts from the left atrium to the right atrium

because the left atrial pressure is normally slightly


higher than the right atrial pressure.
H This pressure difference forces large amounts of
blood through a defect.
H This shunt results in right heart volume overload,
affecting the right atrium, right ventricle, and pulmonary arteries.
H Eventually, the right atrium enlarges, and the right
ventricle dilates to accommodate the increased blood
volume.
H If pulmonary artery hypertension develops, increased
pulmonary vascular resistance and right ventricular
hypertrophy follow.
H Irreversible pulmonary artery hypertension causes
reversal of the shunt direction in some adults, which
results in unoxygenated blood entering the systemic
circulation, causing cyanosis.

Causes
H No known cause
H Ostium primum defects commonly occurring in

patients with Down syndrome

Common characteristics
H Fatigue after exertion
H Early to midsystolic murmur at the second or third

left intercostal space


H Low-pitched diastolic murmur at the left lower ster-

nal border; more pronounced on inspiration


H Fixed, widely split S2
H Systolic click or late systolic murmur at the apex
H Clubbing and cyanosis, if a right-to-left shunt

develops

ALERT
An infant may be cyanotic because he has a cardiac or pulmonary disorder. Cyanosis that worsens
with crying most likely has a cardiac cause because
crying increases pulmonary resistance to blood
flow, resulting in an increased right-to-left shunt.
Cyanosis that improves with crying most likely has
a pulmonary cause because deep breathing improves tidal volume.

Complications
H Physical underdevelopment
H Respiratory infections
H Heart failure
H Atrial arrhythmias
H Mitral valve prolapse

Assessment
History
H Increasing fatigue
H Chest pain
H Dyspnea
H Coughing
H Dizziness or syncope

Physical findings
H Early to midsystolic murmur at the second or third

left intercostal space


H Low-pitched diastolic murmur at the left lower ster-

nal border, more pronounced on inspiration


H Fixed, widely split S2
H Systolic click or late systolic murmur at the apex
H Peripheral edema
H Cyanosis
H Distended jugular veins

Incidence

Test results

H Accounts for about 10% of congenital heart defects


H Appears almost twice as often in females than in

Imaging
H Chest X-ray shows an enlarged right atrium and right
ventricle, a prominent pulmonary artery, and increased pulmonary vascular markings.
Diagnostic procedures
H Electrocardiography results may be normal, but
commonly show right axis deviation, a prolonged
PR interval, varying degrees of right bundle-branch

males, with a strong familial tendency


H Usually benign defect during infancy and childhood

(Delayed development of symptoms and complications makes it one of the most common congenital
heart defects diagnosed in adults.)

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block, right ventricular hypertrophy, atrial fibrillation


(particularly in severe cases in patients older than
age 30) and, in ostium primum defect, left axis deviation.
H Echocardiography measures right ventricular enlargement, may locate the defect, and shows volume
overload in the right side of the heart. It may reveal
right ventricular and pulmonary artery dilation.
H Two-dimensional echocardiography with color
Doppler flow, contrast echocardiography, or both has
supplanted cardiac catheterization as the confirming
test for atrial septal defects (ASDs). Cardiac catheterization is used if inconsistencies exist in the clinical
data or if significant pulmonary hypertension is suspected.

Patient teaching
Be sure to cover:
H pretest and posttest procedures to the child and his
parents (If possible, use drawings or other visual
aids to explain it to the child.)
H postoperative procedures, tubes, dressings, and
monitoring equipment
H antibiotic prophylaxis to prevent infective endocarditis.

Treatment
General
H Activity as tolerated
H Low-fat, low-cholesterol diet

Medications
H Diuretics, such as furosemide and torsemide
H Antibiotics, as appropriate
H Analgesics

Surgery
H Minimally invasive heart surgery may be required for

the patient with an uncomplicated ASD with evidence


of significant left-to-right shunting.
H A large defect may need immediate surgical closure
with sutures or a patch graft.
H Cardiac catheterization closure the insertion of an
umbrella-like patch or septal occluder through a
cardiac catheter may be performed.

Nursing considerations
Key outcomes
The patient will:
H maintain an optimal cardiac output
H maintain hemodynamic stability
H experience no cardiac arrhythmias.

Nursing interventions
H Encourage the child to engage in any activity he can

tolerate.
H Give prescribed drugs.

Monitoring
H Vital signs
H Central venous and intra-arterial pressures
H Intake and output
H Cardiac rhythm
H Oxygenation

Atrial septal defect

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Attention deficit
hyperactivity disorder
Overview
Description
H A behavioral problem characterized by difficulty with

inattention, impulsivity, hyperactivity, and boredom


H Also called ADHD and ADD

Pathophysiology
H Alleles of dopamine genes may alter dopamine, sero-

tonin, and adrenalin transmission in the neural networks.


H During fetal development, bouts of hypoxia and hypotension could selectively damage neurons located
in some of the critical regions of the anatomical networks.

Causes
H Underlying cause unknown
H Limited evidence of a genetic component
H May result from altered neurotransmitter levels in the

brain

Risk factors
H Family history
H History of learning disability
H Mood or conduct disorder

Incidence
H Present at birth, but diagnosis before age 4 or 5 is

difficult; some patients undiagnosed until adulthood


H Occurs in 3% to 5% of school-age children
H Affects males three times more than females

Common characteristics
H Impulsive behavior
H Inattentiveness
H Disorganization in school
H Tendency to jump quickly from one partly completed

project, thought, or task to another


H Difficulty meeting deadlines and keeping track of

school or work tools and materials

Complications
H Emotional and social complications
H Poor nutrition

Assessment
History
H Characterized as a fidgeter and a daydreamer
H Appears inattentive and lazy
H Performs sporadically at school or work

102

Attention deficit hyperactivity disorder

Physical findings
Symptoms of inattention
H Makes careless mistakes
H Struggles to sustain attention
H Fails to finish activities
H Difficulty with organization
H Avoids tasks that require sustained mental effort
H Distracted or forgetful
Symptoms of hyperactivity
H Fidgets
H Cant sit still for sustained period
H Difficulty playing quietly
H Talks excessively
Symptoms of impulsivity
H Interrupts
H Cant wait patiently

DSM-IV-TR criteria
These criteria confirm a diagnosis:
H six symptoms or more from the inattention or hyperactivity-impulsivity categories
H symptoms present for at least 6 months
H symptoms evident before age 7
H impairment present in two or more settings
H symptoms arent accounted for by another mental
disorder.

Test results
H Complete psychological, medical, and neurologic

evaluations rule out other problems; specific tests include continuous performance test, behavior rating
scales, and learning disability.

Treatment
General
H Education regarding the nature and effect of the dis-

order
H Behavior modification
H External structure
H Supportive psychotherapy
H Elimination of sugar, dyes, and additives from diet
H Monitor activity (for safety purposes)

Medications
H Stimulants, such as methylphenidate, dextroampheta-

mine, and pemoline


H Tricyclic antidepressants, such as desipramine and

imipramine
H Mood stabilizers such as bupropion
H Beta-adrenergic blockers such as propranolol
H Selective norepinephrine reuptake inhibitors such as

atomoxetine
H Alpha2-agonists such as clonidine

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Nursing considerations
Key outcomes
The patient (or family) will:
H demonstrate effective social interaction skills in oneon-one and group settings
H report improvement in family and social interactions
H demonstrate effective coping behavior.

Nursing interventions
H Set realistic expectations and limits to avoid frustrat-

ing the patient.


H Maintain a calm and consistent manner.
H Keep all instructions short and simple make one-

step requests.
H Provide praise, rewards, and positive feedback when-

ever possible.
H Provide diversional activities suited to a short atten-

tion span.

Monitoring
H Activity level
H Nutritional status
H Adverse drug reactions
H Response to treatment
H Complications
H Activity (for safety purposes)

Patient teaching
Be sure to cover:
H behavior therapy
H reinforcement of good behavior
H realistic expectations
H medications and possible adverse reactions
H nutrition.

Discharge planning
H Refer the patient to family therapy.

Attention deficit hyperactivity disorder

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Autistic disorder
Overview
Description
H A severe, pervasive developmental disorder
H Degree of impairment varies
H Usually apparent before age 3
H Poor prognosis
H Sometimes called Kanners autism

Pathophysiology
H Defects in the central nervous system (CNS) may

arise from prenatal complications.

Causes
H Exact cause unknown
H Defects in CNS from prenatal complications such as

rubella
H Nutritional deficiency
H Disease caused or triggered by immunizations

Risk factors
H High-risk pregnancy

Incidence
H Affects an estimated 1 in 1,000 children
H Three to four times more likely in males than in

females, usually the firstborn male

Common characteristics
H Unresponsive to social contact
H Gross deficit in intelligence and language develop-

H Pronoun reversal
H Bizarre or self-destructive behavior
H Extreme compulsion for sameness
H Abnormal reaction to sensory stimuli
H Cognitive impairment
H Eating, drinking, and sleeping problems
H Mood disorders

DSM-IV-TR criteria
At least 6 of these 12 characteristics must be present,
including at least 2 items from the first section, 1 from
the second, and 1 from the third.
H Qualitative impairment in social interaction:
Impaired nonverbal behavior
Absence of peer relationships
Failure to seek or share enjoyment, interests, or
achievements
Lack of social or emotional reciprocity
H Qualitative impairment in communication:
Delay or lack of language development
Inability to initiate or sustain conversation
Idiosyncratic or repetitive language
Lack of appropriate imaginative play
H Restricted repetitive and stereotyped patterns of behavior, interests, and activities:
Abnormal preoccupation with a restricted pattern
of interest
Inflexible routines or rituals
Repetitive motor mannerisms
Preoccupation with parts of objects
H The diagnostic criteria also include delays or abnormal functioning in at least one of these areas before
age 3:
Social interaction and language skills
Symbolic or imaginative play

ment
H Ritualistic and compulsive behavior
H Restricted capacity for developmentally appropriate

activities and interests


H Bizarre response to the environment

Complications
H Epileptic seizures
H Depression

During stress
H Catatonic phenomena
H Undifferentiated psychotic state

Treatment
General
H Structured treatment plan
H Behavioral techniques
H Pleasurable sensory and motor stimulation
H Monitor activities (for safety purposes)

Medications
H Serotonin receptor reuptake inhibitors, such as flu-

voxamine and sertratine

Assessment
History
H Becomes rigid or flaccid when held
H Cries when touched
H Shows little or no interest in human contact

Physical findings
H Delayed smiling response
H Severe language impairment
H Lack of socialization and imaginative play
H Echolalia

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Autistic disorder

H Antidepressants, such as doxepin, imipramine, and

clomipramine
H Antipsychotics, such as haloperidol, thioridazine, and

risperidone
H Stimulants, such as dextroamphetamine and

methylphenidate
H Alpha2-agonists such as clonidine
H Bet-adrenergic blockers such as propranolol

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Nursing considerations
Key outcomes
The patient (or family) will:
H identify and contact available resources, as needed
H openly share feelings about the present situation
H as much as possible, demonstrate age-appropriate
skills and behaviors
H practice safety measures and take safety precautions
in the home
H interact with family or friends.

Nursing interventions
H Institute safety measures when appropriate.
H Provide positive reinforcement.
H Encourage development of self-esteem.
H Encourage self-care.
H Prepare the child for change by telling him about it.
H Help family members develop strong one-on-one

relationships with the patient.

Monitoring
H Response to treatment
H Complications
H Adverse drug reactions
H Patterns of behavior
H Nutritional status
H Social interaction
H Communication skills
H Activity

Patient teaching
Be sure to cover:
H physical care for the childs needs
H importance of identifying signs of excessive stress
and coping skills.

Discharge planning
H Refer the parents to resource and support services.

Autistic disorder

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Avian influenza
Overview
Description
H Extremely virulent virus occurring naturally in birds
H Rapidly mutating and has been transmitted from

birds to mammals, including humans


H Risk of pandemic as the virus evolves and more hu-

man cases occur each year


H International concern because virus spreads by mi-

gratory birds

Pathophysiology
H The virus invades the epithelium of the respiratory

tract, causing inflammation.

H Shortness of breath
H Eye infections
H Cytokine storm

Hypotension
Tachycardia
Dyspnea
Fever
Uncontrollable hemmorrhage
Signs of multisystem organ failure from ischemia
or insufficient tissue perfusion

Test results
Laboratory
H Oropharyngeal, nasal, nasopharyngeal, or lower respiratory tract specimen culture shows causative organism.
H Serology for influenza H5N1-specific antibody shows
causative organism.

H The immune system releases inflammatory mediators

(cytokines, oxygen free radicals and coagulation factors).


H Cytokine storm, an inappropriate and exaggerated
immune response, is caused by rapidly proliferating
and active T-cells.
H If the immune response isnt limited, the lungs are
permanently damaged.
H Patients develop acute respiratory distress syndrome,
sepsis, and multisystem organ failure.

Treatment

Causes

captopril, enalapril and lisinopril and angiotensin II


receptor blockers, such as candesartan, valsartan
and irbesartan to treat cytokine storm
H Corticosteroids
H Vaccine produced and approved for distribution by
public-health officials if needed (Further vaccine research is underway.)

H Influenza A, H5N1 virus strain

Incidence
H Few hundred cases per year world-wide
H No recent cases in the United States
H Affects all age-groups and both sexes
H Primarily in those with exposure to infected poultry
H Greater than 50% mortality

Common characteristics
H Influenza-like symptoms

Complications
H Acute respiratory distress
H Viral pneumonia
H Multisystem organ failure

Assessment
History
H Close contact with infected poultry or contaminated

surfaces
H Rarely, close contact with infected human

Physical findings
H Influenza-like symptoms

106

Fever
Cough
Sore throat
Muscle aches

Avian influenza

General
H Supportive measures

Medications
H Antibiotics as appropriate
H Anti-viral medications (effectiveness under study)
H Angiotensin-converting enzyme inhibitors, such as

Nursing considerations
Key outcomes
The patient will:
H develop no complications
H maintain stable vital signs
H express understanding of the disorder and treatment
regimen

Nursing interventions
H Observe standard and respiratory precautions to pre-

vent transmission of the disease.


H Give prescribed drugs.
H Provide supportive care and emotional support.

Monitoring
H Vital signs
H Respiratory status
H Cardiovascular status
H Response to treatment
H Complications

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Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H measures to prevent the spread of disease
H medication administration, dosage, and possible adverse effects
H importance of continuing the prescribed antibiotic
until the entire prescription is finished
H disposal of secretions and the use of proper handwashing technique
H fact that seasonal influenza vaccine doesnt protect
against avian flu

Discharge planning
H Refer the patient to an infectious disease specialist, if

necessary.

Avian influenza

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Basal cell carcinoma


Overview
Description

H Nonmelanoma skin cancer


H Slow-growing, destructive cancerous skin tumor
H Two major types: noduloulcerative and superficial
H Most common malignant tumor that affects whites

(see Identifying basal cell carcinoma)

Pathophysiology
H Although the pathogenesis is uncertain, some experts

hypothesize that it originates when undifferentiated


basal cells become carcinomatous instead of differentiating into sweat glands, sebum, and hair.

Causes
H Prolonged sun exposure (90% of tumors occur on

sun-exposed areas of the body)

Risk factors
H Arsenic ingestion
H Radiation exposure
H Burns
H Immunosuppression
H Vaccinations (rare)
H History of previous nonmelanoma skin cancer

Incidence
H Usually occurs in people older than age 40
H Most prevalent in blond, fair-skinned males

Common characteristics
H Lesion found on face, head, neck, and back
H Five warning signs

An open sore

Identifying basal cell carcinoma


This illustration shows an enlarged nasal nodule in basal
cell carcinoma. Note its depressed center and firm, elevated border.

A reddish patch
A shiny bump
A pink growth
A scarlike area

Complications
H Disfiguring lesions of the eyes, nose, and cheeks

Assessment
History
H Odd-looking skin lesion
H Prolonged exposure to the sun
H Nonhealing sore of varying duration

Physical findings
H Lesions characterized as small, smooth, pinkish, and

translucent papules (early-stage noduloulcerative)


H Telangiectatic vessels across surface and lesions may

be pigmented
H Lesions enlarge with depressed centers and firm and

elevated borders (also called rodent ulcers)


H Multiple oval or irregularly shaped, lightly pigmented

plaques on chest or back


H Head and neck possibly showing waxy, sclerotic, yel-

low to white plaques without distinct borders

Test results
Diagnostic procedures
H Incisional or excisional biopsy and histologic study
may help determine the tumor type and histologic
subtype.
Other
H All types of basal cell carcinomas are diagnosed by
clinical appearance.

Treatment
General
H Depends on the size, location, and depth of the le-

sion
H Irradiation, if the tumor location requires it; pre-

ferred for elderly or debilitated patients who might


not tolerate surgery
H Cryotherapy (liquid nitrogen that freezes the cells
and kills them)
H Well-balanced diet; no restrictions
H Avoidance of sun exposure

Medications
H Chemotherapy such as topical fluorouracil
H Immune response modifier such as topical

imiquimod

Surgery
H Curettage and electrodesiccation

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Basal cell carcinoma

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H Microscopically controlled surgical excision, known

as Mohs surgery, that carefully removes recurrent


lesions until a tumor-free plane is achieved (after
removal of large lesions, skin grafting may be required)
H Simple excision
H Chemosurgery

Nursing considerations
Key outcomes
The patient will:
H express positive feelings about self
H express feelings of increased comfort
H exhibit healing lesions or wounds
H demonstrate effective coping mechanisms.

Nursing interventions
H Encourage verbalization and provide support.
H Provide appropriate wound care.

Monitoring
H Complications of treatment
H Response to treatment
H Signs and symptoms of infection
H Wound healing
H Skin surveillance for additional lesions

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H appropriate wound care
H importance of avoiding excessive sun exposure,
wearing protective clothing, and using a strong sunscreen or sunshade to protect the skin.

Discharge planning
H Refer the patient to resource and support services, as

needed.

Basal cell carcinoma

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Bells palsy
Overview

H Local traumatic injury


H Autoimmune disease
H Lyme disease
H Tumor
H Bacterial infections such as meningitis

Description

Incidence

H Condition in which the impulses from the seventh

H Affects all age-groups


H Most common between ages 20 and 60
H Affects males and females equally

cranial nerve are blocked, causing muscle weakness


or paralysis
H Rapid onset
H Subsides spontaneously in 80% to 90% of patients
H Complete recovery in 1 to 8 weeks
H Delayed recovery in elderly people
H Partial recovery: contractures may develop on the
paralyzed side of the face
H May recur on same or opposite side of the face

Pathophysiology

Common characteristics
H Unilateral facial weakness
H Aching at jaw angle
H Drooping mouth
H Distorted and loss of taste
H Impaired ability to fully close eye on affected side
H Tinnitus

H An inflammatory reaction occurs around the seventh

Complications

cranial nerve (motor innervation of the facial muscles).


H Inflammation is usually at the internal auditory
meatus.
H Unilateral facial weakness or paralysis results.

H Corneal ulceration and blindness


H Impaired nutrition secondary to paralysis of the low-

Causes

Assessment

H Unknown
H Ischemia
H Viral disease, such as herpes simplex or herpes

History

zoster

Facial paralysis in Bells palsy


Unilateral facial paralysis characterizes Bells palsy. The
paralysis produces a distorted appearance and an inability
to wrinkle the forehead, close the eyelid, smile, show the
teeth, or puff out the cheek on the affected side.

er face
H Long-term psychosocial problems

H Pain on the affected side around the angle of the jaw

or behind the ear for a few hours or days before onset of weakness
H Difficulty chewing on the affected side
H Difficulty speaking clearly

Physical findings
H Mouth droops on the affected side (see Facial paral-

ysis in Bells palsy)


H Smooth forehead
H Distorted taste perception
H Inability to raise eyebrow, smile, show teeth, or puff

out cheek
H Impaired ability to close eye on the weak side
H Eye rolls upward (Bells phenomenon) when at-

tempting to close the eye


H Excessive tearing

Test results
H Diagnosis is based on clinical presentation.

Imaging
H Magnetic resonance imaging rules out tumor.

Treatment
General
H Eliminating the source of damage to the nerve immeSMILING

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Bells palsy

diately

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H Oral hygiene maintenance


H Eye protection such as sunglasses
H Hearing protection
H Moist heat
H Diet, as tolerated
H Activity, as tolerated

Medications
H Oral corticosteroids, such as prednisone and

hydrocortisone
H Analgesic such as ibuprofen
H Antiviral such as acyclovir

Surgery
H Exploration of the facial nerve (possibly)
H Facial reanimation, such as direct facial nerve repair

or facial nerve grafting

Nursing considerations
Key outcomes
The patient will:
H experience increased comfort and relief from pain
H consume an adequate amount of calories daily
H express positive feelings about self
H express understanding of the condition and treatment regimen
H exhibit improvement in facial muscle movement.

Nursing interventions
H Provide psychological support.
H Apply moist heat to the affected side of the face.
H Massage the patients face with a gentle upward

motion.
H Provide a facial sling.
H If the patient had surgery, provide preoperative and

postoperative care.
H Administer medication, as ordered.

Monitoring
H Neurologic function
H Response to medications
H Signs and symptoms of peptic ulceration, pancreati-

tis, or other GI adverse effects of prednisone and


hydrocortisone
H Nutritional status
H Facial muscle movement

Patient teaching
Be sure to cover:
H the disorder
H medication and adverse effects
H protection of affected eye
H exercises of the facial muscles
H nutritional management program.

Bells palsy

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Benign prostatic
hyperplasia
Overview
Description
H Enlargement of prostate gland enough to compress

urethra, causing overt urinary obstruction

H Urinary hesitancy and frequency


H Difficulty initiating urination
H Nocturia, hematuria
H Dribbling, incontinence
H Urine retention

Physical findings
H Visible midline mass above the symphysis pubis from

distended bladder
H Enlarged prostate on digital rectal examination

H May be treated surgically or symptomatically, de-

Test results

pending on the size of prostate, age and health of


patient, and extent of obstruction
H Referred to as BPH

Laboratory
H Elevated blood urea nitrogen and serum creatinine
levels suggest impaired renal function.
H Bacterial count that exceeds 100,000/mm3 reveals
hematuria, pyuria, and UTI.
Imaging
H Excretory urography may indicate urinary tract obstruction, hydronephrosis, calculi or tumors, and
bladder filling and emptying defects.
Diagnostic procedures
H Cystourethroscopy determines the best surgical intervention and shows prostate enlargement, bladder
wall changes, calculi, and raised bladder.
Other
H International Prostate Symptom Score classifies
disorders severity.

Pathophysiology
H Changes occur in periurethral glandular tissue.
H Prostate enlarges and may extend into the bladder.
H Compression or distortion of prostatic urethra

obstructs urine outflow.


H BPH may cause diverticulum through the muscula-

ture leading to urinary retention.

Causes
H Unknown
H Possible link with hormonal activity

Risk factors
H Age
H Intact testes

Treatment

Incidence

General

Special populations
BPH occurs in 80% of all males older than age 40,
and in 95% of all males older than age 80.

Common characteristics
H Changes in voiding patterns and urine stream

Complications
H Urinary stasis, urinary tract infection (UTI), or renal

calculi
H Bladder wall trabeculation
H Detrusor muscle hypertrophy
H Bladder diverticula and saccules
H Urethral stenosis
H Hydronephrosis
H Paradoxical (overflow) incontinence
H Acute or chronic renal failure
H Acute postobstructive diuresis

Assessment
History
H Decreased urine stream caliber and force
H Interrupted urinary stream

112

Benign prostatic hyperplasia

H Prostatic massage
H Short-term fluid restriction (prevents bladder disten-

tion)
H Avoidance of lifting, performing strenuous exercises,

and taking long automobile rides for at least 1 month


after surgery
H No sexual intercourse for several weeks after surgery

Medications
H Antibiotics, such as cefepime and levofloxacin, if

infection present
H Alpha-1-adrenergic blockers, such as doxazosin and

terazosin
H 5-Alpha-reductase inhibitors such as dutasteride and

finasteride

Surgery
H For relief of acute urine retention, hydronephrosis,

severe hematuria, and recurrent UTI or for palliative


relief of intolerable symptoms
H Suprapubic (transvesical) prostatectomy
H Perineal prostatectomy
H Retropubic (extravesical) prostatectomy
H Transurethral resection of the prostate
H Balloon dilatation, ultrasound needle ablation, and
use of stents

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Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H express understanding of disorder and treatment
H demonstrate skill in managing urinary elimination
H express feelings about potential or actual changes in
sexual activity.

Nursing interventions
H Give prescribed drugs.
H Avoid giving sedatives, alcohol, antidepressants, or

anticholinergics (which can worsen the obstruction).


H Provide I.V. therapy, as ordered.
H Administer continuous bladder irrigation, as pre-

scribed.
H Keep the head of the bed elevated at least 30 degrees

to prevent pneumonia.
H Encourage coughing, deep breathing, and incentive

spirometer use.

Monitoring
H Vital signs
H Intake and output
H Daily weight

ALERT
Watch for signs of postobstructive diuresis, characterized by polyuria exceeding 2 L in 8 hours and
excessive electrolyte losses. Although usually selflimiting, it can result in vascular collapse and
death if not promptly treated.

After prostatic surgery


H Pain control
H Catheter function and drainage
H Continuous bladder irrigation function
H Signs of infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of UTI that should be reported
H when to seek medical care (fever, unable to void, or
passing bloody urine).

Benign prostatic hyperplasia

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Bipolar disorder
Overview
Description
H An affective disorder marked by severe pathologic

mood swings from hyperactivity and euphoria to


sadness and depression
H In cyclothymia, a variant of bipolar disorder: numerous episodes of hypomania and depressive symptoms
too mild to meet the criteria for major depression or
bipolar disorder (see Cyclothymic disorder)
H Manic episodes that emerge over a period of days to
weeks, but onset possible within hours
H Untreated episodes that can last weeks or as long as
8 to 12 months, with some having an unremitting
course
H Found in 15% of patients, mostly female, rapid cycling, in which four or more episodes of either depression or mania occur in 1 year
H Difficulties in work performance and psychosocial
functioning in about half of all patients with this disorder

Pathophysiology
H Bipolar disorder may be an effect of neurotransmit-

ter imbalance.
H Mood swings may involve membrane changes in

sodium- and potassium-activated adenosine triphosphatase involving disordered intracellular signals.

Common characteristics
Manic phase
H Accelerated speech
H Frequent changes of topic
H Flight of ideas
Depressive phase
H Loss of self-esteem
H Overwhelming inertia
H Social withdrawal
H Feelings of hopelessness
H Apathy or self-reproach
H Suicidal thoughts
Bipolar II disorder
H Meets all the diagnostic criteria for a manic episode
H May experience recurrent depressions, separated by
periods of mild activation and increased energy

Complications
H Emotional and social consequences
H Sexually transmitted disease
H Exhaustion
H Nutritional deficits
H Sleep disturbances
H Suicide

Assessment
History
H Sleeping and eating disturbances
H Exhibits expansive, grandiose, sometimes irritable

mood alternating with symptoms of depression

Causes

Physical findings

H Exact cause unclear


H Autosomal dominant inheritance found in genetic

Mania
H Increased psychomotor activity
H Excessive social extroversion
H Impulsive actions
H Impaired judgment
H Delusions
H Paranoid thinking
H Limited attention span
H Inflated sense of self-esteem
H Rapid responses to external stimuli
Depression
H Slow speech and response
H No obvious disorientation or intellectual impairment
H Psychomotor retardation
H Lethargy
H Low muscle tone
H Weight loss
H Slowed gait

studies
H Some evidence that links to an X chromosome

disorder
H May be triggered by death, separation, or divorce
H Imbalances in the biochemistry that controls food

(biochemical) imbalances

Risk factors
H Family history
H Substance abuse

Incidence
H Affects over 5 million people in the United States
H Equally common in females and males
H Females: likely to have more depressive episodes
H Males: likely to have more manic episodes
H Higher among relatives of affected patients than in

the general population

Special populations
Age of onset is usually between ages 20 and 35, but
35% of patients experience onset between ages 35
and 60.

114

Bipolar disorder

DSM-IV-TR criteria
Diagnosis is confirmed when the patient meets the criteria established for a manic or hypomanic episode:
H experiences a distinct period of abnormally and persistently elevated, expansive, or irritable mood
H during the mood disturbance, at least three of these
symptoms must persist (four, if the mood is only irritable) and be present to a significant degree:

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inflated self-esteem or grandiosity


decreased need for sleep
excessive talking
flight of ideas
easily distracted
psychomotor agitation
excessive involvement in dangerous activities
symptoms dont meet criteria for a mixed episode
impairment in occupational function, usual social
activities, or relations with others severe enough
to require hospitalization to prevent harm to self
or others
substance use or other causative medical conditions not present.

Treatment
General
H Group and individual therapy
H Monitoring of activity when in manic phase
H No dietary restrictions

Medications
H Anticonvulsants, such as carbamazepine and valproic

acid
H Antimanic such as lithium
H Antipsychotics, such as aripiprazole, olanzapine,

quetiapine, risperidone, and ziprasidone


H Antidepressant such as fluoxetine

Nursing considerations
Key outcomes
The patient will:
H identify effective coping techniques
H recognize symptoms and comply with medication
regimen
H express feelings related to self-esteem
H join gradually in self-care and the decision-making
processes.

Nursing interventions
For the manic patient
H Encourage activities that require gross motor movements.
H Assist with personal hygiene; encourage responsibility for personal care.
H Protect from overstimulation.
H Set realistic goals and limits for the patients behavior.
H Provide diversional activities suited to a short attention span.
H Reorient to reality.
H Avoid power struggles.
For the depressed patient
H Avoid overwhelming expectations.
H Allow increased time for activities and responses.
H Provide a structured routine.
H Promote interaction with others.

Cyclothymic disorder
A chronic mood disturbance of at least 2 years duration,
cyclothymic disorder involves numerous episodes of hypomania or depressive symptoms that arent of sufficient
severity or duration to qualify as a major depressive
episode.
In the hypomanic phase, the patient may experience insomnia; hyperactivity; inflated self-esteem; increased productivity and creativity; overinvolvement in pleasurable
activities, including an increased sexual drive; physical
restlessness; and rapid speech. Depressive symptoms
may include insomnia, feelings of inadequacy, decreased
productivity, social withdrawal, loss of libido, loss of interest in pleasurable activities, lethargy, depressed speech,
and crying.
A number of medical disorders (for example, endocrinopathies, such as Cushings disease, stroke, brain tumors, head trauma, and drug overdose) can produce a
similar pattern of mood alteration. These organic causes
must be ruled out before making a diagnosis of cyclothymic disorder.

H Encourage verbalization; provide support.


H Institute safety measures.
H Encourage physical activity.

Monitoring
H Patterns of behavior
H Response to treatment
H Social interaction
H Complications
H Adverse drug reactions
H Nutritional status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible adverse effects
H importance of continuing the prescribed medication
regimen.

Discharge planning
H Refer the patient for psychological counseling.
H Refer the patient to support services.

Bipolar disorder

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Bladder cancer
Overview
Description
H Malignant tumor that develops on the bladder wall

Assessment
History
H Gross, painless, intermittent hematuria, usually with

clots
H Suprapubic pain after voiding suggesting invasive

lesions

surface or grows within the wall and quickly invades


underlying muscles
H Less common bladder tumors: adenocarcinomas,
epidermoid carcinomas, squamous cell carcinomas,
sarcomas, tumors in bladder diverticula, and carcinoma in situ
H Most common cancer of the urinary tract

H Bladder irritability, urinary frequency, nocturia, and

Pathophysiology

Test results

H About 90% of bladder cancers are transitional cell

Laboratory
H Complete blood count helps detect anemia.
H Urinalysis detects blood and malignant cells in the
urine.
Imaging
H Excretory urography can identify a large, early-stage
tumor or an infiltrating tumor; delineate functional
problems in the upper urinary tract; assess hydronephrosis; and detect rigid deformity of the bladder
wall.
H Retrograde cystography evaluates bladder structure
and integrity; it also helps confirm a bladder cancer
diagnosis.
H Bone scan can detect metastasis.
H Computed tomography scan defines the thickness of
the involved bladder wall and discloses enlarged
retroperitoneal lymph nodes.
H Ultrasonography reveals metastasis in tissues beyond
the bladder and can distinguish a bladder cyst from a
bladder tumor.
Diagnostic procedures
H Cystoscopy and biopsy confirm bladder cancer diagnosis; if the test results show cancer cells, further
studies will determine the cancer stage and treatment.
Other
H Bimanual examination may be performed during a
cystoscopy if the patient has received an anesthetic;
this helps to determine whether the bladder is fixed
to the pelvic wall.

carcinomas, arising from the transitional epithelium


of mucous membranes. (They may result from malignant transformation of benign papillomas.)

Causes
H Exact cause unknown
H Associated with chronic bladder irritation and infec-

tion in people with renal calculi, indwelling urinary


catheters, chemical cystitis caused by cyclophosphamide, or pelvic irradiation

Risk factors
H Certain environmental carcinogens, such as

2-naphthylamine, tobacco, nitrates, and coffee


H Occupational exposure to carcinogens

Incidence
H Bladder tumors most prevalent in people older than

age 50
H More common in males than in females
H Occurs more commonly in densely populated indus-

trial areas

Common characteristics
H Asymptomatic in early stages for 25% of patients
H First sign: gross, painless, intermittent hematuria,

with or without clots


H Suprapubic pain after voiding most commonly

associated with invasive lesions

dribbling
H Flank pain possibly indicating an obstructed ureter

Physical findings
H Gross hematuria
H Flank tenderness if ureteral obstruction present

H Bladder irritability
H Urinary frequency
H Nocturia
H Dribbling

Treatment

Complications

H Cancers stage, patients lifestyle, other health prob-

H Bone metastasis
H Problems resulting from tumor invasion of contigu-

ous viscera

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Bladder cancer

General
lems, and mental outlook influencing selection of
therapy
H Initially postoperatively, avoidance of heavy lifting
and contact sports
H After recovery, no activity restrictions

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Medications

Discharge planning

H Intravesical chemotherapy, such as thiotepa and

H Refer the patient to resource and support services.


H Before discharge, arrange for follow-up home nurs-

mitomycin
H Attenuated live bacille Calmette-Gurin vaccine
H Chemotherapy, such as cisplatin and doxorubicin

Surgery

ing care.
H Refer the patient to an enterostomal therapist and for

services provided by the therapist.

H Transurethral resection (cystoscopic approach) and

fulguration (electrically)
H Segmental bladder resection
H Radical cystectomy
H Ureterostomy, nephrostomy, continent vesicostomy

(Kock pouch), ileal bladder, and ureterosigmoidostomy

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid balance
H express feelings of increased comfort and decreased
pain
H exhibit adequate coping mechanisms
H express feelings about potential or actual changes in
sexual activity.

Nursing interventions
H Provide support and encourage verbalization.
H Give prescribed drugs.
H Provide preoperative teaching; discuss procedure

and postoperative course.


H Keep the head of the bed elevated at least 30 degrees

to prevent pneumonia.
H Encourage coughing, deep breathing, and incentive

spirometer use.
H Provide skin care.
H Provide stoma care.

Monitoring
H Vital signs
H Wound site
H Postoperative complications, such as pneumonia,

deep vein thrombosis, and infection


H Intake and output
H Pain control
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H stoma care
H skin care and evaluation
H avoidance of heavy lifting and contact sports (postoperatively with a urinary stoma)
H encouragement of participation in usual athletic and
physical activities.

Bladder cancer

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Blastomycosis
Overview
Description
H Fungal infection that usually affects the lungs and

produces bronchopneumonia
H May develop into extrapulmonary disease
H Also called Gilchrists disease

Pathophysiology
H Blastomycosis is generally contracted by inhalation of

aerosolized conidial forms of the fungus from its natural soil habitat.
H The conidia then transforms to the yeast phase at
body temperature (thermal dimorphism).
H Inflammatory response is evoked by multiplication
of organism.
H Dissemination is possible through the blood and
lymphatics to other organs.

Causes
H Inhalation of the yeastlike fungus Blastomyces

dermatitidis

Incidence
H Generally found in North America, where B. der-

matitidis normally inhabits the soil


H Endemic to the southeastern United States
H More common in males than females
H Onset most common between ages 30 and 50, but

can occur at any age

Common characteristics
H Signs and symptoms of a viral upper respiratory tract

infection
H Small, painless, nonpruritic, and nondistinctive macules or papules on exposed body parts

Complications
H Osteomyelitis
H Central nervous system, skin, and genital disorders
H Addisons disease (adrenal insufficiency)
H Pericarditis
H Arthritis

Physical findings
H Thick sputum (may contain blood)
H Bronchial breath sounds; dullness on chest percus-

sion
H Decreased breath sounds
H Tachypnea
H Decreased pulse oximetry
H Raised and reddened lesions
H Chest pain
H Dyspnea

Extrapulmonary findings
H Skin lesions
H Osteolytic lesions
H Joint swelling

Test results
Laboratory
H Culture from skin lesions, pus, sputum, or pulmonary secretions shows presence of B. dermatitidis.
H White blood cell count and erythrocyte sedimentation
rate are increased.
H Serum globulin levels are slightly increased, and mild
normochromic anemia occurs.
H Alkaline phosphatase level is increased (with bone
lesions).
Imaging
H Chest X-ray may show pulmonary infiltrates.
Diagnostic procedures
H Biopsy of tissue from the skin or lungs or of bronchial washings, sputum, or pus shows infecting
organism.
Other
H Immunodiffusion testing detects antibodies for the A
and B antigens of blastomycosis.

Treatment
General
H Increased fluid intake
H Respiratory treatments
H Rest periods, as needed

Medications
H Antifungals, such as amphotericin B, itraconazole,

and ketoconazole
H Antipyretic such as acetaminophen

Assessment

Nursing considerations

History

Key outcomes

H Fever, chills
H Dry, hacking, productive cough
H Weight loss
H Night sweats
H Pleuritic chest pain
H Malaise
H Myalgia

The patient will:


H maintain adequate oxygenation
H improve skin integrity
H report increased comfort and decreased pain.

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Nursing interventions
H Provide a cool room; if the patient is feverish, admin-

ister a tepid sponge bath.


H Elevate painful joints and apply heat.
H Provide appropriate skin care.
H Give prescribed drugs.

Monitoring
H Vital signs
H Pulse oximetry
H Laboratory tests
H Sputum production for hemoptysis
H Level of consciousness and pupil response
H Hematuria
H Lesion healing
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper administration of medications
H skin care.

Discharge planning
H Stress appropriate follow-up care.

Blastomycosis

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Blepharitis
Overview
Description
H Common inflammation of eyelash follicles and

meibomian glands of the upper or lower eyelids


H May affect both eyes
H May affect upper and lower eyelids
H Ulcerative type: may coexist with seborrheic bleph-

aritis

Pathophysiology
H Inflammatory responses of the eyelids to bacteria or

seborrheic dermatitis occurs.

Causes
Seborrheic blepharitis
H Generally results from seborrhea of the scalp, eyebrows, and ears
Ulcerative blepharitis
H Generally results from a Staphylococcus aureus infection
H Pediculosis

Incidence
H More common in elderly people
H Most common ocular disease

Common characteristics
H Eye drainage
H Burning, itching, and swelling of eyes
H Tends to recur
H May become chronic

Complications
H Ocular involvement
H Keratitis
H Excess tearing or dry eye

Assessment
History
H Eyelids itch or burn
H Feeling of foreign body
H Crusty eyelids, which stick together when awakening
H Loss of eyelashes

Physical findings
H Continual blinking
H Red-rimmed appearance to the eyelid margins
H Swelling of eyelids

Seborrheic blepharitis
H Scales along eyelids, especially upon awakening
H Dandruff on scalp and eyebrows

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Blepharitis

Ulcerative blepharitis
H Flaky scales on eyelashes, especially in morning
H Missing eyelashes
H Ulcerations on eyelid margins

Test results
Laboratory
H Culture of the ulcerated eyelid margin reveals
S. aureus in ulcerative blepharitis.

Treatment
General
H Early treatment to prevent recurrence or complica-

tions
H Daily cleansing (using diluted baby-shampoo on a

cotton-tipped applicator or washcloth) to remove


scales from eyelid margins
H Warm eye compresses
H Removal of nits with forceps for blepharitis caused
by pediculosis
H Avoidance of eye makeup
H Avoidance of contact lens use until resolved

Medications
H Antibiotic eye ointment such as gentamicin
H Ophthalmic physostigmine or other insecticidal

ointment for blepharitis caused by pediculosis

Nursing considerations
Key outcomes
The patient will:
H sustain no harm or injury
H verbalize feelings and concerns
H identify available health resources
H demonstrate appropriate coping skills
H maintain current visual acuity.

Nursing interventions
H Provide eyelid care at least twice daily.
H Apply warm compresses, four times daily.
H Give prescribed drugs.
H Apply ointments, as ordered. (See Applying an

ophthalmic ointment.)
H Maintain infection-control techniques.

Monitoring
H Response to treatment
H Adverse reactions to medication
H Complications

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Applying an ophthalmic ointment


Follow these directions to apply an ophthalmic ointment
cleanly and quickly:
H Tilt the patients head back, and ask him to look toward
the ceiling.
H Gently pull the lower eyelid down, and squeeze a small
ribbon of ointment along the edge of the conjunctival
sac from the inner to the outer canthus.
H Take care to avoid touching the eye with the tip of the
ointment tube.
H Repeat this procedure for the other eye, if ordered.

Patient teaching
Be sure to cover:
H the disorder and treatment
H daily eyelid care
H removal of scales from eyelids
H application of warm compresses
H medications and possible adverse effects
H infection control
H potential complications
H importance of keeping follow-up appointments.

Blepharitis

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Life-threatening disorder

Blood transfusion
reaction

Risk factors
H Multiple transfusions
H Rare blood type

Incidence
H Mild reactions in 1% to 2% of transfusions

Common characteristics

Overview
Description
H A hemolytic reaction following the transfusion of mis-

matched blood

H Mild to severe fever within the first 15 minutes of

transfusion or within 2 hours after its completion


H Chills
H Urticaria
H Shortness of breath

H Accompanies or follows I.V. administration of blood

Complications

components
H Mediated by immune or nonimmune factors
H From mild to severe

H Bronchospasm
H Acute tubular necrosis leading to acute renal failure
H Anaphylactic shock
H Vascular collapse
H Disseminated intravascular coagulation

Pathophysiology
H Recipients antibodies, immunoglobulin (Ig) G or

IgM, attach to donor red blood cells (RBCs), leading


to widespread clumping and destruction of recipients RBCs.
H Transfusion with Rh-incompatible blood triggers a
less serious reaction, known as Rh isoimmunization, within several days to 2 weeks. (See Understanding the Rh system.)
H A febrile nonhemolytic reaction the most common
type of reaction develops when cytotoxic or agglutinating antibodies in the recipients plasma attack
antigens on transfused lymphocytes, granulocytes, or
plasma cells.

Causes
H Transfusion with incompatible blood

Assessment
History
H Transfusion of blood product
H Chills, nausea, vomiting, chest tightness, or chest and

back pain

Physical findings
H Fever, tachycardia, and hypotension
H Dyspnea, anxiety, and restlessness
H Urticaria and angioedema
H Wheezing
H In a surgical patient, blood oozing from mucous

membranes or the incision site


H In a hemolytic reaction: fever, an unexpected de-

Understanding the Rh system


The Rh system contains more than 30 antibodies and
antigens. Of the worlds population, about 85% are Rh
positive, which means that their red blood cells carry the
D or Rh antigen. The rest of the population are Rh negative and dont have this antigen.

Effects of sensitization
When an Rh-negative person receives Rh-positive blood
for the first time, he becomes sensitized to the D antigen
but shows no immediate reaction to it. If he receives Rhpositive blood a second time, he experiences a massive
hemolytic reaction.
For example, an Rh-negative mother who delivers an
Rh-positive baby is sensitized by the babys Rh-positive
blood. During her next Rh-positive pregnancy, her sensitized blood will cause a hemolytic reaction in the fetal circulation.

Preventing sensitization
To prevent the formation of antibodies against Rh-positive
blood, an Rh-negative mother should receive Rho(D) immune globulin (human) (RhoGAM) I.M. within 72 hours
after delivering an Rh-positive baby.

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Blood transfusion reaction

crease in serum hemoglobin level, frank blood in


urine, and jaundice

Test results
Laboratory
H Serum hemoglobin levels are decreased.
H Serum bilirubin levels and indirect bilirubin levels
are elevated.
H Urinalysis reveals hemoglobinuria.
H Indirect Coombs test or serum antibody screen is
positive for serum anti-A or anti-B antibodies.
H Prothrombin time is increased and fibrinogen level is
decreased.
H Blood urea nitrogen and serum creatinine levels are
increased.

Treatment
General
H Immediate halt of transfusion
H Dialysis (may be necessary if acute tubular necrosis

occurs)

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H Diet, as tolerated
H Bed rest

Medications
H Osmotic or loop diuretics, such as mannitol and

furosemide
H I.V. normal saline solution
H I.V. vasopressors, such as dopamine and phenyl-

ephrine

Patient teaching
Be sure to cover:
H signs and symptoms of transfusion reaction (before
transfusion begins)
H importance of notifying health care providers of
history of reaction
H wearing or carrying rare blood type identification.

H Adrenergic such as epinephrine


H Antihistamine such as diphenhydramine
H Corticosteroid such as dexamethasone
H Antipyretic such as acetaminophen

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H show no signs of active bleeding
H maintain adequate ventilation
H express understanding of disorder.

Nursing interventions
H Stop the blood transfusion.
H Maintain a patent I.V. line with normal saline

solution.
H Insert an indwelling urinary catheter.
H Report early signs of complications.
H Cover the patient with blankets to ease chills.
H Administer supplemental oxygen, as needed.
H Document the transfusion reaction on the patients

chart, noting the duration of the transfusion and the


amount of blood absorbed.
H Follow your facilitys blood transfusion policy and
procedure.

ALERT
Double-check the patients name, identification
number, blood type, and Rh status before administering blood. If you find any discrepancy, dont administer the blood. Notify the blood bank immediately and return the unopened unit.

Monitoring
H Vital signs
H Intake and output
H Signs of shock
H Laboratory results
H Respiratory status
H Cardiac status
H Pulse oximetry

Blood transfusion reaction

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Bone tumors, primary


malignant

Assessment

Overview

History

Description
H Rare type of bone cancer (less than 1% of all malig-

nant tumors)
H Also known as osteoblastoma or

H Hemorrhage
H Local recurrence
H Pathologic fractures

osteosarcoma

H Localized, dull bone pain


H Weight loss
H Impaired mobility
H Pathologic fracture

Pathophysiology

Physical findings

H Proliferation of cancerous cells clump together to

H Palpable mass
H Cachectic appearance
H Abnormal gait
H Swelling and redness at the site

form a tumor, which is able to spread beyond the


original site.
H Osseous bone tumors arise from the bony structure
itself and include osteogenic sarcoma (most common), parosteal osteogenic sarcoma, chondrosarcoma (chondroblastic), and malignant giant cell tumor.
H Nonosseous bone tumors arise from hematopoietic,
vascular, and neural tissues and include Ewings sarcoma, fibrosarcoma (fibroblastic), and chordoma.

Causes
H No immediately apparent cause in most cases
H Genetic abnormalities (retinoblastoma, Rothmund-

Thomson syndrome)
H Exposure to carcinogens
H Heredity, trauma, and excessive radiation therapy,

Test results
Laboratory
H Serum alkaline phosphatase levels are elevated (with
sarcoma).
Imaging
H Bone X-rays and radioisotope bone and computed
tomography (CT) scans show tumor size.
H Bone scans and CT scans of the lungs reveal metastatic disease.
Diagnostic procedures
H Incision or aspiration biopsy confirms primary
malignancy.

according to theories

Incidence

Treatment

H Account for less than 0.2% of all cancers


H More common in males than females
H Higher incidence in children and adolescents, al-

General

though some types occurring in patients between


ages 35 and 60 (see Types of primary malignant
bone tumors)

Special populations
Osteogenic and Ewings sarcomas are the most
common bone tumors in children.

Common characteristics
H Localized, dull bone pain
H Usually more intense at night
H Presence of a mass or tumor

Special populations
Limb pain, refusal to walk, and limited range of
motion (ROM) are common findings in children
with bone tumors.

Complications
H Infection

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Bone tumors, primary malignant

H High-protein, high-calorie diet


H Rest periods, as needed
H Physical therapy
H Radiation therapy

Medications
H Chemotherapy, such as gemcitabine and docetaxel
H Analgesics, such as morphine, oxycodone, hydro-

codone, and fentanyl

Surgery
H Excision of the tumor
H Radical surgery, such as hemipelvectomy or inter-

scapulothoracic or limb amputation

Nursing considerations
Key outcomes
The patient will:
H maintain weight within an acceptable range
H maintain joint mobility and ROM
H express feelings of comfort and decreased pain
H express feelings and fears.

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Types of primary malignant bone tumors


Type

Clinical features

Treatment

Chondrosarcoma

Develops from cartilage


Painless; grows slowly; locally recurrent and invasive
Occurs most commonly in pelvis, proximal femur, ribs, and
shoulder girdle
Usually in males ages 30 to 50

Hemipelvectomy, surgical resection (ribs)


Radiation (palliative)
Chemotherapy

Malignant
giant cell tumor

Arises from benign giant cell tumor


Found most commonly in long bones, especially in the knee
area
Usually in females ages 18 to 50

Curettage
Total excision
Radiation for recurrent disease

Osteogenic
sarcoma

Osteoid tumor present in specimen


Tumor arises from bone-forming osteoblast and bonedigesting osteoclast
Occurs most commonly in femur, but also tibia and humerus; occasionally, in fibula, ileum, vertebra, or mandible
Usually in males ages 10 to 30

Surgery (tumor resection, high


thigh amputation, hemipelvectomy, interscapulothoracic
surgery)
Chemotherapy

Parosteal
osteogenic
sarcoma

Develops on surface of bone instead of interior


Progresses slowly
Occurs most commonly in distal femur, but also in tibia,
humerus, and ulna
Usually in females ages 30 to 40

Surgery (tumor resection, possible amputation, interscapulothoracic surgery, hemipelvectomy)


Chemotherapy
Combination of the above

OSSEOUS ORIGIN

NONOSSEOUS ORIGIN

Chordoma

Derived from embryonic remnants of notochord


Progresses slowly
Usually found at end of spinal column and in sphenooccipital, sacrococcygeal, and vertebral areas
Characterized by constipation and visual disturbances
Usually in males ages 50 to 60

Surgical resection (commonly


resulting in neural defects)
Radiation (palliative, or when
surgery not applicable, as in
occipital area)

Ewings sarcoma

Originates in bone marrow and invades shafts of long and


flat bones
Usually affects lower extremities, most commonly femur,
innominate bones, ribs, tibia, humerus, vertebra, and fibula;
may metastasize to lungs
Pain increasingly severe and persistent
Usually in males ages 10 to 20
Prognosis poor

High-voltage radiation (tumor is


radiosensitive)
Chemotherapy to slow growth
Amputation only if theres no evidence of metastasis

Fibrosarcoma

Relatively rare
Originates in fibrous tissue of bone
Invades long or flat bones (femur, tibia, mandible) but also
involves periosteum and overlying muscle
Usually in males ages 30 to 40

Nursing interventions

Amputation
Radiation
Chemotherapy
Bone grafts (with low-grade fibrosarcoma)

H Cardiovascular status

H Encourage communication, and help the patient set

realistic goals.
H Administer prescribed I.V. infusions and drugs.
H Postoperative care, including coughing, deep breath-

ing, incentive spirometer use, and turning.


H Keep the head of the bed elevated at least 30 degrees.
H Elevate the foot of the bed or place the affected

stump on a pillow for the first 24 hours. (Be careful not to leave the stump elevated for more than
48 hours because this may lead to contractures.)

Monitoring
H Vital signs
H Circulation to the affected extremity
H Wound dressings
H Respiratory status

Patient teaching
Be sure to cover:
H use of assistive devices
H wound care
H reporting new pain or masses
H the need for antibiotic prophylaxis when undergoing
dental procedures (with bone grafts or prosthetic
implants).

Discharge planning
H Refer the patient to the American Cancer Society for

information and support.

Bone tumors, primary malignant

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Life-threatening disorder

Common characteristics
H Symptoms 18 to 30 hours after ingestion of con-

Botulism

taminated food; may be delay of up to 10 days before


symptoms appear
H Range in severity and can mimic other illnesses,
especially neurologic disorders

Overview

Complications

Description
H Life-threatening paralytic illness
H Results from an exotoxin produced by the gram-

positive, anaerobic bacillus Clostridium botulinum


H Occurs as botulism food poisoning, wound botulism,

and infant botulism (see Infant botulism)

H Respiratory failure
H Paralytic ileus
H Death

Assessment

H Mortality about 25%, with death most commonly

History

caused by respiratory failure during the first week of


illness
H Critical and potentially fatal illness signaled by onset
within 24 hours

H Consumption of home-canned food 18 to 30 hours

before onset of symptoms

H Clostridium botulinum bacteria

H Vertigo
H Sore throat
H Weakness
H Nausea and vomiting
H Constipation or diarrhea
H Diplopia
H Blurred vision
H Dysarthria
H Dysphagia
H Dyspnea
H Heroin use

Risk factors

Physical findings

H Eating improperly preserved foods


H Use of injectable street drugs

H Ptosis
H Dilated, nonreactive pupils
H Appearance of dry, red, and crusted oral mucous

Pathophysiology
H Endotoxin acts at the neuromuscular junction of

skeletal muscle, preventing acetylcholine release and


blocking neural transmission, eventually resulting in
paralysis.

Causes

Incidence
H Occurs worldwide
H Average yearly occurrence of about 110 cases in the

United States
H Affects adults more than children

membranes
H Abdominal distention with absent bowel sounds
H Descending weakness or paralysis of muscles in the

extremities or trunk
H Deep tendon reflexes may be intact, diminished, or

absent

Infant botulism
Infant botulism, which usually afflicts neonates and infants between 3 and 20 weeks old, is commonly caused
by ingesting the spores of botulinum bacteria, which then
grow in the intestines and release toxin. This disorder can
produce floppy infant syndrome, characterized by constipation, a feeble cry, a depressed gag reflex, and an inability to suck. The infant also exhibits a flaccid facial expression, ptosis, and ophthalmoplegia the result of cranial
nerve deficits.
As the disease progresses, the infant develops generalized weakness, hypotonia, areflexia, and sometimes a
striking loss of head control. Almost 50% of affected infants develop respiratory arrest.
Intensive supportive care allows most infants to recover
completely. Antitoxin therapy isnt recommended because
of the risk of anaphylaxis.

H Unexplained orthostatic hypotension


H Urine retention
H Photophobia
H Slurred speech

Test results
Laboratory
H Mouse bioassay detects toxin thats found in the patients serum, stool, or gastric contents.
Diagnostic procedures
H Electromyography shows diminished muscle action
potential after a single supramaximal nerve stimulus.

Treatment
General
H Supportive measures
H Early tracheotomy and ventilatory assistance in respi-

ratory failure
H Nasogastric (NG) suctioning

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Botulism

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H Total parenteral nutrition


H Bed rest

Medications
H I.V. or I.M. botulinum antitoxin

Surgery
H Debridement of wounds to remove source of toxin-

producing bacteria

Nursing considerations
Key outcomes
The patient will:
H maintain tissue perfusion and cellular oxygenation
H maintain adequate ventilation
H maintain stable neurologic status.

Nursing interventions
H Administer I.V. fluids, as ordered.
H Administer oxygen as needed.
H Perform NG suctioning as needed.

ALERT
Immediately report all cases of botulism to the
local board of health.

Monitoring
H Neurologic status
H Cardiac and respiratory function
H Cough and gag reflexes
H Intake and output
H Arterial blood gas analysis
H Pulse oximetry

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper techniques in processing and preserving
foods
H never tasting food from a bulging can or one with a
peculiar odor
H sterilizing utensils by boiling what came in contact
with suspected contaminated food
H not feeding honey to infants (can be fatal if contaminated).

Discharge planning
H If botulism exposure appears to be related to adverse

socioeconomic conditions, refer the patient to the


appropriate community agency.

Botulism

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Brain tumor
Overview
Description
H Abnormal growth among cells within the intracranial

space
H May affect brain tissue, meninges, pituitary gland,
and blood vessels
H In adults, most common tumor types: gliomas and
meningiomas (usually benign), which usually occur
above the covering of the cerebellum, and supratentorial tumors
H In children, most common tumor types: astrocytomas, medulloblastomas, ependymomas, and brain
stem gliomas

Pathophysiology
H Tumor is classified based on histology or grade of

cell malignancy.
H Central nervous system changes occur due to cancer

cells invading and destroying tissues and by secondary effect mainly compression of the brain, cranial nerves, and cerebral vessels; cerebral edema;
and increased intracranial pressure (ICP).

Causes
H Unknown

Risk factors
H Preexisting cancer

Incidence
H Slightly more common in males than in females
H Gliomas, meningiomas, and schwannomas: overall

incidence of 4.5 per 100,000


H Can occur at any age, but most in children before age

1 or between ages 2 and 12


H In adults, incidence highest between ages 40 and 60

Common characteristics
H Increased ICP
H Headache
H Decreased motor strength and coordination
H Seizures
H Altered vital signs
H Nausea and vomiting
H Papilledema

Complications
H Radiation encephalopathy

Special populations
Brain tumors are the most common cause of cancer death in children.

Life-threatening complications from


increased ICP
H Coma
H Respiratory or cardiac arrest
H Brain herniation

Assessment
History
H Insidious onset
H Headache
H Nausea and vomiting

Physical findings
H May vary according to size and location of tumor

Signs and symptoms of increased ICP


H Vision disturbances
H Weakness, paralysis
H Aphasia, dysphagia
H Ataxia, incoordination
H Seizure
H Decreased level of consciousness

Test results
Imaging
H Skull X-rays confirm presence of tumor.
H Brain scan confirms presence of tumor.
H Computed tomography scan confirms presence of
tumor.
H Magnetic resonance imaging confirms presence of
tumor.
H Cerebral angiography confirms presence of tumor.
H Positron-emission tomography confirms presence of
tumor.
Diagnostic procedures
H Tissue biopsy confirms type of tumor.
Other
H Lumbar puncture shows increased cerebrospinal
fluid (CSF) pressure, which reflects ICP, increased
protein levels, decreased glucose levels and, occasionally, tumor cells in CSF.

Treatment
General
H Specific treatments varying with the tumors histolog-

ic type, radiosensitivity, and location


H No dietary restrictions unless swallowing impaired
H Possibly altered physical ability based on neurologic

status

Medications
H Chemotherapy, such as carmustine, cisplatin, and

lomustine
H Steroid such as dexamethasone
H Histamine-receptor antagonists, such as cimetidine,

famotidine, and ranitidine


H Anticonvulsants, such as phenytoin and fosphenytoin
H Analgesic such as codeine

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Surgery
For glioma
H Resection by craniotomy
H Radiation therapy and chemotherapy follow resection
For low-grade cystic cerebellar astrocytoma
H Surgical resection
For astrocytoma
H Repeated surgeries, radiation therapy, and shunting
of fluid from obstructed CSF pathways
For oligodendroglioma and ependymoma
H Surgical resection and radiation therapy
For medulloblastoma
H Surgical resection
H Possibly, intrathecal infusion of methotrexate or
another antineoplastic drug
For meningioma
H Surgical resection, including dura mater and bone
For schwannoma
H Microsurgical technique

Patient teaching
Be sure to cover:
H the disease process, diagnosis, and treatment
H signs of infection or bleeding that may result from
chemotherapy
H adverse effects of chemotherapy and other treatments
and actions that may alleviate them
H early signs of tumor recurrence.

Discharge planning
H Consult with occupational and physical therapy staff

for postdischarge care plan.


H Refer the patient to resource and support services.

Nursing considerations
Key outcomes
The patient will:
H recognize limitations imposed by illness and express
feelings about them
H continue to function in usual roles as much as
possible
H enlist support from available sources
H express feelings of increased comfort.

Nursing interventions
H Maintain a patent airway.
H Take steps to protect the patients safety.
H Give prescribed drugs.
H After supratentorial craniotomy, elevate the head of

the bed about 30 degrees.


H After infratentorial craniotomy, keep the patient flat

for 48 hours.
H As appropriate, instruct the patient to avoid Valsalvas

maneuver and isometric muscle contractions when


moving or sitting up in bed.
H Provide postoperative care.
H Encourage incentive spirometer use.
H Consult with occupational, speech, and physical
therapists.
H Provide emotional support.

Monitoring
H Neurologic status
H Vital signs
H Wound site
H Postoperative complications
H Pulse oximetry
H Respiratory status
H Pain level, location, and effectiveness of treatment
H Cardiovascular status

Brain tumor

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Breast cancer
Overview
Description
H Malignant proliferation of epithelial cells lining the

ducts or lobules of the breast


H Early detection and treatment influencing the prognosis considerably

ALERT
The most reliable detection method of breast cancer is regular breast self-examination, followed by
an immediate professional evaluation of any abnormality. (Theoretically, slow-growing breast cancer may take up to 8 years to become palpable at
1 cm.)
H With adjunctive therapy, 10-year (or longer) 70% to

75% survival in females with negative nodes, compared to 20% to 25% survival in females with positive
nodes

Pathophysiology
H Breast cancer spreads by way of the lymphatic system

H Estrogen therapy
H Antihypertensive therapy
H Alcohol and tobacco use
H Preexisting fibrocystic disease

Incidence
H A female living in the United States to age 80 a

1-in-8 chance of developing invasive breast cancer


sometime during her life
H The second-leading cause of cancer death in females
after lung cancer
H Most common after age 50; but may develop anytime
after puberty
H Seldom occurs in males

Special populations
Breast cancer is the leading cause of cancer deaths
among females ages 35 to 54.

Common characteristics
H Lump or mass in the breast (see Breast tumor

sources and sites)


H Breast pain
H Change in symmetry or size of breast
H Change in skin, such as thickening, scaly skin around

the nipple, dimpling, edema, or ulceration

and the bloodstream through the right side of the


heart to the lungs and to the other breast, chest wall,
liver, bone, and brain.
Classification
H Adenocarcinoma (ductal) arises from the epithelium.
H Intraductal cancer develops within the ducts (includes Pagets disease).
H Infiltrating cancer occurs in the breasts parenchymal
tissue.
H Inflammatory cancer (rare) grows rapidly and causes overlying skin to become edematous, inflamed,
and indurated.
H Lobular carcinoma in situ involves the lobes of glandular tissue.
H Medullary or circumscribed cancer is an enlarged tumor with a rapid growth rate.

H Nipple discharge

Causes

H Clear, milky, or bloody discharge from the nipple,

H Unknown

Risk factors
H Family history of breast cancer, particularly first-

degree relatives, including mother, sister, maternal


grandmother, and maternal aunt
H Positive tests for genetic mutations (BRCA1)
H A female older than age 45 and premenopausal
H Long menstrual cycles
H Early onset of menses, late menopause
H Nulliparous or first pregnancy after age 30
H High-fat diet
H Endometrial or ovarian cancer
H History of unilateral breast cancer
H Radiation exposure

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Breast cancer

Complications
H Distant metastasis
H Infection
H Central nervous system effects
H Respiratory effects

Assessment
History
H Detection of a painless lump or mass in the breast
H Change in breast tissue
H History of risk factors

Physical findings
nipple retraction, scaly skin around the nipple, and
skin changes, such as dimpling or inflammation
H Arm edema
H Hard lump, mass, or thickening of breast tissue
H Lymphadenopathy

Test results
Laboratory
H Hormonal receptor assay determines whether the
tumor is estrogen- or progesterone-dependent; also
guides decisions to use therapy that blocks the action
of the estrogen hormone that supports tumor growth.
H In Vitro Diagnostic Multivariate Index Assay predicts
the odds that an early-stage breast cancer will metastasize in 5 to 10 years.

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Imaging
H Mammography can reveal a tumor thats too small to
palpate.
H Ultrasonography can distinguish between a
fluid-filled cyst and solid mass.
H Chest X-rays can pinpoint metastasis in the chest.
H Scans of the bone, brain, liver, and other organs can
detect distant metastasis.
Diagnostic procedures
H Fine-needle aspiration and excisional biopsy provide
cells for histologic examination that may confirm the
diagnosis.

Breast tumor sources and sites


About 90% of all breast tumors arise from the epithelial
cells lining the ducts. About half of all breast cancers develop in the breasts upper outer quadrant the section
containing the most glandular tissue.
The second most common cancer site is the nipple,
where all the breast ducts converge.
The next most common site is the upper inner quadrant,
followed by the lower outer quadrant and, finally, the lower inner quadrant.

Treatment
General

50%

H The choice of treatment usually depends on: stage

15%

and type of disease, age, menopausal status, and any


disfiguring effects of surgery
H Therapy may include: any combination of surgery,
radiation, chemotherapy, and hormone therapy
H Arm motion and exercises possibly needed after
surgery
H Primary radiation therapy
H Preoperative breast irradiation

18%
11%
6%

Medications
H Chemotherapy, such as a combination of drugs, in-

cluding anastrozole, capecitabine, cyclophosphamide, docetaxel, epirubicin, ememestane, fluorouracil, methotrexate, doxorubicin, vincristine,
paclitaxel, prednisone, and trastuzumab
H Regimen of cyclophosphamide, methotrexate, and
fluorouracil (used in premenopausal and postmenopausal females)
H Antiestrogen therapy such as tamoxifen
H Hormonal therapy, including estrogen, progesterone,
androgen, or antiandrogen aminoglutethimide
therapy

Surgery
H Lumpectomy
H Partial, total, or modified radical mastectomy

Nursing considerations
Key outcomes
The patient will:
H recognize limitations imposed by illness and express
feelings about these limitations
H express positive feelings about self
H report feelings of comfort
H express increased sense of well-being
H use situational supports to reduce fear.

Nursing interventions

H Provide emotional support.


H Provide postoperative care, such as turning, cough-

ing, deep breathing, and incentive spirometer use.


H Keep the head of the bed elevated at least 30 degrees

to prevent pneumonia.
H Encourage early ambulation.

Monitoring
H Wound site
H Postoperative complications
H Vital signs
H Intake and output
H White blood cell count
H Pain control
H Psychological status
H Respiratory status

Patient teaching
Be sure to cover:
H all procedures and treatments
H activities or exercises that promote healing
H breast self-examination
H risks and signs and symptoms of recurrence
H avoidance of venipuncture or blood pressure monitoring on the affected arm.

H Provide information about the disease process, diag-

Discharge planning

nostic tests, and treatment.


H Give prescribed drugs.

H Refer the patient to local and national support

groups.

Breast cancer

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Bronchiectasis

H Dramatically decreased incidence over the past 20

Overview

years due to the availability of antibiotics to treat


acute respiratory infections
H Highest among Inuit populations in the northern
hemisphere and the Maoris of New Zealand

Description

Common characteristics

H Lung disease characterized by abnormal dilation of

H Chronic cough productive for copious, foul-smelling,

the bronchi and destruction of the bronchial walls


H Results from conditions associated with repeated
damage to bronchial walls and with abnormal mucociliary clearance, causing a breakdown of supporting tissue adjacent to the airways
H Can occur throughout the tracheobronchial tree, or
may be confined to one segment or lobe
H Usually bilateral and involves the basilar segments of
the lower lobes
H Occurs in three forms: cylindrical (fusiform), varicose, and saccular (cystic)

Pathophysiology
H Hyperplastic squamous epithelium, denuded of cilia,

replaces ulcerated columnar epithelia.

mucopurulent secretions
H Dyspnea
H Weight loss
H Malaise

Complications
H Chronic malnutrition
H Amyloidosis
H Right-sided heart failure
H Cor pulmonale
H Respiratory failure

Assessment

H Abscess formation occurs, involving all layers of the

History

bronchial walls, which produces inflammatory cells


and fibrous tissues, resulting in dilation and narrowing of the airways.
H Sputum stagnates in the dilated bronchi and leads to
secondary infection, characterized by inflammation
and leukocytic accumulations.
H Additional debris collects in the bronchi and occludes them.
H Building pressure from the retained secretions induces mucosal injury.
H Extensive vascular proliferation of bronchial circulation occurs and produces frequent hemoptysis.

H Frequent bouts of pneumonia


H Coughing up of blood or blood-tinged sputum
H Chronic cough that produces copious, foul-smelling,

Causes
H Cystic fibrosis
H Mucoviscidosis
H Immune disorders
H Recurrent bacterial respiratory tract infections
H Complications of measles, pneumonia, pertussis, or

influenza
H Obstruction with recurrent infection
H Inhalation of corrosive gas
H Repeated aspiration of gastric juices
H Congenital anomalies (rare) such as bronchomalacia
H Various rare disorders such as immotile cilia syn-

drome

Risk factors
H Occupational exposure to damaging inhalants
H Risky behaviors that lead to immunodeficiency disor-

ders, such as human immunodeficiency virus and acquired immunodeficiency syndrome

Incidence
H Affects people of both sexes and of all ages

132

Bronchiectasis

mucopurulent secretions
H Dyspnea
H Weight loss
H Malaise

Physical findings
H Sputum that may show a cloudy top layer, a central

layer of clear saliva, and a heavy, thick, purulent bottom layer upon settling
H Clubbed fingers and toes
H Cyanotic nail beds
H Dullness over affected lung fields, if pneumonia or
atelectasis present
H Diminished breath sounds
H Crackles during inspiration over affected area
H Occasional wheezes

Test results
Laboratory
H Sputum culture and Gram stain show predominant
pathogens.
H Complete blood count reveals anemia and leukocytosis.
Imaging
H Computed tomography scan shows bronchiectasis.
H Bronchography shows location and extent of disease.
H Chest X-rays show peribronchial thickening, atelectatic areas, and scattered cystic changes.
Diagnostic procedures
H Bronchoscopy may show the source of secretions or
the bleeding site in hemoptysis.
H Pulmonary function studies show decreased vital
capacity, expiratory flow, and hypoxemia.

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Other
H A sweat electrolyte test may show cystic fibrosis as
the underlying cause.

Treatment
General
H Postural drainage and chest percussion
H Bronchoscopy to remove secretions
H Well-balanced, high-calorie diet
H Adequate hydration
H Activity, as tolerated

Medications
H Antibiotics, such as cefdinir, cefpodoxime, and

levofloxacin
H Bronchodilators, such as albuterol and aformoterol
H Oxygen
H Mucolytic such as acetylcysteine

Surgery
For poor pulmonary function
H Segmental resection
H Bronchial artery embolization
H Lobectomy

Nursing considerations

H Arterial blood gas results


H Complications
H Chest tube drainage after surgery
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H proper disposal of secretions
H infection control techniques
H frequent rest periods
H preoperative and postoperative instructions, if
surgery is required
H postural drainage and percussion
H coughing and deep-breathing techniques
H avoidance of air pollutants and people with known
upper respiratory tract infections
H immunizations
H balanced, high-protein diet
H avoidance of milk products
H adequate hydration.

Discharge planning
H Refer the patient to a smoking-cessation program, if

indicated.

Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate ventilation
H utilize energy conservation techniques
H demonstrate effective coping mechanisms.

Nursing interventions
H Perform preoperative and postoperative teaching.
H Give prescribed drugs.
H Provide supportive care.
H Administer oxygen, as needed.
H Perform chest physiotherapy.
H Provide a warm, quiet, comfortable environment.
H Alternate rest and activity periods.
H Provide well-balanced, high-calorie meals.
H Offer small, frequent meals.
H Provide adequate hydration.
H Provide frequent mouth care.
H Encourage incentive spirometer use, coughing, and

deep breathing.
H Provide postoperative care.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H Vital signs
H Intake and output
H Respiratory status
H Cardiac status
H Sputum production
H Pulse oximetry

Bronchiectasis

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Bronchitis, chronic
Overview
Description
H An inflammation of the lining of the bronchial tubes
H Form of chronic obstructive pulmonary disease
H Characterized by excessive production of tracheo-

bronchial mucus with a cough for at least 3 months


each year for 2 consecutive years
H Severity linked to the amount of cigarette smoke or
other pollutants inhaled and inhalation duration
H Respiratory tract infections that typically exacerbate
the cough and related symptoms
H Development of significant airway obstruction seen in
few patients with chronic bronchitis

Pathophysiology
H Hypertrophy and hyperplasia of the bronchial mu-

cous glands, increased goblet cells, ciliary damage,


squamous metaplasia of the columnar epithelium,
and chronic leukocytic and lymphocytic infiltration
of bronchial walls results.
H Additional effects include widespread inflammation,
airway narrowing, and mucus within the airways
all producing resistance in the small airways and, in
turn, a severe ventilation-perfusion imbalance. (See
What happens in chronic bronchitis.)

Causes
H Cigarette smoking
H Possible genetic predisposition
H Environmental pollution
H Organic or inorganic dusts and noxious gas exposure

Incidence
H About 20% of males affected
H More than 8.8 million people in the United States di-

agnosed annually
H More prevalent in females than in males
H Children of parents who smoke: higher risk for con-

tracting chronic bronchitis than children of parents


who dont smoke

Common characteristics
H Long-time smoker
H Frequent upper respiratory tract infections
H Productive cough
H Exertional dyspnea

Complications
H Cor pulmonale
H Pulmonary hypertension
H Right ventricular hypertrophy
H Acute respiratory failure

Assessment
History
H Longtime smoker
H Frequent upper respiratory tract infections
H Productive cough
H Exertional dyspnea
H Cough, initially prevalent in winter, but gradually

becoming year-round
H Increasingly severe coughing episodes
H Worsening dyspnea

Physical findings
H Cough producing copious gray, white, or yellow

sputum
H Cyanosis
H Accessory respiratory muscle use
H Tachypnea
H Substantial weight gain
H Pedal edema
H Jugular vein distention
H Wheezing
H Prolonged expiratory phase
H Rhonchi

Test results
Laboratory
H Arterial blood gas analysis shows decreased partial
pressure of oxygen and normal or increased partial
pressure of carbon dioxide.
H Sputum culture reveals microorganisms and neutrophils.
Imaging
H Chest X-ray may show hyperinflation and increased
bronchovascular markings.
Diagnostic procedures
H Pulmonary function tests show increased residual
volume, decreased vital capacity and forced expiratory flow, and normal static compliance and diffusing
capacity.
H Electrocardiography may show atrial arrhythmias;
peaked P waves in leads II, III, and aVF; and right
ventricular hypertrophy.

Treatment
General
H Smoking cessation
H Avoidance of air pollutants
H Chest physiotherapy
H Ultrasonic or mechanical nebulizer treatments
H Adequate fluid intake
H High-calorie, protein-rich diet
H Activity, as tolerated with frequent rest periods

Medications
H Oxygen
H Antibiotics, such as cefdinir, cefpodoxime, and

levofloxacin

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Bronchitis, chronic

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What happens in chronic bronchitis


In chronic bronchitis, irritants inhaled
for a prolonged period inflame the tracheobronchial tree. The inflammation
leads to increased mucus production
and a narrowed or blocked airway.
As inflammation continues, the
mucus-producing goblet cells undergo
hypertrophy, as do the ciliated epithelial cells that line the respiratory tract.
Hypersecretion from the goblet cells
blocks the free movement of the cilia,
which normally sweep dust, irritants,
and mucus from the airways.
As a result, the airway stays
blocked, and mucus and debris accumulate in the respiratory tract.

CROSS SECTION OF THE NORMAL


BRONCHIAL TREE

Cilia

Cilia

Goblet cell

H Bronchodilators, such as aformoterol, salmeterol,

and tiotropium
H Corticosteroids, such as fluticasone, hydrocortisone,
methylprednisolone, and prednisone
H Diuretics such as furosemide

Surgery

NARROWED BRONCHIAL TUBE IN


CHRONIC BRONCHITIS

Epithelial cell

Goblet cell

Epithelial cell

H Daily weight
H Edema
H Response to treatment
H Cardiovascular status

Patient teaching

H Tracheostomy in advanced disease

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H identify measures to prevent or reduce fatigue
H express understanding of the illness
H maintain a patent airway.

Nursing interventions
H Give prescribed drugs.
H Encourage expression of fears and concerns.
H Include the patient and his family in care decisions.
H Perform chest physiotherapy.
H Provide a high-calorie, protein-rich diet.
H Offer small, frequent meals.
H Encourage energy-conservation techniques.
H Ensure adequate oral fluid intake.
H Provide frequent mouth care.
H Encourage daily activity.
H Provide diversional activities, as appropriate.
H Provide frequent rest periods.
H Encourage coughing, deep breathing, and incentive

Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H infection control practices
H influenza and pneumococcus immunizations
H home oxygen therapy, if required
H postural drainage and chest percussion
H coughing and deep-breathing exercises
H inhaler use
H high-calorie, protein-rich meals
H adequate hydration
H avoidance of inhaled irritants
H prevention of bronchospasm
H respiratory hygiene and cough etiquette.

Discharge planning
H Refer the patient to a smoking-cessation program, if

indicated.
H Refer the patient to the American Lung Association

for information and support.


H Refer the patient to support services for respiratory

care equipment and supplies.

spirometer use.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H Vital signs
H Intake and output
H Sputum production
H Respiratory status, including breath sounds and

pulse oximetry

Bronchitis, chronic

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Brucellosis
Overview
Description
H An acute febrile illness transmitted to humans from

animals
H Also known as undulant fever, Malta fever, or

Bangs disease

Pathophysiology
H Brucellosis is transmitted through the consumption

of unpasteurized dairy products or uncooked or undercooked contaminated meat, and through contact
with infected animals or their secretions or excretions.

Causes
H The nonmotile, nonspore-forming, gram-negative

coccobacilli of the genus Brucella, notably B. suis


(found in swine), B. melitensis (in goats), B. abortus (in cattle), and B. canis (in dogs)

Risk factors
H Occupational exposure to animals

Incidence
H Most common among farmers, stock handlers,

butchers, and veterinarians


H Six times more common in males than in females
H Less common in children
H People with chlorhydria particularly susceptible be-

cause hydrochloric acid in gastric juices kills Brucella bacteria


H Most prevalent in the Middle East, Africa, Russia, India, South America, and Europe; uncommon in the
United States

Common characteristics
Acute phase
H Fever
H Chills
H Profuse sweating
H Fatigue
H Headache
H Backache
H Enlarged lymph nodes
H Hepatosplenomegaly
H Weight loss
H Abscess and granuloma formulation in subcutaneous
tissues, lymph nodes, liver, and spleen
Chronic phase
H Recurrent depression
H Sleep disturbances
H Fatigue
H Headache
H Sweating
H Sexual impotence

136

Brucellosis

H Hepatosplenomegaly
H Enlarged lymph nodes

Complications
H Abscesses in the testes, ovaries, kidneys, and brain

(meningitis and encephalitis)


H Osteomyelitis
H Orchitis
H Subacute bacterial endocarditis
H Pleural effusions
H Pneumothorax
H Eczematous rashes, petechiae, purpura

Assessment
History
H Direct exposure to animals
H Ingestion of unpasteurized dairy products
H Recent travel to an endemic area
H Fatigue
H Headache
H Intermittent fever
H Profuse sweating
H Anxiety
H General aching

Physical findings
H Excessive perspiration
H Chills
H Weakness
H Lymphadenopathy
H Hepatosplenomegaly
H Tenderness in the right upper quadrant

Test results
Laboratory
H Agglutinin titers are 1:160 or higher.
H Definitive diagnosis is provided by three to six
cultures of blood and bone marrow and biopsies
of infected tissue (for example, the spleen).
H Erythrocyte sedimentation rate is increased.
H White blood cell count is either normal or reduced.

Treatment
General
H Bed rest during the acute phase
H High-calorie, high-protein diet
H Secretion precautions until lesions stop draining

Medications
H Antibiotic such as tetracycline
H Antipyretic such as acetaminophen
H Corticosteroids, such as hydrocortisone, methylpred-

nisolone, and prednisone

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Nursing considerations
Key outcomes
The patient will:
H be free from signs and symptoms of infection
H attain relief from immediate symptoms
H experience feelings of comfort or absence of pain
H regain or maintain skin integrity.

Nursing interventions
H Keep suppurative granulomas and abscesses dry.
H Maintain contact precautions: double-bag and prop-

erly dispose of all secretions and soiled dressings.


H Reassure the patient that this infection is curable.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H Vital signs
H Complications
H Depression and disturbed sleep pattern
H Lesion healing
H Neurologic status

Patient teaching
Be sure to cover:
H continuing medication for the prescribed duration
H preventing recurrence by cooking meat thoroughly
and avoiding unpasteurized milk
H advice to meat packers and other people at risk for
occupational exposure to wear rubber gloves and
goggles.

Brucellosis

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Buergers disease
Overview

H Digital ischemia
H Trophic nail changes
H Absent or diminished radial, ulnar, or tibial pulses
H Ischemic ulcers on the toes, feet, or fingers
H Superficial thrombophlebitis

Description

Test results

H An inflammatory, nonatheromatous occlusive condi-

Imaging
H Doppler ultrasonography shows diminished circulation in the peripheral vessels.
H Arteriography locates lesions and rules out atherosclerosis.
Diagnostic procedures
H Plethysmography helps detect decreased circulation
in the peripheral vessels.
Other
H Allens test results are abnormal. (See Performing
Allens test.)

tion that impairs circulation to the legs, feet and, occasionally, hands
H Sometimes called thromboangiitis obliterans

Pathophysiology
H Polymorphonuclear leukocytes infiltrate the walls of

small and medium-sized arteries and veins.


H Thrombus develops in the vascular lumen, eventually

occluding and obliterating portions of the small vessels, resulting in decreased blood flow to the feet and
legs.
H This diminished blood flow may produce ulceration
and, eventually, gangrene.

Treatment

Causes

General

H Unknown
H Linked to smoking (suggesting a hypersensitivity

H Smoking cessation
H Nothing by mouth, if surgery is needed
H Exercise program that uses gravity to fill and drain

reaction to nicotine)

Incidence
H More common in males than females
H Most patients ages 20 to 45
H Affects natives of India, Japan, and Korea and Ashke-

nazic Jews

Common characteristics

the blood vessels

Medications
H Antibiotics, such as cefuroxime, gentamicin, and

tobramycin, for secondary infection


H Analgesics, such as morphine, hydromorphone, and

ketarolac

H Intermittent claudication of the instep, aggravated by

Surgery

exercise and relieved by rest


H Initially, coldness, cyanosis, and numbness in feet
during exposure to low temperature; later, redness,
heat, and tingling
H Impaired peripheral pulses and migratory superficial
thrombophlebitis

H In severe disease, a lumbar sympathectomy to in-

Complications
H Ulceration
H Muscle atrophy
H Gangrene

Assessment
History
H Exposure to secondhand smoke
H Use of nicotine patch
H Use of chewing tobacco
H Smoking
H Painful, intermittent claudication of the instep, aggra-

vated by exercise and relieved by rest

Physical findings
H Feet that are cold, numb, and cyanotic when exposed

to low temperatures

138

Buergers disease

crease blood supply to the skin


H Amputation for nonhealing ulcers, intractable pain,

or gangrene

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H maintain tissue integrity
H carry out previous roles without the limitations of the
disease process
H develop adequate coping mechanisms.

Nursing interventions
H Position the patient for comfort with the head of the

bed elevated at least 30 degrees.


H Provide a padded footboard or bed cradle to prevent

pressure from bed linens.


H Protect the feet with soft padding.
H Provide emotional support.
H Administer medications, as ordered.

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Performing Allens test


Dont obtain an arterial blood gas specimen from the radial artery until you assess collateral arterial blood supply using the
Allens test.
Direct the patient to close his hand
while you occlude his radial and ulnar
arteries for 10 to 30 seconds, watching for the hand to blanch.

Tell the patient to open his hand.

Release pressure on the ulnar artery.


Color should return to the patients
hand in 15 seconds. If the color
doesnt return, select another site
for an arterial puncture.

Monitoring
H Skin integrity
H Peripheral circulation
H Infection
H Pain control

Patient teaching
Be sure to cover:
H avoiding precipitating factors, such as emotional
stress, exposure to extreme temperatures, and
trauma
H proper foot care, especially the importance of wearing well-fitting shoes and cotton or wool socks.

Discharge planning
H Refer the patient to a self-help group to help him

stop smoking.
H Refer the patient for psychological counseling, if

needed.
H If the patient has undergone amputation, refer him

to physical therapists, occupational therapists, and


social service agencies, as needed.

Buergers disease

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Bulimia nervosa
Overview
Description
H Behavioral disorder characterized by eating binges

followed by feelings of guilt, humiliation, and


self-deprecation
H Self-induced vomiting, the use of laxatives or diuretics, or strict dieting or fasting to overcome the effects
of the binges
H Seldom incapacitating

Pathophysiology
H Decreased caloric intake depletes body fat and pro-

H Distinguished for participation in competitive activi-

ties

Complications
H Dental caries
H Erosion of tooth enamel
H Parotitis
H Gum infections
H Electrolyte imbalances
H Dehydration
H Arrhythmias
H Cardiac failure
H Sudden death
H Esophageal tears
H Gastric ruptures
H Mucosal damage to intestine
H Suicide

tein stores.
H Estrogen deficiency occurs in women due to lack of

lipid substrate for synthesis, causing amenorrhea.


H Testosterone levels fluctuate in men, causing de-

creased erectile function and sperm count.


H Ketoacidosis occurs from increased use of fat as en-

ergy fuel.

Causes
H Exact cause unknown

Risk factors
H Family disturbance or conflict
H Sexual abuse
H Maladaptive learned behavior
H Struggle for control or self-identity
H Cultural overemphasis on physical appearance
H Parental obesity
H Female gender
H Adolescent or young adult

Incidence
H Affects nine females for every one male
H Between 1% and 3% of adolescent and young fe-

males meeting the diagnostic criteria; 5% to 15%


having some symptoms of the disorder

Assessment
History
H Episodic binge eating
H Continues eating until abdominal pain, sleep, or the

presence of another person interrupts it


H Preferred food usually sweet, soft, and high in calo-

ries and carbohydrate content


H Exaggerated sense of guilt
H Depression
H Childhood trauma
H Parental obesity
H Unsatisfactory sexual relationships

Physical findings
H Thin or slightly overweight
H Use of diuretics, laxatives, vomiting, and exercise
H Abdominal and epigastric pain
H Amenorrhea
H Painless swelling of the salivary glands
H Unusual swelling of cheeks or jaw area
H Hoarseness
H Throat irritation or lacerations
H Calluses of the knuckles or abrasions and scars on

the dorsum of the hand

Special populations
Bulimia has been found to begin in adolescence or
early adulthood.

Common characteristics
H Strongly associated with depression
H Can occur simultaneously with anorexia nervosa
H More prone to psychoactive substance abuse
H Hyperactivity
H Peculiar eating habits or rituals
H Frequent weighing
H Perceived by others as a perfect student, mother,

or career woman

140

Bulimia nervosa

DSM-IV-TR criteria
Diagnosis of bulimia nervosa can be confirmed when
these criteria are met, on average, twice per week for
3 months:
H recurrent episodes of binge eating
H repeated inappropriate behaviors to prevent weight
gain.

Test results
Laboratory
H Serum electrolyte studies show elevated bicarbonate,
decreased potassium, and decreased sodium levels.
Other
H The Beck Depression Inventory may identify coexisting depression.

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Treatment
General
H Inpatient or outpatient psychotherapy
H Self-help groups
H Drug rehabilitation
H Balanced diet
H Monitoring of eating pattern
H Monitoring of activity

Medications
H Antidepressant such as fluoxetine

Nursing considerations
Key outcomes
The patient will:
H acknowledge change in body image
H participate in decision-making about her case
H express positive feelings about self
H achieve expected state of wellness.

Nursing interventions
H Supervise mealtime and for a specified period after

meals, usually up to 1 hour.


H Set a time limit for each meal.
H Provide a pleasant, relaxed environment for eating.
H Use behavior modification techniques.
H Establish a food contract, specifying the amount and

type of food to be eaten at each meal.


H Encourage verbalization and provide support.

Monitoring
H Suicide potential
H Elimination patterns
H Eating patterns
H Complications
H Response to treatment
H Activity

Patient teaching
Be sure to cover:
H importance of keeping a food journal
H risks of laxative, emetic, and diuretic abuse
H assertiveness training
H medication administration, dosage, and possible
adverse effects.

Discharge planning
H Refer the patient to support services or specialized

inpatient care.
H Refer the patient for psychological counseling.

Bulimia nervosa

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Burns
Overview
Description
H Heat or chemical injury to tissue
H May be permanently disfiguring and incapacitating
H May be partial thickness or full thickness

Pathophysiology
Superficial, partial-thickness burns
H These burns cause localized injury to the epidermis
that isnt life-threatening.
Deep, partial-thickness burns
H These burns cause destruction of the epidermis and
some dermis resulting in thin-walled and fluid-filled
blisters.
H Nerve endings are exposed to air as blisters break.
H Pain develops when blisters are exposed to air.
H Barrier function of the skin is lost.
Full-thickness burns
H These burns affect every body system and organ and
extend into the subcutaneous tissue layer damaging
muscle, bone, and interstitial tissues.
H Interstitial fluids result in edema and an immediate
immunologic response occurs.
H These burns carry a threat of wound sepsis.
H Depending on the level of nerve damage, the patient
may have no pain.

Causes
H Residential fires
H Motor vehicle accidents
H Improper use or handling of matches
H Improperly stored gasoline
H Space heater or electrical malfunctions
H Improper handling of firecrackers
H Scalding accidents
H Child or elder abuse
H Contact, ingestion, inhalation, or injection of acids,

alkali, or vesicants
H Contact with faulty electrical wiring
H Contact with high-voltage power lines
H Chewing electric cords
H Friction or abrasion
H Sun exposure

Incidence
H Affects more than 2 million people each year
H 70,000 hospitalizations
H 20,000 specialized burn unit admissions

Common characteristics
Superficial, partial-thickness burns
H Localized pain
H Erythema
H Blanching
H Chills
H Headache
142

Burns

H Nausea and vomiting

Deep, partial-thickness burns


H Thin-walled, fluid-filled blisters
H Mild to moderate pain
H White, waxy appearance of damaged area
Full-thickness burns
H Pale, white, brown, or black leathery tissue
H Visible thrombosed vessels
H No blister formation
H Painless
Electrical burns
H Silver-colored, raised area at contact site
H Smoke inhalation and pulmonary damage
H Singed nasal hair
Mucosal burns
H Sores in mouth or nose
H Voice changes
H Coughing, wheezing
H Darkened sputum

Complications
H Respiratory complications
H Sepsis
H Hypovolemic shock
H Anemia
H Malnutrition
H Multiple organ dysfunction syndrome

Assessment
History
H Cause of the burn revealed
H Preexisting medical conditions

Physical findings
H Depth and size of the burn assessed
H Severity of the burn estimated
H Major more than 10% of the patients body sur-

face area (BSA); more than 20% of a childs BSA


H Moderate 3% to 10% of a patients BSA; 10% to

20% of a childs BSA


H Minor less than 3% of a patients BSA; less than

10% of a childs BSA


H Respiratory distress and cyanosis
H Edema
H Alteration in pulse rate, strength, and regularity
H Stridor, wheezing, crackles, and rhonchi
H S3 or S4
H Hypotension

Test results
Laboratory
H Arterial blood gas levels show hypoxia.
H Complete blood count shows decreased hemoglobin
level and hematocrit, if blood loss has occurred.
H Electrolyte levels are abnormal due to fluid losses
and shifts.
H Blood urea nitrogen levels are increased with fluid
losses.

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H Glucose level is decreased in children due to limited

glycogen storage.
H Urinalysis shows myoglobinuria and hemoglobinuria.
H Carboxyhemoglobin level is increased.
Diagnostic procedures
H Electrocardiography may show myocardial ischemia,
injury, or arrhythmias, especially in electrical burns.
H Fiber-optic bronchoscopy may show airway edema.

Treatment
General
H Burn source cessation
H Airway secured
H Hypoxia prevention
H Giving I.V. fluids through a large-bore I.V. line

Adult: maintain urine output of 30 to 50 ml/hour.


Child less than 66 lb (30 kg): maintain urine output of 1 ml/kg/hour.
H Nasogastric tube and urinary catheter insertion
H Wound care
H Nothing by mouth until severity of burn established,
then high-protein, high-calorie diet
H Increased hydration with high-calorie, high-protein
drinks, not free water
H Total parenteral nutrition if unable to take food by
mouth
H Activity limitation based on extent and location of
burn
H Physical therapy

Medications
H Booster of tetanus toxoid
H Analgesic such as morphine
H Antibiotics, such as gentamicin, tobramycin, and

H Remove constricting items.


H Encourage coughing, deep breathing, and incentive

spirometer use.
H Perform appropriate wound care.
H Keep the head of the bed elevated at least 30 degrees.
H Provide adequate hydration.
H Weigh the patient daily.
H Encourage verbalization and provide support.
H Perform range-of-motion exercises.

Monitoring

F
T
f

F
E

H Wound healing
H Vital signs
H Respiratory status, including pulse oximetry
H Signs of infection
H Intake and output
H Hydration and nutritional status
H Pain control
H Cardiac status

S
E

Patient teaching

Be sure to cover:
H the injury, diagnosis, and treatment
H appropriate wound care
H medication administration, dosage, and possible
adverse effects
H developing a dietary plan
H signs and symptoms of complications.

Discharge planning
H Refer the patient to rehabilitation, if appropriate.
H Refer the patient to psychological counseling, if

needed.
H Refer the patient to resource and support services.

vancomycin
H Antianxiety agent such as lorazepam

Surgery
H Loose tissue and blister debridement
H Escharotomy
H Skin grafting

Nursing considerations
Key outcomes
The patient will:
H report increased comfort and decreased pain
H attain the highest degree of mobility
H maintain fluid balance within the acceptable range
H maintain a patent airway
H demonstrate effective coping techniques.

Nursing interventions
H Apply immediate, aggressive burn treatment.
H Use strict sterile technique.
H Remove clothing thats still smoldering; soak first

with normal saline solution if its stuck to patients


skin.

Burns

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Campylobacteriosis

H More common in the summer months

Overview

H Mild or severe diarrhea


H Abdominal cramps
H Malaise

Description

Common characteristics

H In humans and animals, intestinal infection caused

Complications

by the Campylobacter organism, a spiral-shaped


bacteria
H Signs and symptoms developing 2 to 5 days after exposure to Campylobacter
H May spread to the bloodstream in persons with compromised immune systems, causing a life-threatening
infection

H Bacteremia
H Severe dehydration and electrolyte disturbances
H Guillain-Barr syndrome
H Reiters syndrome

Pathophysiology

History

H The organism invades and destroys the epithelial

H Exposure to contaminated food or water


H Acute onset of diarrhea
H Recent close contact with a person who has diarrhea

cells of the jejunum, ileum, and colon.


H This produces an increase in motility and secretions
that results in diarrhea.

Causes
H Ingestion of contaminated food or water or unpas-

teurized milk
H Occasionally from infected pets or wild animals
H Contact with an infected persons stool

Risk factors
H Occupational exposure to cattle, sheep, and other

Assessment

Physical findings
H Cramping abdominal pain
H Nausea and vomiting
H Fever
H Traces of blood in the stool

Test results
Laboratory
H Stool culture identifies Campylobacter.

farm animals
H Laboratory worker
H Homosexual men

Treatment

Incidence

General

H Most common bacterial cause of diarrheal illness in

H Contact precautions (see Contact precautions)


H Correction of fluid and electrolyte imbalances
H Increased fluid intake
H Activity as tolerated

the United States

Contact precautions
In addition to standard precautions, follow these precautions:
H Place the patient in a private room. If a private room
isnt available, consult with infection control personnel.
As an alternative, he may be placed in a room with a
patient who has an active infection with the same microorganism.
H Wear gloves whenever you enter the patients room. Always change them after contact with infected material.
Remove them before leaving the room. Wash your
hands immediately with an antimicrobial soap, or rub
them with a waterless antiseptic. Then avoid touching
contaminated surfaces.
H Wear a gown when entering the patients room if you
think your clothing will have extensive contact with him
or anything in his room or if he has diarrhea or is incontinent. Remove the gown before leaving the room.
H Limit the patients movement from the room, and
check with infection control personnel whenever he
must leave it.

Medications
H Oral antibiotics, such as doxycycline, minocycline,

and tetracycline

Nursing considerations
Key outcomes
The patient will:
H regain or maintain normal fluid and electrolyte balance
H have an elimination pattern that returns to normal.

Nursing interventions
H Follow contact precautions for those with active diar-

rhea.
H Isolate a patient who cant practice good hygiene.
H Give prescribed drugs.
H Replace lost fluids and electrolytes through diet or

I.V. fluids.

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Monitoring
H Intake and output
H Vital signs
H Signs of dehydration
H Electrolytes
H Amount and characteristics of stool
H Abdominal status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H proper food-handling practices
H medications and possible adverse effects
H complications and when to notify the physician
H preventive measures.

Campylobacteriosis

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Candidiasis
Overview
Description
H Mild, superficial fungal infection
H Can lead to severe disseminated infections and

fungemia in immunocompromised patient, transplant


recipient, burn patient, low-birth-weight neonate, or
patient on hyperalimentation
H Prognosis variable, depending on patients resistance
H Also known as candidosis and moniliasis

Pathophysiology
H Change in the patients resistance to infection, his im-

munocompromised state, and antibiotic use permit


the sudden proliferation of Candida albicans.

Causes

H Total parenteral nutrition


H Surgery
H Use of antibiotic agents

Incidence
H Affects 14% of immunocompromised patients
H Affects males and females equally
H Can occur at any age

Common characteristics
H Causative fungi infecting the nails (paronychia), skin

(diaper rash), or mucous membranes, especially the


oropharynx (thrush), vagina (vaginitis), esophagus,
and GI tract (see Identifying thrush)
H Systemic infection predominating among drug
abusers and diabetic and immunosuppressed
patients

Complications
H Dissemination with organ failure of the kidneys,

brain, GI tract, eyes, lungs, and heart

H In most cases, infection with C. albicans or C. tropi-

calis

Risk factors
H Maternal vaginitis present during vaginal delivery
H Preexisting diabetes mellitus, cancer, or immunosup-

pressant illness
H Immunosuppressant drug use
H Radiation
H Aging
H Irritation from dentures
H I.V. or urinary catheterization
H Drug abuse

Identifying thrush
Candidiasis of the oropharyngeal mucosa (thrush) causes
cream-colored or bluish white pseudomembranous patches on the tongue, mouth, or pharynx (as shown). Fungal
invasion may extend to circumoral tissues.

Assessment
History
H Underlying illness
H Recent course of antibiotic or antineoplastic therapy
H Drug abuse
H Hyperalimentation

Physical findings
H Scaly, erythematous, papular rash, possibly covered

with exudate and erupting in breast folds, between


fingers, and at the axillae, groin, and umbilicus
H Red, swollen, darkened nailbeds; occasionally, purulent discharge; possibly nail separation from the
nailbed
H Scales in the mouth and throat
H White or yellow vaginal discharge, with local excoriation; white or gray raised patches on vaginal walls,
with local inflammation
H Cream-colored or bluish white lacelike patches of
exudate on the tongue, mouth, or pharynx revealing
bloody engorgement when scraped
H Hemoptysis, cough; coarse breath sounds in the
infected lung fields
H Flank pain, dysuria, hematuria, cloudy urine with
casts
H Headache, nuchal rigidity, seizures, focal neurologic
deficits
H Blurred vision, orbital or periorbital pain, eye exudate, floating scotomata, and lesions with a white,
cotton-ball appearance seen during ophthalmoscopy
H Chest pain and arrhythmias
H Septic shock

Test results
Laboratory
H Fungal serological panel shows the presence of the
candidal organism.
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Treatment
General
H Treatment of predisposing condition
H No dietary restrictions unless oral infection
H With oral infection, spicy food only as tolerated
H Activity as tolerated

Medications
H Antifungals, such as amphotericin B, anidulafungin,

clotrimazole, and nystatin

Surgery
H Abscess drainage; surgically or percutaneously

Nursing considerations
Key outcomes
The patient will:
H express increased comfort
H avoid or have minimal complications
H maintain skin integrity
H express understanding of disorder and treatment.

Nursing interventions
H Follow standard precautions.
H Give prescribed drugs.
H Provide a nonirritating mouthwash to loosen tena-

cious secretions and a soft toothbrush to avoid irritation.


H Observe high-risk patients daily for patchy areas, irritation, sore throat, oral and gingival bleeding, and
other signs of superinfection.
H Assess the patient for underlying systemic causes.

Monitoring
H Vital signs
H Intake and output
H Blood urea nitrogen, serum creatinine, and urine

blood and protein levels


H Potassium levels

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H good oral hygiene practices
H (for a woman in her third trimester of pregnancy)
the need for examination for vaginitis to protect her
neonate from thrush infection at birth.

Candidiasis

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Life-threatening disorder

Cardiac tamponade
Overview
Description
H Rapid increase in intrapericardial pressure caused

by fluid accumulation in the pericardial sac


H Impaired diastolic filling of the heart

Pathophysiology
H Progressive accumulation of fluid in the pericardial

sac causes compression of the heart chambers.


H Compression of the heart chambers obstructs blood

flow into the ventricles and reduces the amount of


blood pumped out with each contraction.
H With each contraction, more fluid accumulates,
decreasing cardiac output. (See Understanding
cardiac tamponade.)

Causes
H May be idiopathic
H Effusion in cancer, bacterial infections, tuberculosis

and, rarely, acute rheumatic fever


H Trauma
H Hemorrhage from nontraumatic cause
H Viral, postirradiation, or idiopathic pericarditis
H Acute myocardial infarction
H Chronic renal failure
H Drug reaction
H Connective tissue disorders
H Cardiac catheterization
H Cardiac surgery

Incidence
H More common in males than in females
H Occurs with 2% of penetrating chest traumas

Common characteristics
H Systemic hypotension
H Muffled heart sounds
H Jugular vein distention

Physical findings
H Vary with volume of fluid and speed of fluid accumu-

lation
H Diaphoresis
H Anxiety and restlessness
H Pallor or cyanosis
H Jugular vein distention
H Edema
H Rapid, weak pulses
H Hepatomegaly
H Decreased arterial blood pressure
H Increased central venous pressure
H Pulsus paradoxus
H Narrow pulse pressure
H Muffled heart sounds

Test results
Imaging
H Chest X-rays show slightly widened mediastinum and
enlargement of the cardiac silhouette.
Diagnostic procedures
H Electrocardiography may show low voltage complexes in the precordial leads.
H Hemodynamic monitoring shows equalization of
mean right atrial, right ventricular diastolic, pulmonary artery wedge, and left ventricular diastolic pressures.
H Echocardiography may show an echo-free space, indicating fluid accumulation in the pericardial sac.

Treatment
General
H Pericardiocentesis, if necessary
H Diet, as tolerated
H Bed rest with the head of the bed elevated at least 30

degrees

Medications
H Intravascular volume expansion
H Inotropic agents, such as digoxin, milrinon, and

inamrinone
H Oxygen

Surgery

H Cardiogenic shock
H Death

H Pericardial window
H Subxiphoid pericardiotomy
H Complete pericardectomy
H Thoracotomy

Assessment

Nursing considerations

History

Key outcomes

H Presence of one or more causes


H Dyspnea
H Shortness of breath
H Chest pain

The patient will:


H maintain hemodynamic stability
H maintain adequate cardiac output
H not develop arrhythmias
H express understanding of disorder and treatment.

Complications

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Understanding cardiac tamponade


The pericardial sac, which surrounds
and protects the heart, is composed of
several layers. The fibrous pericardium
is the tough outermost membrane; the
inner membrane, called the serous
membrane, consists of the visceral and
parietal layers. The visceral layer clings
to the heart and is also known as the
epicardial layer of the heart. The parietal layer lies between the visceral layer
and the fibrous pericardium. The pericardial space between the visceral
and parietal layers contains 10 to
30 ml of pericardial fluid. This fluid
lubricates the layers and minimizes
friction when the heart contracts.

NORMAL HEART AND PERICARDIUM

Aorta
Superior vena cava
Parietal pericardium
Visceral pericardium
Fibrous pericardium
Pericardial space
Attachment of fibrous
pericardium to diaphragm

Diaphragm

In cardiac tamponade, blood or fluid


fills the pericardial space, compressing
the heart chambers, increasing intracardiac pressure, and obstructing venous
return. As blood flow into the ventricles
falls, so does cardiac output. Without
prompt treatment, low cardiac output
can be fatal.

CARDIAC TAMPONADE

Aorta
Superior vena cava
Fibrous pericardium
Parietal pericardium
Visceral pericardium
Pericardial space filled
with excess fluid
Compressed heart

Diaphragm

Nursing interventions
H Give prescribed drugs.
H Provide reassurance.
H Assist with pericardiocentesis, if necessary.
H Infuse I.V. solutions, as ordered.
H Administer oxygen therapy, as needed.
H Maintain the chest drainage system, if used.

Monitoring
H Vital signs
H Intake and output
H Signs and symptoms of increasing tamponade
H Cardiovascular status, including cardiac rhythm
H Hemodynamics
H Arterial blood gas levels
H Respiratory status
H Complications

H Pulse oximetry
H Jugular vein distention
H Chest tube drainage

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H preoperative and postoperative care
H emergency procedures.

Cardiac tamponade

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Cardiomyopathy, dilated
Overview
Description
H Disease of the heart muscle fibers
H Also called congestive cardiomyopathy

Pathophysiology
H Extensively damaged myocardial muscle fibers re-

duce contractility of left ventricle.


H The hearts pumping ability is reduced.
H As systolic function declines, cardiac output falls.
H The sympathetic nervous system is stimulated to increase heart rate and contractility.
H When compensatory mechanisms can no longer
maintain cardiac output, the heart begins to fail.
(See Understanding dilated cardiomyopathy.)

H Dry cough at night


H Shortness of breath
H Fatigue
H Weight gain

Complications
H Intractable heart failure
H Arrhythmias
H Emboli

Assessment
History
H Possible history of a disorder that can cause cardio-

myopathy
H Gradual onset of shortness of breath, orthopnea,

dyspnea on exertion, paroxysmal nocturnal dyspnea,


fatigue, dry cough at night, palpitations, and vague
chest pain

Causes

Physical findings

H Viral or bacterial infections


H Hypertension
H Peripartum syndrome related to toxemia
H Ischemic heart disease
H Valvular disease
H Drug hypersensitivity
H Chemotherapy
H Cardiotoxic effects of drugs or alcohol

H Peripheral edema
H Jugular vein distention
H Ascites
H Peripheral cyanosis
H Tachycardia even at rest and pulsus alternans in late

Incidence
H Most commonly affects middle-aged males but can

occur in any age-group and females

Common characteristics
H Dyspnea on exertion

Understanding dilated cardiomyopathy

stages
H Hepatomegaly and splenomegaly
H Narrow pulse pressure
H Irregular rhythms, diffuse apical impulses, pansys-

tolic murmur
H S3 and S4 gallop rhythms
H Pulmonary crackles

ALERT
Dilated cardiomyopathy may need to be differentiated from other types of cardiomyopathy. (See Assessment findings in cardiomyopathies.)

Test results

H Greatly increased chamber size


H Thinning of left ventricular muscle
H Increased atrial chamber size
H Increased myocardial mass
H Normal ventricular inflow resistance
H Decreased contractility

150

Cardiomyopathy, dilated

Imaging
H Chest X-rays demonstrate moderate to marked cardiomegaly and possible pulmonary edema.
H Echocardiography may reveal ventricular thrombi,
global hypokinesis, and the degrees of left ventricular
dilation and systolic dysfunction.
H Gallium scans may identify patients with dilated cardiomyopathy and myocarditis.
Diagnostic procedures
H Cardiac catheterization evaluates heart structure and
function.
H Transvenous endomyocardial biopsy may be useful in
determining underlying disorder in some patients.
H Electrocardiography evaluates ischemic heart disease
and identifies arrhythmias and intraventricular conduction defects.

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Assessment findings in cardiomyopathies


Type

Assessment findings

Dilated cardiomyopathy

Generalized weakness, fatigue


Chest pain, palpitations
Syncope
Tachycardia
Narrow pulse pressure
Pulmonary congestion, pleural effusions
Jugular vein distention, peripheral edema
Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion

Hypertrophic cardiomyopathy

Angina, palpitations
Syncope
Orthopnea, dyspnea on exertion
Pulmonary congestion
Loud systolic murmur
Life-threatening arrhythmias
Sudden cardiac arrest

Restrictive cardiomyopathy

Generalized weakness, fatigue


Bradycardia
Dyspnea
Jugular vein distention, peripheral edema
Liver congestion, abdominal ascites

Treatment
General
H No ingestion of alcohol if cardiomyopathy caused by

alcoholism
H Low-sodium diet supplemented by vitamin therapy
H Rest periods

H develop no complications of excess fluid volume


H recognize and accept limitations of chronic illness
H express feelings of increased energy and decreased

fatigue.

Nursing interventions
H Administer prescribed medications.
H Alternate periods of rest with required activities of

daily living.

Special populations
A woman of childbearing age with dilated cardiomyopathy should avoid pregnancy.

Medications
H Cardiac glycoside such as digoxin
H Diuretic such as furosemide
H Angiotensin-converting enzyme inhibitors, such as

benazepril and captopril


H Oxygen
H Anticoagulant such as warfarin
H Vasodilator such as isosorbide
H Antiarrhythmic such as esmolol
H Beta-adrenergic blocker such as metoprolol

Surgery
H Heart transplantation
H Possible cardiomyoplasty

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output and hemodynamic
stability
H maintain adequate ventilation

H Consult with dietitian to provide a low-sodium diet.


H Administer oxygen, as needed.
H Check serum potassium levels for hypokalemia, es-

pecially if therapy includes a cardiac glycoside.


H Offer support and let the patient express his feelings.
H Allow patient and family to express fears and con-

cerns; help them identify effective coping strategies.

Monitoring
H Vital signs and hemodynamics
H Cardiac rhythm
H Intake and output
H Daily weights
H Cardiovascular status
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H sodium and fluid restrictions
H signs and symptoms of worsening heart failure.

Discharge planning
H Refer family members to community cardiopul-

monary resuscitation classes.

Cardiomyopathy, dilated

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Cardiomyopathy,
hypertrophic
Overview
Description

Common characteristics
H Dyspnea
H Fatigue
H Signs of heart failure

Complications
H Pulmonary hypertension
H Heart failure
H Ventricular arrhythmias

H Primary disease of cardiac muscle characterized by

left ventricular hypertrophy


H Also known as idiopathic hypertrophic subaortic

stenosis, hypertrophic obstructive cardiomyopathy, and muscular aortic stenosis

Pathophysiology
H The hypertrophied ventricle becomes stiff, noncom-

pliant, and unable to relax during ventricular filling.


H Ventricular filling time is reduced as compensation

to tachycardia.
H Reduced ventricular filling leads to low cardiac output. (See Understanding hypertrophic cardiomyopathy.)

Causes

Assessment
History
H Generally, no visible clinical features until disease

well advanced
H Atrial fibrillation
H Possible family history of hypertrophic cardiomyop-

athy
H Orthopnea
H Dyspnea on exertion
H Anginal pain
H Fatigue
H Syncope, even at rest

H Transmission by autosomal dominant trait (about

Physical findings

one-half of all cases)


H Associated with hypertension

H Rapidly rising carotid arterial pulse possible


H Pulsus bisferiens
H Double or triple apical impulse, possibly displaced

Incidence
H More common in males than females
H Affects 5 to 8 people per 100,000 in the United States
H More common in blacks

laterally
H Bibasilar crackles if heart failure present
H Harsh systolic murmur heard after S1 at the apex

near the left sternal border

H Possible S4

Understanding hypertrophic
cardiomyopathy

ALERT
Hypertrophic cardiomyopathy may need to be differentiated from other types of cardiomyopathy.
(See Assessment findings in cardiomyopathies, page
151.)

Test results

H Normal right and decreased left chamber size


H Left ventricular hypertrophy
H Thickened interventricular septum (hypertrophic
obstructive cardiomyopathy)
H Atrial chamber size increased on left
H Increased myocardial mass
H Increased ventricular inflow resistance
H Increased or decreased contractility

152

Cardiomyopathy, hypertrophic

Imaging
H Chest X-rays may show a mild to moderate increase
in heart size.
H Thallium scan usually reveals myocardial perfusion
defects.
H Angiography reveals a dilated, diffusely hypokinetic
left ventricle.
Diagnostic procedures
H Echocardiography shows left ventricular hypertrophy
and a thick, asymmetrical intraventricular septum in
obstructive hypertrophic cardiomyopathy, whereas
hypertrophy affects various ventricular areas in
nonobstructive hypertrophic cardiomyopathy.
H Cardiac catheterization reveals elevated left ventricular end-diastolic pressure and, possibly, mitral insufficiency.

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H Electrocardiography usually shows left ventricular

hypertrophy, ST-segment and T-wave abnormalities,


Q waves in leads II, III, aVF, and in V4 to V6 (because
of hypertrophy, not infarction), left anterior hemiblock, left axis deviation, and ventricular and atrial
arrhythmias.

Treatment
General
H Cardioversion for atrial fibrillation
H Low-fat, low-sodium diet
H Fluid restrictions
H Avoidance of alcohol
H Activity limitations individualized
H Bed rest, if necessary

Medications
H Beta-adrenergic blocker such as propranolol
H Calcium channel blocker such as diltiazam
H Antiarrhythmic such as amiodarone (if atrioventricu-

lar block isnt present)

ALERT
If beta-adrenergic blockers will be discontinued,
dont stop the drug abruptly; doing so may cause
rebound effects, resulting in myocardial infarction
or sudden death.
H Offer support and let the patient express his feelings.
H Allow the patient and his family to express their fears

and concerns and identify effective coping strategies.

Monitoring
H Vital signs
H Cardiac rhythm
H Hemodynamics
H Intake and output
H Cardiovascular status
H Respiratory status (amiodarone may cause lung

toxicity)
H Emotional status

Patient teaching

H Antibiotic prophylaxis such as amoxicillin

ALERT
Angiotensin-converting enzyme inhibitors, nitrates, other beta-adrenergic blockers, and digoxin
are contraindicated in hypertrophic cardiomyopathy.

Surgery
H Ventricular myotomy alone or combined with mitral

valve replacement
H Heart transplantation

Nursing considerations
Key outcomes

Be sure to cover:
H that propranolol can cause depression and the need
to notify the physician if symptoms occur
H instructions to take medication as ordered
H the need to notify any physician caring for the patient
that he shouldnt be given nitroglycerin, digoxin, or
diuretics because they can worsen the obstruction
H the need for antibiotic prophylaxis before dental
work or surgery to prevent infective endocarditis
H warnings against strenuous activity, which may precipitate syncope or sudden death
H the need to avoid Valsalvas maneuver or sudden
position changes.

Discharge planning
H Refer family members to community cardiopulmo-

nary resuscitation classes.

The patient will:


H maintain adequate cardiac output and hemodynamic
stability
H develop no complications of excess fluid volume
H carry out activities of daily living (ADLs) without excess fatigue or decreased energy
H express feelings of comfort and decreased pain
H develop adequate coping mechanisms.

Nursing interventions
H Alternate periods of rest with required ADLs and

treatments.
H Provide personal care, as needed, to prevent fatigue.
H Provide active or passive range-of-motion exercises.
H Obtain daily weight.
H Administer prescribed medications.

Cardiomyopathy, hypertrophic

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Cardiomyopathy,
restrictive

Common characteristics

Overview

H Fatigue
H Dyspnea
H Orthopnea
H Chest pain
H Edema
H Systolic murmurs

Description

Complications

H Disease of the heart muscle fibers resulting in re-

H Heart failure
H Arrhythmias
H Systemic or pulmonary embolization
H Sudden death

strictive filling and reduced diastolic volume of one


or both ventricles
H Irreversible if severe

Pathophysiology
H Stiffness of the ventricle is caused by left ventricular

hypertrophy and endocardial fibrosis and thickening,


thus reducing the ventricles ability to relax and fill
during diastole.
H Failure of the rigid myocardium to contract completely during systole causes decreased cardiac output. (See Understanding restrictive cardiomyopathy.)

Causes
H Idiopathic or associated with other disease (for ex-

ample, amyloidosis or endomyocardial fibrosis)


H Heart transplant
H Mediastinal radiation
H Carcinoid heart disease

Incidence
H Rare; accounts for 5% of all cases of primary heart

disease
H Occurs equally in males and females

Understanding restrictive
cardiomyopathy

Assessment
History
H Fatigue
H Viral infection
H Dyspnea
H Chest pain

Physical findings
H Peripheral edema
H Liver engorgement
H Peripheral cyanosis
H Pallor
H S3 or S4 gallop rhythms (due to heart failure)
H Systolic murmurs

ALERT
Restricted cardiomyopathy may need to be differentiated from other types of cardiomyopathy. (See
Assessment findings in cardiomyopathies, page 151.)

Test results
Laboratory
H Complete blood count reveals eosinophilia.
Imaging
H Chest X-ray may reveal cardiomegaly.
H Echocardiography may reveal left ventricular muscle
mass, normal or reduced left ventricular cavity size,
and decreased systolic function.
Diagnostic procedures
H Electrocardiography may reveal low-voltage hypertrophy, arterioventricular conduction defects, and arrhythmias.
H Cardiac catheterization shows reduced systolic function and increased left ventricular end-diastolic pressures.

H Decreased ventricular chamber size


H Left ventricular hypertrophy
H Increased atrial chamber size
H Normal myocardial mass
H Increased ventricular inflow resistance
H Decreased contractility

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Cardiomyopathy, restrictive

Treatment
General
H Treatment of underlying cause
H Low-sodium diet
H Initially, bed rest, then activity, as tolerated

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Medications
H Cardiac glycoside such as digoxin
H Diuretic such as furosemide
H Vasodilator such as isosorbide
H Angiotensin-converting enzyme inhibitor such as

captopril
H Anticoagulant such as warfarin
H Corticosteroid such as prednisone

Surgery
H Permanent pacemaker
H Heart transplantation

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output and hemodynamic
stability
H express understanding of the disorder
H recognize and accept limitations of chronic illness
H seek support and establish coping mechanisms.

Nursing interventions
H Give prescribed drugs.
H Provide psychological support.
H Provide appropriate diversionary activities for the pa-

tient restricted to prolonged bed rest.

Monitoring
H Cardiac rhythm
H Vital signs
H Intake and output
H Hemodynamics
H Daily weight
H Cardiovascular status
H Respiratory status

Patient teaching
Be sure to cover:
H signs of digoxin toxicity
H importance of recording daily weight and reporting
weight gain of 2 lb (0.9 kg) or more
H dietary restrictions.

Discharge planning
H Refer for psychosocial counseling, as necessary, for

assistance in coping with restricted lifestyle.

Cardiomyopathy, restrictive

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Carpal tunnel syndrome

Pathophysiology
H Space-occupying lesion or direct pressure within the

carpal canal increases pressure on the median nerve,


resulting in compression.
H Compression of the median nerve interrupts normal
function. (See The carpal tunnel.)

Overview
Description
H Compression of the median nerve in the wrist
H Most common nerve entrapment syndrome
H May pose a serious occupational health problem

Causes
H Exact cause unknown
H Repetitive wrist motions involving excessive flexion

or extension

The carpal tunnel


The carpal tunnel is clearly visible in this palmar view and
cross section of a right hand. Note the median nerve, flexor tendons of fingers, and blood vessels passing through
the tunnel on their way from the forearm to the hand.

Flexor
tendons
of fingers

Radial nerve
Median nerve
CARPAL
TUNNEL

Ulnar nerve

H Dislocation
H Acute sprain that may damage the median nerve
H Tumors
H Gout
H Amyloidosis
H Edema-producing conditions

Risk factors
H Diabetes
H Pregnancy
H Alcoholism
H Hypothyroidism
H Renal failure

Incidence
H Most common in females ages 30 to 60
H Occurs in people who move their wrists continually

Common characteristics
H Weakness, pain, burning, numbness, tingling in the

hand
H Thumb, forefinger, middle finger, and half of fourth

finger affected by paresthesia


H Inability to clench fist
H Atrophic nails
H Dry and shiny skin

Complications
H Tendon inflammation
H Compression
H Neural ischemia
H Permanent nerve damage with loss of movement and

sensation

Assessment
History
H Occupation or hobby requiring strenuous or repeti-

tive use of the hands


H Condition that causes swelling in carpal tunnel struc-

tures
H Weakness, pain, burning, numbness, or tingling that

occurs in one or both hands


Flexor tendons
of fingers

Transverse
carpal ligament

H Paresthesia that worsens at night and in the morning


H Pain that spreads to the forearm and, in severe cases,

as far as the shoulder


H Pain can be relieved by:

shaking hands vigorously


dangling the arms at sides

156

Carpal tunnel syndrome

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Physical findings
H Inability to make a fist
H Fingernails may be atrophied, with surrounding dry,

shiny skin

Test results
Imaging
H Electromyography shows a median nerve motor conduction delay of more than 5 milliseconds.
H Digital electrical stimulation shows median nerve
compression by measuring the length and intensity of
stimulation from the fingers to the median nerve in
the wrist.
Other
H Compression test result supports the diagnosis.

H the prescribed medication regimen


H adverse reactions to drugs
H avoidance of NSAIDs in pregnancy.

Discharge planning
H Refer the patient for occupational counseling if a job

change is necessary.

Treatment
General
H Conservative initially:

Splinting the wrist for 1 to 2 weeks


Possible occupational changes
Correction of any underlying disorder
H Activity, as tolerated

Medications
H Nonsteroidal anti-inflammatory drug (NSAID) such

as ibuprofen
H Corticosteroid such as prednisone
H Vitamin supplement such as vitamin B complex

Surgery
H Decompression of the nerve
H Neurolysis

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and pain relief
H maintain muscle strength
H maintain joint mobility and range of motion
H perform activities of daily living.

Nursing interventions
H Promote self-care.
H Give prescribed analgesics.

Monitoring
H Response to analgesia
H After surgery, vital signs
H Color, sensation, and motion of the affected hand

Patient teaching
Be sure to cover:
H splint application
H hand exercises in warm water

Carpal tunnel syndrome

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Cataract
Overview
Description
H Opacity of the lens or lens capsule of the eye
H Common cause of gradual vision loss
H Commonly affects both eyes
H Traumatic cataracts usually unilateral

Pathophysiology
H The clouded lens blocks light shining through the

cornea.
H Images cast onto the retina are blurred.
H A hazy image is interpreted by the brain.

Causes
H Classified according to cause

Senile cataracts
H Chemical changes in lens proteins in elderly patients
Congenital cataracts
H Inborn errors of metabolism
H Maternal rubella infection during the first trimester
H Congenital anomaly
H Genetic causes (usually autosomal dominant)
H Recessive cataracts may be sex-linked
Traumatic cataracts
H Foreign bodies causing aqueous or vitreous humor
to enter lens capsule
Complicated cataracts
H Uveitis
H Glaucoma
H Retinitis pigmentosa
H Retinal detachment
H Diabetes
H Hypoparathyroidism
H Atopic dermatitis
H Ionizing radiation or infrared rays
Toxic cataracts
H Drug or chemical toxicity:
ergot
dinitrophenol
naphthalene
phenothiazines

Incidence
H Most prevalent in people older than age 70

Common characteristics
H Painless, gradual vision loss
H Glare
H Milky white pupil

Complications

H Hyphema
H Pupillary block glaucoma
H Retinal detachment
H Infection

Assessment
History
H Painless, gradual vision loss
H Blinding glare from headlights with night driving
H Poor reading vision
H Annoying glare
H Poor vision in bright sunlight
H Better vision in dim light than in bright light (central

opacity)

Physical findings
H Milky white pupil on inspection with a penlight
H Grayish white area behind the pupil (advanced

cataract)
H Red reflex lost (mature cataract)

Test results
Diagnostic procedures
H Indirect ophthalmoscopy reveals a dark area in the
normally homogeneous red reflex.
H Slit-lamp examination confirms lens opacity.
H Visual acuity test establishes the degree of vision loss.

Treatment
General
H Before surgery, eyeglasses and contact lenses that

may help to improve vision


H Sunglasses in bright light and lamps that provide re-

flected lighting rather than direct lighting, decreasing


glare and aiding vision
H Restricted activity according to vision loss

Medications
For cataract removal
H Nonsteroidal anti-inflammatory drugs, such as
ketorolac and bromfenac

Surgery
H Lens extraction and implantation of intraocular lens

(see Comparing methods of cataract removal)


H Extracapsular cataract extraction
H Intracapsular cataract extraction
H Phacoemulsification

Nursing considerations

H Complete vision loss

Key outcomes

Possible complications of surgery


H Loss of vitreous
H Wound dehiscence

The patient will:


H maintain current health status
H sustain no harm or injury

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Cataract

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Comparing methods of cataract removal


Cataracts can be removed by intracapsular or extracapsular techniques.

Intracapsular cataract extraction

Lens

Cryoprobe

In this technique, the surgeon makes a partial incision at


the superior limbus arc. He then removes the lens using
specially designed forceps or a cryoprobe, which freezes
and adheres to the lens to facilitate its removal.

Cornea

Extracapsular cataract extraction


In this technique, the surgeon may use irrigation and aspiration or phacoemulsification. In the former approach, the surgeon makes an incision at the limbus, opens the anterior lens capsule with a cystotome, and exerts pressure from below
to express the lens. He then irrigates and suctions the remaining lens cortex.
In phacoemulsification, he uses an ultrasonic probe to break the lens into minute particles, which are aspirated by the
probe.
PHACOEMULSIFICATION

IRRIGATION AND ASPIRATION


Cortical and nuclear cataract
material aspirated through
needle

Nucleus and cortex fragmented


and aspirated by probe

Cystotome

Lens
Ultrasonic probe

Lens

H voice feelings and concerns


H regain visual function.

Nursing interventions
H Perform routine postoperative care.
H Assist with early ambulation.
H Apply an eye shield or eye patch postoperatively, as

ordered.

Monitoring
H Vital signs
H Visual acuity
H Complications of surgery

Patient teaching
Be sure to cover:
H the need to avoid activities that increase intraocular
pressure, such as straining with coughing, bowel
movements, or lifting
H the need to abstain from sexual intercourse until the
patient receives physicians approval
H proper instillation of ophthalmic ointment or drops.

ALERT
If the patient has increased eye discharge, sharp
eye pain thats unrelieved by analgesics, or deterioration in vision, instruct him to notify his physician immediately.

Cataract

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Celiac disease
Overview
Description
H A multisystem intestinal intramucosal enzyme defect
H Characterized by poor food absorption and inability

to digest gluten, a protein found in wheat and wheat


products, rye, barley and, possibly, oats
H Also known as idiopathic steatorrhea, nontropical
sprue, gluten enteropathy, celiac sprue

Pathophysiology
H A toxic reaction in response to the ingestion of gluten

causes damage to the small intestines mucosal surface.


H Villi in the small intestine atrophy.
H Activity and amount of enzymes in the surface of the
epithelium decrease.
H Interference with nutrient absorption results.

Causes
H Exact mechanism unknown
H Environmental factors
H Genetic predisposition (associated with a group of

genes on chromosome 6)
H May be autoimmune in nature
H Strongly associated with two human leukocyte antigen haplotypes, DR3 and DQw2
H Can appear at any time in a persons life
H Triggers include surgery, infection, severe emotional
stress, and childbirth

Risk factors
H Family history

Incidence
H Affects 1 in every 133 persons in United States
H Affects twice as many females as males
H Primarily affects whites and those of European ances-

try
H Commonly associated with type 1 diabetes mellitus,

lactose intolerance, thyroid disease, Down syndrome,


liver disease, and autoimmune disorders, such as
rheumatoid arthritis and systemic lupus erythematosus

Common characteristics
H Varying significantly from person to person
H Some people asymptomatic

Complications
Prognosis usually good with treatment compliance
Without treatment:
H Anemia
H Central and peripheral nervous system disorders
H Intestinal lymphomas
H Neurologic changes
H Osteoporosis or osteopenia

160

Celiac disease

H Pancreatic insufficiency
H Skin disorders (dermatitis herpetiformis)
H Unexplained infertility or miscarriage
H Vitamin K deficiency with risk of hemorrhage
H Vitamin and mineral deficiencies

Assessment
History
H GI symptoms, including chronic diarrhea or consti-

pation (or both) and recurrent attacks of steatorrhea


(pale, foul-smelling, or fatty stool)
H Abdominal pain
H Anorexia or increased appetite without weight gain
H Fatigue
H Bone or joint pain (especially in lower back, rib
cage, and pelvis)
H Muscle cramps
H Mood changes and irritability
H Tingling or numbness in the legs
H Seizures
H Amenorrhea
H Itchy skin rash

Physical findings
H Abdominal distention
H Muscle wasting
H Compression fractures
H Unexplained short stature
H Peripheral neuropathy
H Dry skin, eczema, psoriasis, dermatitis herpetiformis,

or acne rosacea
H Generalized fine, sparse, prematurely gray hair
H Brittle nails
H Localized hyperpigmentation on the face, lips, and

mucosa
H Pale sores inside the mouth, called aphthous ulcers
H Tooth discoloration or loss of enamel

Special populations
Infants, toddlers, and children are commonly
found to have delayed growth, failure to thrive,
rickets, vomiting, a bloated abdomen, and behavioral changes.

Test results
Laboratory
H Alkaline phosphatase level is elevated possibly due to
bone loss.
H Cholesterol, albumen, and serum carotene levels are
decreased and may reflect malabsorption and malnutrition.
H Unexplained decrease in hemoglobin level and
hematocrit is noted; white blood cell and platelet
counts are reduced.
H Liver enzyme levels are mildly elevated.
H Prothrombin time is decreased.

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H Antibody blood testscombined are sensitive and

specific indicator.

Patient teaching

H Total serum immunoglobulin A (IgA), IgA anti-

endomysium antibodies (AEA), anti-tissue transglutaminase (tTGA), and antigliadin (IgA and IgG) levels
are elevated.
Diagnostic procedures
H Small-bowel biopsy specimens obtained by esophagogastroduodenoscopy show histologic changes that
confirm the diagnosis.

Treatment
General

Be sure to cover:
H the disorder and its treatment
H the reasons for not beginning a gluten-free diet before a diagnosis is made
H foods that are allowed on a gluten-free diet
H food product labels and how to identify ingredients
that may contain hidden gluten
H that gluten may be used as a binder in some medications and vitamins as well as stamp and envelope adhesives
H importance of contacting a dietitian
H testing of family members.

H Life-long gluten-free dietfull return to normal in

months or may never occur


H Eliminate all wheat, barley, rye, and oat products as

well as foods made from these grains, such as breads


and baked goods

Medications
H Corticosteroids for short-term use
H Supportive treatment with vitamin B12, iron, folic

acid, and vitamin K

Nursing considerations
Key outcomes
The patient will:
H express understanding of the disease and treatment
regimen
H consume an adequate number of calories daily
H express feelings of comfort and decreased pain
H develop a normal bowel elimination pattern
H demonstrate adaptive coping behaviors.

Nursing interventions
H Assess the patients acceptance and understanding of

the disease and treatment regimen.


H Observe the patients nutritional status and progress

by daily calorie counts and weight checks.


H Assess the patients pain and administer pain medica-

tion as ordered.
H Provide fluid replacement as ordered, and observe

for signs and symptoms of dehydration and electrolyte imbalance.


H Encourage the patient to use support systems to assist with coping.

Monitoring
H Signs and symptoms of complications
H Compliance with dietary restrictions
H Nutritional status
H Frequency and characteristics of stools

Celiac disease

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Cellulitis
Overview
Description
H Acute infection of the dermis and subcutaneous tis-

Complications
H Sepsis
H Deep vein thrombosis (DVT)
H Progression of cellulitis
H Local abscesses
H Thrombophlebitis
H Lymphangitis
H Amputation

sue causing inflammation of the cells


H May follow damage to the skin, such as a bite or

wound
H Prognosis usually good with timely treatment
H With other comorbidities, such as diabetes, in-

creased risk of developing or spreading cellulitis

Pathophysiology
H A break in skin integrity almost always precedes in-

fection.
H As the offending organism invades the compromised

area, it overwhelms the defensive cells, including the


neutrophils, eosinophils, basophils, and mast cells,
that normally contain and localize the inflammation.
H As cellulitis progresses, the organism invades tissue
around the initial wound site.

Causes
H Bacterial infections, usually by Staphylococcus au-

reus and group A beta-hemolytic streptococci


H Fungal infections
H Extension of a skin wound or ulcer
H Furuncles or carbuncles

Risk factors
H Venous and lymphatic compromise
H Edema
H Diabetes mellitus
H Underlying skin lesion
H Prior trauma

Special populations
Cellulitis of the lower extremity is more likely to
develop into thrombophlebitis in an elderly patient.

Incidence
H Occurs most commonly in the lower extremities
H Affects males and females equally

Special populations
Perianal cellulitis occurs more commonly in children, especially boys.

Assessment
History
H Presence of one or more risk factors
H Tenderness
H Pain at the site and possibly surrounding area
H Erythema and warmth
H Edema
H Possible fever, chills, malaise

Physical findings
H Erythema with indistinct margins
H Fever
H Warmth and tenderness of the skin
H Regional lymph node enlargement and tenderness
H Red streaking visible in skin proximal to area of cel-

lulitis

Test results
Laboratory
H White blood cell count shows mild leukocytosis.
H Erythrocyte sedimentation rate shows mild elevation.
H Culture and Gram stain may show the causative
organism.

Treatment
General
H Immobilization and elevation of the affected

extremity
H Moist heat
H Well-balanced diet
H Bed rest, with the head of bed elevated at least

30 degrees, possibly necessary in severe infection

Medications
H Antibiotics, such as cefuroxime and cephalexin
H Topical antifungal such as mupirocin
H Analgesics, such as ibuprofen and acetaminophen

Surgery
H Tracheostomy possibly needed for severe cellulitis of

head and neck

Common characteristics
H Tenderness
H Pain
H Erythema
H Warmth
H Edema

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Cellulitis

H Possible abscess drainage


H Amputation (with gas-forming cellulitis [gangrene])

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Nursing considerations
Key outcomes
The patient will:
H avoid injury
H express feelings of increased comfort
H remain free from signs and symptoms of infection
H verbalize feelings and concerns.

Nursing interventions
H Give prescribed drugs.
H Elevate affected extremity.
H Apply moist heat, as ordered.
H Encourage a well-balanced diet.
H Encourage adequate fluid intake.
H Encourage verbalization of feelings and concerns.
H Institute safety precautions.
H Institute contact precautions if a draining wound is

present.

Monitoring
H Vital signs
H Pain control
H Edema
H Laboratory results
H Signs and symptoms of infection
H Complications
H Cellulitis progression

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H use of warm compresses
H signs and symptoms of infection
H prevention of injury and trauma
H infection control
H signs and symptoms of DVT.

Discharge planning
H Refer the patient for management of diabetes melli-

tus, as indicated.

Cellulitis

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Cerebral contusion
Overview
Description
H Ecchymosis of brain tissue resulting from injury to

the head

Pathophysiology
H Trauma to the head causes tearing or twisting of the

structures and blood vessels of the brain.


H Scattered hemorrhages form over the surface.
H Functional disruption occurs and may be prolonged.

Causes

Test results
Imaging
H Computed tomography scan shows contusion.

Treatment
General
H Establishment of a patent airway
H Administration of oxygen as needed
H Administration of I.V. fluids
H Minimization of environmental stimuli
H Activity based on neurologic status
H Initially, bed rest with the head of bed elevated at

least 30 degrees
H Avoidance of contact sports

H Acceleration-deceleration or coup-contrecoup

Medications

injuries
H Head trauma

H Analgesics, such as codeine and acetaminophen

Risk factors

H Craniotomy

Surgery

H Unsteady gait
H Participation in contact sports
H Receiving anticoagulant therapy

Nursing considerations

Incidence

Key outcomes

H Occurs at any age

The patient will:


H use support systems to assist with coping
H maintain a stable neurologic state
H express feelings of comfort and pain relief
H maintain adequate fluid volume.

Common characteristics
H Change in level of consciousness
H Hypertension
H Dizziness
H Headache
H Nausea and vomiting
H Pupil changes
H Hemiparesis
H Memory loss or forgetfulness
H Seizure

Nursing interventions
H Perform neurologic examinations.
H Maintain a patent airway.
H Give prescribed drugs (no aspirin).
H Protect from injury.
H Institute seizure precautions.

Complications

Monitoring

H Intracranial hemorrhage
H Hematoma
H Tentorial herniation
H Increased intracranial pressure (see What happens

H Vital signs
H Neurologic and respiratory status
H Check for cerebrospinal fluid (CSF) leakage
H Pain control

with increased ICP)

Assessment
History
H Head injury or motor vehicle accident
H Loss of consciousness

Physical findings
H Unconscious patient: pale and motionless; altered

vital signs
H Conscious patient: drowsy or easily disturbed
H Scalp wound
H Possible involuntary evacuation of bowel and bladder
H Hemiparesis

164

Cerebral contusion

Patient teaching
Be sure to cover:
H the need to avoid coughing, sneezing, or blowing the
nose until after recovery
H observation for CSF drainage
H how to detect and report mental status changes
H signs and symptoms of infection.

Discharge planning
H Refer the patient to a neurologist for follow-up, as

indicated.
H Refer the patient for rehabilitation, as needed.

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What happens with increased ICP


Intracranial pressure (ICP) is the pressure exerted within the intact skull by the intracranial volume, which is comprised of
about 10% blood, 10% cerebrospinal fluid (CSF), and 80% brain tissue. The rigid skull allows very little space for expansion
of these substances. When ICP increases to pathologic levels, brain damage can result.
The brain compensates for increases in ICP by regulating the volumes of the three substances in the following ways:
H limiting blood flow to the head
H displacing CSF into the spinal canal
H increasing absorption or decreasing production of CSF withdrawing water from brain tissue into the blood and excreting it through the kidneys.
When compensatory mechanisms become overworked, small changes in volume lead to large changes in pressure.
Brain insult
Trauma (contusion, laceration, intracranial hemorrhage)
Cerebral edema (following surgery, stroke, infection, hypoxia)
Hydrocephalus
Space-occupying lesion (tumor, abscess)

Slight increase in ICP

Attempt at normal regulation of ICP by decreased blood flow to head

Slight decrease in cerebral perfusion pressure (CPP)

Loss of autoregulatory mechanism of constriction or dilation


of cerebral blood vessels if increased ICP persists

Passive dilation

Increased cerebral blood flow; venous congestion

Further increase in ICP

Cellular hypoxia

Uncal or central herniation

Further decrease in CPP

BRAIN DEATH

Cerebral contusion

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Cerebral palsy

H Poisoning
H Any condition resulting in cerebral thrombus or em-

bolus

Overview
Description
H Most common crippling neuromuscular disease in

children
H Comprises several neuromuscular disorders
H Results from prenatal, perinatal, or postnatal central

nervous system (CNS) damage


H Three types (sometimes occur in mixed forms):
spastic (affecting about 70% of children with cerebral palsy)
athetoid (affecting about 20%)
ataxic (affecting about 10%)
H Motor impairment may be minimal or severely disabling
H Associated defects:
seizures
speech disorders
mental retardation
H Prognosis varies

Pathophysiology
H A lesion or an abnormality occurs in the early stages

of brain development.
H Structural and functional defects occur, impairing

Incidence
H Highest in premature neonates and in those who are

small for gestational age


H Slightly more common in boys than in girls
H More common in whites

Common characteristics
H Excessive lethargy or irritability
H High-pitched cry
H Poor head control
H Weak sucking reflex
H Delayed motor development
H Abnormal head circumference
H Abnormal postures
H Abnormal reflexes
H Abnormal muscle tone and performance

Complications
H Seizure disorders
H Speech, vision, and hearing problems
H Language and perceptual deficits
H Mental retardation (in up to 40% of patients)
H Dental problems
H Respiratory difficulties
H Poor swallowing and gag reflexes

motor or cognitive function.


H Defects may not be distinguishable until months after

birth.

Assessment

Causes

History

H Conditions that result in cerebral anoxia, hemor-

H Maternal or patient history revealing possible cause

rhage, or other CNS damage


Prenatal causes
H Rh factor incompatibility
H ABO blood type incompatibility
H Maternal infection (especially rubella in the first
trimester)
H Maternal diabetes
H Irradiation
H Anoxia
H Toxemia
H Malnutrition
H Abnormal placental attachment
H Isoimmunization
Parturition causes
H Trauma during delivery
H Depressed maternal vital signs from general or spinal
anesthesia
H Asphyxia from the cord wrapping around the neck
H Prematurity
H Prolonged or unusually rapid labor
H Multiple births (neonates born last in a multiple
birth have an especially high rate of cerebral palsy)
Postnatal causes
H Infections, such as meningitis and encephalitis
H Head trauma

166

Cerebral palsy

(see When to suspect cerebral palsy)

Physical findings
H Child with retarded growth and development
H Difficulty chewing and swallowing

Spastic cerebral palsy


H Underdevelopment of affected limbs
H Characteristic scissors gait
H Walks on toes
H Crosses one foot in front of the other
H Hyperactive deep tendon reflexes
H Increased stretch reflexes
H Rapid alternating muscle contraction and relaxation
H Muscle weakness
H Impaired fine and gross motor skills
H Contractures in response to manipulation of muscles
Athetoid cerebral palsy
H Involuntary movements
H Grimacing
H Wormlike writhing
H Dystonia
H Sharp jerks that impair voluntary movement
H Involuntary facial movements (speech difficult)
H Drooling

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Ataxic cerebral palsy


H Lack of leg movement during infancy
H Wide gait when child begins to walk
H Disturbed balance
H Incoordination (especially of the arms)
H Hypoactive reflexes
H Nystagmus
H Muscle weakness
H Tremors

Test results
Imaging
H Computed tomography scan and magnetic resonance
imaging of the brain may show structural abnormalities of the brain such as cerebral atrophy.
H EEG may show the source of seizure activity.

When to suspect cerebral palsy


Early detection of cerebral palsy is essential for effective
treatment and requires careful clinical observation during
infancy and precise neurologic assessment. Suspect cerebral palsy whenever a neonate:
H has difficulty sucking or keeping the nipple or food in
his mouth
H seldom moves voluntarily or has arm or leg tremors
with voluntary movement
H crosses his legs when lifted from behind rather than
pulling them up or bicycling like a normal neonate
H has legs that are hard to separate, making diaper
changing difficult
H persistently uses only one hand or, as he gets older,
uses his hands well but not his legs.

Treatment

H Provide a safe physical environment.


H Keep the head of the bed elevated at least 30 degrees.

General

Monitoring

H Braces or splints
H Special appliances, such as adapted eating utensils

H Pain control
H Seizure activity
H Speech
H Visual and auditory acuity
H Respiratory status
H Swallowing function
H Neurologic status
H Nutritional status
H Skin integrity
H Motor development
H Muscle strength

and low toilet seat with arms


H Range-of-motion (ROM) exercises
H Prescribed exercises to maintain muscle tone

Medications
H Anticonvulsant such as phenytoin
H Muscle relaxant such as dantrolene
H Antianxiety agent such as lorazepam

Surgery
H Orthopedic surgery
H Neurosurgery

Patient teaching

Nursing considerations

Be sure to cover:
H the prescribed medication regimen
H adverse drug reactions
H daily skin inspection and massage
H the need to place food far back in patients mouth to
facilitate swallowing
H the need to chew food thoroughly
H drinking through a straw
H sucking lollipops to develop muscle control
H proper nutrition
H opportunities for learning, such as summer camps or
Special Olympics
H correct use of assistive devices.

Key outcomes
The patient will:
H consume calorie requirements daily
H express positive feelings about self
H maintain joint mobility and ROM
H develop adequate coping mechanisms
H develop effective communication skills.

Nursing interventions
H Speak slowly and distinctly.
H Give all care in an unhurried manner.
H Allow participation in care decisions.
H Provide a diet with adequate calories. Stroking the

throat may aid swallowing.


H Provide frequent mouth and dental care.
H Provide skin care.
H Perform prescribed exercises to maintain muscle
tone.
H Care for associated hearing and vision disturbances,
as necessary.
H Postoperatively, give analgesics, as ordered.

Discharge planning
H Refer family members to community support groups

such as the local chapter of the United Cerebral Palsy


Association.

Cerebral palsy

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Cervical cancer

Incidence
H Typically occurs between ages 30 and 45; rarely,

before age 20

Overview
Description
H Proliferation of cancer cells in the cervix
H Third most common cancer of the female reproduc-

tive system
H Classified as either preinvasive (curable in 75% to
90% of patients with early detection and proper
treatment) or invasive

Pathophysiology
Preinvasive cancer
H Preinvasive cancer ranges from minimal cervical dysplasia, in which the lower third of the epithelium
contains abnormal cells, to carcinoma in situ, in
which the full thickness of the epithelium contains
abnormally proliferating cells.
Invasive cancer
H Cancer cells penetrate the basement membrane and
can spread directly to contiguous pelvic structures or
disseminate to distant sites by way of lymphatic
routes.
H Most (95%) cases are squamous cell carcinoma; 5%
of cases are adenocarcinomas.

Common characteristics
H Abnormal vaginal bleeding

Complications
H Renal failure
H Distant metastasis
H Vaginal stenosis
H Ureterovaginal or vesicovaginal fistula
H Proctitis
H Cystitis
H Bowel obstruction

Assessment
History
H One or more risk factors present

Preinvasive cancer
H No symptoms or other clinical changes
Invasive cancer
H Abnormal vaginal bleeding or discharge
H Gradually increasing flank pain

Physical findings

H Unknown

H Vaginal discharge
H Postcoital bleeding
H Irregular bleeding

Risk factors

Test results

H Frequent intercourse at a young age (younger than

Imaging
H Lymphangiography can show metastasis.
H Cystography can show metastasis.
H Organ and bone scans can show metastasis.
Diagnostic procedures
H Papanicolaou (Pap) test shows abnormal cells, and
colposcopy shows the source of the abnormal cells
seen on the Pap test. (See Testing for cervical cancer.)
H Cone or punch biopsy is performed if endocervical
curettage is positive.
H Vira Pap test permits examination of the specimens
deoxyribonucleic acid structure to detect HPV.

Causes

age 16)
H Multiple sexual partners
H Multiple pregnancies
H Human papillomavirus (HPV) infection
H Bacterial or viral venereal infections
H Exposure to diethylstilbestrol in utero
H Human immunodeficiency virus
H Smoking (see Preventing cervical cancer)

Prevention

Preventing cervical cancer


Cervical cancer can be prevented by following these
guidelines:
H Delay sexual intercourse.
H Limit the number of sexual partners.
H Avoid sexual activity with people who have had many
other sexual partners.
H Use barrier protection.
H Dont smoke.
H Receive the human papilloma virus vaccine.

168

Cervical cancer

Treatment
General
H Accurate clinical staging used to determine type of

treatment
H Well-balanced diet, as tolerated

Medications
H Chemotherapy, such as bleomycin, cisplatin, ifos-

famide, and topotecan

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Testing for cervical cancer


To analyze cervical cells, the ThinPrep may be collected in
the same manner as a Papanicolaou (Pap) test using a cytobrush and plastic spatula. The specimens are deposited in
a bottle provided with a fixative and sent to the laboratory.
A filter is then inserted into the bottle and excess mucus,
blood, and inflammatory cells are filtered out by centrifuge.
Remaining cells are then placed on a slide in a uniform, thin
layer and read as a Pap test. This causes fewer slides to be
classified as unreadable, significantly reducing the incidence
of false negatives and the need for repeat tests.
When the ThinPrep test is used, screening can also be
easily done for the human papillomavirus (HPV), of which
certain strains have been identified as the primary cause of
cervical cancer. The Digene hc2 HPV deoxyribonucleic acid
(DNA) test has been approved by the Food and Drug Administration to determine if those identified as high risk for developing cervical cancer have been exposed to HPV. The

Surgery
Preinvasive lesions
H Total excisional biopsy
H Cryosurgery
H Laser destruction
H Conization, followed by frequent Pap test follow-ups
H Hysterectomy (rare)
Invasive squamous cell carcinoma
H Radical hysterectomy and radiation therapy (internal,
external, or both)
H Pelvic exenteration (rare; may be performed for recurrent cervical cancer)

specimen is collected as a Pap smear but is dispersed with


ThinPrep solution. Separate aliquots are used for each test,
from brushings of the endocervix. The brush is then inserted
into the specialized tube and snapped off at the shaft, capping securely. The target solution in the tube disrupts the
virus and releases target DNA, which combines with specific
ribonucleic acid (RNA) probes creating RNA:DNA hybrids.
The hybrids are captured, bound, and able to be magnified
and measured using a luminometer.
If a patient is positive for HPV, it means she had been infected with the virus. Depending on the type of HPV found
through DNA testing, those harboring high-risk HPV strains
have a high risk of developing cervical cancer. These patients should have a colposcopy in which the cervix is
viewed under microscope and a biopsy taken from the tissue
sample.

Patient teaching
Be sure to cover:
H the disease process, diagnosis, and treatment
H importance of follow-up care
H how treatment wont radically alter the patients
lifestyle or prohibit sexual intimacy
H medication administration, dosage, and possible
adverse effects.

Discharge planning
H Refer the patient to resource and support services.

Nursing considerations
Key outcomes
The patient will:
H express increased comfort and decreased pain
H express feelings and perceptions about changes in
sexual activity
H maintain joint mobility and range of motion
H experience no signs or symptoms of infection
H use support systems and develop coping strategies.

Nursing interventions
H Encourage verbalization and provide support.
H Give prescribed drugs.

Monitoring
H Vital signs
H Complications
H Pain control
H Vaginal discharge
H Renal status
H Response to treatment

Cervical cancer

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Chalazion

H Infection
H Vision disturbance

Overview

Assessment

Description

History

H Painless, slowly growing nodule on the eyelid


H Common disorder of the sebaceous gland in the

H Nodule on eyelid
H Rosacea or blepharitis

eyelid
H May become large enough to press on the eyeball,

Physical findings

producing astigmatism
H May be chronic

H Palpable small lump in the eyelid


H Red, elevated area on the conjunctival surface (see

Pathophysiology

Recognizing chalazion)

H Granulomatous inflammation in the upper or lower

Test results

eyelid is the result of an obstruction of the meibomian (sebaceous) gland duct.


H Edema is usually contained on the conjunctival portion of the eyelid.

Other
H Visual examination and palpation of the eyelid
reveals chalazion.
H Biopsy rules out meibomian cancer.

Causes
H Rosacea
H Chronic blepharitis
H Seborrhea
H Meibomian cancer

Treatment
General
H Warm compresses to the affected eyelid

Incidence

Medications

H Higher incidence in fair-skinned males than in other

H Antibiotic such as sulfacetamide


H Corticosteroid such as dexamethasone

groups, possibly because of that groups higher incidence of rosacea and blepharitis
H More common in adults ages 30 to 50

Common characteristics

Surgery
H Incision and curettage of the chalazion under local

anesthetic (possibly)

H Painless, hard lump that usually points toward the

conjunctival side of the eyelid

Complications
H Cosmetic deformity
H Bleeding after surgery

Recognizing chalazion
A chalazion is a nontender granulomatous inflammation of
a meibomian gland on the upper or lower eyelid.

Nursing considerations
Key outcomes
The patient will:
H report improvement of condition of eyelid
H maintain positive outlook regarding body image
H remain free from signs of bleeding or infection.

Nursing interventions
H Apply warm compress after surgery.
H Apply eye patch to the affected eye for 24 hours. (See

Applying an eye patch.)


H Instill eyedrops, as ordered.

Monitoring
H Bleeding (after surgery)

Patient teaching
Be sure to cover:
H proper instillation of eyedrops
H signs and symptoms of infection
H reporting recurrence.

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Chalazion

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Applying an eye patch


You may apply an eye patch for various reasons: to protect the eye after injury or surgery, to prevent accidental damage to
an anesthetized eye, to promote healing, to absorb secretions, to protect the eye from drying when the patient is comatose
or unable to close the eye as in Bells palsy, or to prevent the patient from touching or rubbing his eye.
A thicker patch, called a pressure patch, may be used to help corneal abrasions heal, compress postoperative edema, or
control hemorrhage from traumatic injury. Application requires an ophthalmologists prescription and supervision.
To apply a patch, choose a gauze pad of appropriate size
for the patients face, place it gently over the closed eye (as
shown), and secure it with two or three strips of tape. Extend the tape from midforehead across the eye to below
the earlobe.

A pressure patch, which is markedly thicker than a singlethickness gauze patch, exerts extra tension against the
closed eye. After placing the initial gauze pad, build it up
with additional gauze pieces. Tape it firmly so that the
patch exerts even pressure against the closed eye (as
shown).

For increased protection of an injured eye, place a plastic


or metal shield (as shown) on top of the gauze pads and
apply tape over the shield.
Occasionally, you may use a head dressing to secure a
pressure patch. The dressing applies additional pressure
or, in burn patients, holds the patch in place without tape.

ALERT
Tell the patient to start applying warm compresses
at the first sign of lid irritation to increase the
blood supply and keep the lumen open.

Discharge planning
H Encourage follow-up care, as ordered.

Chalazion

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Chancroid

H More common in males than in females


H Occurs at any age but is most common among young,

sexually active people

Overview

Common characteristics

Description

H Multiple papules that ulcerate


H Lesions possibly healing spontaneously and usually

H Sexually transmitted disease


H Characterized by painful genital ulcers and inguinal

adenitis
H Common cause of genital ulcers in patients in devel-

oping countries

Pathophysiology
H Organisms are carried from the site of entry through

the lymphatics to regional lymph nodes, resulting in


node swelling.
H The initial lesion is a papule that ulcerates within
24 hours. (See Chancroidal lesion.)
H Untreated infections disseminate to other organs,
causing systemic inflammation and specific organ
dysfunction.

Causes
H Haemophilus ducreyi, a short, nonmotile, gram-

negative bacillus

Risk factors
H Poor personal hygiene
H Unprotected sex
H Multiple sex partners
H Uncircumcised males

Incidence
H Increasing in the United States

Chancroidal lesion
Chancroid produces a soft, painful chancre, similar to that
of syphilis. Without treatment, it may progress to inguinal
adenitis and formation of buboes (enlarged, inflamed
lymph nodes).

responding well to treatment when no secondary


infections present

Complications
H Phimosis and urethral fistulas in males
H Secondary infection
H Abscess formation
H Inguinal adenitis and formation of buboes

Assessment
History
H May report unprotected sexual contact with an infect-

ed person or with unknown or multiple partners


H Pain from ulcers and lymphadenopathy
H Headaches and malaise

Physical findings
H Genital area initially with single or multiple papules

surrounded by redness that rapidly become pustular


and then ulcerate
H Ulcers nonindurated with ragged edges, a base of
granulation tissue, and bleed easily; range from 1 to
2 mm in diameter
H Lesions on the tongue, lip, or breast
H Suppuration with bubo formation in the untreated
patient; rupture of abscess may follow
H Tender, fluctuant inguinal nodes

Test results
Laboratory
H Cultures from the lesion show H. ducreyi.

Treatment
General
H Aspiration of fluid-filled nodes
H Good personal hygiene
H Abstinence from sexual activity (until genital lesions

are healed)
H Evaluation of patient for syphilis, herpes simplex

virus, and human immunodeficiency virus (HIV)

Medications
H Antibiotics, such as azithromycin, doxycycline,

erythromycin, minocylcine, and tetracycline

Surgery
H Surgical drainage for large abscess

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Chancroid

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Nursing considerations
Key outcomes
The patient will:
H communicate feelings about changes in body image
H regain skin integrity with decrease in size of chancroids
H state infection risk factors
H voice feelings about changes in sexual activity.

Nursing interventions
H Follow standard precautions.
H Give prescribed drugs.
H Wash the affected area with soap and water, followed

by a bactericidal agent.
H Dry the affected area thoroughly.
H Report all cases of chancroid to the local board of

health.

Monitoring
H Response to treatment
H Adverse effects of medications
H Compliance with treatment regimen
H Complications

Patient teaching
Be sure to cover:
H need to avoid applying creams, lotions, or oils on or
near genitalia or on other lesion sites
H abstaining from sexual contact until follow-up shows
that healing is complete
H proper washing techniques of the genitalia
H HIV infection and recommend testing
H following safer sex practices.

Discharge planning
H Refer the patient and affected sexual partners for

treatment.

Chancroid

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Chlamydial infections
Overview
Description
H Infection that results in urethritis in males, cervicitis

in females, and lymphogranuloma venereum in both


sexes
H Trachoma inclusion conjunctivitis: seldom occurs in
United States, but is leading cause of blindness in developing countries
H Most common sexually transmitted disease (STD) in
the United States

H Urethral and rectal strictures


H Perihepatitis
H Cervical cancer
H Trachoma
H Urethritis and epididymitis (in males)
H Sterility
H Stillbirth, neonatal death, premature labor (with in-

fected pregnant females)

Assessment
History
H Unprotected sexual contact with an infected person
H Previous STD

Pathophysiology

Physical findings

H Chlamydial infections are transmitted by direct con-

H Two-thirds of patients asymptomatic

tact (such as sexual).


H Infection produces local inflammation.
H Endometritis and salpingitis occur as the organism
ascends the genitourinary tract.

Female
H Pelvic or abdominal pain
H Dyspareunia
H Cervical erosion
H Mucopurulent discharge
H Dysuria
H Urinary frequency
Male
H Dysuria
H Urinary frequency
H Pruritus
H Urethral discharge (copious and purulent)
H Meatal erythema
H Severe scrotal pain
Lymphogranuloma venereum
H Painless vesicle or nonindurated ulcer, 2 to 3 mm in
diameter, on the glans or shaft of the penis; on the
labia, vagina, or cervix; or in the rectum
H Enlarged inguinal lymph nodes
H Regional nodes appearing as series of bilateral
buboes
H Untreated buboes possibly rupturing and forming
sinus tracts that discharge thick, yellow, granular
secretion

Causes
H Transmission of Chlamydia trachomatis, by sexual

contact (oral, anal, or vaginal)


H Neonate infection caused by transport through the

infected mothers birth canal

Risk factors
H Multiple sex partners or new sex partner
H Unprotected sex
H Coinfection with another STD

Incidence
H About 4 million cases annually
H Affects primarily the Native American population of

the southwest United States


H Occurs more commonly among minorities and lower

socioeconomic groups and people living in urban


areas

Special populations
Chlamydial infections have a 10% incidence
among sexually active adolescent girls.

Common characteristics
H Primarily occurring after vaginal or rectal inter-

course or oral-genital contact with an infected person


H Late appearance of signs and symptoms during the
course of the disease
H No symptoms in 75% of females, 50% of males
H Sexual transmission of organism that occurs unknowingly

Complications
H Infertility
H Pelvic inflammatory disease

174

Chlamydial infections

Test results
Laboratory
H Swab culture of the infection site shows C. trachomatis. (See Chlamydia trachomatis.)
H Culture of aspirated blood, pus, or cerebrospinal
fluid establishes epididymitis, prostatitis, and
lymphogranuloma venereum.
H Serologic studies reveal previous exposure.
H Enzyme-linked immunosorbent assay shows C. trachomatis antibody.

Treatment
General
H Symptomatic treatment (sex partners also treated)
H Abstinence from sexual activity until infection re-

solved

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Medications
H Antibiotics, such as azithromycin, doxycycline,

erythromycin, levofloxacin, and tetracycline

Chlamydia trachomatis
In chlamydial infections, microscopic examination reveals
Chlamydia trachomatis, a unicellular parasite with a rigid
cell wall.

Nursing considerations
Key outcomes
The patient will:
H voice feelings about changes in sexuality
H express concern about self-concept, self-esteem, and
body image
H exhibit improved or healed lesions or wounds
H express relief from pain.

Nursing interventions
H Follow standard precautions.
H Check the neonate of an infected mother for signs of

infection.
H Give prescribed drugs.
H Provide appropriate skin care.
H Report cases of chlamydial infection to the local

board of health.

Monitoring
H Response to treatment
H Adverse effects of medication
H Complications

Patient teaching
Be sure to cover:
H the disorder, signs and symptoms, and treatment
H proper hand-washing technique
H abstinence from intercourse or use of condoms
H importance of getting tested for the human immunodeficiency virus
H dealing with long-term risks and complications from
infection
H transmission of infection
H prevention of STDs by following safer sex practices
H follow-up care
H complications.

Discharge planning
H Refer the patient to support services.
H Advise rescreenings at 3 to 4 months and annual

screenings for sexually active teens and females ages


20 to 25.

Chlamydial infections

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Cholelithiasis,
cholecystitis,
and related disorders
Overview
Description
Cholelithiasis
H Leading biliary tract disease
H Formation of calculi (gallstones) in the gallbladder
Cholecystitis
H Related disorder that arises from formation of gallstones
H Acute or chronic inflammation of gallbladder
H Usually caused by a gallstone lodged in the cystic
duct
H Acute form most common during middle age
H Chronic form most common among elderly persons
Choledocholithiasis
H Related disorder arising from formation of gallstones
H Partial or complete biliary obstruction due to gallstones lodged in the common bile duct
Cholangitis
H Related disorder that arises from formation of gallstones
H Infected bile duct
H Commonly linked to choledocholithiasis
H Rapid response of nonsuppurative type to antibiotic
treatment
H Poor prognosis of suppurative type unless surgery to
correct obstruction and drain infected bile performed promptly
Gallstone ileus
H Related disorder that arises from obstruction of the
small bowel by a gallstone
H Most common in elderly persons

Pathophysiology
H Calculi formation in the biliary system causes ob-

struction.

immobility, chronic dieting, adhesions, prolonged


anesthesia, and opioid abuse)

Risk factors
H High-calorie, high-cholesterol diet
H Obesity
H Elevated estrogen levels due to hormonal contracep-

tive use, postmenopausal hormone-replacement


therapy, or pregnancy
H Diabetes mellitus, ileal disease, hemolytic disorders,
hepatic disease (cirrhosis), or pancreatitis
H Rapid weight loss

Incidence
H Six times more common in females ages 20 to 50
H Males and females equal after age 50; increases with

each succeeding decade

Common characteristics
H Epigastric or right upper quadrant abdominal pain
H Nausea, vomiting
H Low-grade fever
H Abdominal distention

Complications
Cholelithiasis
H Cholangitis
H Cholecystitis
H Choledocholithiasis
H Gallstone ileus
Cholecystitis
H Gallbladder complications, such as empyema,
hydrops or mucocele, and gangrene
H Chronic cholecystitis and cholangitis
Choledocholithiasis
H Cholangitis
H Obstructive jaundice
H Pancreatitis
H Secondary biliary cirrhosis
Cholangitis
H Septic shock
H Death
Gallstone ileus
H Bowel obstruction

H Obstruction of hepatic duct leads to intrahepatic re-

tention of bile; increased release of bilirubin into the


bloodstream occurs.
H Obstruction of cystic duct leads to inflammation of
the gallbladder; increased gallbladder contraction
and peristalsis occurs.
H Obstruction of bile causes impairment of digestion
and absorption of lipids.

Causes
H Calculi formation; type of disorder that develops de-

pendent on where in the gallbladder or biliary tract


the calculi collect
H Acute cholecystitis also a result of conditions that alter gallbladders ability to fill or empty (trauma, reduced blood supply to the gallbladder, prolonged

176

Assessment
History
H Gallbladder disease possibly producing no symptoms

(even when X-rays reveal gallstones)


Acute cholecystitis
H Sudden onset of severe steady or aching pain in the
midepigastric region or the right upper abdominal
quadrant
H Pain radiating to the back, between the shoulder
blades or over the right shoulder blade, or just to the
shoulder area
H Attack occurring after eating a fatty meal or a large
meal after fasting for an extended time
H Attack occurring in the middle of the night

Cholelithiasis, cholecystitis, and related disorders

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H Nausea, vomiting, and chills


H Low-grade fever
H History of milder GI symptoms that preceded the

acute attack; indigestion, vague abdominal discomfort, belching, and flatulence after eating meals or
snacks rich in fats

H Bile salts
H Analgesics
H Antispasmodics
H Anticholinergics
H Antiemetics
H Antibiotics

Physical findings

Surgery

H Severe pain
H Pallor
H Diaphoresis
H Low-grade fever (high in cholangitis)
H Exhaustion
H Jaundice (chronic)
H Dark-colored urine and clay-colored stools
H Tachycardia
H Tenderness over the gallbladder, which increases on

H Cholecystectomy (laparoscopic or abdominal), cho-

inspiration (Murphys sign)

lecystectomy with operative cholangiography, choledochostomy, or exploration of the common bile duct

Other
H Endoscopic retrograde cholangiopancreatography to

visualize and remove calculi


H Lithotripsy

H Palpable, painless, sausagelike mass (calculus-filled

Nursing considerations

gallbladder without ductal obstruction)


H Hypoactive bowel sounds

Key outcomes

Test results
Laboratory
H Blood studies may reveal elevated levels of serum alkaline phosphatase, lactate dehydrogenase, aspartate
aminotransferase, icteric index, and total bilirubin;
white blood cell count is slightly elevated during
cholecystitis attack.
Imaging
H Plain abdominal X-rays show gallstones if they contain enough calcium to be radiopaque. X-rays are
also helpful in identifying porcelain gallbladder, limy
bile, and gallstone ileus.
H Ultrasonography of the gallbladder confirms
cholelithiasis in most patients and distinguishes between obstructive and nonobstructive jaundice; calculi as small as 2 mm can be detected.
H Oral cholecystography confirms the presence of gallstones, although this test is gradually being replaced
by ultrasonography.
H Technetium-labeled iminodiacetic acid scan of the
gallbladder indicates cystic duct obstruction and
acute or chronic cholecystitis if the gallbladder cant
be seen.
Diagnostic procedures
H Percutaneous transhepatic cholangiography, imaging
performed under fluoroscopic guidance, supports
the diagnosis of obstructive jaundice and is used to
visualize calculi in the ducts.

Treatment
General
H Low-fat diet
H Nothing by mouth if surgery required
H Activity, as tolerated

Medications

The patient will:


H express feelings of increased comfort
H show no signs of infection
H have laboratory values that return to within normal
parameters
H avoid complications.

Nursing interventions
H Position the patient for comfort and reposition at

least every 2 hours.


H Keep the head of the bed elevated at least 30 degrees.
H Give prescribed drugs.
H Encourage coughing, deep breathing, and incentive

spirometer use.
H Encourage early ambulation postoperatively.
H Maintain nothing-by-mouth status.

Monitoring
H Vital signs
H Intake and output
H Pain control
H Abdominal status
H Respiratory status

After surgery
H T tube patency and drainage
H Cardiac status
H Postoperative complications

Patient teaching
Be sure to cover:
H the disease, diagnosis, and treatment
H how to breathe deeply, cough, expectorate, and perform leg exercises that are necessary after surgery
H dietary modifications
H medication administration, dosage, and possible
adverse effects
H wound care.

H Gallstone dissolution therapy

Cholelithiasis, cholecystitis, and related disorders

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Cholera
Overview
Description
H Acute enterotoxin-mediated GI infection
H Transmitted through food and water contaminated

with fecal material from carriers or people with active infections


H Food poisoning caused by Vibrio parahaemolyticus,
a similar bacterium (see Vibrio parahaemolyticus
food poisoning)
H Also known as Asiatic cholera or epidemic cholera

Pathophysiology
H Humans are the only hosts and victims of V. choler-

ae, a motile, aerobic organism.


H The incubation period is several hours to 5 days.
H Enterotoxins cause profuse watery diarrhea and vom-

iting without nausea.


H Massive fluid and electrolyte loss occurs and, if not

corrected, leads to metabolic acidosis, uremia, and


possibly coma and death.
H Infection doesnt confer permanent immunity.

Causes
H Gram-negative bacillus V. cholerae

Risk factors
H Deficiency or absence of hydrochloric acid

Incidence
H Most common in Africa, Southern and Southeast

Asia, and the Middle East, although outbreaks have


occurred in Japan, Australia, and Europe
H Occurs during the warmer months; most prevalent
among lower socioeconomic groups
H Common among children ages 1 to 5 in India, but
equally distributed among all age-groups in other
endemic areas

Common characteristics
H Acute, painless, profuse, watery diarrhea
H Effortless vomiting (without preceding nausea)

Complications
H Dehydration
H Hypovolemic shock
H Metabolic acidosis
H Uremia
H Coma and death

Assessment
History
H Profuse, watery diarrhea
H Vomiting
H Intense thirst
H Weakness
H Muscle cramps (especially in the extremities)

Physical findings
H Stools containing white flecks of mucus (rice-water

stools)

Vibrio parahaemolyticus food poisoning


Vibrio parahaemolyticus is a common cause of gastroenteritis in Japan. Outbreaks also occur on American cruise
ships and in the eastern and southeastern coastal areas of
the United States, especially during the summer.
V. parahaemolyticus, which thrives in a salty environment, is transmitted through the ingestion of uncooked or
undercooked contaminated shellfish, particularly crab and
shrimp. After an incubation period of 2 to 48 hours,
V. parahaemolyticus causes watery diarrhea, moderately
severe cramps, nausea, vomiting, headache, weakness,
chills, and fever. Food poisoning is usually self-limiting
and subsides spontaneously within 2 days. Occasionally,
however, its more severe and may even be fatal in debilitated or elderly persons.
Diagnosis requires bacteriologic examination of vomitus, blood, stool smears, or fecal specimens collected by
rectal swab. Diagnosis must rule out not only other causes of food poisoning but also other acute GI disorders.
Treatment is supportive, consisting primarily of bed rest
and oral fluid replacement. I.V. replacement therapy is seldom necessary, but oral tetracycline may be prescribed.
Thorough cooking of seafood prevents this infection.

178

Cholera

H Loss of skin turgor, wrinkled skin, sunken eyes


H Pinched facial expression
H Cyanosis
H Tachycardia
H Tachypnea
H Thready or absent peripheral pulses
H Hypotension
H Fever
H Inaudible, hypoactive bowel sounds

Test results
Laboratory
H A culture of V. cholerae from feces or vomitus indicates cholera.
H Microscopic examination of fresh feces shows rapidly moving bacilli (like shooting stars).
H Agglutination reveals reactions to group- and typespecific antisera.
Other
H In endemic areas or during epidemics, typical clinical features strongly suggest cholera.

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Treatment
General
H Standard precautions
H Supportive care
H Increased fluid intake

Medications
H Rapid I.V. infusion of large amounts (50 to 100 ml/

minute) of isotonic saline solution, alternating with


sodium bicarbonate or sodium lactate
H Antibiotic such as tetracycline

Nursing considerations
Key outcomes
The patient will:
H regain and maintain adequate fluid and electrolyte
balance
H have normal elimination patterns
H have stable vital signs
H produce adequate urine volume.

Nursing interventions
H Maintain standard precautions.
H Carefully observe jugular veins.
H Administer prescribed medications.

Monitoring
H Vital signs
H Intake and output
H Laboratory values
H I.V. infusion
H Jugular veins
H Respiratory status
H GI status

Patient teaching
Be sure to cover:
H administration of cholera vaccine to travelers in
endemic areas
H proper hand-washing technique
H need for increased fluid intake.

Discharge planning
H Explain the use of oral tetracycline to family mem-

bers.
H If the physician orders a cholera vaccine, tell the

patient that hell need a booster 3 to 6 months later


for continuing protection.

Cholera

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Chronic fatigue and


immune dysfunction
syndrome
Overview

Incidence
H Affects people of all ages, occupations, and income

levels
H More common in females than in males or children,

especially females younger than age 45


H Sporadic incidence and epidemic clusters
H Estimated to affect about 200 out of every 100,000

persons in the United States

Special populations

Description
H Characterized by prolonged overwhelming fatigue
H Also called chronic fatigue syndrome, chronic

Epstein-Barr virus, myalgic encephalomyelitis,


and Yuppie flu

Chronic fatigue and immune dysfunction syndrome is most prevalent among professionals in
their 20s and 30s.

Pathophysiology

Common characteristics

H Infectious agents or environmental factors trigger

H Suggests viral illness in some cases


H Characterized by incapacitating fatigue
H Waxing and waning symptoms
H Severely debilitating; can last for months or years
H Depression and anxiety after the syndromes onset
H Fever
H Pharyngitis
H Lymphadenopathy

an abnormal immune response and hormonal alterations.

Causes
H Exact cause unknown
H Possibly cytomegalovirus, herpes simplex virus types

1 and 2, human herpesvirus 6, Inoue-Melnick virus,


human adenovirus 2, enteroviruses, measles virus, or
a retrovirus that resembles human T-cell lymphotropic virus type II
H May result from overactive immune system

Risk factors
H Genetic predisposition
H Hormonal balance
H Neuropsychiatric factors
H Gender
H Previous illness
H Stressful environment

Diagnosing chronic fatigue syndrome


Chronic fatigue and immune dysfunction syndrome is defined by:
H New or relapsing fatigue that isnt the result of ongoing
exertion or alleviated by rest and reduces occupational,
educational, social, or personal activities or efforts.
H Four or more of the following symptoms, occurring for
6 months or more:
self-reported impairment in short-term memory or
concentration
sore throat
tender cervical or axillary nodes
muscle pain
multiple joint pain without redness or swelling
headaches of a new pattern or severity
nonrefreshing sleep
postexertional malaise lasting 24 hours or longer.

180

Complications
H Social and occupational impairment

Assessment
History
H Characteristic complaints of prolonged, overwhelm-

ing fatigue (see Diagnosing chronic fatigue syndrome)

Physical findings
H Myalgia
H Cognitive dysfunction

Test results
Laboratory
H Lymphocyte differential reveals reduced natural killer
cell cytotoxicity, abnormal CD4+:CD8+ T-cell ratios,
and mild lymphocytosis.
H Immunoglobulin profile shows decreased immunoglobulin subclasses.
H Immune complex profile reveals circulating immune
complexes.
H Antimicrosomal antibody testing reveals increased
levels of antimicrosomal antibodies.

Chronic fatigue and immune dysfunction syndrome

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Treatment
General
H Focus on supportive care
H Psychiatric evaluation
H Behavioral therapy
H Well-balanced diet high in vitamins and minerals
H Physical therapy
H Frequent rest periods, as needed
H Avoidance of strenuous activities

Medications
H Nonsteroidal anti-inflammatory drug such as ibu-

profen
H Antidepressants, such as sertraline and paroxetine
H Antihistamines, such as loratidine and fexofenidine

Nursing considerations
Key outcomes
The patient will:
H verbally report having an increased energy level
H express feelings about diminished capacity to
perform usual roles
H recognize limitations imposed by illness
H make decisions regarding the course of treatment
and management of the illness
H voice feelings related to self-esteem.

Nursing interventions
H Provide emotional support.
H Begin a graded exercise program.
H Administer prescribed medications.

Monitoring
H Response to treatment
H Adverse effects of medication
H Complications

Patient teaching
Be sure to cover:
H the need to decrease activities when fatigue is
greatest
H the need to avoid bed rest, which has no proven
therapeutic value
H medication administration, dosage, and possible
adverse effects
H appropriate activity planning.

Discharge planning
H Refer the patient to support services.

Chronic fatigue and immune dysfunction syndrome

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Cirrhosis
Overview
Description
H Chronic hepatic disease
H Several types

Pathophysiology
H Diffuse destruction and fibrotic regeneration of

hepatic cells occurs.


H Necrotic tissue yields to fibrosis.
H Liver structure and normal vasculature are altered.
H Blood and lymph flow are impaired.
H Hepatic insufficiency occurs.

Causes
Lannecs or micronodular cirrhosis
(alcoholic or portal cirrhosis)
H Chronic alcoholism
H Malnutrition
Postnecrotic or macronodular cirrhosis
H Complication of viral hepatitis
H Possible after exposure to such liver toxins as
arsenic, carbon tetrachloride, and phosphorus
Biliary cirrhosis
H Prolonged biliary tract obstruction or inflammation
Idiopathic cirrhosis (cryptogenic)
H No known cause
H Sarcoidosis
H Chronic inflammatory bowel disease

Risk factors
H Alcoholism
H Toxins
H Biliary obstruction
H Hepatitis
H Metabolic disorders

Incidence
H Tenth most common cause of death in the United

States
H Most common among those ages 45 to 75
H Occurs in twice as many males as females

Common characteristics
H Abdominal pain
H Pruritus
H Jaundice
H Ascites
H Indigestion
H Anemia

Complications
H Portal hypertension
H Bleeding esophageal varices
H Hepatic encephalopathy
H Hepatorenal syndrome
H Death

182

Cirrhosis

Assessment
History
H Chronic alcoholism
H Malnutrition
H Viral hepatitis
H Exposure to liver toxins such as arsenic and certain

medications
H Prolonged biliary tract obstruction or inflammation

Early stage
H Vague signs and symptoms
H Abdominal pain
H Diarrhea, constipation
H Fatigue
H Nausea, vomiting
H Muscle cramps
Later stage
H Chronic dyspepsia
H Constipation
H Pruritus
H Weight loss
H Bleeding tendency, such as frequent nosebleeds, easy
bruising, and bleeding gums

Physical findings
H Telangiectasis on the cheeks
H Spider angiomas on the face, neck, arms, and trunk
H Gynecomastia
H Umbilical hernia
H Distended abdominal blood vessels
H Ascites
H Testicular atrophy
H Menstrual irregularities
H Palmar erythema
H Clubbed fingers
H Thigh and leg edema
H Ecchymosis
H Jaundice
H Palpable, large, firm liver with a sharp edge (early

finding)
H Enlarged spleen
H Asterixis
H Slurred speech, paranoia, hallucinations

Test results
Laboratory
H Liver enzyme levels, such as alanine aminotransferase, aspartate aminotransferase, total serum bilirubin, and indirect bilirubin are elevated.
H Total serum albumin and protein levels are decreased.
H Prothrombin time is prolonged.
H Hemoglobin, hematocrit, and serum electrolyte levels
are decreased.
H Vitamins A, C, and K are deficient.
H Urine levels of bilirubin and urobilinogen are increased; fecal urobilinogen levels are decreased.

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Imaging
H Abdominal X-rays show an enlarged liver and spleen
and cysts or gas in the biliary tract or liver; liver calcification; and massive ascites.
H Computed tomography and liver scans determine
liver size, identify liver masses, and visualize hepatic
blood flow and obstruction.
H Radioisotope liver scans show liver size, blood flow,
or obstruction.
Diagnostic procedures
H Liver biopsy is the definitive test for cirrhosis, revealing hepatic tissue destruction and fibrosis.
H Esophagogastroduodenoscopy reveals bleeding
esophageal varices, stomach irritation or ulceration,
and duodenal bleeding and irritation.

Treatment

H Provide appropriate skin care.


H Maintain patient safety.

Monitoring
H Vital signs
H Laboratory values
H Hydration and nutritional status
H GI status
H Cardiovascular status
H Hemodynamic status
H Respiratory status
H Abdominal girth
H Weight
H Bleeding tendencies
H Skin integrity
H Changes in mentation, behavior
H Neurologic status

General

Patient teaching

H Removal or alleviation of underlying cause


H I.V. fluids
H Blood transfusion
H Restricted sodium consumption
H Restricted fluid intake
H No alcohol intake
H High-calorie diet
H Frequent rest periods, as needed
H Paracentesis
H Esophageal balloon tamponade
H Sclerotherapy

Be sure to cover:
H the disorder, diagnosis, and treatment
H over-the-counter medications that may increase
bleeding tendencies
H dietary modifications
H the need to avoid infections and abstain from alcohol
H the need to avoid sedatives and acetaminophen (hepatotoxic)
H high-calorie diet and small, frequent meals.

Medications

H Refer the patient to Alcoholics Anonymous, if appro-

H Vitamin supplementation such as thiamine


H Posterior pituitary hormone such as vasopressin
H Potassium-sparing diuretic such as spirolactone
H Ammonia detoxicant such as lactoluse
H Antiemetic such as metoclopramide
H Antidiarrheal such as octreotide

Discharge planning
priate.
H Refer the patient for psychological counseling, if

needed.

Surgery
H May be required to divert ascites into venous circula-

tion; if so, peritoneovenous shunt used


H Portal-systemic shunts
H Transjugular intrahepatic portosystemic shunt

Nursing considerations
Key outcomes
The patient will:
H maintain caloric intake, as required
H maintain normal fluid volume
H incur no injuries
H exhibit no bleeding.

Nursing interventions
H Give prescribed I.V. fluids and blood products.
H Give prescribed drugs.
H Encourage verbalization and provide support.

Cirrhosis

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Cleft lip and cleft palate


Overview
Description
H Imperfect fusion of front and sides of the face and

the palatine shelves during pregnancy


H May occur separately or in combination
H Can occur unilaterally, bilaterally or, rarely, in the

midline
H May affect just the lip or extend into the upper jaw or

nasal cavity (see Types of cleft deformities)

Pathophysiology
H Chromosomal abnormality, exposure to teratogens,

genetic abnormality, or environmental factors cause


the lip or palate to fuse imperfectly during the second month of pregnancy.
H A complete cleft includes the soft palate, the bones of
the maxilla, and the alveolus on one or both sides of
the premaxilla.
H A double cleft runs from the soft palate forward to either side of the nose, separating the maxilla and premaxilla into freely moving segments. The tongue and
other muscles can displace the segments, enlarging
the cleft.

ALERT
Isolated cleft palate occurs more commonly with
congenital defects other than isolated cleft lip. The
constellation of U-shaped cleft palate, mandibular
hypoplasia, and glossoptosis known as Robin sequence can occur as an isolated defect or one feature of many different syndromes.These infants
should have comprehensive genetic evaluation. Because of their mandibular hypoplasia and glossoptosis, the airway in infants with Robin sequence
must be carefully evaluated and managed.

Common characteristics
H Obvious cleft lip or cleft palate
H Feeding difficulties from incomplete fusion of the

palate

Complications
H Malnutrition
H Hearing impairment
H Permanent speech impediment

Assessment
History
H Family history of cleft defects
H Maternal exposure to teratogens during pregnancy
H Clinical presentation obvious at birth

Physical findings
H Cleft that runs from the soft palate forward to either

side of the nose

Test results
Imaging
H Prenatal targeted ultrasound reveals abnormality.

Treatment
General
H Orthodontic prosthesis to improve sucking
H Use of a contoured speech bulb attached to the pos-

terior of a denture to occlude the nasopharynx when


a wide horseshoe defect makes surgery impossible
(to help the child develop intelligible speech)
H Use of a large, soft nipple with large holes, such as a
lambs nipple, to improve feeding patterns and promote adequate nutrition

Medications
ALERT

Causes
H Chromosomal or Mendelian syndrome (cleft defects

caused by more than 300 syndromes)


H Exposure to teratogens during fetal development
H Combined genetic and environmental factors

Incidence
H Twice as common in males than in females
H More common in children with a family history of

cleft defects
H Cleft lip with or without cleft palate occurs in about 1

in 1,000 births among Whites; incidence higher in


Asians (1.7 in 1,000) and Native Americans (more
than 3.6 in 1,000), but lower in Blacks (1 in 2,500)

184

Cleft lip and cleft palate

Daily use of folic acid before conception decreases


the risk for isolated (not associated with another
genetic or congenital malformation) cleft lip or
palate by up to 25%. Women of childbearing age
should be encouraged to take a daily multivitamin
containing folic acid until menopause or until
theyre no longer fertile.

Surgery
H Surgical correction of cleft lip in the first few days of

life and again at 12 to 18 months, after the infant


gains weight and is infection-free

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Nursing considerations
Key outcomes
The patient will:
H exhibit normal growth and development patterns
within the confines of the disorder
H not aspirate feedings.
The family will:
H express an understanding of the condition and
treatment
H seek appropriate resources to assist with coping.

Types of cleft deformities


These illustrations show variations of cleft lip and cleft
palate.
NOTCH IN THE VERMILLION BORDER
(JUNCTION OF THE LIP AND SURROUNDING SKIN)

Nursing interventions
H Encourage the mother of an infant with cleft lip to

breast-feed if the cleft doesnt prevent effective


sucking.
H Suction, as necessary.
H Help the parents deal with their feelings about the
childs deformity.

UNILATERAL CLEFT LIP AND PALATE

ALERT
Never place a child with Robin sequence on his
back because his tongue could fall back and obstruct his airway. Place the infant on his side for
sleeping. Most other infants with a cleft palate can
sleep on their backs without difficulty.

Monitoring

BILATERAL CLEFT LIP AND PALATE

H Swallowing ability
H Weight gain
H Intake and output

Patient teaching
Be sure to cover:
H treatment plan
H how to best feed the infant
H burping the infant frequently
H gently cleaning the palatal cleft with a cotton-tipped
applicator dipped in half-strength hydrogen peroxide
or water after each feeding.

CLEFT PALATE

Discharge planning
H Refer the patient to speech therapy to correct speech

patterns.
H Refer the parents to a social worker who can guide

them to community resources, if needed, and to a


genetic counselor to determine the recurrence risk.

Cleft lip and cleft palate

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Clostridium difficile
infection
Overview
Description
H A gram-positive anaerobic bacterium commonly

resulting in antibiotic-associated diarrhea

H Hemorrhage
H Pseudomembranous colitis

Assessment
History
H Recent antibiotic therapy
H Abdominal pain
H Cramping

H Symptoms ranging from asymptomatic carrier states

Physical findings

to severe pseudomembranous colitis caused by


exotoxins (Toxin A is an enterotoxin and toxin B
is a cytotoxin.)
H Within 14 to 30 days of treatment, recurrence with
the same organism possible in 10% to 20% of
patients

H Soft, unformed, or watery diarrhea (more than three

Pathophysiology
H Antibiotics may trigger toxin production.
H Toxin A mediates alteration in fluid secretion, en-

hances inflammation, and causes leakage of albumin


from the postcapillary venules.
H Toxin B causes damage and exfoliation to the superficial epithelial cells and inhibits adenosine diphosphate ribosylation of Rho proteins.
H Both toxins cause electrophysiologic alterations of
colonic tissue.

Causes
H Antibiotics that disrupt the bowel flora
H Enemas and intestinal stimulants
H Transmission from infected person
H Some antifungal and antiviral agents

Risk factors

stools in a 24-hour period) that may be foul smelling


or grossly bloody
H Abdominal tenderness
H Fever

Test results
Laboratory
H Cell cytotoxin test shows toxins A and B.
H Enzyme immunoassay identifies C. difficile; its
slightly less sensitive than cell cytotoxin test but
has a turnaround time of only a few hours.
H Stool culture identifies C. difficile.

Treatment
General
H Withdrawal of causative antibiotic
H Avoidance of antimotility agents
H Good skin care
H Well-balanced diet
H Increased fluid intake, if appropriate
H Rest periods, if fatigued

H Contaminated equipment and surfaces


H Antibiotics
H Abdominal surgery
H Antineoplastic agents that have an antibiotic activity
H Immunocompromised state

Medications

Incidence

Key outcomes

H More common in people in nursing homes and day-

care facilities
H One of the most common nosocomial infections
(contracted by about 20% of hospitalized patients
taking antibiotics)

The patient will:


H maintain stable vital signs
H maintain normal electrolyte levels
H maintain adequate fluid volume
H maintain skin integrity.

Common characteristics

Nursing interventions

H Watery, foul-smelling diarrhea

H Give prescribed drugs.


H Institute contact precautions for those with active

Complications
H Electrolyte abnormalities
H Hypovolemic shock
H Toxic megacolon
H Colonic perforation
H Peritonitis
H Sepsis

186

Clostridium difficile infection

H Antibiotics, such as vancomycin and metronidazole

Nursing considerations

diarrhea.
H Wash your hands with an antiseptic soap after direct

contact with the patient or his immediate environment.


H Make sure reusable equipment is disinfected with a
bleach-based solution before its used on another
patient.

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Monitoring
H Vital signs
H Intake and output
H Complications
H Serum electrolytes
H Adverse effects of medication
H Response to treatment
H Amount and characteristics of stools
H Skin integrity
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H proper disinfection of contaminated clothing or
household items
H adequate fluid intake
H signs and symptoms of dehydration
H medications and possible adverse effects
H complications and when to notify the physician
H perirectal skin care.

Clostridium difficile infection

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Clubfoot

H Heredity
H Idiopathic
H Suspected muscle abnormalities, leading to varia-

tions in length and tendon insertions

Overview

Incidence

Description
H Foot deformity caused by a deformed talus and short-

ened Achilles tendon, giving the foot a characteristic


clublike appearance
H In talipes equinovarus: foot points downward (equinus) and turns inward (varus), and front of foot
curls toward the heel (forefoot adduction)
H Also known as talipes: most common congenital disorder of lower extremities

H 1 per 1,000 live births


H Usually occurs bilaterally
H Twice as common in boys as in girls
H May be linked to other birth defects, such as

myelomeningocele, spina bifida, and arthrogryposis

Common characteristics
H Inward deformity of the foot (see Recognizing club-

foot)

Pathophysiology

Complications

H Unknown, but contributing factors may include:

H Abnormal gait
H Stress changes on lateral side of the foot
H Residual deformity

defective cartilage with ligamentous laxity


muscle imbalance
abnormal intrauterine position
central nervous system anomaly
persistence of a normal fetal relationship.

Assessment

Causes

History

H Combination of genetic and environmental factors in

H Family history
H Muscular atrophy or dystrophy

utero

Recognizing clubfoot
Clubfoot (talipes) may have
various names, depending
on the orientation of the deformity, as shown in the illustrations at right.

188

Clubfoot

TALIPES EQUINUS

TALIPES CALCANEUS

TALIPES CAVUS

TALIPES VARUS

TALIPES EQUINOVARUS

TALIPES CALCANEOVARUS

TALIPES VALGUS

TALIPES CALCANEOVALGUS

TALIPES EQUINOVALGUS

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Physical findings
H Deformed talus with a shortened Achilles tendon, the

H Proper foot alignment


H Pain control

calcaneus somewhat shortened and flattened


H Shortened, underdeveloped calf muscles, with soft

tissue contractures at the site of the deformity

Patient teaching

H Foot tight in its deformed position and resistant of

manual efforts to push it back into normal position

Test results
Imaging
H X-rays show superimposition of the talus and the
calcaneus and a ladderlike appearance of the
metatarsals.

Treatment

Be sure to cover:
H the need for prompt treatment
H signs of circulatory impairment
H proper skin care
H use of exercise, night splints, and orthopedic shoes
to maintain alignment.

Discharge planning
H Refer the patient to rehabilitation resources, as

needed.

General
H Correction of the deformity
H Activity according to ability
H Maintaining the correction until the foot regains nor-

mal muscle balance


H Close observation to prevent the deformity from re-

curring
Sequential correction
H For forefoot adduction: uncurling the front of the
foot away from the heel (forefoot abduction)
H For varus deformity: turning the foot so the sole faces
outward (eversion)
H For equinus: casting the foot with the toes pointing
up (dorsiflexion)

Medications
H Analgesics

Surgery
H Subcutaneous tenotomy of the Achilles tendon and

posterior capsulotomy of the ankle joint (may need


to be done with the equinus stage of correction)
H In severe cases, bone surgery, such as wedge resections, osteotomy, or astragalectomy possibly appropriate (After surgery, a cast is applied to preserve
the correction.)

Nursing considerations
Key outcomes
The patient will:
H maintain joint mobility and range of motion
H maintain muscle strength
H show no evidence of complications.

Nursing interventions
H After casting, elevate the childs feet with pillows.
H Perform proper skin and cast care.

Monitoring
H Neurovascular status of affected extremity after cast-

ing or surgery

Clubfoot

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Coarctation of the aorta


Overview
Description
H A narrowing of the aorta, usually just below the left

subclavian artery, near the site where the ligamentum


arteriosum (the remnant of the ductus arteriosus, a
fetal blood vessel) joins the pulmonary artery to the
aorta
H May occur with aortic valve stenosis (usually of a bicuspid aortic valve) and with severe cases of hypoplasia of the aortic arch, patent ductus arteriosus
(PDA), and ventricular septal defect
H Ineffective pumping of the heart and increased risk
due to heart failure caused by the obstruction of
blood flow

Pathophysiology
H Coarctation of the aorta may develop as a result of

spasm and constriction of the smooth muscle in the


ductus arteriosus as it closes.
H This contractile tissue extends into the aortic wall,
causing narrowing.
H The obstructive process causes hypertension in the
aortic branches above the constriction (arteries that
supply the arms, neck, and head) and diminished
pressure in the vessel below the constriction.
H Restricted blood flow through the narrowed aorta increases the pressure load on the left ventricle and
causes dilation of the proximal aorta and ventricular
hypertrophy.
H As oxygenated blood leaves the left ventricle, a portion travels through the arteries that branch off the
aorta proximal to the coarctation.
H If PDA is present, the rest of the blood travels
through the coarctation, mixes with deoxygenated
blood from the PDA, and travels to the legs.
H If PDA is closed, the legs and lower portion of the
body must rely solely on the blood that gets through
the coarctation.

Causes
H Unknown
H Turners syndrome

Incidence
H Accounts for about 7% of all congenital heart defects

in children
H Twice as common in males as in females
H In females, commonly linked to Turners syndrome, a

chromosomal disorder that causes ovarian dysgenesis

Common characteristics
H Resting systolic hypertension in the upper body
H Absent or diminished femoral pulses

190

Coarctation of the aorta

H Wide pulse pressure


H Signs and symptoms of heart failure

Complications
H Heart failure
H Severe hypertension
H Cerebral aneurysms and hemorrhage
H Rupture of the aorta
H Aortic aneurysm
H Infective endocarditis
H Hypoperfusion of lower extremities

Assessment
History
H Tachypnea
H Dyspnea
H Failure to thrive
H Headache
H Vertigo
H Epistaxis
H Claudication

Physical findings
H Pallor
H Hypertension
H Crackles
H Edema
H Tachycardia
H Cardiomegaly
H Hepatomegaly
H Hypertension
H Pink upper arms and cyanotic legs
H Absent or diminished femoral pulses
H Arm blood pressure greater than leg blood pressure
H Chest and arms more developed than legs

Test results
Imaging
H Chest X-rays may show left ventricular hypertrophy,
heart failure, a wide ascending and descending aorta,
and notching of the ribs undersurfaces due to erosion by collateral circulation. (See Recognizing
coarctation of the aorta.)
H Echocardiography may show increased left ventricular muscle thickness, coexisting aortic valve abnormalities, and the coarctation site.
Diagnostic procedures
H Electrocardiography may reveal left ventricular hypertrophy.
H Cardiac catheterization evaluates collateral circulation and measures pressure in the right and left ventricles and in the ascending and descending aortas
(on both sides of the obstruction).
H Aortography locates the site and extent of coarctation.

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Treatment
General
H Low-sodium diet
H Fluid restrictions
H Limited activity

Recognizing coarctation of the aorta


Collateral circulation develops to bypass the occluded aortic lumen, and can be seen on X-ray as notching of the
ribs. By adolescence, palpable, visible pulsations may be
evident.
Coarctation

Medications
H Cardiac glycoside such as digoxin
H Diuretic such as furosemide
H Oxygen
H Sedative such as chloral hydrate
H Prostaglandin infusion to keep the ductus open
H Antibiotic prophylaxis such as amoxicillin
H Antihypertensive such as enalaprilat

Surgery
H A flap of the left subclavian artery may be used to

reconstruct the aorta.


H Balloon angioplasty or resection with end-to-end

anastomosis or use of a tubular graft may also be


performed.

Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without weakness or
fatigue
H maintain hemodynamic stability
H remain free from signs and symptoms of infection.

Nursing interventions
H Offer emotional support.
H Regulate environmental temperature.
H Give prescribed drugs.

Monitoring
H Hemodynamics
H Vital signs
H Intake and output
H Respiratory status
H Blood glucose levels
H Postoperative pain
H Signs of infection
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H exercise restrictions
H endocarditis prophylaxis.

Discharge planning
H Stress the need for follow-up care, as ordered.

Coarctation of the aorta

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Coccidioidomycosis
Overview
Description
H Fungal infection occurring primarily as a respiratory

tract infection, although generalized dissemination


may occur
H Also known as valley fever or San Joaquin Valley
fever

Pathophysiology

Assessment
History
H Living or traveling to an endemic area
H Fever
H Dry cough
H Pleuritic chest pain
H Sore throat
H Chills
H Malaise
H Headache
H Joint pain

H After spores are inhaled, cell activation and cytokine

Physical findings

formation stimulate inflammatory cells and facilitate


killing of the organism.
H Immunosuppression may delay resolution of the infection.

H Fever
H Itchy macular rash
H Hemoptysis
H Local swelling and redness in involved sites (with

Causes

H Bronchial breath sounds

H Inhaled spores of Coccidioides immitis found in

the soil or dust from dressings or plaster casts of infected persons

Risk factors
H Occupational exposure to dust, such as with farmers

and construction workers


H Impaired immune system

Incidence
H Disseminated illness more common in dark-skinned

males, pregnant females, and patients taking an immunosuppressant


H Endemic to the southwestern United States, especially
between the San Joaquin Valley in California and
southwestern Texas; also found in Mexico, Guatemala, Honduras, Venezuela, Colombia, Argentina,
and Paraguay
H Generally affects Filipino Americans, Mexican Americans, Native Americans, and Blacks because of population distribution and an occupational link (common in migrant farm laborers)

Common characteristics
Primary coccidioidomycosis
H Acute or subacute respiratory signs and symptoms
H Fever that persists for weeks
Disseminated coccidioidomycosis
H Fever
H Abscesses throughout the body, especially in skeletal,
central nervous system, splenic, hepatic, renal, and
subcutaneous tissues

Complications
H Meningitis
H Bronchiectasis
H Osteomyelitis
H Hepatosplenomegaly
H Liver failure

192

Coccidioidomycosis

musculoskeletal involvement)

Test results
Laboratory
H Serum precipitins (immunoglobulins) are positive.
H C. immitis spores is detected through immunodiffusion testing of sputum, pus from lesions, and tissue
biopsy.
H Antibodies are present in pleural and joint fluid and
a rising serum or body fluid antibody titer indicates
dissemination.
H White blood cell count is increased.
H Eosinophil count is increased.
H Erythrocyte sedimentation rate is increased.
Imaging
H Chest X-ray shows bilateral diffuse infiltrates.
Other
H Coccidioidin skin test result is abnormal.

Treatment
General
H Bed rest
H Symptomatic measures

Medications
H I.V. fluids
H Antifungal such as amphotericin B
H Analgesics, such as acetaminophen and morphine
H Oxygen

Surgery
H Excision or drainage of lesions
H Lobectomy for severe pulmonary lesions

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Nursing considerations
Key outcomes
The patient will:
H be free from pain
H maintain a patent airway
H cough effectively.

Nursing interventions
H Administer prescribed medications.
H Administer oxygen as prescribed.
H Encourage coughing, deep breathing, and incentive

spirometer use.
H Maintain a patent airway.
H Encourage bed rest, with head of the bed elevated

30 degrees.
H Encourage adequate fluid intake.
H Provide measures to relieve pain and increase

comfort.

Monitoring
H Pain control
H Intake and output
H Vital signs
H Sputum color, consistency, and amount
H Respiratory status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H wound care.

Coccidioidomycosis

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Colorectal cancer
Overview
Description
H Malignant tumors of colon or rectum almost always

adenocarcinomas (about one-half are sessile lesions


of rectosigmoid area; all others, polypoid lesions)
H Slow progression
H Five-year survival rate 50%; potentially curable in
75% of patients if early diagnosis allows resection
before nodal involvement
H Second most common visceral neoplasm in United
States and Europe

Pathophysiology
H Most lesions of the large bowel are moderately differ-

entiated adenocarcinomas.
H Tumors tend to grow slowly and produce no symp-

toms for long periods.


H Tumors in the sigmoid and descending colon under-

go circumferential growth and constrict the intestinal


lumen.
H Tumors in the ascending colon are usually large at
diagnosis and are palpable on physical examination.

Assessment
History
H Right colon tumors: no signs and symptoms in early

stages because stool is liquid in that part of colon


H Transverse colon tumors: may cause cramps, gas,

partial or complete obstruction


H Descending colon tumors and rectal tumors: may

cause pencil-shaped stools if the tumor partially


obstructs the intestine
H Black, tarry stools
H Abdominal aching, pressure, or dull cramps
H Weakness
H Diarrhea, anorexia, obstipation, weight loss, and
vomiting
H Rectal bleeding
H Intermittent abdominal fullness
H Rectal pressure
H Urgent need to defecate on arising

Physical findings
H Abdominal distention or visible masses
H Enlarged abdominal veins
H Enlarged inguinal and supraclavicular nodes
H Abnormal bowel sounds
H Abdominal masses (right-side tumors that usually

H Unknown

feel bulky; tumors of transverse portion more easily


detected)
H Generalized abdominal tenderness

Risk factors

Test results

H Excessive intake of saturated animal fat


H Digestive tract diseases
H Older than age 40
H History of ulcerative colitis
H Familial polyposis
H Family history of colon cancer
H High-protein, low-fiber diet

Laboratory
H Fecal occult blood test may show blood in stools, a
warning sign of rectal cancer.
H Carcinoembryonic antigen allows patient monitoring
before and after treatment to detect metastasis or
recurrence.
Imaging
H Excretory urography verifies bilateral renal function
and allows inspection for displacement of the kidneys, ureters, or bladder by a tumor pressing against
these structures.
H Barium enema studies use a dual contrast of barium
and air and reveal the location of lesions that arent
detectable manually or visually. Barium examination
shouldnt precede colonoscopy or excretory urography because barium sulfate interferes with these
tests.
H Computed tomography scan allows better visualization if a barium enema yields inconclusive results or
if metastasis to the pelvic lymph nodes is suspected.
Diagnostic procedures
H Proctoscopy or sigmoidoscopy permits visualization
of the lower GI tract. It can detect up to 66% of colorectal cancers.
H Colonoscopy permits visual inspection and photography of the colon up to the ileocecal valve and provides access for polypectomies and biopsies of suspected lesions.

Causes

Incidence
H Equally distributed among males and females
H Greater in areas of higher economic development

Common characteristics
H Changes in bowel habits
H Symptoms of direct extension to bladder, prostate,

ureters, vagina, or sacrum


H Symptoms of local obstruction

Complications
H Abdominal distention and intestinal obstruction as

tumor growth encroaches on abdominal organs


H Anemia

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Other
H Digital rectal examination can be used to detect almost 15% of colorectal cancers; specifically, it can
be used to detect suspicious rectal and perianal lesions.

Treatment
General
H Radiation preoperatively and postoperatively to

induce tumor regression


H High-fiber diet
H After surgery, avoidance of heavy lifting and contact

sports

Medications
H Antibiotics such as metronidazole postoperatively
H Chemotherapy, such as bevacizumab, capecitabine,

cetuximab, fluorouracil, irinotecan, oxaliplatin, and


panitumunab
H Analgesic such as morphine

Surgery
H Resection or right hemicolectomy for advanced dis-

ease; may include resection of the terminal segment


of the ileum, cecum, ascending colon, and right half
of the transverse colon with corresponding mesentery for tumor of cecum and ascending colon
H Right colectomy that includes the transverse colon
and mesentery corresponding to midcolic vessels, or
segmental resection of the transverse colon and associated midcolic vessels for proximal and middle
transverse colon tumor
H Resection usually limited to the sigmoid colon and
mesentery for sigmoid tumor
H Anterior or low anterior resection for upper rectal
tumor
H Abdominoperineal resection and permanent sigmoid
colostomy required for lower rectal tumor

Monitoring
H Stools
H Diet

Postoperative
H Vital signs
H Intake and output
H Hydration and nutritional status
H Electrolyte levels
H Wound and stoma site
H Postoperative complications
H GI status
H Pain control
H Psychological status
H Respiratory status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disease process, treatment, and postoperative
course
H stoma care
H avoidance of heavy lifting
H the need for keeping follow-up appointments
H risk factors and signs of recurrence.

Discharge planning
H Refer the patient to resource and support services.

Nursing considerations
Key outcomes
The patient will:
H maintain normal fluid volume
H maintain intact mucous membranes
H report feeling less pain
H express increased sense of well-being
H use support systems and employ coping strategies.

Nursing interventions
H Encourage early ambulation postoperatively.
H Encourage coughing, deep breathing, and incentive

spirometer use.
H Keep the head of the bed elevated at least 30 degrees

to prevent pneumonia.
H Provide support and encourage verbalization.
H Give prescribed drugs.
H Provide stoma care.

Colorectal cancer

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Common cold
Overview
Description
H Acute, usually afebrile viral infection that causes in-

flammation of the upper respiratory tract


H Transmission through airborne respiratory droplets

or through contact with contaminated objects, including hands


H Accounts for 30% to 50% of time lost from work by
adults and 60% to 80% of time lost from school by
children, more than any other illness
H Communicable for 2 to 3 days after onset of symptoms
H Usually benign and self-limiting

Pathophysiology
H Rhinoviruses may infect cells by attaching to specific

receptors.
H Infiltration with neutrophils, lymphocytes, plasma
cells, and eosinophils occurs.
H Mucus-secreting glands become hyperactive and
nasal turbinates become engorged. (See What happens in the common cold.)

Causes

Complications
H Secondary bacterial infection causing sinusitis, otitis

media, pharyngitis, or lower respiratory tract infection

Assessment
History
H Exposure to persons with the common cold
H Sore throat
H Fatigue
H Malaise
H Myalgia
H Fever

Physical findings
H Copious nasal discharge that commonly irritates the

nose
H Increased erythema of nasal and pharyngeal mucous

membranes
H Nasal quality to voice
H Excoriated skin around nose

Test results
H There isnt an explicit diagnostic test.

Laboratory
H White blood cell count and differential are within
normal limits.

H Viral infection of the upper respiratory tract passages

and consequent mucous membrane inflammation responsible for 90% of cases


H More than 200 viruses, including rhinoviruses, coronaviruses, myxoviruses, adenoviruses, coxsackieviruses, and echoviruses
H Mycoplasma

Risk factors
H Exposure to an infected person or contact with con-

taminated objects
H Compromised immune system

Incidence
H Most common infectious disease
H More prevalent in children, adolescent boys, and

adult females
H In temperate climates, occurring more commonly in
the colder months
H In the tropics, occurring more commonly during the
rainy season

Common characteristics
H Initial complaints of nasal congestion, headache, and

burning, watery eyes, chills, myalgia, arthralgia,


malaise, lethargy, sore throat, and a hacking, nonproductive or nocturnal cough
H Most patients afebrile, although fever possibly occurring, especially in children

196

Common cold

Treatment
General
H Use of humidified inspired air
H Prevention of chilling
H Increased fluid intake
H Rest periods, as needed

Medications
H Antipyretic such as acetaminophen
H Throat lozenges
H Antitussive such as dextromethorphan
H In infants, saline nose drops and mucus aspiration

with a bulb syringe

Nursing considerations
Key outcomes
The patient will:
H express feeling of increased comfort
H cope effectively with illness
H reestablish normal temperature
H have respiratory secretions that remain clear and
odorless
H maintain adequate air exchange.

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What happens in the common cold

Virus-infected droplets enter the body and


attack the cells lining the throat and nose.
The virus particles then multiply rapidly.

Body cell

The immune system responds by sending lymphocytes to the infected mucosa,


causing blood vessels in the nasal
mucosa to swell. This swelling causes
secretion of excess fluid the classic
cold symptom of a runny nose.

Infected
nasal lining
Virus
particles

Blood vessel
Lymphocyte

Phagocytes engulf and destroy dead virus


particles and damaged cells. Soon the cold
symptoms disappear.
Antibodies
Phagocyte

Some lymphocytes
immobilize the virus
particles with virusspecific proteins
(antibodies); others
kill infected cells with
a chemical substance.

Chemicals
Damaged
virus particles

Nursing interventions
H Give prescribed drugs.
H Provide a lubricant for nostrils to decrease irritation.
H Relieve throat irritation with sugarless hard candy or

cough drops.
H A warm bath or heating pad can reduce aches and

pains.
H Suggest a hot or cold steam vaporizer to relieve nasal

congestion.

Monitoring

Lymphocyte

Patient teaching
Be sure to cover:
H advice against overuse of nose drops or sprays
H how to avoid spreading colds
H proper hand-washing technique.

Discharge planning
H Refer the patient for medical care if a high fever per-

sists, level of consciousness changes, or significant


respiratory symptoms develop.

H Body temperature
H Respiratory status
H Response to treatment
H Adverse effects of medication
H Complications

Common cold

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Complex regional pain


syndrome
Overview
Description
H A chronic pain disorder resulting from abnormal

healing after minor or major injury to a bone,


muscle, or nerve
H Also known as reflex sympathetic dystrophy
(RSD/CRPS1) or causalgia (CRPS2)

Pathophysiology
H Abnormal functioning of the sympathetic nervous sys-

tem causes development of symptoms commonly disproportionate to the injurys severity.


H Interference with normal signals for sensations, temperature, and blood flow may be caused by impaired
communication between the damaged nerves of the
sympathetic nervous system and the brain.

Causes

H Muscle wasting (see Stages of complex regional

pain syndrome)

Test results
Imaging
H Bone X-rays rule out other conditions.

Treatment
General
H Physical therapy
H Activity, as tolerated

Medications
H Anti-inflammatory such as ibuprofen
H Antidepressant such as venlafaxine
H Analgesics, such as diclofenac and oxycodone

Surgery
H Nerve or regional blocks

Nursing considerations

H Exact cause unknown

Key outcomes

Precipitating factors
H Trauma
H Neurologic disorder
H Herpes zoster infection
H Myocardial infarction
H Musculoskeletal disorder (shoulder rotator cuff
injury)
H Malignancy

The patient will:


H express increased comfort
H use support systems and develop coping techniques
H demonstrate effective relaxation techniques.

Incidence
H Can occur at any age but is less common in children
H Reported more commonly in women

Common characteristics

Nursing interventions
H Offer emotional support.
H Apply antiembolism stockings.
H Apply heat or cold therapy.

Monitoring
H Pain control
H Effects of medications
H Blood glucose level

H Severe, constant pain

Complications
H Impaired mobility
H Depression

Assessment
History
H Injury
H Severe pain that worsens after activity

Physical findings
H Altered blood flow, feeling either warm or cool to the

touch, with discoloration, sweating, or swelling to the


affected extremity
H Skin, hair, and nail changes
H Impaired mobility and weakness

198

Complex regional pain syndrome

Patient teaching
Be sure to cover:
H the disease and treatment
H relaxation techniques
H medication administration, dosage, and possible
adverse effects.

Discharge planning
H Refer the patient for home therapy.
H Refer the patient to a pain care specialist.
H Refer the patient for psychological counseling and

support groups, as indicated.

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Stages of complex regional pain syndrome


Complex regional pain syndrome is divided into three stages. The stages arent always distinct and not all of the signs may
be present.

Stage

Duration

Pain, swelling,
and immobility

Skin

Hair and
nails

Osteoporosis

Symptoms
begin within
hours, days,
or weeks of
the injury; this
stage lasts
several weeks

Gradual or abrupt
onset of severe
aching, throbbing,
and burning pain at
site of injury
Pain may be accompanied by sensitivity
to touch, swelling,
muscle spasm, stiffness, and limited
mobility

Warm, red,
dry skin at
onset;
changes to
bluish and
becomes cold
and sweaty

Accelerated
hair and nail
growth

Early
osteoporosis
symptoms

Continuous burning,
aching, or throbbing
pain thats more severe than stage I
Swelling spreads
and changes from
soft to brawny and
firm
Loss of range of
motion, muscle
wasting

Cool, pale,
bluish,
sweaty

Altered hair
growth;
cracked,
grooved, or
ridged nails

More apparent
osteoporosis

Pain spreads proximally and may be intractable, but sometimes lessens and
stabilizes
More distinct dystrophic changes and
irreversible tissue
damage
Muscle atrophy and
contractures

Thin, shiny

Increasingly
brittle and
ridged nails

Marked diffuse
osteoporosis

I (Acute)

II (Subacute or dystrophic)

Lasts 3 to
6 months

III (Chronic or atrophic)

Lasts more
than 6 months

Complex regional pain syndrome

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Concussion
Overview
Description
H Blow to the head forceful enough to jostle the brain

and make it strike the skull


H Acceleration-deceleration injury
H Causes temporary (less than 48 hours) neural dys-

function

Assessment
History
H Trauma to head
H Short-term loss of consciousness
H Vomiting
H Antegrade and retrograde amnesia
H Change in level of consciousness (LOC)
H Dizziness
H Nausea
H Severe headache

Pathophysiology

Physical findings

H Concussion causes diffuse soft tissue damage.


H Inflammation occurs.
H Structural damage is usually minimal.

H Tenderness or hematomas on skull palpation

Causes
H Trauma to the head

Incidence
H More than 2 million instances of concussion per year

in the United States


H May occur in up to 20% of football players
H More common in males than in females
H Most commonly affects those ages 15 to 24

Common characteristics
H Short-term loss of consciousness
H Nausea and vomiting
H Dizziness
H Retrograde amnesia
H Erratic behavior
H Headache
H Blurred vision

Complications
H Seizures
H Persistent vomiting
H Intracranial hemorrhage (rare)

What to look for after a concussion


Before the patients discharge, follow these teaching
guidelines: Instruct the caregiver to awaken the patient
every 2 hours through the night and to ask his name and
whether he can identify the caregiver.
Advise the caregiver to return the patient to the facility
immediately if he is difficult to arouse, is disoriented,
has seizures, or experiences a persistent or worsening
headache, forceful or constant vomiting, blurred vision,
changes in personality, abnormal eye movements, a staggering gait, or twitching. If the patient is a child, explain to
the parents that some children have no apparent ill effects
immediately after a concussion but may grow lethargic or
somnolent a few hours later. Teach the patient the signs of
postconcussion syndrome headache, vertigo, anxiety,
personality changes, memory loss, and fatigue. Explain
that these signs may persist for several weeks.

200

Concussion

Test results
Imaging
H Computed tomography scan and magnetic resonance
imaging help rule out fractures and more serious
injuries.

Treatment
General
H Observation for changes in mental status
H Clear liquids if vomiting occurs
H Bed rest initially with head of the bed elevated at

least 30 degrees
H Avoidance of contact sports until fully recovered

Medications
H Nonopioid analgesic such as acetaminophen

Nursing considerations
Key outcomes
The patient will:
H state appropriate interactions for pain relief
H maintain stable vital signs
H identify factors that increase the potential for injury
H recover or be rehabilitated from physical injuries to
the extent possible.

Nursing interventions
H Give prescribed drugs, and avoid opioids that may

decrease LOC.
H Reorient the patient to time and place, if necessary.

Monitoring
H Vital signs
H Neurologic status
H Pain control

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Patient teaching
Be sure to cover:
H the injury, diagnosis, and treatment
H nonopioid analgesics for a headache and avoidance
of products containing aspirin
H change in LOC or projectile vomiting, which requires
a return to the hospital
H signs and symptoms of increased intracranial pressure.

Discharge planning
H Arrange for continued observation at home. (See

What to look for after a concussion.)

Concussion

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Conjunctivitis

H Transmission by contaminated towels, washcloths, or

ones own hand


H Systemic diseases, such as erythema multiforme and

thyroid disease

Overview

H Candidal infection

Description

Incidence

H Inflammation of palpebral or bulbar conjunctiva


H Characterized by hyperemia of the conjunctiva
H Usually spreads rapidly from one eye to the other
H Usually benign and self-limiting
H Seldom affects vision
H If chronic, may signal degenerative changes or dam-

H Most common eye disorder in the Western hemi-

age from repeated acute attacks


H Acute bacterial conjunctivitis (pink eye) usually lasting about 2 weeks
H Other viral conjunctival infections lasting 2 to
3 weeks; chronic and may produce severe disability

Pathophysiology
H Conjunctivitis is an inflammatory response of the

conjunctiva that usually begins in one eye and may


rapidly spread to the other eye.
H Vernal conjunctivitis is linked to a severe form of immunoglobulin E-mediated mast cell hypersensitivity
reaction.

sphere
H Responsible for about 30% of all eye complaints

Common characteristics
H Reddened conjunctiva
H Edema of eyelid
H Pain in the eye
H Increased lacrimation
H Burning in eyes

Complications
H Tic
H Corneal infiltrates
H Corneal ulcers
H Eye loss

Assessment

Causes

History

H Allergens
H Bacteria
H Viruses
H Chemical irritations

H Eye pain
H Photophobia
H Burning, itching, and sensation of a foreign body in

the eye
H Sore throat and fever, in children

Physical findings
Recognizing conjunctival papillae
If you see papillae in the conjunctiva of the upper eyelid,
your patient may have vernal (allergic) conjunctivitis.
These cobblestone bumps are the telltale sign. They result
from swollen lymph tissue within the conjunctival membrane.

H Conjunctival hyperemia
H Discharge
H Tearing
H Crust of sticky, mucopurulent discharge (in bacterial

conjunctivitis)
H Profuse, purulent discharge (in gonococcal conjunc-

tivitis)
H Copious tearing and minimal discharge (in viral con-

junctivitis)
H Conjunctival papillae (in vernal conjunctivitis) (see

Recognizing conjunctival papillae)


H Ipsilateral preauricular lymph node enlargement (in

viral conjunctivitis)

Test results
Laboratory
H Culture and sensitivity tests may identify the bacterial
pathogen.
H Stained smears of conjunctival scrapings may show
mostly monocytes with viral conjunctivitis; polymorphonuclear cells (neutrophils) are predominate with
bacterial conjunctivitis; and eosinophils are predominate with allergic conjunctivitis.

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Conjunctivitis

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Treatment
General
H Warm compresses
H Depends on cause

Medications
H Antibiotics, such a ciprofloxacin, erythromycin, and

mixofloxacin
H Antiviral such as acyclovir
H Corticosteroid such as dexamethasone
H Histamine-1 receptor antagonist such as azelastine
H Oral antihistamine such as loratidine

Nursing considerations
Key outcomes
The patient will:
H maintain current health status
H sustain no harm or injury
H exhibit no signs of infection
H regain visual function.

Nursing interventions
H Apply warm compresses.
H Apply therapeutic ointment or eyedrops, as ordered.
H Avoid irrigating the eye to prevent the spread of in-

fection.
H Notify public health officials if culture results identify

Neisseria gonorrhoeae.
H Obtain culture specimens before antibiotic therapy.

Monitoring
H Response to treatment
H Signs and symptoms of complications
H Adverse reactions
H Visual acuity

Patient teaching
Be sure to cover:
H proper hand-washing technique
H instillation of eyedrops and ointments
H completing the prescribed antibiotics
H methods for preventing disease transmission
H importance of avoiding chemical irritants
H avoiding eye makeup and contact lens use until the
infection has cleared.

ALERT
Caution the patient to avoid rubbing the infected
eye so that he can prevent the spread of infection
to the other eye or to other people.

Conjunctivitis

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Corneal abrasion
Overview
Description

Test results
Diagnostic procedures
H Fluorescein staining of the injured area of the cornea
appears green when illuminated.
H Slit-lamp examination discloses the depth of the
abrasion.

H Scratch on the epithelial surface of the cornea


H Prognosis usually good with appropriate treatment

Treatment

Pathophysiology

General

H Epithelial layers of cornea are lost due to trauma.


H Superficial abrasions dont involve Bowmans mem-

H Eye irrigation (see Performing eye irrigation)


H Removal of foreign body
H Warm compresses
H Eye patch for 24 hours
H Eye protection with potentially dangerous activities

brane.
H Deep abrasions penetrate Bowmans membrane.

Causes
H Eye trauma
H Foreign bodies embedded under eyelid
H Contact lenses
H Chemicals
H Fingernails
H Hair brushes
H Tree branches
H Dust

Incidence

Medications
H Antibiotic eyedrops or ointment, such as ciproflox-

acin, erythromycin, gentamicin, and tobramycin


H Corticosteroid such as dexamethasone

Surgery
H Surgical repair of corneal lacerations by an ophthal-

mologist

H Affects males and females equally

Nursing considerations

Common characteristics

Key outcomes

H Difficulty opening the eye


H Eye pain
H Erythema
H Feeling of foreign body in eye
H Increased lacrimation

The patient will:


H regain visual function
H sustain no harm or injury
H express feelings of increased comfort
H verbalize feelings and concerns.

Complications

Nursing interventions

H Corneal erosion
H Corneal ulceration
H Permanent vision loss
H Secondary infection

H Use a flashlight to inspect the cornea.


H Check visual acuity before treatment begins.
H If a foreign body is present, irrigate the eye with

Assessment
History
H Eye trauma
H Prolonged contact lens wear
H Sensation of foreign body in eye
H Sensitivity to light
H Decreased visual acuity
H Eye pain

Physical findings
H Redness in eye
H Increased tearing
H Possibly a foreign object embedded under the eyelid,

uncovered by eyelid eversion


H Disruption of corneal surface

204

Corneal abrasion

normal saline solution.


H Give prescribed antibiotics and cycloplegics.
H Instill prescribed topical anesthetics.

ALERT
Never give the patient topical anesthetic drops for
self-administration. Abuse of this medication can
delay healing, especially if the patient rubs the
numb eye and further injures it.

Monitoring
H Visual acuity
H Response to treatment

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Performing eye irrigation


SQUEEZE BOTTLE

I.V. TUBE

MORGAN LENS

For moderate-volume irrigation to


remove eye secretions, for example
apply sterile ophthalmic irrigant to the
eye directly from the squeeze bottle
container. Direct the stream at the inner canthus and position the patient so
that the stream washes across the
cornea and exits at the outer canthus.

For copious irrigation to treat chemical burns, for example set up an


I.V. bag and tubing without a needle.
Use the procedure described for moderate irrigation to flush the eye for at
least 15 minutes. Alkali burns may require irrigation for several hours.

Connected to irrigation tubing, a Morgan lens permits continuous lavage


and delivers medication to the eye.
Use an adapter to connect the lens to
the I.V. tubing and the solution container. Begin the irrigation at the prescribed flow rate. To insert the device,
ask the patient to look down as you insert the lens under the upper eyelid.
Then have her look up as you retract
and release the lower eyelid over the
lens.

ALERT
Pulse oximeter probes should be applied to the
middle, ring, or preferably little finger, but never
the index finger, in order to minimize the likelihood of corneal abrasion, especially as patients
emerge from anesthesia.

Patient teaching
Be sure to cover:
H healing process
H proper instillation of antibiotic eyedrops or ointment
H effects of untreated corneal infection
H need to wear safety glasses in the workplace, if
appropriate
H contact lens care and instructions for wear.

Corneal abrasion

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Coronary artery disease


Overview
Description
H Heart disease that results from narrowing of coro-

nary arteries over time due to atherosclerosis


H Primary effect: loss of oxygen and nutrients to myo-

cardial tissue because of diminished coronary blood


flow

Pathophysiology
H Increased blood levels of low-density lipoprotein

(LDL) irritate or damage the inner layer of coronary


vessels.
H LDL enters the vessel after damaging the protective
barrier, accumulates, and forms a fatty streak.
H Smooth muscle cells move to the inner layer to engulf the fatty substance, produce fibrous tissue, and
stimulate calcium deposition.
H Cycle continues, resulting in transformation of the
fatty streak into fibrous plaque and, eventually, a
coronary artery disease (CAD) lesion evolves.
H Oxygen deprivation forces the myocardium to shift
from aerobic to anaerobic metabolism, leading to
accumulation of lactic acid and reduction of cellular pH.
H The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular
function.
H The strength of contractions in the affected myocardial region is reduced as the fibers shorten inadequately, resulting in less force and velocity.
H Wall motion is abnormal in the ischemic area, resulting in less blood being ejected from the heart with
each contraction.

Causes
H Atherosclerosis
H Dissecting aneurysm
H Infectious vasculitis
H Syphilis
H Congenital defects
H Coronary artery spasm

Risk factors
H Family history
H High cholesterol level
H Smoking
H Diabetes
H Hormonal contraceptives
H Obesity
H Sedentary lifestyle
H Stress
H Increased homocystine levels

Incidence
H Occurs after age 40

206

Coronary artery disease

H Males eight times more susceptible than premeno-

pausal females
H Risk increased by positive family history
H White males more susceptible than nonwhite males;

nonwhite females more susceptible than white females


H Occurs in about 11 million Americans

Common characteristics
H Angina

Complications
H Arrhythmias
H Myocardial infarction (MI)
H Heart failure

Assessment
History
H Angina that may radiate to the left arm, neck, jaw, or

shoulder blade
H Commonly occurring after physical exertion but pos-

sibly following emotional excitement, exposure to


cold, or ingestion of a large meal
H May develop during sleep; symptoms wake the
patient
H Nausea
H Vomiting
H Fainting
H Sweating
H Stable angina (predictable and relieved by rest or nitrates)
H Unstable angina (increases in frequency and duration and is more easily induced and generally indicates extensive or worsening disease and, untreated,
may progress to MI)
H Crescendo angina (an effort-induced pain occurring
with increasing frequency and decreasing provocation)
H Prinzmetals or variant angina pectoris (severe noneffort-produced pain occurs at rest without provocation due to spasm)

Physical findings
H Cool extremities
H Xanthoma
H Arteriovenous nicking of the eye
H Obesity
H Hypertension
H Positive Levines sign (holding fist to chest)
H Decreased or absent peripheral pulses

Test results
Imaging
H Myocardial perfusion imaging with radionucleotide
during treadmill exercise shows ischemic areas of
the myocardium, visualized as cold spots.
H Pharmacologic myocardial perfusion imaging in arteries with stenosis shows decrease in blood flow
proportional to the percentage of occlusion.

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H Coronary angiography reveals the location and de-

gree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery
beyond the narrowing.
H Stress echocardiography may show abnormal wall
motion.
H Multiple-gated acquisition scanning demonstrates
cardiac wall motion and reflects injury to cardiac
tissue.
Diagnostic procedures
H Electrocardiography may be normal between anginal
episodes. During angina, it may show ischemic
changes.
H Exercise stress testing may be performed to detect
ST-segment changes during exercise, indicating
ischemia, and to determine a safe exercise prescription.

Treatment
General

Preventing coronary artery disease


Because coronary artery disease is so widespread, prevention is important. Dietary restrictions aimed at reducing the intake of calories (in obesity) and of salt, fats, and
cholesterol minimize the risk, especially when supplemented with regular exercise. Abstention from smoking
and reduction of stress are also essential.
Other preventive actions include control of hypertension
(with diuretics or sympathetic beta-adrenergic blockers),
control of elevated serum cholesterol or triglyceride levels
(with antilipemics such as HMG-CoA reductase inhibitors,
including atorvastatin, pravastatin, or simvastatin), and
measures to minimize platelet aggregation and the danger
of blood clots (with aspirin, for example).

Nursing interventions
H Ask the patient to grade the severity of his pain on a

scale of 0 to 10.
H Keep nitroglycerin available for immediate use. In-

and maintaining ideal body weight (see Preventing


coronary artery disease)
H Low-fat, low-sodium diet
H Activity restrictions possible
H Regular exercise

struct the patient to call immediately whenever he


feels pain and before taking nitroglycerin.
H Observe for signs and symptoms that may signify
worsening of condition.
H Maintain bed rest immediately postoperatively with
the head of the bed elevated at least 30 degrees.
H Encourage coughing, deep breathing, and incentive
spirometer use postoperatively.
H Encourage early ambulation after surgery.

Medications

Monitoring

H Antianginals, such as ranolazine and nitroglycerin


H Beta-adrenergic blocker such as metoprolol
H Calcium channel blocker such as diltiazem
H Antiplatelets, such as ticlopidine and aspirin
H Antilipemic such as simvastatin
H Antihypertensive such as lisinopril

H Vital signs
H Hemodynamic status
H Intake and output
H Effectiveness of pain medication during anginal

Surgery

H Respiratory status
H Chest tube drainage, after surgery
H Cardiac rate and rhythm
H Cardiovascular status

H Stress reduction techniques essential, especially if

known stressors precipitate pain


H Lifestyle modifications, such as smoking cessation

H Coronary artery bypass graft


H Keyhole or minimally invasive surgery
H Angioplasty
H Endovascular stent placement
H Laser angioplasty
H Atherectomy

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H plan menus appropriate to prescribed diet
H demonstrate understanding of the disease process
H express concern about self-concept, self-esteem, and
body image
H express feelings of increased comfort and decreased
pain.

episodes
H Abnormal bleeding and distal pulses following inter-

vention procedures

Patient teaching
Be sure to cover:
H risk factors for CAD
H avoidance of activities that precipitate pain
H effective coping mechanisms to deal with stress
H the need to follow the prescribed drug regimen
H low-sodium and low-calorie diet
H the importance of regular, moderate exercise.

Discharge planning
H Refer the patient to a weight-loss program, if needed.
H Refer the patient to a smoking-cessation program, if

needed.
H Refer the patient to a cardiac rehabilitation program,

if indicated.

Coronary artery disease

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Cor pulmonale

H In response to hypoxia, the bone marrow produces

more red blood cells, causing polycythemia.


H The bloods viscosity increases, further aggravating

pulmonary hypertension. This increases the right


ventricles workload, causing heart failure. (See Cor
pulmonale: An overview.)

Overview
Description
H Hypertrophy and dilation of the right ventricle sec-

Causes

ondary to disease affecting the structure or function


of the lungs or their vasculature
H Can occur at the end stage of various chronic disorders of the lungs, pulmonary vessels, chest wall, or
respiratory control center
H Also called right-sided heart failure

H Disorders affecting the pulmonary parenchyma


H Chronic obstructive pulmonary disease
H Bronchial asthma
H Primary pulmonary hypertension
H Vasculitis
H Pulmonary emboli
H External vascular obstruction resulting from a tumor

Pathophysiology
H An occluded vessel impairs the hearts ability to gen-

erate enough pressure.


H Increased blood flow creates pulmonary hyperten-

sion.
H Pulmonary hypertension increases the hearts work-

load.
H To compensate, the right ventricle hypertrophies to

force blood through the lungs.

or aneurysm
H Kyphoscoliosis
H Pectus excavatum (funnel chest)
H Muscular dystrophy
H Poliomyelitis
H Obesity
H High altitude

Incidence
H Accounts for 6% to 7% of all types of adult heart

disease in the United States

Cor pulmonale: An overview


Although pulmonary restrictive disorders (such as fibrosis
or obesity), obstructive disorders (such as bronchitis), or
primary vascular disorders (such as recurrent pulmonary
emboli) may cause cor pulmonale, these disorders share
this common pathway.

H Affects males and females equally

Common characteristics
H Dyspnea
H Tachypnea
H Signs of heart failure

Complications
Pulmonary disorder

Anatomic alterations in the pulmonary blood vessels and


functional alterations in the lung

H Right- and left-sided heart failure


H Hepatomegaly
H Edema
H Ascites
H Pleural effusions
H Thromboembolism due to polycythemia

Assessment
Increased pulmonary vascular resistance

Pulmonary hypertension

History
H Dyspnea
H Chronic productive cough
H Fatigue
H Weakness

Physical findings

Right ventricular hypertrophy (cor pulmonale)

HEART FAILURE

208

Cor pulmonale

H Wheezing respirations
H Tachypnea
H Dependent edema
H Enlarged, tender liver
H Hepatojugular reflux
H Jugular vein distention
H Tachycardia
H Pansystolic murmur at the lower left sternal border

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Test results

Monitoring

Laboratory
H Arterial blood gas analysis detects decreased
partial pressure of arterial oxygen (usually less
than 70 mm Hg and rarely more than 90 mm Hg).
H Hematocrit is typically over 50%.
H Serum hepatic tests may show an elevated level of
aspartate aminotransferase levels.
Imaging
H Echocardiography demonstrates right ventricular
enlargement.
H Angiography shows right ventricular enlargement.
H Chest X-rays reveal large central pulmonary arteries
and right ventricular enlargement.
H Magnetic resonance imaging measures the right ventricular mass, wall thickness, and ejection fraction.
H Cardiac catheterization measures pulmonary vascular
pressures.
Diagnostic procedures
H Electrocardiography shows arrhythmias, such as premature atrial and ventricular contractions and atrial
fibrillation during severe hypoxia, and also right
bundle-branch block, right axis deviation, prominent
P waves, and an inverted T wave in right precordial
leads.
H Pulmonary function studies reflect underlying pulmonary disease.
Other
H Pulmonary artery catheterization shows increased
right ventricular and pulmonary artery pressures.

H Vital signs
H Oxygenation
H Intake and output
H Laboratory values
H Respiratory status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary restrictions
H medication administration and possible adverse effects.

Discharge planning
H Refer the patient for home services, as indicated.

Treatment
General
H Low-sodium diet
H Fluid restrictions
H Limited activity or bed rest
H Phlebotomy, if necessary

Medications
H Cardiac glycoside such as digoxin
H Antibiotics, such as amoxicillin and ampicillin
H Vasodilator such as isosorbide
H Oxygen

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain adequate ventilation
H use support services and develop coping mechanisms.

Nursing interventions
H Reposition the patient often.
H Give prescribed drugs.
H Administer oxygen as prescribed.

Cor pulmonale

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Life-threatening disorder

Creutzfeldt-Jakob
disease

H Sporadic form of unknown etiology


H Iatrogenic or acquired form due to inadvertent expo-

sure to CJD-contaminated equipment or material as


a result of brain surgery, corneal grafts, or use of human pituitary-derived growth hormones or gonadotropin

Incidence

Overview
Description
H Rapidly progressive infectious disease attacking the

central nervous system (CNS)


H Manifested by progressive dementia, tremors, and

muscle wasting

H About one case in 1 million people worldwide

annually
H Most cases sporadic, accounting for about 85% of all

cases
H About 5% to 15% of cases familial, with an autoso-

mal dominant pattern of inheritance


H Usually patients older than age 55; median age of

death in the United States: 68

H Always fatal
H Not transmitted by normal casual contact (although

H Affects males and females of diverse ethnic back-

iatrogenic transmission can occur)


H Has a 15- to 20-month incubation period
H Typical duration: 6 months
H New variant of Creutzfeldt-Jakob disease emerged in
Europe in 1996 (see Understanding new-variant
Creutzfeldt-Jakob disease)
H No cure and cant slow progression
H Also known as CJD

H Most cases in Libya, North Africa, and Slovakia

Pathophysiology

grounds

Common characteristics
H Rapidly progressive dementia
H Prominent myoclonus

Complications
H Severe, progressive dementia
H CNS abnormalities
H Death

H CJD is caused by the abnormal accumulation or me-

tabolism of prion proteins.


H These modified proteins are resistant to proteolytic

digestion and aggregate in the brain to produce rodlike particles.


H The accumulation of these modified cellular proteins
results in neuronal degeneration and spongiform
changes in brain tissue.

Causes
H Familial or genetically inherited form

Understanding new-variant
Creutzfeldt-Jakob disease
Like conventional Creutzfeldt-Jakob disease (CJD), variant
CJD (vCJD) is a rare, fatal neurodegenerative disease.
Most cases have been reported in the United Kingdom,
and its most likely caused by exposure to bovine spongiform encephalopathy (BSE), a fatal brain disease in cattle
also known as mad cow disease. Ingestion of beef products from cattle with BSE is the most probable route of
exposure.
vCJD affects patients at a much younger age than CJD,
and the duration of the illness is much longer (14 months
versus 6 months).
Regulations have been established in Europe to control
outbreaks of BSE in cattle and to prevent contaminated
meat from entering the food supply. vCJD and its relationship with BSE are still being explored by the Centers for
Disease Control and Prevention and the World Health Organization.

210

Creutzfeldt-Jakob disease

Assessment
History
H Mood changes
H Emotional lability
H Poor concentration
H Lethargy
H Impaired judgment
H Memory loss
H Involuntary muscle movements
H Vision disturbances or other types of hallucinations
H Gait disturbances

Physical findings
H Dementia
H Myoclonus
H Spasticity
H Agitation
H Tremor
H Clumsiness
H Ataxia
H Hypokinesis and rigidity
H Hyperreflexia

Test results
Laboratory
H Cerebral spinal fluid (CSF) immunoassay may show
abnormal protein species.
H CSF analysis may show mildly elevated protein level.

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Imaging
H Computed tomography scan and magnetic resonance
imaging of the brain may show evidence of generalized cortical atrophy.
Diagnostic procedures
H EEG may show burst suppression changes in brainwave activity.
H Brain biopsy may show spongiform changes.
Other
H Autopsy of brain tissue allows definitive diagnosis.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and supportive treatment
H prevention of disease transmission
H effective coping strategies
H safety precautions.

Discharge planning
H Refer the patient and his family to CJD support

Treatment

groups.
H Refer the patient for hospice care, as appropriate.

General
H Palliative care to make the patient comfortable and to

ease symptoms
H Well-balanced diet
H Adequate fluid intake
H Activity, as tolerated

Medications
H Antiparkinsonian such as amantadine

Surgery
H Possible brain biopsy for diagnosis

Nursing considerations
Key outcomes
The patient will:
H verbalize feelings of anxiety and fear
H demonstrate effective coping techniques
H remain free from injury
H maintain social interaction to the extent possible
H utilize support systems.

Nursing interventions
H Assist the patient and his family through the grieving

process.
H Follow standard precautions.
H Encourage verbalization of concerns and fears.
H Encourage involvement of the patient and his family

in care decisions.

Monitoring
H Vital signs
H Intake and output
H Neurologic status

Creutzfeldt-Jakob disease

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Crohns disease

H Perforation
H Nutritional deficiencies caused by malabsorption and

maldigestion

Overview
Description

Assessment

H Inflammatory bowel disease possibly affecting any

History

part of the GI tract but commonly involving the terminal ileum


H Fifty percent of cases involving colon and small bowel; 33% involving terminal ileum; 10% to 20% involving only colon
H Extends through all layers of the intestinal wall; possibly involving regional lymph nodes and mesentery

H Gradual onset of signs and symptoms, marked by pe-

Pathophysiology
H Crohns disease involves slow, progressive inflamma-

tion of the bowel.

riods of remission and exacerbation


H Fatigue and weakness
H Fever, flatulence, nausea
H Steady, colicky, or cramping abdominal pain usually

occurring in the right lower quadrant


H Diarrhea possibly worsening after emotional upset

or ingestion of poorly tolerated foods, such as milk,


fatty foods, and spices
H Weight loss

H Lymphatic obstruction is caused by enlarged lymph

Physical findings

nodes.
H Edema, mucosal ulceration, fissures, and abscesses
occur.
H Elevated patches of closely packed lymph follicles
(Peyers patches) develop in the small intestinal lining.
H Fibrosis occurs, thickening the bowel wall and causing stenosis.
H Inflamed bowel loops adhere to other diseased or
normal loops.
H The diseased bowel becomes thicker, shorter, and
narrower.

H Possible soft or semiliquid stool, usually without

Causes
H Exact cause unknown
H Lymphatic obstruction and infection among con-

tributing factors

Risk factors
H History of allergies
H Immune disorders
H Genetic predisposition 10% to 20% of patients

with the disease have one or more affected relatives;


sometimes occurs in monozygotic twins

Incidence
H Occurs equally in males and females
H More common in Jewish people
H Onset usually before age 30

Common characteristics
H Diarrhea
H Abdominal pain
H Weight loss

gross blood
H Right lower quadrant tenderness or distention
H Possible abdominal mass, indicating adherent loops

of bowel
H Hyperactive bowel sounds
H Bloody diarrhea
H Perianal and rectal abscesses

Test results
Laboratory
H Occult blood is seen in stools.
H Hemoglobin level and hematocrit are decreased.
H White blood cell count and erythrocyte sedimentation
rate are increased.
H Serum potassium, calcium, and magnesium levels
are decreased.
H Hypoproteinemia is present due to intestinal protein
loss.
H Vitamin B12 and folate levels are decreased.
Imaging
H Small-bowel X-rays may show irregular mucosa, ulceration, and stiffening.
H Barium enema reveals the string sign (segments of
stricture separated by normal bowel) and may also
show fissures and narrowing of the lumen.
Diagnostic procedures
H Sigmoidoscopy and colonoscopy show patchy areas
of inflammation and may also reveal the characteristic coarse irregularity (cobblestone appearance) of
the mucosal surface.
H Biopsy reveals granulomas in up to half of all specimens.

Complications

Treatment

H Anal fistula
H Perineal abscess
H Fistulas of the bladder or vagina or to the skin in an

General

old scar area


H Intestinal obstruction

212

Crohns disease

H Stress reduction
H Avoidance of foods that worsen diarrhea
H Adequate caloric, protein, and vitamin intake

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H Parenteral nutrition, if necessary


H Reduced physical activity

Medications
H Corticosteroid such as budesonide
H Immunosuppressants, such as adalimumab and

infliximab
H Sulfonamide such as sulfasalazine
H Antibacterials and antiprotozoals, such as metronida-

zole and nitazoxanide


H Antidiarrheal such as octreotide
H Opioid such as morphine
H Vitamin supplements, such as vitamin B12 and folate
H Antispasmodic such as alosetron
H Iron supplement such as ferrous sulfate

Surgery
H Indicated for acute intestinal obstruction
H Colectomy with ileostomy

Patient teaching
Be sure to cover:
H information about the disease, symptoms, and complications
H ordered diagnostic tests and pretest guidelines
H the importance of adequate rest
H how the patient can identify and reduce sources of
stress
H prescribed dietary changes
H prescribed medications, administration, and possible
adverse effects.

Discharge planning
H Refer the patient to a smoking-cessation program, if

appropriate.
H Refer the patient to enterostomal therapist, if indi-

cated.

Nursing considerations
Key outcomes
The patient will:
H maintain adequate caloric intake
H maintain normal fluid volume
H regain normal bowel movements
H verbalize understanding of the disease process and
treatment regimen
H exhibit adequate coping mechanisms and seek
appropriate sources of support.

Nursing interventions
H Provide emotional support to the patient and his

family.
H Provide meticulous skin care after each bowel

movement.
H Schedule patient care to include rest periods

throughout the day.


H Assist with dietary modification.
H Give prescribed iron supplements and blood

transfusions.
H Give prescribed analgesics.

Monitoring
H GI status
H Vital signs
H Intake and output, including amount of stool
H Daily weight
H Serum electrolyte, glucose, and Hb levels and stools

for occult blood


H Signs of infection or obstruction
H Bleeding, especially with steroid use
H Pain control
H Skin integrity

Crohns disease

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Croup
Overview
Description
H Viral infection causing severe inflammation and ob-

struction of the upper airway


H Childhood disease manifested by acute laryngotracheobronchitis (most commonly), laryngitis, acute
spasmodic laryngitis, and febrile rhinitis
H Incubation period about 3 to 6 days; contagious
while febrile
H Recovery usually complete

Pathophysiology
H Viral invasion of the laryngeal mucosa leads to in-

flammation, hyperemia, edema, epithelial necrosis,


and shedding.
H This leads to irritation and cough, reactive paralysis
and continuous stridor, or collapsible supraglottic or
inspiratory stridor and respiratory distress.
H A thin, fibrinous membrane covers the mucosa of the
epiglottis, larynx, and trachea. (See How croup affects the upper airways.)

Causes
H Parainfluenza viruses
H Adenoviruses
H Respiratory syncytial virus
H Influenza viruses
H Measles viruses
H Bacteria (pertussis and diphtheria)

Incidence
Special populations
Occurs mainly in children ages 3 months to 5
years.
H Affects boys more commonly than girls
H Usually occurs in late autumn and early winter

Special populations
Acute spasmodic laryngitis affects children
between ages 1 and 3, particularly those with
allergies.

Common characteristics
H Sharp, barklike, or brassy cough progressing to

stridor
H Hoarse or muffled vocal sounds

Complications
H Airway obstruction
H Respiratory failure

214

Croup

H Dehydration
H Ear infection
H Pneumonia
H Hypoxia
H Hypercapnia

Assessment
History
H Recent upper respiratory infection

Laryngotracheobronchitis
H Fever and breathing problems usually occurring at
night
H Difficulty exhaling
Laryngitis in children
H Mild sore throat
H Cough
H Marked hoarseness (rare)
H No respiratory distress
Laryngitis in infants
H Respiratory distress
Acute spasmodic laryngitis
H Mild to moderate hoarseness
H Nasal discharge
H Characteristic cough and noisy inspiration
H Anxiety
H Increased dyspnea
H Transient cyanosis

Physical findings
H Rhinorrhea
H Use of accessory muscles
H Nasal flaring
H Barklike cough
H Hoarse, muffled vocal sounds
H Inspiratory stridor
H Diminished breath sounds

Laryngotracheobronchitis
H Edema of bronchi and bronchioles
H Decreased breath sounds
H Expiratory rhonchi
H Scattered crackles
Laryngitis
H Suprasternal and intercostal retractions
H Inspiratory stridor
H Dyspnea, tachypnea
H Diminished breath sounds
H Severe dyspnea and exhaustion in later stages
Acute spasmodic laryngitis
H Labored breathing with retractions
H Clammy skin
H Rapid pulse rate

Test results
Laboratory
H Throat cultures show bacteria and sensitivity to
antibiotics.

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Imaging
H Neck X-ray may show upper airway narrowing and
edema in subglottic folds; helps to differentiate croup
from bacterial epiglotidititis.
H Computed tomography scan helps differentiate between croup, epiglotidititis, and noninfection.
Diagnostic procedures
H Laryngoscopy may reveal inflammation and obstruction in epiglottal and laryngeal areas.

How croup affects the upper airways


In croup, inflammatory swelling and spasms constrict the
larynx, thereby reducing airflow. This cross-sectional
drawing (from chin to chest) shows the upper airway
changes caused by croup. Inflammatory changes almost
completely obstruct the larynx (which includes the epiglottis) and significantly narrow the trachea.

Treatment
General
H Home or hospitalized care
H Humidification during sleep
H Intubation if other means of preventing respiratory

failure unsuccessful
H Diet, as tolerated
H Parenteral fluids, if required
H Rest periods

Medications
H Oxygen therapy, as needed
H Antipyretic such as acetaminophen
H Antibiotics, such as cefuroxime and cefprozil, if

Inflamed
laryngeal area
Inflamed
subglottic tissue

Narrowed
trachea

cause is bacterial
H Adrenergic, aerosolized racemic epinephrine for

moderately severe croup


H Corticosteroids for acute laryngotracheobronchitis

Surgery
H Tracheostomy (rare)

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain normal temperature
H maintain a patent airway
H use effective coping strategies
H verbalize understanding of the disorder.

Nursing interventions
H Maintain a patent airway.
H Adminster oxygen, as prescribed.
H Administer I.V. fluids, as prescribed.
H Give prescribed drugs.
H Provide quiet diversional activities.
H Engage parents in the care of the infant or child.
H Position an infant in an infant seat or prop him up

H Use sponge baths and hypothermia blanket, as or-

dered, for temperatures above 102 F (38.9 C).

Monitoring
H Vital signs
H Intake and output
H Respiratory status
H Signs and symptoms of dehydration

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H humidification
H hydration
H signs and symptoms of ear infection
H signs and symptoms of pneumonia.

with a pillow.
H Position an older child in Fowlers position.
H Provide humidification.
H Avoid milk-based fluids if the patient has thick mucus

or swallowing difficulties.
H Provide frequent mouth care.
H Isolate patients for respiratory syncytial virus and

parainfluenza infections.

Croup

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Cryptococcosis
Overview
Description
H Fungal infection that usually begins as asymptomatic

pulmonary infection in patient who presents with


meningoencephalitis
H Also known as torulosis and European blastomycosis

Pathophysiology
H Small granulomas and cysts in the cerebral cortex

and, later, in deep cerebral tissues produce a minimal inflammatory response.


H In chronic cases, dense basilar arachnoiditis occurs.
H Lung lesions with intense granulomatous inflammation occur.

Causes
H Airborne fungus Cryptococcus neoformans found in

dust particles contaminated by pigeon stool


H Transmission by inhalation of cryptococci

Incidence
H Prevalent in immunocompromised patients and those

taking immunosuppressant drugs


H Increasing, especially in patients with acquired im-

munodeficiency syndrome

Common characteristics
H Disseminates to extrapulmonary sites, including the

central nervous system (CNS), skin, bones, prostate


gland, liver, and kidneys
H Without treatment, leads to CNS infection and death
H Mortality dramatically reduced with treatment; neurologic deficits, such as paralysis and hydrocephalus,
not necessarily reduced with treatment

Complications
H Optic atrophy
H Ataxia
H Hydrocephalus
H Deafness
H Paralysis
H Organic mental syndrome
H Personality changes
H Coma
H Death

Assessment
History
H Human immunodeficiency virus infection or another

immunosuppressive disorder
H Usually asymptomatic but patient may complain of

dull chest pain and cough producing slight amount


of white, blood-streaked sputum

216

Cryptococcosis

Physical findings
H Progressively severe frontal and temporal headache
H Diplopia, blurred vision, and papilledema
H Tinnitus, dizziness, ataxia, and aphasia
H Vomiting
H Memory changes, inappropriate behavior, irritability,

and psychosis
H Facial weakness
H Hyperactive reflexes and seizures in the late stage
H Pain in the long bones, skull, spine, and joints
H Red facial papules and other skin abscesses, with or

without ulceration
H Rarely, pleural friction rub or crackles
H Photophobia

Test results
Imaging
H Chest X-ray or computed tomography scan of the
chest reveals lesions in pulmonary cryptococcosis.
Laboratory
H Analysis or cultures of the sputum, urine, prostatic
secretions, or bone marrow aspirate show C. neoformans.
H Tissue or neural biopsy shows myriad cryptococci.
H India ink preparation of cerebrospinal fluid (CSF)
diagnosing CNS infection when C. neoformans is
detected.
H Blood cultures are positive only in severe infection.
H Antigen titer in serum and CSF is elevated in disseminated infection.
H Protein levels and white blood cell count are elevated
in CNS infection.
H CSF glucose levels are moderately decreased in about
50% of patients.
Other
H Lumbar puncture shows increased CSF pressure.

Treatment
General
H Early treatment for cryptococcal disease

Medications
H Combination of antifungal antibiotics amphotericin B

and flucytosine, or amphotericin B alone

Nursing considerations
Key outcomes
The patient will:
H be free from pain
H be free from injury
H maintain patent airway
H increase activity, as tolerated.

Nursing interventions
H Maintain a patent airway.
H Keep the head of the bed elevated at least 30 degrees.
H Give prescribed drugs.

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H Before therapy, obtain electrolyte and creatinine

levels.
H Observe for adverse effects such as diarrhea.
H Evaluate the need for long-term venous access for

administering amphotericin B.
H Provide psychological support to help the patient

cope with long-term treatment.


H If vision loss occurs, provide a safe environment.
H Encourage verbalization and provide support.

Monitoring
H Vital signs
H Neurologic checks
H Respiratory status
H Headache, vomiting, and nuchal rigidity
H Intake and output
H Blood urea nitrogen, creatinine levels, and complete

blood count results


H Urinalysis results
H Magnesium and potassium levels and liver function

test results
H Blood levels of flucytosine

Patient teaching
Be sure to cover:
H the disorder and treatment
H medication therapy, including dosage, desired drug
actions, adverse effects, and need for long-term treatment.

Discharge planning
H Urge the patient to return for follow-up care and

evaluation every few months for 1 year.


H Refer the patient for resource and support services,

as needed.

Cryptococcosis

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Cryptorchidism

H True undescended testes remain along the path of

Overview

Causes

normal descent, while ectopic testes deviate from


that path.

Description
H Congenital disorder in which one or both testes fail

to descend into the scrotum, remaining in the abdomen or inguinal canal or at the external ring
H May be bilateral, but more commonly affects the
right testis (see Varieties of cryptorchidism)

H Hormonal factors
H Testosterone deficiency
H Structural factors
H Genetic predisposition

Incidence
H Occurs in 30% of premature male neonates, but in

only 3% of those born at term

Pathophysiology

H In about 80% of affected infants: testes descend

H In the male fetus, testosterone normally stimulates

the formation of the gubernaculum. A fibromuscular


band connects the testes to the scrotal floor.
H This band probably helps pull the testes into the
scrotum by shortening as the fetus grows.
H Thus, cryptorchidism may result from inadequate
testosterone levels or a defect in the testes or the gubernaculum.
H Because the testis is maintained at a higher temperature, spermatogenesis is impaired, leading to reduced fertility.

spontaneously during first year; in the rest: testes


may descend later

Common characteristics
H Testis on the affected side not palpable in the scro-

tum; underdeveloped scrotum (unilateral cryptorchidism)


H Scrotum enlarged on the unaffected side
H Infertility

Varieties of cryptorchidism
Descent interrupted beyond
external inguinal ring

Descended but not to


bottom of scrotum

218

Cryptorchidism

Partially descended

Testis retained in
abdomen

Normal

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Complications
H Sterility
H Increased risk for testicular cancer
H Increased vulnerability of the testes to trauma

Assessment
Physical findings
H Nonpalpable testes
H Underdeveloped scrotum

Test results
Laboratory
H Buccal smear (cells from oral mucosa) determines
genetic sex (a male sex chromatin pattern).
H Serum gonadotropin confirms the presence of testes
by showing presence of circulating hormone.

Treatment
Medications
H Human chorionic gonadotropin

Surgery
H Orchiopexy

Nursing considerations
Key outcomes
The patient will:
H express or demonstrate feelings of increased comfort
H be free from complications.

Nursing interventions
H Encourage the parents of the child with undescended

testes to express their concern about his condition.


H Tell the parents that a rubber band may be taped to

the patients thigh for about 1 week after surgery to


keep the testis in place. Explain that his scrotum may
swell but shouldnt be painful.

Monitoring
After surgery
H Vital signs
H Intake and output
H Operative site
H Pain control

Patient teaching
Be sure to cover:
H the disorder, treatment, and effect on reproduction
H surgery or medications prescribed.

Cryptorchidism

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Cushings syndrome

H Menstrual disturbances
H Sexual dysfunction
H Psychiatric problems, ranging from mood swings to

Overview

frank psychosis

Description

Assessment

H Clinical manifestations of glucocorticoid excess, par-

ticularly cortisol
H May also reflect excess secretion of mineralocorti-

coids and androgens


H Classified as primary, secondary, or iatrogenic, depending on etiology
H Prognosis dependent on early diagnosis, identification of underlying cause, and effective treatment

Pathophysiology
H A loss of normal feedback inhibition by cortisol

occurs.
H Elevated levels of cortisol dont suppress hypothala-

mic and anterior pituitary secretion of corticotropinreleasing hormone and adrenocorticotropic hormone (ACTH).
H The result is excessive levels of circulating cortisol.

Causes
H Pituitary microadenoma
H Excess production of corticotropin
H Corticotropin-producing tumor in another organ
H Chronic use of synthetic glucocorticoids or corti-

cotropin
H Cortisol-secreting adrenal tumor

Special populations
In neonates, the usual cause of Cushings syndrome
is adrenal carcinoma.

Incidence
H More common in females than in males
H Can affect a person at any age

Common characteristics
H Adiposity of the face, neck, and trunk
H Purple striae on the skin
H Truncal weight gain
H Glucose intolerance

Complications
H Osteoporosis and pathologic fractures
H Peptic ulcer
H Dyslipidemia
H Impaired glucose tolerance
H Diabetes mellitus
H Frequent infections
H Slow wound healing
H Suppressed inflammatory response
H Hypertension
H Ischemic heart disease; heart failure

220

Cushings syndrome

History
H Use of synthetic steroids
H Fatigue
H Muscle weakness
H Sleep disturbances
H Polyuria
H Thirst
H Frequent infections
H Water retention
H Amenorrhea
H Decreased libido
H Irritability; emotional instability
H Symptoms resembling those of hyperglycemia
H Impotence
H Headache

Physical findings
H Thin hair
H Moon-shaped face
H Hirsutism
H A buffalo-humplike back
H Thin extremities
H Muscle wasting and weakness
H Petechiae, ecchymoses, and purplish striae
H Delayed wound healing
H Swollen ankles
H Hypertension
H Central obesity
H Acne

Test results
Laboratory
H Salivary free cortisol level is elevated.
H ACTH is decreased in adrenal disease and excess
pituitary or ectopic secretion of ACTH is increased.
H Blood chemistry may show hypernatremia, hypokalemia, hypocalcemia, and elevated blood glucose
level.
H Urinary free cortisol level is elevated.
H Serum cortisol level is elevated in the morning.
H Glycosuria occurs.
Imaging
H Ultrasonography, computed tomography scan, and
magnetic resonance imaging may show the location
of a pituitary or adrenal tumor.
Diagnostic procedures
H A low-dose dexamethasone suppression test shows
failure of plasma cortisol levels to be suppressed.

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Treatment
General
H Management to restore hormone balance and re-

verse Cushings syndrome, including radiation, drug


therapy, or surgery
H High-protein, high-potassium, low-calorie, lowsodium diet
H Activity, as tolerated

Medications
H Antihypertensive such as atenolol
H Diuretic such as furosemide
H Glucocorticoid such as dexamethasone
H Potassium supplements
H Antihormone agents, such as ketoconazole, amino-

glutethimide, and mitotane


H Pituitary hormone such as pitressin

ALERT
Glucocorticoid administration on the morning of
surgery can help prevent acute adrenal insufficiency during surgery. Cortisol therapy is essential during and after surgery to help the patient tolerate
the physiologic stress caused by removal of the
pituitary or adrenal glands.

Surgery
H Possible hypophysectomy or pituitary irradiation
H Bilateral adrenalectomy
H Excision of nonendocrine, corticotropin-producing

tumor, followed by drug therapy

Nursing considerations
Key outcomes
The patient will:
H maintain skin integrity
H remain free from infection
H perform activities of daily living as tolerated within
the confines of the disorder
H express positive feelings about self
H express understanding of disorder.

With transsphenoidal approach to


hypophysectomy
H Keep the head of the bed elevated at least 30 degrees.
H Maintain nasal packing.
H Provide frequent mouth care.
H Avoid activities that increase intracranial pressure
(ICP).

Monitoring
H Vital signs
H Intake and output
H Daily weights
H Serum electrolyte results

After bilateral adrenalectomy and


hypophysectomy
H Neurologic status
H Severe nausea, vomiting, and diarrhea
H GI status
H Adrenal hypofunction
H Increased ICP
H Hypopituitarism
H Transient diabetes insipidus
H Hemorrhage and shock
After transsphenoidal approach to
hypophysectomy
H Cerebrospinal fluid leak

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H lifelong steroid replacement
H signs and symptoms of adrenal crisis
H medical identification bracelet
H prevention of infection
H stress reduction strategies.

Discharge planning
H Refer the patient to a mental health professional for

additional counseling, if necessary.

Nursing interventions
H Give prescribed drugs.
H Consult a dietitian.
H Use protective measures to reduce the risk of

infection.
H Use meticulous hand-washing technique.
H Schedule adequate rest periods.
H Institute safety precautions.
H Provide meticulous skin care.
H Encourage verbalization of feelings.
H Offer emotional support.
H Help to develop effective coping strategies.

Cushings syndrome

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Cystic fibrosis
Overview
Description
H Chronic, progressive, inherited, incurable disease af-

fecting exocrine (mucus-secreting) glands


H Transmitted as an autosomal recessive trait
H Genetic mutation that involves chloride transport

across epithelial membranes (more than 100 specific mutations of the gene identified)
H Characterized by major aberrations in sweat gland,
respiratory, and GI functions
H Accounts for almost all cases of pancreatic enzyme
deficiency in children
H Signs and symptoms apparent soon after birth or not
for several years
H Death typically from pneumonia, emphysema, or
atelectasis

Pathophysiology
H The viscosity of bronchial, pancreatic, and other mu-

cous gland secretions increases, obstructing glandular ducts.


H The accumulation of thick, tenacious secretions in
the bronchioles and alveoli causes respiratory
changes, eventually leading to severe atelectasis and
emphysema.
H The disease also causes characteristic GI effects in
the intestines, pancreas, and liver.
H Obstruction of the pancreatic ducts results in a deficiency of trypsin, amylase, and lipase. This prevents
the conversion and absorption of fat and protein in
the intestinal tract and interferes with the digestion of
food and absorption of fat-soluble vitamins.
H In the pancreas, fibrotic tissue, multiple cysts, thick
mucus, and fat replace the acini, producing signs of
pancreatic insufficiency.

Causes

H Dyspnea
H Poor weight gain

Complications
H Bronchiectasis
H Pneumonia
H Atelectasis
H Dehydration
H Distal intestinal obstructive syndrome
H Malnutrition
H Gastroesophageal reflux
H Cor pulmonale
H Hepatic disease
H Diabetes
H Arthritis
H Biliary disease
H Clotting problems
H Retarded bone growth
H Delayed sexual development
H Azoospermia in males
H Secondary amenorrhea in females
H Electrolyte imbalances
H Cardiac arrhythmias
H Potentially fatal shock
H Death

Assessment
History
H Recurring bronchitis and pneumonia
H Nasal polyps and sinusitis
H Wheezing
H Dry, nonproductive cough
H Shortness of breath
H Abdominal distention, vomiting, constipation
H Frequent, bulky, foul-smelling, and pale stool with a

high fat content


H Poor weight gain
H Poor growth
H Ravenous appetite
H Hematemesis

H Autosomal recessive mutation of gene on chromo-

some 7
H Causes of symptoms: increased viscosity of bronchial,

pancreatic, and other mucous gland secretions and


consequent destruction of glandular ducts

Incidence
H Most common fatal genetic disease of white children
H Twenty-five percent chance of transmission with each

pregnancy: both parents carriers of the recessive


gene
H Highest in people of northern European ancestry
H Less common in Blacks, Native Americans, and people of Asian ancestry
H Equally common in both sexes

Common characteristics
H Wheezy respirations
H Dry, nonproductive, paroxysmal cough

222

Cystic fibrosis

Special populations
Neonates may exhibit meconium ileus and develop
symptoms of intestinal obstruction, such as abdominal distention, vomiting, constipation, dehydration, and electrolyte imbalance.

Physical findings
H Wheezy respirations
H Dry, nonproductive, paroxysmal cough
H Dyspnea
H Tachypnea
H Bibasilar crackles and hyperresonance
H Barrel chest
H Cyanosis, and clubbing of the fingers and toes
H Distended abdomen
H Thin extremities

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H Sallow skin with poor turgor


H Delayed sexual development
H Neonatal jaundice
H Hepatomegaly
H Rectal prolapse
H Failure to thrive

Test results
Laboratory
H Sweat test reveals sodium and chloride values.
H Stool specimen analysis shows absence of trypsin.
H Deoxyribonucleic acid testing shows presence of the
delta F 508 deletion.
H Liver enzyme tests may show hepatic insufficiency.
H Sputum culture may show such organisms as
Pseudomonas and Staphylococcus.
H Serum albumin level is decreased.
H Serum electrolytes may show hypochloremia and
hyponatremia.
H Arterial blood gas shows hypoxemia.
Imaging
H Chest X-rays may show early signs of lung obstruction.
H High-resolution chest computed tomography scan
shows bronchial wall thickening, cystic lesions, and
bronchiectasis.
Diagnostic procedures
H Pulmonary function tests show decreased vital capacity, elevated residual volume, and decreased forced
expiratory volume in 1 second.

Treatment
General
H Based on organ systems involved
H Chest physiotherapy, nebulization, and breathing ex-

ercises several times per day


H Postural drainage
H Gene therapy (experimental)
H Salt supplements
H High-fat, high-protein, high-calorie diet
H Activity, as tolerated, encouraged

Medications
H Pulmonary enzyme, such as dornase alfa, given by

aerosol nebulizer
H Antibiotic, as appropriate
H Oxygen therapy, as needed
H Oral pancreatic enzymes such as pancreatin
H Bronchodilator such as albuterol
H Corticosteroid such as prednisone
H Vitamin A, D, E, and K supplements
H Annual influenza vaccination

Surgery
H Heart-lung transplantation
H Feeding tube placement for nutritional support

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway and adequate ventilation
H consume adequate calories daily
H use a support system to assist with coping
H express an understanding of the illness.

Nursing interventions
H Give prescribed drugs.
H Administer pancreatic enzymes with meals and

snacks.
H Perform chest physiotherapy and postural drainage.
H Administer oxygen therapy, as needed.
H Provide a well-balanced, high-calorie, high-protein

diet; include adequate fats.


H Provide vitamin A, D, E, and K supplements, if indi-

cated.
H Ensure adequate oral fluid intake.
H Provide exercise and activity periods.
H Encourage breathing exercises.
H Provide the young child with play periods.
H Enlist the help of the physical therapy department

and play therapists, if available.


H Provide emotional support.
H Include family members in all phases of the childs

care.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Hydration and nutrition
H Pulse oximetry
H Respiratory status
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H aerosol therapy
H chest physiotherapy
H signs and symptoms of infection
H complications.

Discharge planning
H Refer family members for genetic counseling, as

appropriate.
H Refer the patient and his family to a local support

group such as the Cystic Fibrosis Foundation.

Cystic fibrosis

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Cytomegalovirus
infection
Overview
Description
H Infection with a member of the herpesvirus group
H Also called generalized salivary gland disease and

cytomegalic inclusion disease

Neonatal complications
H Stillbirth
H Neonatal retinitis
H Microcephaly
H Mental retardation
H Seizures
H Hearing loss
H Thrombocytopenia
H Hemolytic anemia

Assessment

Pathophysiology

History

H Cytomegalovirus (CMV) is found in the saliva, urine,

H Immunosuppressive condition

semen, breast milk, feces, blood, and vaginal and


cervical secretions of infected people. It can be detected in body fluids for weeks or months after infection.
H CMV usually remains latent, but reactivation occurs
when T-lymphocyte-mediated immunity is compromised, as in organ transplantation, lymphoid neoplasms, and certain acquired immunodeficiencies.
H CMV spreads through the body in lymphocytes or
mononuclear cells to the lungs, liver, GI tract, eyes,
and central nervous system (CNS), typically producing inflammatory reactions.

Causes
H Results from a deoxyribonucleic acid virus belonging

to the herpes family


H Transmitted by human contact; once infected, CMV

carried for life


H Transmission through direct contact with secretions

and excretions, through blood transfusions, transplacentally, and through transplanted organs

Risk factors
H Poor hygiene
H Immunosuppression
H Child care workers

Incidence
H Occurs worldwide
H Occurs in approximately 30% to 50% of acquired

immunodeficiency syndrome patients


H One of the most opportunistic pathogens in patients

infected with human immunodeficiency virus

Common characteristics
H Mild fatigue, myalgia, and headache or no clinical

symptoms

Complications
H Pneumonia
H Hepatitis
H Ulceration of the GI tract and esophagus
H Retinitis
H Encephalopathy

224

Cytomegalovirus infection

Physical findings
H Fever common
H Lethargy
H In immunocompetent patient with CMV mononucleo-

sis, 3 or more weeks of irregular high fever may be


only finding
H Tachypnea
H Dyspnea
H Cyanosis
H Cough
H Jaundice
H Spider angiomas
H Hepatomegaly
H Splenomegaly
H In infants, CNS damage (mental retardation, hearing
loss, seizures), jaundice, petechial rash, respiratory
distress

Test results
Laboratory
H Isolating the virus or demonstrating increasing serologic titers by complement fixation studies, hemagglutination inhibition antibody tests and, in congenital infections, indirect immunofluorescent tests for
CMV immunoglobulin M antibody allows diagnosis.
Imaging
H Chest X-ray reveals bilateral, diffuse, white infiltrates.
H Computed tomography scan or magnetic resonance
imaging shows CNS involvement.
Diagnostic procedures
H Endoscopy shows GI involvement.
H Fundoscopy may show retinitis.

Treatment
General
H Rest, as needed

Medications
H Antivirals, such as cidofovir and ganciclovir
H Immune serum such as cytomegalovirus immune

globulin

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Nursing considerations
Key outcomes
The patient will:
H maintain normal temperature
H maintain adequate caloric intake
H demonstrate skill in conserving energy while carrying
out daily activities to tolerance level
H verbally report having an increased energy level
H articulate factors that intensify pain and modify behavior accordingly
H maintain respiratory rate within 5 breaths of baseline
H express feeling of comfort while maintaining air
exchange.

Nursing interventions
H Institute standard precautions.
H Give prescribed drugs.
H If vision impairment occurs, provide a safe environ-

ment and encourage optimal independence.

Monitoring
H Intake and output
H Ventilation and oxygenation if the respiratory system

involved
H Vital signs

Patient teaching
Be sure to cover:
H proper hand-washing technique
H need for parents to wear gloves when in contact with
secretions or changing diapers and to dispose of diapers or soiled articles properly and wash hands thoroughly
H need for female health care workers trying to get
pregnant to have CMV titers drawn to identify their
risk of contracting the infection
H need for an immunosuppressed or pregnant patient
to avoid contact with any person who has confirmed
or suspected CMV infection
H need for an immunosuppressed patient whos CMVseronegative to carry this information with him so he
wont be given CMV-positive blood.

Discharge planning
H Provide emotional support and counseling to the

parents of a child with severe CMV infection. Help


them find support systems, and coordinate referrals
to other health care professionals.
H For information and support, refer the patient and
his family to a local chapter of the National Center for
Infectious Diseases.

Cytomegalovirus infection

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Dacryocystitis
Overview
Description

H Infection of the lacrimal sac resulting from obstruc-

tion of the nasolacrimal duct

H Acute, chronic, or congenital

Pathophysiology

H The lacrimal excretory system is a mucous mem-

brane-lined tract thats contiguous with conjuctival


and nasal mucosa.
H Conjuctival and nasal mucosa are normally colonized
with bacteria.
H Inability to drain tears due to a blocked lacrimal
drainage system results in infection. (See A close
look at tears.)

Causes
Acute form
H Staphylococcus aureus
H Beta-hemolytic streptococci
Chronic form
H Streptococcus pneumonia
H Fungus, such as Actinomyces or Candida albicans
H Chronic mucosal degeneration
H Secondary tumors from sinuses, nose, and eye orbits

Risk factors
H Congenital blockage of nasolacrimal duct

Incidence
H More common in adults older than age 40
H More common on the left side than the right side
H Rare in blacks
H Affects females more commonly than males

Common characteristics
Acute form
H Sudden onset of pain
H Redness in the medial canthal region
Chronic form
H Incidious onset of watery eyes

Complications
H Hemorrhage
H Infection
H Cerebrospinal fluid leakage

Assessment
History
H Eye pain
H Fever

A close look at tears


Tears begin in the lacrimal gland and drain through the nasolacrimal duct into the nose.
Lacrimal gland

Punctum
Lacrimal canals
Lacrimal sac

Nasolacrimal duct

226

Dacryocystitis

Iris
Pupil
Sclera

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Physical findings
H Severe erythematous swelling around nasal aspect of

lower eyelid
H Tenderness of eyelid
H Tearing
H Conjunctival injection
H Palpable mass inferior to the medial canthal tendon
H Decreased visual acuity
H Orbital cellulitis

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H applying warm compresses and eyedrops
H reporting signs of worsening infection.

Test results
Laboratory
H Culture of discharge shows causative organism.
H Complete blood count shows elevated white blood
cell count.
Imaging
H X-ray after injection of radiopaque medium locates
atresia.
H Dacryocystography and dacryoscintigraphy identify
anatomical abnormalities of the nasolacrimal
drainage system.

Treatment
General
H Warm compresses
H Activity, as tolerated

Medications
H Antibiotic eyedrops such as polymyxin/trimethoprim
H Antibiotics, such as gentamicin, amoxicillin, and

clavulanate potassium

Surgery
H Incision and drainage
H Dacryocystorhinostomy (chronic cases)

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H remain free from signs of infection.

Nursing interventions
H Administer prescribed antibiotics.
H Apply compresses.

Monitoring
H Temperature
H Pain
H Visual acuity

Dacryocystitis

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Dermatitis
Overview
Description
H Skin condition characterized by inflammation
H Can be acute or chronic
H Occurs in several forms, including contact, seborrhe-

ic, nummular, exfoliative, and stasis dermatitis (see


Types of dermatitis, pages 230 and 231)
H Typically associated with other atopic diseases

Pathophysiology
H The allergic mechanism of hypersensitivity results in

a release of inflammatory mediators through sensitized antibodies of immunoglobulin (Ig) E.


H Histamine and other cytokines induce an inflammatory response resulting in edema, skin breakdown,
and pruritus.

Causes
H Exact cause unknown
H Possible underlying metabolic or biochemical causes
H Possible genetic link to elevated serum IgE levels
H Possible defective T-cell function
H Precipitating factors:

Infections
Allergens
Temperature extremes
Humidity
Sweating
Stress

Incidence
H Common in infants and toddlers between ages 6

H Exposure to an allergen or irritant


H Intense itching

Physical findings
H Depend on type of dermatitis
H Erythematous patches in excessively dry areas

Special populations
In children, look for lesions on the forehead,
cheeks, and extensor surfaces of the arms and legs.
H Lesions usually at flexion points in adults
H During a flare-up: edema, scaling, and vesiculation;

pus-filled vesicles
H In chronic disease: multiple areas of dry, scaly skin,

with white dermatographism, blanching, and lichenification

Test results
H Results depend on type of dermatitis.

Laboratory
H Serum analysis shows elevated IgE levels.
H Tissue cultures may rule out bacterial, viral, or fungal superinfections.
H Allergy testing may disclose allergic rhinitis or
asthma.
Diagnostic procedures
H Patch testing and distribution of lesions are used to
pinpoint the provoking allergen.
Other
H Firm stroking of the patients skin with a blunt instrument causes a white not reddened hive to appear on the skin of 70% of patients with atopic dermatitis.
H Food elimination diet may help to identify at least one
allergen.

months and 2 years


H Common in those with strong family histories of

atopic disease

Treatment

Common characteristics

General

H Pruritus
H Skin lesions

H Dependent on type of dermatitis


H Elimination of allergens
H Avoidance of precipitating factors
H Ultraviolet B light therapy to increase the thickness of

Complications
H Permanent skin damage
H Lichenification
H Altered pigmentation
H Scarring
H Bacterial, fungal, and viral infections
H Kaposis varicelliform eruption

Assessment
History
H Depends on type of dermatitis
H Family history of atopic dermatitis

228

Dermatitis

the stratum corneum


H Avoidance of food allergens
H Avoidance of overheating

Medications
H Antihistamines, such as diphenhydramine
H Corticosteroids, such as betamethasone and hydro-

cortisone
H Antibiotics such as gentamicin
H Antifungals such as ketoconazole
H Antivirals such as acyclovir
H Antipruritics such as hydroxyzine hydrochloride

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Surgery
H Vein stripping, sclerotherapy, or skin grafts in stasis

dermatitis

Nursing considerations
Key outcomes
The patient will:
H exhibit improved or healed lesions or wounds
H avoid complications
H demonstrate understanding of skin care regimen
H verbalize feelings about altered body image.

Nursing interventions
Nursing interventions are guided by the type of dermatitis.
H Assist with daily skin care, and avoid using perfumed
soaps.
H Apply intermittent occlusive dressings to lichenified
skin.
H Apply cool, moist compresses.
H Encourage verbalization of feelings.
H Offer emotional support and reassurance.
H Administer medications as prescribed.
H Prevent rubbing and scratching of the affected area.

Monitoring
H Adverse reactions
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H skin care
H prescribed medications and possible adverse effects
H signs and symptoms of corticosteroid overdose and
notifying the practitioner immediately if they occur
H control of pruritus
H meticulous hand washing and good personal hygiene
H use of plain, tepid water (96 F [35.6 C]) and nonperfumed soaps
H application of occlusive dressings when skin is
lichenified
H application of wet-to-dry dressings
H identification and avoidance of aggravating factors
H avoidance of temperature extremes.

Discharge planning
H Refer the patient to the American Academy of Derma-

tology.

Dermatitis

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Types of dermatitis
Type

Causes

Assessment
findings

Diagnosis

Treatment
and intervention

Thick, lichenified, single or multiple lesions


on any part of the
body (commonly on
the hands)
Inflammation and
scaling
Recurrence after long
remissions

No characteristic pattern or
course; diagnosis based on
detailed history
and physical
findings

Elimination of known allergens and decreased exposure


to irritants, wearing protective
clothing such as gloves, and
washing immediately after
contact with irritants or allergens
Antibiotics for secondary infection
Avoidance of excessive washing and drying of hands and
of accumulation of soaps and
detergents under rings
Use of emollients with topical
steroids

Mild irritants and allergens: erythema and


small vesicles that
ooze, scale, and itch
Strong irritants: blisters and ulcerations
Classic allergic response: clearly defined lesions, with
straight lines following points of contact
Severe allergic reaction: marked edema
of affected areas

Patient history
Patch testing
to identify allergens
Shape and distribution of lesions

Same as for chronic dermatitis


Topical anti-inflammatories
(such as steroids), systemic
steroids for edema and bullae,
antihistamines, and local applications of Burows solution
(for blisters)
Other nursing interventions
similar to those for atopic dermatitis

Generalized dermatitis, with acute loss of


stratum corneum, and
erythema and scaling
Sensation of tight skin
Hair loss
Possibly fever, sensitivity to cold, shivering, gynecomastia,
and lymphadenopathy

Identification
of the underlying cause

Hospitalization, with protective isolation and hygienic


measures to prevent secondary bacterial infection
Open wet dressings, with colloidal baths
Bland lotions over topical
steroids
Maintenance of constant environmental temperature to prevent chilling or overheating
Careful monitoring of renal
and cardiac status
Systemic antibiotics and
steroids
Other nursing interventions
similar to those for atopic dermatitis

CHRONIC DERMATITIS

Characterized by
inflammatory
eruptions of the
hands and feet

Usually unknown but may


result from progressive contact
dermatitis
Secondary factors: trauma,
infections, redistribution of
normal flora,
photosensitivity,
and food sensitivity, which
may perpetuate
this condition

CONTACT DERMATITIS

Commonly,
sharply demarcated skin inflammation and irritation
due to contact
with concentrated
substances to
which the skin is
sensitive, such as
perfumes or
chemicals

Mild irritants:
chronic exposure to detergents or solvents
Strong irritants:
damage on contact with acids
or alkalis
Allergens: sensitization after
repeated exposure

EXFOLIATIVE DERMATITIS

Severe, chronic
skin inflammation
characterized by
redness and widespread erythema
and scaling

Progression of
preexisting skin
lesions to exfoliative stage, as
in contact dermatitis, drug reaction, lymphoma, or
leukemia

LOCALIZED NEURODERMATITIS (LICHEN SIMPLEX CHRONICUS, ESSENTIAL PRURITUS)

Superficial skin
inflammation
characterized by
itching and papular eruptions that
appear on thickened, hyperpigmented skin

230

Dermatitis

Chronic
scratching or
rubbing of a
primary lesion
or insect bite,
or other skin
irritation

Intense, sometimes
continual scratching
Thick, possibly dry,
scaly lesions, with
sharp borders and
raised papules
Usually affects easily
reached areas, such
as ankles, lower legs,
anogenital area, back
of neck, and ears

Physical findings

Scratching must stop; then


erosions will disappear in
2 weeks
Fixed dressing or Unnas boot
to cover affected area
Topical steroids (occlusive
dressings or intralesional injections)
Antihistamines and open wet
dressings
Emollients

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Types of dermatitis (continued)


Type

Causes

Assessment
findings

Diagnosis

Treatment
and intervention

Round, nummular
(coin-shaped) lesions,
usually on arms and
legs, with distinct borders of crusts and
scales
Possibly oozing and
severe itching
Summertime remissions common, with
wintertime recurrence

Physical findings and patient history;


history of
atopic dermatitis in middleaged or older
patient
Exclusion of
fungal infections, atopic or
contact dermatitis, and
psoriasis

Elimination of known irritants


Measures to relieve dry skin:
increased humidification, limited frequency of baths and
use of bland soap and bath
oils, and application of emollients
Wet dressings in acute phase
Topical steroids (occlusive
dressings or intralesional injections) for persistent lesions
Tar preparations and antihistamines for itching and antibiotics for infection
Other interventions similar to
those for atopic dermatitis

Eruptions in areas
with many sebaceous
glands (usually scalp,
face, and trunk) and
in skin folds
Itching, redness, and
inflammation of affected areas; lesions
that may appear
greasy; possibly
fissures
Indistinct, occasionally yellowish scaly
patches from excess
stratum corneum
(dandruff may be mild
seborrheic dermatitis)

Patient history
and physical
findings, especially distribution of lesions
in sebaceous
gland areas
Exclusion of
psoriasis

Removal of scales by frequent


washing and shampooing
with selenium sulfide suspension, zinc pyrithione, tar and
salicylic acid shampoo or ketoconazole shampoo
Application of topical steroids
and antifungal agents to nonhairy areas
For infants, baby shampoo

Varicosities and
edema common, but
obvious vascular insufficiency not always
present
Usually affects the
lower leg, just above
internal malleolus, or
sites of trauma or irritation
Early signs: dusky red
deposits of hemosiderin in skin, with
itching and dimpling
of subcutaneous tissue; later signs:
edema, redness, and
scaling of large area
of legs
Possibly fissures,
crusts, and ulcers

Positive history of venous


insufficiency
and physical
findings such
as varicosities

Measures to prevent venous


stasis: avoidance of prolonged
sitting or standing, use of
support stockings, and weight
reduction for obese patients
Corrective surgery for underlying cause
After ulcer develops, rest periods with legs elevated; open
wet dressings; Unnas boot
(provides continuous pressure to areas); and antibiotics
for secondary infection after
wound culture

NUMMULAR DERMATITIS

Chronic form of
dermatitis characterized by coinshaped, vesicular,
crusted scales
and, possibly, pruritic lesions

Possibly precipitated by stress;


or dryness, irritants, or
scratching

SEBORRHEIC DERMATITIS

An acute or subacute disease that


affects the scalp,
face and, occasionally, other areas and is characterized by lesions
covered with yellow or brownish
gray scales

Unknown;
stress and neurologic conditions may be
predisposing
factors

STASIS DERMATITIS

Condition usually
caused by impaired circulation
and characterized
by eczema of the
legs with edema,
hyperpigmentation, and persistent inflammation

Secondary to
peripheral vascular diseases
affecting legs,
such as recurrent thrombophlebitis and resultant chronic
venous insufficiency

Dermatitis

231

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Developmental
dysplasia of the hip

H Can be unilateral or bilateral


H Occurs in three forms of varying severity (see De-

Overview

H Excessive or abnormal movement of the joint during

Description
H An abnormality of the hip joint present at birth
H Most common disorder affecting the hip joints in

children younger than age 3

Degrees of hip dysplasia


Normally, the head of the femur fits snugly into the
acetabulum, allowing the hip to move properly. In
developmental hip dysplasia, flattening of the acetabulum
prevents the head of the femur from rotating adequately.
The childs hip may be unstable, subluxated (partially
dislocated), or completely dislocated, with the femoral
head lying totally outside the acetabulum. The degree of
dysplasia and the childs age are considered in
determining the treatment choice.

grees of hip dysplasia)

Pathophysiology
a traumatic birth may cause dislocation.
H Displacement of bones within the joint may damage

joint structures, including articulating surfaces,


blood vessels, tendons, ligaments, and nerves.
H Disruption of blood flow to the joint may lead to ischemic necrosis.

Causes
H Unknown

Risk factors
H Breech delivery
H Elevated maternal relaxin (hormone secreted by the

corpus luteum during pregnancy that causes relaxation of pubic symphysis and cervical dilation)
H Large neonates and twins

Incidence
H About 85% of cases: female

NORMAL HIP

Common characteristics
H Level of knees uneven
H Limited abduction on the dislocated side
H Buttock fold on the affected side higher with the

Acetabulum
Head of the femur

child lying prone (see Ortolanis and Trendelenburgs signs)

Complications
H Degenerative hip changes
H Abnormal acetabular development
H Lordosis (abnormally increased concave curvature of

the lumbar and cervical spine)


SUBLUXATED HIP

H Joint malformation
H Sciatic nerve injury (paralysis)
H Avascular necrosis of femoral head
H Soft tissue damage
H Permanent disability

Assessment
History
DISLOCATED HIP

H Traumatic birth
H Large birth size
H Twin

Physical findings
H Extra fold on the thigh of the affected side
H Limited abduction on the dislocated side
H Level of knees uneven
H Swaying from side to side (duck waddle) because

of uncorrected bilateral dysplasia


H Limp due to uncorrected unilateral dysplasia

232

Developmental dysplasia of the hip

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Test results
Imaging
H X-rays show the location of the femur head and a
shallow acetabulum.
H Computed tomography scan shows the location and
extent of the deformity.
H Sonography and magnetic resonance imaging assess
reduction.
Other
H Physical examination helps to confirm the diagnosis.

Treatment
Treatment of developmental dysplasia of the hip varies
with the patients age.
Younger than age 3 months:
H Gentle manipulation to reduce the dislocation, followed by splint-brace or Pavlik harness
H Splint-brace or Pavlik harness worn continuously for
2 to 3 months, then a night splint for another month
Older than age 3 months:
H Bilateral skin traction (in infants) or skeletal traction
(in children who have started walking)
H Bryants traction or divarication traction (both extremities placed in traction, even if only one is affected, to help maintain immobilization) for children
younger than 3 years and weighing less than 35 lb
(15.9 kg) for 2 to 3 weeks
H Immobilization in a spica cast for about 3 months for
children ages 6 to 12 months

Special populations
Treatment begun after age 5 rarely restores satisfactory hip function.

General
H Activity, as tolerated
H No dietary restrictions

Surgery
H Gentle closed reduction under general anesthesia to

further abduct the hips, followed by a spica cast for 3


months (if traction fails)
H In children older than age 18 months, open reduction and pelvic or femoral osteotomy to correct bony
deformity, followed by immobilization in a spica cast
for 6 to 8 weeks
H In children ages 2 to 5 years, skeletal traction and
subcutaneous adductor tenotomy (surgical cutting of
the tendon)

Ortolanis and Trendelenburgs signs


A positive Ortolanis or Trendelenburgs sign confirms
developmental dysplasia of the hip.

Ortolanis sign

H Place the infant on his back, with hip flexed and in


abduction. Adduct the hip while pressing the femur
downward.
H Next, abduct the hip while moving the femur upward. A
click or a jerk (produced by the femoral head moving
over the acetabular rim) indicates subluxation in an
infant younger than 1 month. The sign indicates
subluxation or complete dislocation in an older infant.

Trendelenburgs sign

H When the child rests his weight on the side of the


dislocation and lifts his other knee, the pelvis drops on
the normal side because abductor muscles in the
affected hip are weak.
H However, when the child stands with his weight on the
normal side and lifts the other knee, the pelvis remains
horizontal.

H achieve the highest level of mobility possible within

the confines of the disease.

Nursing interventions
H Provide reassurance to the parents.
H Turn the child every 2 hours.
H Provide appropriate cast care.

Monitoring
H Parental care of cast or equipment
H Skin integrity
H Color, sensation, and motion of the infants legs and

feet
H Comfort

Patient teaching
Be sure to cover:
H how to correctly splint or brace the hips, as ordered
H good hygiene
H signs and symptoms of cast compression (cyanosis,
cool extremities, or pain).

Discharge planning
H Stress the need for frequent checkups.
H Refer the child and parents to a child life specialist to

ensure continued developmental progress.

Nursing considerations
Key outcomes
The patient will:
H maintain joint mobility and range of motion
H maintain muscle strength

Developmental dysplasia of the hip

233

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Diabetes insipidus
Overview
Description
H Disorder in which secretion of antidiuretic hormone

is inadequate, causing an inability to concentrate


urine
H Two types: primary and secondary
H May occur transiently during pregnancy, usually after
the fifth or sixth month of gestation
H Impaired or absent thirst mechanism increasing risk
of complications
H If uncomplicated, prognosis good
H If complicated by underlying disorder, such as cancer, prognosis variable
H Also referred to as DI

Pathophysiology
H Vasopressin (antidiuretic hormone) is synthesized in

the hypothalamus and stored by the posterior pituitary gland.


H Once released into the general circulation, vasopressin acts on the distal and collecting tubules of
the kidneys.
H Vasopressin increases the water permeability of the
tubules and causes water reabsorption.
H The absence of vasopressin allows filtered water to
be excreted in the urine instead of being reabsorbed.

Causes
H Failure of vasopressin secretion in response to nor-

mal physiologic stimuli


H Failure of the kidneys to respond to vasopressin,
called nephrogenic DI
H Familial
H Idiopathic
H Congenital malformation of the central nervous system (CNS)
H Infection
H Trauma
H Tumors
H Neurosurgery, skull fracture, or head trauma
H Granulomatous disease
H Vascular lesions
H Psychogenic
H Pregnancy (gestational DI)
H Damage to hypothalamus or pituitary gland
H Certain medications such as lithium

Incidence
H Affects males and females equally
H Primary DI in 50% of patients

Common characteristics
H Polyuria with low specific gravity and osmolality
H Nocturia
H Dehydration

234

Diabetes insipidus

H Polydipsia
H Weight loss
H Fatigue

Complications
H Hypovolemia
H Hyperosmolality
H Circulatory collapse
H Loss of consciousness
H CNS changes
H Bladder distention
H Hydroureter
H Hydronephrosis

Assessment
History
H Abrupt onset of extreme polyuria
H Extreme thirst
H Extraordinarily large oral fluid intake
H Weight loss
H Dizziness; weakness; fatigue
H Constipation
H Nocturia

Special populations
In children, reports of enuresis, sleep disturbances,
irritability, anorexia, thirst, and decreased weight
gain and linear growth are common.

Physical findings
H Signs of dehydration
H Fever
H Dyspnea
H Pale, voluminous urine
H Poor skin turgor
H Tachycardia
H Decreased muscle strength
H Hypotension

Test results
Laboratory
H Urinalysis shows colorless urine with specific gravity
1.005 or less and osmolality less than 200 mOsm/kg.
H 24-hour urine sample shows decreased specific gravity and increased volume.
H Serum chemistries show elevated sodium, blood urea
nitrogen (BUN), and creatinine levels.
H Serum osmolality is increased.
H Serum vasopressin level is decreased.
Diagnostic procedures
H Dehydration test or water deprivation test shows an
increase in urine osmolality after vasopressin administration exceeding 9%.
H Magnetic resonance imaging may show a pituitary tumor or brain tumor.

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H Computed tomography scan may reveal head trauma,

pituitary tumor, or brain tumor.

Treatment
General
H Identification and treatment of underlying cause
H Control of fluid balance; administration of I.V. fluids

to match urine output


H Dehydration prevention
H Free access to oral fluids
H With nephrogenic DI, low-sodium diet

Medications
H Posterior pituitary hormones, such as vasopressin

and desmopressin
H Thiazide diuretics, such as hydrochlorothiazide, in

nephrogenic DI
H I.V. fluids:

If serum sodium > 150 mEq/L: 5% dextrose in


water
If serum sodium < 150 mEq/L: normal saline solution

H Signs and symptoms of hypovolemic shock


H Changes in mental or neurologic status
H Cardiac rhythm

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the practitioner
H signs and symptoms of dehydration
H daily weight
H intake and output
H use of a hydrometer to measure urine specific gravity
H need for medical identification jewelry
H need for ongoing medical care.

Discharge planning
H Refer the patient to a mental health professional for

additional counseling, as indicated.

Surgery
H Not indicated, unless required to treat underlying

cause such as a tumor

Nursing considerations
Key outcomes
The patient will:
H demonstrate balanced fluid volume
H display adaptive coping behaviors
H avoid complications
H demonstrate normal laboratory values.

Nursing interventions
H Administer I.V. fluid to match urine output.
H Administer medications, as ordered.
H Provide meticulous skin and mouth care.

ALERT
Use caution when administering vasopressin to a
patient with coronary artery disease because it can
cause coronary artery constriction.
H Encourage verbalization of feelings.
H Offer encouragement while providing a realistic as-

sessment of the situation.


H Help the patient develop effective coping strategies.

Monitoring
H Intake and output
H Vital signs
H Daily weight
H Urine specific gravity
H Serum electrolytes and BUN

Diabetes insipidus

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Diabetes mellitus
Overview
Description
H Chronic disease of absolute or relative insulin defi-

ciency or resistance
H Characterized by disturbances in carbohydrate, pro-

tein, and fat metabolism

Complications
H Ketoacidosis
H Hyperosmolar hyperglycemic nonketotic syndrome
H Cardiovascular disease
H Peripheral vascular disease
H Retinopathy, blindness
H Nephropathy
H Diabetic dermopathy
H Impaired resistance to infection
H Cognitive depression
H Hypoglycemia

H Two primary forms:

Type 1, characterized by absolute insufficiency


Type 2, characterized by insulin resistance with
varying degrees of insulin secretory defects

Pathophysiology
H The effects of diabetes mellitus (DM) result from in-

sulin deficiency or resistance to endogenous insulin.

Special populations
Neonates of diabetic mothers have a two to three
times greater incidence of congenital malformations and fetal distress, unless the mothers blood
glucose levels are well-controlled before conception
and during pregnancy.

H Insulin allows glucose transport into the cells for use

as energy or storage as glycogen.


H Insulin also stimulates protein synthesis and free fatty

acid storage in the adipose tissues.


H Insulin deficiency compromises the body tissues ac-

cess to essential nutrients for fuel and storage.

Causes
H Genetic factors
H Autoimmune disease (type 1)

Risk factors
H Viral infections (type 1)
H Obesity (type 2)
H Physiologic or emotional stress
H Sedentary lifestyle (type 2)
H Pregnancy
H Medication, such as thiazide diuretics, adrenal corti-

costeroids, and hormonal contraceptives

Incidence
H Type 1 usually occurs before age 30, although it

may occur at any age


H More common in males
H Type 2 usually occurs in obese adults after age 30,

although it may be seen in obese North American


youths of African-American, Native American, or Hispanic descent
H Affects about 8% of the population of the United
States
H About one-third of patients undiagnosed
H Increases with age (type 2)

Common characteristics
H Polyuria
H Polydipsia
H Polyphagia
H Weight loss
H Fatigue

236

Diabetes mellitus

Assessment
History
H Polyuria, nocturia
H Dehydration
H Polydipsia
H Dry mucous membranes
H Poor skin turgor
H Weight loss and hunger
H Weakness; fatigue
H Vision changes
H Frequent skin and urinary tract infections
H Dry, itchy skin
H Sexual problems
H Numbness or pain in the hands or feet
H Postprandial feeling of nausea or fullness
H Nocturnal diarrhea

Type 1
H Rapidly developing symptoms
Type 2
H Vague, long-standing symptoms that develop
gradually
H Family history of DM
H Pregnancy
H Severe viral infection
H Other endocrine diseases
H Recent stress or trauma
H Use of drugs that increase blood glucose levels

Physical findings
H Retinopathy or cataract formation
H Skin changes, especially on the legs and feet
H Muscle wasting and loss of subcutaneous fat (type 1)
H Obesity, particularly in the abdominal area (type 2)
H Poor skin turgor
H Dry mucous membranes
H Decreased peripheral pulses
H Cool skin temperature
H Diminished deep tendon reflexes

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H Orthostatic hypotension
H Characteristic fruity breath odor in ketoacidosis
H Possible hypovolemia and shock in ketoacidosis and

hyperosmolar hyperglycemic state

Test results
Laboratory
H Fasting plasma glucose level is greater than or equal
to 126 mg/dl on at least two occasions.
H Random blood glucose level is greater than or equal
to 200 mg/dl.
H Two-hour postprandial blood glucose level is greater
than or equal to 200 mg/dl.
H Glycosylated hemoglobin (Hb A1C) level is increased.
H Urinalysis may show acetone or glucose.
Diagnostic procedures
H Ophthalmologic examination may show diabetic
retinopathy.

Treatment
General
H Exercise and diet control
H Tight glycemic control for prevention of complica-

tions

H Provide meticulous skin care, especially to the feet

and legs.
H Treat all injuries, cuts, and blisters immediately.
H Avoid constricting hose, slippers, or bed linens.
H Encourage adequate fluid intake.
H Encourage verbalization of feelings.
H Offer emotional support.
H Help to develop effective coping strategies.

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Serum glucose
H Urine acetone
H Renal status
H Cardiovascular status
H Signs and symptoms of:

Hypoglycemia
Hyperglycemia
Hyperosmolar coma
Urinary tract and vaginal infections
Diabetic neuropathy

Patient teaching

H Modest caloric restriction for weight loss or mainte-

Nursing considerations

Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the practitioner
H prescribed meal plan
H prescribed exercise program
H signs and symptoms of:
urinary tract and vaginal infection
hypoglycemia
hyperglycemia
diabetic neuropathy
H self-monitoring of blood glucose
H complications of hyperglycemia
H foot care
H annual regular ophthalmologic examinations
H safety precautions
H management of diabetes during illness.

Key outcomes

Discharge planning

The patient will:


H maintain optimal body weight
H remain free from infection
H avoid complications
H verbalize understanding of the disorder and treatment
H demonstrate adaptive coping behaviors.

H Refer the patient to a dietitian.


H Refer the patient to a podiatrist, if indicated.
H Refer the patient to an ophthalmologist.
H Refer the adult patient who is planning a family for

nance
H American Diabetes Association recommendations to

reach target glucose, Hb A1c lipid, and blood pressure levels


H Regular aerobic exercise

Medications
H Exogenous insulin (type 1 or possibly type 2)
H Oral antidiabetics (type 2), such as arcabose, exe-

natide, glimeperide, glipizide, glyburide, metformin,


pioglitazone, and sitagliptin

Surgery
H Pancreas transplantation

Nursing interventions

preconception counseling.
H Refer the patient to the Juvenile Diabetes Research

Foundation, the American Association of Diabetes


Educators, and the American Diabetes Association to
obtain additional information.

H Administer prescribed drugs.


H Give rapidly absorbed carbohydrates for hypo-

glycemia or, if the patient is unconscious, glucagon


or I.V. dextrose, as ordered.
H Administer I.V. fluids and insulin replacement for hyperglycemic crisis, as ordered.

Diabetes mellitus

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Diphtheria
Overview
Description
H Acute, highly contagious, toxin-mediated infection

that usually infects the respiratory tract primarily


the tonsils, nasopharynx, and larynx
H GI and urinary tracts, conjunctivae, and ears rarely
involved

Pathophysiology
H The organism proliferates at the site of implantation.
H Endotoxins are produced, absorbed by the blood,

and transported to the heart and central nervous system.

Causes
H Corynebacterium diphtheriae, a gram-positive rod
H Transmission usually through intimate contact, air-

borne respiratory droplets, or a break in the skin

Risk factors
H Crowded living conditions
H Poor hygiene

H In cutaneous diphtheria, yellow spots or skin lesions

(resembles impetigo)

Complications
H Thrombocytopenia
H Myocarditis
H Neurologic involvement (primarily affecting motor

fibers but possibly also sensory neurons)


H Renal involvement
H Pulmonary involvement (bronchopneumonia)

Assessment
History
H Fever
H Sore throat
H Rasping cough
H Malaise
H Vomiting
H Dysphagia

Physical findings
H Hoarseness or stridor
H Thick, patchy, grayish green membrane over the mu-

Incidence

cous membranes of the pharynx, larynx, tonsils, soft


palate, and nose
H Swelling of the palate
H Yellow spots or lesions (cutaneous)

H More prevalent during the colder months


H Rare in many parts of the world, including the United

Test results

States
H Cutaneous diphtheria on the increase since 1972, especially in the Pacific Northwest and the Southwest
H More prevalent in children younger than age 15

Laboratory
H Throat culture or culture of other suspect lesions
grows C. diphtheriae.
H Arterial blood gas results may reveal hypoxemia.

Common characteristics
H Thick, patchy, grayish green membrane over the mu-

cous membranes of the pharynx, larynx, tonsils, soft


palate, and nose
H Symptoms similar to croup
H Bleeding when membrane dislodged

Droplet precautions
Droplet precautions prevent the spread of infectious diseases transmitted by contact with nasal or oral secretions
(droplets arising from coughing or sneezing) from the infected patient with the mucous membranes of the susceptible host.
Effective droplet precautions require a single room
(not necessarily a negative-pressure room), and the door
doesnt need to be closed. Persons having direct contact
with, or who will be within 3 feet of, the patient should
wear a surgical mask covering the nose and mouth.
When handling infants or young children who require
droplet precautions, you may also need to wear gloves
and a gown to prevent soiling of clothing with nasal and
oral secretions.

238

Diphtheria

Treatment
General
H Symptomatic
H Droplet precautions (see Droplet precautions)
H Activity, as tolerated
H Diet, as tolerated
H Endotracheal intubation and mechanical ventilation,

as necessary

Medications
H Diphtheria antitoxin
H Antibiotics, such as penicillin and erythromycin
H Oxygen therapy

Surgery
H Tracheotomy (if airway obstruction occurs)

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Nursing considerations
Key outcomes
The patient will:
H maintain patent airway
H have adequate ventilation
H remain free from signs and symptoms of infection.

Nursing interventions
H Enforce droplet precautions.
H Administer prescribed drugs.
H Obtain cultures, as ordered.
H Report all cases to local public health authorities.
H Keep the head of the bed elevated at least 30 degrees.
H Maintain a patent airway.

Monitoring
H Vital signs
H Pulse oximetry
H Respiratory status
H Signs of shock
H Cardiac rhythm and cardiovascular status
H Intake and output

Patient teaching
Be sure to cover:
H proper disposal of nasopharyngeal secretions
H maintaining isolation precautions until two consecutive negative nasopharyngeal cultures at least 1
week after drug therapy stops.

Discharge planning
H Stress the need for childhood immunizations to all

parents.

Diphtheria

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Dislocations and
subluxations
Overview
Description
H Dislocation displacement of joint bones so that ar-

ticulating surfaces totally lose contact (see Common


dislocation)
H Subluxation partial displacement of articulating
surfaces
H May accompany fractures of joints

Pathophysiology
H Trauma causes displacement of the joint.
H Joint structures (blood vessels, ligaments, tendons,

and nerves) are damaged.

Common dislocation
The elbow is a common site of dislocation.
NORMAL ELBOW JOINT

H Injuries may result in deposition of fracture frag-

ments between joint surfaces, damaging surrounding


structures.
H Joint function is impaired.

Causes
H Congenital
H Trauma
H Pagets disease of surrounding joint tissues

Risk factors
H Participation in contact sports

Incidence
H Shoulder dislocations more than half of disloca-

tions seen in emergency departments


H Hip dislocations from trauma, more common in

those younger than age 35; from falls, more common


in those older than age 65

Common characteristics
H Visible deformity of affected extremity
H Shortening of affected extremity
H Local pain
H Swelling
H Limitation of function
H Numbness of affected extremity

Complications
H Damage to surrounding muscle, ligaments, nerves,

and blood vessels


H Avascular necrosis
H Bone necrosis

Assessment
History
H Trauma or fall
H Extreme pain at injury site
H Participation in contact sports

Physical findings
ELBOW JOINT WITH
LATERAL DISLOCATION

H Joint surface fractures


H Deformity around the joint
H Change in the length of the involved extremity
H Impaired joint mobility
H Point tenderness

Test results
Imaging
H X-rays confirm the diagnosis and reveal any associated fractures.

Treatment
General
H Ice application
H Immediate reduction and immobilization

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Dislocations and subluxations

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H Nothing by mouth if surgery scheduled


H Activity limitations based on injury
H Active range-of-motion (ROM) exercises for adjacent

joints not immobilized

Medications
H Sedative, such as lorazepam
H Analgesics, such as ibuprofen and oxycodone
H Muscle relaxants, such as carisoprodol and cy-

H medication administration, dosage, and possible ad-

verse effects.

Discharge planning
H Refer the patient to a rehabilitation program, if ap-

propriate.
H Refer the patient for home health care, if appropri-

ate.

clobenzaprine

Surgery
H Open reduction
H Skeletal traction
H Ligament repair

Nursing considerations
Key outcomes
The patient will:
H identify factors that intensify pain
H identify factors that increase the risk for injury
H maintain muscle strength and tone
H maintain joint ROM.

Nursing interventions
H Administer prescribed drugs.
H Provide proper positioning of the affected area.
H Apply ice, as ordered.
H Encourage ROM exercises, as ordered, for adjacent

nonmobilized joints.
H Provide meticulous skin care.

ALERT
Immediately report signs and symptoms of severe
vascular compromise, such as pallor, pain, loss of
pulse, paralysis, and paresthesia; the patient needs
an immediate orthopedic examination and emergency reduction.

Monitoring
H Respiratory status when I.V. sedatives used
H Neurovascular status of involved extremity
H Integrity of skin

Patient teaching
Be sure to cover:
H the need to report numbness, pain, cyanosis, and
coldness of the extremity below the cast or splint
H how to evaluate skin integrity
H how to assess neurovascular status
H the use of assistive devices
H the importance of follow-up visits

Dislocations and subluxations

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Life-threatening disorder

Disseminated
intravascular
coagulation
Overview
Description

Common characteristics
H Abnormal bleeding
H Hemorrhage

Complications
H Cardiac tamponade
H Hemothorax
H Renal failure
H Hepatic damage
H Stroke
H Ischemic bowel
H Respiratory distress
H Death (mortality is greater than 50%)
H Intracerebral bleed

H Syndrome of activated coagulation characterized by

bleeding or thrombosis
H Complicates diseases and conditions that accelerate

clotting, causing occlusion of small blood vessels, organ necrosis, depletion of circulating clotting factors
and platelets, and activation of the fibrinolytic system
H Also known as DIC, consumption coagulopathy,
and defibrination syndrome

Pathophysiology
H Typical accelerated clotting results in generalized ac-

tivation of prothrombin and a consequent excess of


thrombin.
H Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation.
H This process consumes exorbitant amounts of coagulation factors (especially platelets, factor V, prothrombin, fibrinogen, and factor VIII), causing
thrombocytopenia, deficiencies in factors V and VIII,
hypoprothrombinemia, and hypofibrinogenemia.
H Circulating thrombin activates the fibrinolytic system,
which lyses fibrin clots into fibrinogen degradation
products (FDPs).
H The hemorrhage that occurs may be due largely to
the anticoagulant activity of FDPs and depletion of
plasma coagulation factors.

Causes
H Infection, sepsis
H Obstetric complications
H Neoplastic disease
H Disorders that produce necrosis, such as extensive

burns and trauma


H Other disorders, such as heatstroke, shock, incom-

patible blood transfusion, drug reactions, cardiac arrest, surgery necessitating cardiopulmonary bypass,
acute respiratory distress syndrome, diabetic ketoacidosis, pulmonary embolism, and sickle cell anemia
H Snakebite

Incidence
H Dependent on the cause

242

Disseminated intravascular coagulation

Assessment
History
H Abnormal bleeding without a history of a serious

hemorrhagic disorder; bleeding possibly occurring


at all bodily orifices
H Possible presence of one of the causes of DIC
H Possible signs of bleeding into the skin, such as
cutaneous oozing, petechiae, ecchymoses, and
hematomas
H Possible bleeding from surgical or invasive procedure sites, such as incisions or venipuncture sites
H Possible nausea and vomiting; severe muscle, back,
and abdominal pain; chest pain; hemoptysis; epistaxis; seizures; and oliguria
H Possible GI bleeding, hematuria

Physical findings
H Petechiae
H Acrocyanosis
H Dyspnea, tachypnea
H Mental status changes, including confusion

Test results
Laboratory
H Serum platelet count is less than 150,000/mm3.
H Serum fibrinogen level is less than 170 mg/dl.
H Prothrombin time is more than 19 seconds.
H Partial thromboplastin time is more than 40 seconds.
H FDPs are increased (commonly greater than 45
mcg/ml, or positive at less than 1:100 dilution).
H Result of D-dimer test (specific fibrinogen test for
DIC) is positive at less than 1:8 dilution.
H Thrombin time is prolonged.
H Blood clotting factors V, VIII, X, XII, and protein C
are diminished.
H Complete blood count shows decreased hemoglobin
level (less than 10 g/dl).
H Blood urea nitrogen level is greater than 25 mg/dl,
and serum creatinine level is greater than 1.3 mg/dl.
H Antithrombin III level is decreased.

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Treatment

H Limit venipunctures whenever possible.


H Watch for transfusion reactions and signs of fluid

General

H Measure the amount of blood lost, weigh dressings

H Treatment of underlying condition


H Possibly supportive care alone if the patient not ac-

H Weigh the patient daily, particularly in renal involve-

tively bleeding
H Activity, as tolerated
H Fluid replacement
H Oxygen therapy
H Endotracheal intubation and mechanical ventilation,

as necessary

Medications
If the patient is actively bleeding
H Administration of blood, fresh frozen plasma,
platelets, or packed red blood cells
H Cryoprecipitate
H Antithrombin III and gabexate
H Anticoagulant such as heparin
H Analgesics such as morphine

Nursing considerations
Key outcomes
The patient will:
H maintain balanced intake and output
H maintain adequate ventilation
H express feelings of increased comfort and decreased
pain
H have laboratory values return to normal
H use available support systems to assist in coping with
fears.

overload.
and linen, and record drainage.
ment.
H Elevate the head of the bed at least 30 degrees.
H Provide nutritional support.
H Maintain bed rest with range-of-motion exercises.

Monitoring
H Vital signs
H Results of serial blood studies
H Signs of shock
H Intake and output, especially when administering

blood products
H Cardiovascular status
H Respiratory status, including pulse oximetry

Patient teaching
Be sure to cover (for the patient and his family):
H an explanation of the disorder
H the signs and symptoms of the problem, diagnostic
procedures required, and treatment that the patient
will receive.

Nursing interventions
ALERT
Focus on early recognition of signs of abnormal
bleeding, prompt treatment of the underlying disorders, and prevention of further bleeding.
H Provide emotional support.
H Provide adequate rest periods.
H Give prescribed analgesics as necessary.
H Reposition the patient every 2 hours, and provide

meticulous skin care.


H Give prescribed oxygen therapy.
H Maintain a patent airway.

ALERT
To prevent clots from dislodging and causing fresh
bleeding, dont vigorously rub the affected areas
when bathing.
H Protect the patient from injury.
H If bleeding occurs, use pressure and topical hemo-

static agents to control bleeding.

Disseminated intravascular coagulation

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Diverticular disease

Complications

Overview

H Intestinal obstruction
H Rectal hemorrhage
H Portal pyemia
H Fistula
H Sepsis

H Ruptured diverticula that cause abdominal abscesses

or peritonitis

Description
H Bulging pouches (diverticula) in GI wall pushing the

mucosal lining through surrounding muscle


H Sigmoid colon most common site, but possibly devel-

oping anywhere, from proximal end of the pharynx


to the anus
H Other typical sites:
The duodenum, near the pancreatic border or the
ampulla of Vater
The jejunum
H Diverticular disease of the ileum (Meckels diverticulum) most common congenital anomaly of the GI
tract
H Two clinical forms:
Diverticulosis: diverticula present but dont cause
symptoms
Diverticulitis: diverticula inflamed and may cause
complications

Pathophysiology
H Pressure in the intestinal lumen is exerted on weak

areas, such as points where blood vessels enter the


intestine, causing a break in the muscular continuity
of the GI wall, creating a diverticulum.
H Diverticulitis occurs when retained undigested food
mixed with bacteria accumulates in the diverticulum,
forming a hard mass (fecalith). This substance cuts
off the blood supply to the diverticulums thin walls,
increasing its susceptibility to attack by colonic bacteria.
H Inflammation follows bacterial infection, causing abdominal pain.

Causes
H Diminished colonic motility and increased intralumi-

nal pressure
H Defects in colon wall strength

Risk factors
H Age
H Low-fiber diet

Incidence
H Most common in adults ages 45 and older
H Affects 30% of adults older than age 60

Common characteristics
H Left lower quadrant abdominal pain
H Generalized abdominal pain
H Diarrhea or constipation
H Palpable mass
H Nausea, vomiting

244

Diverticular disease

Assessment
History
Diverticulosis
H May be symptom-free
H Occasional intermittent pain in the left lower abdominal quadrant, which may be relieved by defecation
or the passage of flatus
H Alternating bouts of constipation and diarrhea
Diverticulitis
H History of diverticulosis
H Low fiber consumption
H Recent consumption of foods containing seeds or
kernels or indigestible roughage, such as celery and
corn
H Complaints of moderate dull or steady pain in the left
lower abdominal quadrant, aggravated by straining,
lifting, or coughing
H Mild nausea, gas, diarrhea, or intermittent bouts of
constipation, sometimes accompanied by rectal
bleeding

Physical findings
Diverticulitis
H Distressed appearance
H Left lower quadrant abdominal tenderness
H Low-grade fever
H Palpable mass
Acute diverticulitis
H Muscle spasms
H Signs of peritoneal irritation
H Guarding and rebound tenderness

Test results
Laboratory
H Complete blood count reveals leukocytosis.
H Erythrocyte sedimentation rate is elevated (in diverticulitis).
H Stool test is positive for occult blood (in 25% of patients with diverticulitis).
Imaging
H Barium studies reveal barium-filled diverticula or
outlines, but barium doesnt fill diverticula blocked
by impacted stools. This procedure isnt performed
for acute diverticulitis due to potential rupture.
H Radiography may reveal colonic spasm if irritable
bowel syndrome accompanies diverticular disease.
H Abdominal X-rays rule out perforation.

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Diagnostic procedures
H Colonoscopy or flexible sigmoidoscopy shows diverticula or inflamed mucosa. It isnt usually performed
in the acute phase.
H Biopsy results may rule out cancer.
H Computed tomography scan of the abdomen evaluates the presence of abscess.

Treatment
General
H For asymptomatic diverticulosis, no treatment
H Bed rest

For symptomatic diverticulosis


H Liquid or low-residue diet (if experiencing pain)
H Increased water consumption, if appropriate
H High-residue diet
For severe diverticulitis
H Nothing by mouth
H Nasogastric (NG) decompression

Medications
For diverticulosis
H Stool softeners such as docusate sodium
H Bulk medication such as calcium polycarbophil
For diverticulitis
H Antibiotics, such as metronidazole and ceftazidime
H Analgesics such as morphine
H I.V. therapy for severe diverticulitis

Surgery
H Colon resection
H May require temporary colostomy to drain abscesses

or to rest the colon for 6 to 8 weeks


H Needed for rupture or to correct cases refractory to

medical treatment

Nursing considerations
Key outcomes

H Maintain bed rest for acute diverticulitis.


H Maintain the prescribed diet.
H If surgery is scheduled, provide routine preoperative

care.
After colon resection
H Provide meticulous wound care.
H Encourage coughing and deep breathing and incentive spirometer use to prevent atelectasis.
H Administer I.V. fluids and prescribed drugs.
H Provide colostomy care, if appropriate.
H Apply sequential compression device.
H Encourage early ambulation.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H GI status
H Vital signs
H Pain control
H Stools for color, consistency, and frequency
H NG drainage, if appropriate
H Signs and symptoms of complications

After colon resection


H Signs of infection and postoperative bleeding
H Intake and output

Patient teaching
Be sure to cover:
H bowel and dietary habits (in uncomplicated diverticulosis)
H the disorder, diagnosis, and treatment
H preoperative teaching (for a patient needing surgery)
H postoperative teaching (for a patient who must care
for his colostomy)
H the desired actions and possible adverse effects of
prescribed medications.

Discharge planning
H Refer the patient to an enterostomal therapist, if ap-

propriate.
H Refer the patient to a dietitian, if needed.

The patient will:


H express feelings of increased comfort
H maintain normal fluid volume
H have bowel movements that return to normal
H verbalize understanding of the disease process and
treatment regimen.

Nursing interventions
ALERT
Remember that diverticulitis produces more serious signs and symptoms as well as complications,
and requires more interventions than diverticulosis.
H If the patient is anxious, provide psychological sup-

port.
H Administer prescribed drugs.

Diverticular disease

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Down syndrome
Overview
Description
H A chromosomal aberration that results in mental and

physical abnormalities
H Average IQ between 30 and 50 (some higher)
H Also known as mongolism and trisomy 21 syn-

drome

Pathophysiology
H Down syndrome is an aberration in which chromo-

some 21 has three copies instead of the normal two


because of faulty meiosis (nondisjunction) of the
ovum or, sometimes, the sperm.
H Theres unbalanced translocation, in which the long
arm of chromosome 21 breaks and attaches to another chromosome.
H The result is a karyotype of 47 chromosomes instead
of the normal 46.

Causes
H Trisomy 21
H Mosaicism and trisomy 21
H Robertsonian translation and partial trisomy 21

Risk factors
H Maternal age, especially older than age 35

Incidence
H Occurs in 1 per 800 to 1,000 live births
H Increases with maternal age, especially after age 35

Common characteristics
H Mental retardation
H Abnormal facial features
H Heart defects
H Other congenital defects

Complications
H Death
H Congenital heart defects
H Premature senile dementia
H Leukemia
H Acute and chronic infections
H Diabetes mellitus
H Thyroid disorders

H Brushfields spots on the iris


H Small skull
H Flat bridge across the nose
H Flattened face
H Small external ears
H Short neck with excess skin
H Dry, sensitive skin with decreased elasticity
H Umbilical hernia
H Short stature
H Short extremities with broad, flat, and squarish

hands and feet


H Dysplastic middle phalanx of the fifth finger
H Wide space between the first and second toes
H Abnormal fingerprints and footprints
H Impaired reflex development
H Absent Moros reflex and hyperextensible joints
H Impaired posture, coordination, and balance
H Clubfoot
H Imperforate anus
H Cleft lip and palate
H Pelvic bone abnormalities

Test results
Laboratory
H Karyotype analysis or chromosome mapping shows
the chromosomal abnormality and confirms the diagnosis of Down syndrome.
H Prenatal serum alpha-fetoprotein reveals reduced
levels of alpha-fetoprotein.
Imaging
H Prenatal ultrasonography can suggest Down syndrome if a duodenal obstruction or an atrioventricular canal defect is present.
H Amniocentesis allows prenatal diagnosis.
Other
H Developmental screening tests show severity and
progress of retardation.

Treatment
General
H Early intervention
H Special education programs
H Special athletic programs
H Maximal environmental simulation for infants
H Safety precautions for children and adults in a con-

trolled environment

Medications
H Antibiotics, depending on the infective organism, for

Assessment
History
H Neonate lethargic and a poor feeder

Physical findings
H Slanting, almond-shaped eyes
H Small, open mouth, protruding tongue
H Single transverse palmar crease

246

Down syndrome

recurrent infections
H Thyroid hormone replacement with levothyroxine for

hypothyroidism

Surgery
H Open-heart surgery to correct cardiac defects, such

as ventricular or atrial septal defects


H Plastic surgery to correct congenital abnormalities,

such as protruding tongue, cleft lip, and cleft palate

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Nursing considerations
Key outcomes
The patient will:
H demonstrate age-appropriate skills and behaviors to
the extent possible
H perform health maintenance activities according to
level of ability
H participate in developmental stimulation programs to
increase skill levels.

Nursing interventions
H Establish a trusting relationship with the childs par-

ents.
H Encourage verbalization and provide support.
H Encourage the parents to hold and nurture their

child.

Monitoring
H Response to treatment
H Signs and symptoms of infection
H Complications
H Nutritional status
H Growth and development
H Thyroid function test results
H Cardiovascular status

Patient teaching
Be sure to cover:
H the need for adequate exercise and maximal environmental stimulation
H realistic goals for the parents and child
H information about a balanced diet
H the importance of remembering the emotional needs
of other children in the family.

Discharge planning
H Refer the parents to infant stimulation classes.
H Refer the parents and older siblings for genetic and

psychological counseling, as appropriate.


H Refer the patient and his parents to support services.

Down syndrome

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Dysmenorrhea
Overview
Description

H Obesity
H Smoking

Incidence
H Affects more than 45% of females of reproductive age
H Usually peaks in the early 20s, then slowly decreases

H Painful menstruation unassociated with pelvic dis-

Common characteristics

ease
H Most common gynecologic complaint
H A primary disorder that begins 6 to 12 months after
the onset of ovulation
H A secondary disorder that typically begins between
ages 20 and 30, but possible any time after menarche

H Sharp, intermittent, cramping, lower abdominal pain,

Pathophysiology
H Pain may result from increased prostaglandin secre-

tion in menstrual blood, which intensifies normal


uterine contractions.
H Prostaglandins intensify myometrial smooth muscle
contraction and uterine blood vessel constriction,
thereby worsening the uterine hypoxia normally associated with menstruation.
H Intense muscle contractions and hypoxia cause the
intense pain of dysmenorrhea.

Causes
Primary
H Increased prostaglandin secretion caused by sloughing endometrial cells
Secondary
H Endometriosis
H Cervical stenosis
H Uterine leiomyomas (benign fibroid tumors)
H Pelvic inflammatory disease
H Pelvic tumors (see Causes of pelvic pain)

Risk factors
Primary
H Early-onset menarche
H Null parity

Causes of pelvic pain


The characteristic pelvic pain of dysmenorrhea must be
distinguished from the acute pain caused by many other
disorders, such as:
H GI disorders: appendicitis, acute diverticulitis, acute or
chronic cholecystitis, chronic cholelithiasis, acute pancreatitis, peptic ulcer perforation, intestinal obstruction
H urinary tract disorders: cystitis, renal calculi
H reproductive disorders: acute salpingitis, chronic inflammation, degenerative fibroid, ovarian cyst torsion
H pregnancy disorders: impending abortion (pain and
bleeding early in pregnancy), ectopic pregnancy, abruptio placentae, uterine rupture, leiomyoma degeneration,
toxemia
H emotional conflicts: psychogenic (functional) pain.
Other conditions that may mimic dysmenorrhea include
ovulation and normal uterine contractions experienced in
pregnancy.

usually radiating to the back, thighs, groin, and vulva


H Pain typically starting with or immediately before

menstrual flow and peaking within 24 hours

Complications
H Dehydration

Assessment
History
H Pelvic disease
H Urinary frequency
H Nausea
H Vomiting
H Diarrhea
H Headache
H Backache
H Chills
H Depression
H Irritability

Physical findings
H Abdominal tenderness
H Painful breasts

Test results
Imaging
H Laparoscopy, hysteroscopy, and pelvic ultrasound
help diagnose underlying disorders (in secondary
dysmenorrhea).
Other
H Pelvic examination and a detailed patient history help
identify the cause.

Treatment
General
H Heat applied locally to the lower abdomen
H Increased fluid intake
H Activity, as tolerated

Medications
H Analgesics, such as acetaminophen, diclofenac, and

ketoprofen
H Prostaglandin inhibitors, such as aspirin and ibupro-

fen

Surgery
H Surgical treatment of underlying disorders, such as

endometriosis or uterine leiomyomas (secondary)

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Nursing considerations
Key outcomes
The patient will:
H remain free from pain
H express understanding of disorder.

Nursing interventions
H Provide emotional support.
H Administer prescribed analgesics.

Monitoring
H Depression
H Hydration
H Pain control
H Menstrual cycle

Patient teaching
Be sure to cover:
H explanation of normal female anatomy and physiology as well as the nature of dysmenorrhea
H information on pregnancy and contraception
H keeping a detailed record of her menstrual cycle and
symptoms
H seeking medical care if symptoms persist.

Discharge planning
H Refer the patient for psychological counseling, if

appropriate.

Dysmenorrhea

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Life-threatening disorder

Ebola virus infection

Risk factors
H Travel to endemic areas of Africa
H Exposure to animals, humans, or contaminated nee-

dles

Incidence

Overview

H Not endemic to the United States


H Affects males and females of all ages

Description

Common characteristics

H An unclassified ribonucleic acid virus that results in

H Flulike symptoms
H Severe diarrhea
H Vomiting
H Internal and external hemorrhage
H Macular papular rash

bleeding
H Four known strains: Ebola Zaire (EBO-Z), Ebola Sudan (EBO-S), Ebola Tai (EBO-C), and Ebola Reston
(affects only monkeys)
H Poor prognosis

Pathophysiology
H The virus is transmitted by direct contact with infect-

ed blood, body secretions, or infected tissues.


H It can be transmitted by nosocomial and community-

acquired modes.
H Viral replication causes focal tissue necrosis, most

Complications
H Liver and kidney dysfunction
H Dehydration
H Hemorrhage
H Abortion
H Myocarditis
H Pulmonary edema

severely in the liver.


H Microvasculature damage causes increased vascular

permeability and bleeding.


H Ebola virus remains contagious even after the patient

has died.

Causes
H EBO-Z, EBO-S, or EBO-C virus strains

Prevention

Preventing the spread of Ebola virus


The Centers for Disease Control and Prevention recommends the following guidelines to help prevent the spread
of this deadly disease:
H Keep the patient in isolation throughout the course of
the disease.
H If possible, place the patient in a negative-pressure
room at the beginning of hospitalization to avoid the
need for transfer as the disease progresses.
H Restrict nonessential staff members from entering the
patients room.
H Make sure that anyone who enters the patients room
wears gloves and a gown to prevent contact with any
surface in the room that may have been soiled.
H Use barrier precautions to prevent skin and mucous
membrane exposure to blood or other body fluids, secretions, or excretions when caring for the patient.
H If you must come within 3 (1 m) of the patient, also
wear a face shield or a surgical mask and goggles or
eyeglasses with side shields.
H Dont reuse gloves or gowns unless they have been
completely disinfected.
H Make sure any patient who dies of the disease is
promptly buried or cremated. Precautions to avoid
contact with the patients body fluids and secretions
should continue even after the patients death.

250

Ebola virus infection

Assessment
History
H Contact with an infected person
H Headache
H Malaise
H Myalgia
H Fever
H Cough
H Sore throat
H Nausea
H Vomiting

Physical findings
H Conjunctival injection
H Bruising
H Maculopapular eruptions
H Melena
H Hematemesis
H Bleeding gums

Test results
Laboratory
H Blood studies show specific antigens or antibodies
and may show the isolated virus.
H Blood studies show neutrophil leukocytosis, hypofibrinogenemia, thrombocytopenia, and microangiopathic hemolytic anemia.
H Blood studies show elevated blood urea nitrogen and
creatinine levels.
H Blood studies show elevated aspartate aminotransferase and alanine aminotransferase levels.

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Treatment
General
H Supportive care
H Strict isolation (see Preventing the spread of Ebola

virus)
H Diet as tolerated or total parental nutrition
H Bed rest or limited activity

Medications
H I.V. fluids
H Blood transfusions

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid balance
H remain hemodynamically stable
H understand the implications of his illness.

Nursing interventions
H Enforce strict isolation.
H Provide emotional support.
H Administer prescribed I.V. solutions and blood prod-

ucts.
H Provide safety precautions.
H Provide nutritional support.

Monitoring
H Vital signs
H Signs of bleeding
H Intake and output
H Laboratory studies
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of bleeding
H isolation precautions.

Discharge planning
H Refer the patient for home care, if appropriate.
H Stress to the patient the need for continued follow-up

care.

Ebola virus infection

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Ectopic pregnancy
Overview
Description
H Implantation of a fertilized ovum outside the uterine

cavity, most commonly in the fallopian tube (see Implantation sites of ectopic pregnancy)
H Prognosis good with prompt diagnosis, appropriate
surgical intervention, and control of bleeding
H Very few fetuses carried to term; rarely, with abdominal implantation, fetus survives to term
H About one in three chance of giving birth to live
neonate in subsequent pregnancy

H Previous surgery, such as tubal ligation or resection


H Transmigration of the ovum
H Congenital defects in reproductive tract
H Ectopic endometrial implants in the tubal mucosa
H Sexually transmitted tubal infection
H Intrauterine device
H Smoking
H Hormonal contraceptives

Incidence
H In whites, about 1 of 200 pregnancies
H In nonwhites, about 1 of 120 pregnancies

Common characteristics

Pathophysiology

H Abdominal tenderness
H Abdominal discomfort
H Minimal vaginal bleeding
H Amenorrhea

H The transport of a blastocyst to the uterus is delayed.


H The blastocyst implants at another available vascular-

Complications

ized site, usually the fallopian tube lining.


H Normal signs of pregnancy are initially present.
H Uterine enlargement occurs in about 25% of cases.
H Human chorionic gonadotropin (HCG) hormonal
levels are lower than in uterine pregnancies.
H If not interrupted, internal hemorrhage occurs with
rupture of the fallopian tube.

H Rupture of fallopian tube


H Hemorrhage
H Shock
H Peritonitis
H Infertility
H Disseminated intravascular coagulation
H Death

Causes
H Abnormal reproductive organ anatomy
H Delay in reproductive events such as movement of

zygote to uterus
H Unknown

Assessment
History
H Amenorrhea
H Abnormal menses (after fallopian tube implantation)
H Slight vaginal bleeding
H Unilateral pelvic pain over the mass
H If fallopian tube ruptures, sharp lower abdominal

Risk factors
H Endosalpingitis
H Diverticula
H Tumors pressing against the tube

pain, possibly radiating to the shoulders and neck

Implantation sites of ectopic pregnancy


In about 95% of patients with ectopic pregnancy, the
ovum implants in part of the fallopian tube: the fimbria,
ampulla, or isthmus. Other possible abnormal sites of implantation include the interstitium, ovarian ligament,
ovary, abdominal viscera, and internal cervical os.

ALERT
Ectopic pregnancy sometimes produces symptoms
of normal pregnancy or no symptoms other than
mild abdominal pain (especially in abdominal
pregnancy), making diagnosis difficult.

Physical findings

Ampulla
Fimbria

Isthmus

H Possible extreme pain when cervix is moved and ad-

nexa palpated

Interstitium

H Boggy and tender uterus


H Adnexa possibly enlarged

Test results
Ovary
Ovarian ligament

252

Ectopic pregnancy

Internal cervical os

Laboratory
H Serum HCG level is abnormally low; when repeated
in 48 hours, it remains lower than levels found in a
normal intrauterine pregnancy.
Imaging
H Real-time ultrasonography shows intrauterine pregnancy or ovarian cyst.

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Diagnostic procedures
H Laparoscopy may reveal pregnancy outside the
uterus.

Treatment

H Signs of impending shock


H Cardiovascular status

Patient teaching

Medications

Be sure to cover:
H the disorder, diagnosis, and treatment
H postoperative care
H prevention of recurrent ectopic pregnancy
H prompt treatment of pelvic infections
H risk factors for ectopic pregnancy, including surgery
involving the fallopian tubes and pelvic inflammatory
disease.

H Transfusion with packed red blood cells


H Broad-spectrum I.V. antibiotics, according to isolated

Discharge planning

General
H Initially, in the event of pelvic-organ rupture, man-

agement of shock
H Diet determined by clinical status
H Activity determined by clinical status

organism
H Supplemental iron

H Refer the patient to a mental health professional for

additional counseling, if necessary.

Surgery
H Laparotomy and salpingectomy; possibly after lap-

aroscopy to remove affected fallopian tube and control bleeding


H Microsurgical repair of the fallopian tube for patients
who wish to have children
H Oophorectomy for ovarian pregnancy
H Hysterectomy for interstitial pregnancy
H Laparotomy to remove the fetus for abdominal pregnancy

Nursing considerations
Key outcomes
The patient will:
H have stable vital signs
H express feelings about the current situation
H use available support systems to aid in coping.

Nursing interventions
H Prepare the patient with excessive blood loss for

emergency surgery.
H Administer prescribed blood transfusions.
H Provide emotional support.
H Give prescribed analgesics.
H Administer Rho(D) immune globulin (RhoGAM), as

ordered, if the patient is Rh-negative.


H Determine the date and description of her last men-

strual period.
H Provide a quiet, relaxing environment.
H Encourage the patient to express her feelings of fear,

loss, and grief.


H Help the patient to develop effective coping strate-

gies.

Monitoring
H Vital signs
H Vaginal bleeding
H Pain control
H Intake and output
H Signs of hypovolemia

Ectopic pregnancy

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Life-threatening disorder

Electric shock
Overview
Description
H Electric current passing through body
H Physical damage depending on intensity of current,

resistance of the tissues it passes through, type of


current, and frequency and duration of current flow
H Classified as lightning, low voltage (less than 600 V),
and high voltage (greater than 600 V)
H Burns the most common injury

Pathophysiology
H Electrical energy results in altered cell membrane

resting potential, causing depolarization in muscles


and nerves.
H Electric shock alters normal electrical activity of the
heart and brain.
H Electric shock resulting from a high-frequency current generates more heat in tissues than a lowfrequency current, resulting in burns and local tissue
coagulation and necrosis.
H Muscle tetany is elicited.
H Tissue destruction and coagulative necrosis occur.

Causes
H Accidental contact with an exposed part of an electri-

cal appliance or wiring


H Lightning
H Flash of electric arcs from high-voltage power lines

or machines

Incidence

Assessment
History
H Exposure to electricity or lightning
H Loss of consciousness
H Muscle pain
H Fatigue
H Headache
H Nervous irritability

Physical findings
H Determined by voltage exposure
H Burns
H Local tissue coagulation
H Entrance and exit injuries
H Cyanosis
H Apnea
H Markedly decreased blood pressure
H Cold skin
H Unconsciousness
H Numbness or tingling or sensorimotor deficits

Test results
Laboratory
H Laboratory test results evaluate internal damage and
guide treatment:
Arterial blood gas analysis may show hypoxemia
and acid-base imbalance.
Urine may test positive for myoglobin.
Blood urea nitrogen and creatinine levels may be
elevated.
Imaging
H If chest injury or shortness of breath occurred, chest
X-rays evaluate internal damage and guide treatment.
Diagnostic procedures
H Electrocardiography evaluates internal damage and
guides treatment.

H Causes more than 1,000 deaths annually


H More common in males ages 20 to 40

Treatment

Common characteristics

General

H Cutaneous burn
H Variable deep tissue damage

H Separation of victim from current source


H Stabilization of cervical spine
H Emergency measures to maintain airway, breathing,

Complications
H Sepsis
H Neurologic dysfunction
H Cardiac dysfunction
H Psychiatric dysfunction
H Renal failure
H Electrolyte abnormalities
H Peripheral nerve injuries
H Vascular disruption
H Thrombi
H Death

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Electric shock

and circulation
H Treatment of acid-base imbalance
H Vigorous fluid replacement
H No dietary restrictions if swallowing ability intact
H Activity based on outcome of interventions

Medications
H Tetanus prophylaxis with tetanus toxoid

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Nursing considerations
Key outcomes
The patient will:
H maintain stable cardiac rhythm
H maintain cardiac output
H regain skin integrity
H have wounds and incisions that appear clean, pink,
and free from purulent drainage.

Nursing interventions
H Separate the victim from the current source.
H Provide emergency treatment to maintain airway,

breathing, and circulation.


H Give rapid I.V. fluid infusion.
H Obtain a 12-lead electrocardiogram.
H Administer prescribed drugs.
H Provide wound care.

Monitoring
H Vital signs
H Cardiac rhythm (continuously) and cardiovascular

status
H Intake and output (hourly)
H Neurologic status
H Sensorimotor deficits
H Peripheral neurovascular status
H Respiratory status

Patient teaching
Be sure to cover:
H information about the injury, diagnosis, and treatment
H how to avoid electrical hazards at home and at work
H electrical safety regarding children.

Electric shock

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Emphysema
Overview
Description
H Progressive, chronic lung disease characterized by

permanent enlargement of air spaces distal to the


terminal bronchioles and by exertional dyspnea
H One of several diseases usually labeled collectively as
chronic obstructive pulmonary disease or chronic
obstructive lung disease

Pathophysiology
H Recurrent inflammation associated with the release

of proteolytic enzymes from lung cells causes abnormal, irreversible enlargement of the air spaces distal
to the terminal bronchioles.
H This enlargement leads to the destruction of alveolar
walls, which results in a breakdown of elasticity. (See
What happens in emphysema.)

Causes
H Cigarette smoking
H Air pollutants

Risk factors
H Genetic deficiency of alpha1-antitrypsin

Incidence
H Most common cause of death from respiratory dis-

ease in the United States


H More prevalent in males than in females
H About 2 million U.S. residents affected
H Affects 1 in 3,000 neonates

Common characteristics
H Exertional dyspnea
H Chronic cough
H Shortness of breath
H Anorexia and weight loss
H Malaise

Complications

Physical findings
H Barrel chest
H Pursed-lip breathing
H Use of accessory muscles
H Cyanosis
H Clubbed fingers and toes
H Tachypnea
H Decreased tactile fremitus
H Decreased chest expansion
H Hyperresonance
H Decreased breath sounds
H Crackles
H Inspiratory wheeze
H Prolonged expiratory phase with grunting respira-

tions
H Distant heart sounds

Test results
Laboratory
H Arterial blood gas analysis shows decreased partial
pressure of oxygen; partial pressure of carbon dioxide remains normal until late in the disease.
H Red blood cell count shows an increased hemoglobin level late in the disease.
Imaging
H Chest X-ray may show:
a flattened diaphragm
reduced vascular markings at the lung periphery
overaeration of the lungs
a vertical heart
enlarged anteroposterior chest diameter
large retrosternal air space.
Diagnostic procedures
H Pulmonary function tests typically show:
increased residual volume and total lung capacity
reduced diffusing capacity
increased inspiratory flow.
H Electrocardiography may show tall, symmetrical P
waves in leads II, III, and aVF; a vertical QRS axis;
and signs of right ventricular hypertrophy late in the
disease.

Treatment

H Recurrent respiratory tract infections


H Cor pulmonale
H Respiratory failure
H Peptic ulcer disease
H Spontaneous pneumothorax
H Pneumomediastinum

General

Assessment

Medications

History
H Smoking
H Shortness of breath
H Chronic cough
H Anorexia and weight loss
H Malaise

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Emphysema

H Chest physiotherapy
H Possible transtracheal catheterization and home oxy-

gen therapy
H Adequate hydration
H High-protein, high-calorie diet
H Activity, as tolerated

H Bronchodilators such as formoterol


H Anticholinergics such as tiotropium
H Mucolytics such as acetylcysteine
H Corticosteroids such as fluticasone
H Antibiotics according to the isolated organism
H Oxygen

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H Immunizations, such as influenza virus vaccine and

pneumococcal vaccine

Surgery
H Chest tube insertion for pneumothorax
H Lung volume reduction surgery

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway and adequate ventilation
H demonstrate energy conservation techniques
H express understanding of the illness
H demonstrate effective coping strategies.

What happens in emphysema


In normal, healthy breathing, air moves in and out of the
lungs to meet metabolic needs. A change in airway size
compromises the lungs ability to circulate sufficient air.
In a patient with emphysema, recurrent pulmonary inflammation damages and eventually destroys the alveolar
walls, creating large air spaces. This breakdown leaves the
alveoli unable to recoil normally after expanding and results in bronchiolar collapse on expiration. This traps air
within the lungs.
Associated pulmonary capillary destruction usually allows a patient with severe emphysema to match ventilation to perfusion and thus avoid cyanosis.
NORMAL ALVEOLI
Bronchiole

Nursing interventions
H Administer prescribed drugs.
H Provide supportive care.
H Help the patient adjust to lifestyle changes necessitat-

ed by a chronic illness.
H Encourage the patient to express his fears and con-

cerns.
H Perform chest physiotherapy.
H Provide a high-calorie, protein-rich diet.
H Give small, frequent meals.
H Encourage daily activity and diversional activities.
H Provide frequent rest periods.
H Keep the head of the bed elevated at least 30 degrees.
H Encourage oral fluid intake.

Alveoli

ABNORMAL ALVEOLI

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Complications
H Respiratory status
H Activity tolerance
H Cardiovascular status
H Nutritional status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the practitioner
H avoidance of smoking and areas where smoking is
permitted
H avoidance of crowds and people with known infections
H home oxygen therapy, if indicated
H transtracheal catheter care, if needed
H coughing and deep-breathing exercises
H the proper use of handheld inhalers
H high-calorie, protein-rich diet
H adequate oral fluid intake
H avoidance of respiratory irritants
H signs and symptoms of pneumothorax.

ALERT
Urge the patient to notify the practitioner if he experiences a sudden onset of worsening dyspnea or
sharp pleuritic chest pain exacerbated by chest
movement, breathing, or coughing.

Discharge planning
H Refer the patient to a smoking-cessation program, if

indicated.
H Refer the patient for influenza and pneumococcal

pneumonia immunizations, as needed.


H Refer the family of patients with familial emphysema

for alpha1-antitrypsin deficiency screening.

Emphysema

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Encephalitis
Overview
Description
H Severe inflammation of the brain

Pathophysiology
H Intense lymphocytic infiltration of brain tissues and

the leptomeninges results in:


cerebral edema
degeneration of the brains ganglion cells
diffuse nerve cell destruction (gray matter more
than white).

Causes
H Mosquito- or tick-borne arboviruses specific to rural

areas

H Sore throat and upper respiratory tract symptoms


H Sudden onset of altered level of consciousness
H Seizures

Physical findings
H Confusion, disorientation, or hallucinations
H Tremors
H Cranial nerve palsies
H Exaggerated deep tendon reflexes and absent superfi-

cial reflexes
H Paresis or paralysis of the arms and legs
H Stiff neck when the head is bent forward
H Fever
H Nausea and vomiting
H Cerebral hemispheres
H Aphasia
H Involuntary movements
H Ataxia
H Sensory defects

H Enteroviruses in urban areas (coxsackievirus, po-

Test results

liovirus, and echovirus)


H Herpesvirus
H Mumps virus
H Adenoviruses
H Demyelinating diseases after measles, varicella,
rubella, or vaccination
H Human immunodeficiency virus

Laboratory
H Blood analysis identifies the virus.
H Serologic studies in herpes encephalitis show rising
titers of complement-fixing antibodies.
Imaging
H Magnetic resonance imaging locates the lesion.
H Computed tomography scan shows cerebral edema.
Diagnostic procedures
H Cerebrospinal fluid (CSF) analysis identifies the
virus.
H Lumbar puncture discloses CSF pressure.
H EEG shows slowing of waveforms.

Incidence
H About 1,500 cases annually in the United States
H More common in elderly people and infants

Common characteristics
H Dysuria; pyuria
H Fever
H Nausea and vomiting
H Myalgia
H Photophobia
H Stiff neck; headache
H Localized seizures
H Acute confusion or amnesic state

Complications
H Bronchial pneumonia
H Urinary retention and urinary tract infection
H Pressure ulcers
H Coma
H Epilepsy
H Parkinsonism
H Mental deterioration

Assessment
History
H Headache
H Muscle stiffness and malaise

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Encephalitis

Treatment
General
H Supportive measures
H Airway maintenance
H Oxygen administration
H Adequate fluid and electrolyte intake
H Diet as tolerated
H Activity as tolerated

Medications
H Osmotic diuretics such as mannitol
H Corticosteroids such as dexamethasone
H Anticonvulsants such as phenytoin
H Antipyretics such as acetaminophen
H Antibiotics according to isolated organism
H Antivirals such as vidarabine
H Oxygen
H Stool softeners such as docusate sodium

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Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H exhibit fluid balance within normal limits
H exhibit temperature within normal limits
H consume adequate calorie requirements daily
H verbalize feelings of increased comfort and relief
from pain.

Nursing interventions
H Ensure adequate fluid intake.
H Administer prescribed drugs.
H Position and turn the patient often.
H Assist with range-of-motion exercises.
H Maintain adequate nutrition.
H Administer laxatives or stool softeners.
H Administer mouth care.
H Maintain a quiet environment.
H Start seizure precautions, if necessary.
H Reorient the patient often, if necessary.
H Keep the head of the bed elevated, as ordered.

Monitoring
H Vital signs
H Neurologic status
H Intake and output
H Response to medications
H Intracranial pressure (severe cases)
H Respiratory status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H transient behavior changes
H the medication regimen
H adverse effects of medication
H follow-up care.

Discharge planning
H Refer the patient to an outpatient rehabilitation pro-

gram, as indicated.

Encephalitis

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Endocarditis
Overview
Description
H Inflammation or infection of the endocardium, heart

valves, or cardiac prosthesis


H Classified as infective (bacterial or fungal) or noninfective

Pathophysiology
H Fibrin, neutrophils, lymphocytes, and platelets clus-

ter on valve tissue and engulf bacteria, fungi, or


necrotic tissue. (See Degenerative changes in endocarditis.)
H This produces vegetation, which may cover the valve
surfaces, causing deformities and destruction of
valvular tissue, and may extend to the chordae
tendineae, causing them to rupture, leading to valvular insufficiency.
H Vegetative growth on the heart valves, endocardial
lining of a heart chamber, or the endothelium of a
blood vessel may embolize to the spleen, kidneys,
central nervous system, and lungs.

Causes
H Bacterial or fungal infection
H Advanced stages of cancer
H Immune system disorders

Risk factors
H Cardiac valvular disease
H I.V. drug use
H Rheumatic heart disease
H Prosthetic heart valves
H Congenital heart disease
H Mitral valve prolapse
H Degenerative heart disease
H Calcific aortic stenosis (in elderly patients)
H Asymmetrical septal hypertrophy
H Marfan syndrome
H Syphilitic aortic valve
H Long-term hemodialysis
H Streptococcal infection
H Systemic lupus erythematosus

Incidence
H No underlying heart disease in up to 40% of patients

Native valve endocarditis


H More common in males than in females
H Most patients older than age 50
H Uncommon in children
H Rheumatic valvular disease in about 25% of cases
H Mitral valve most commonly involved valve
H Drug abusers with endocarditis (frequently young
males)

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Endocarditis

Common characteristics
H Heart murmur

Complications
H Valve stenosis or regurgitation
H Myocardial erosion
H Embolic debris lodged in the small vasculature of the

visceral tissue causing multiple organ infarcts


H Stroke
H Myocardial infarction
H Heart failure
H Acute renal failure

Assessment
History
H Predisposing condition
H Complaint of nonspecific symptoms, such as weak-

ness, fatigue, weight loss, anorexia, arthralgia, night


sweats, and intermittent fever, that may recur for
weeks

Physical findings
H Petechiae on the skin (especially common on the up-

per anterior trunk) and on the buccal, pharyngeal,


or conjunctival mucosa
H Splinter hemorrhages under the nails
H Clubbing of the fingers in long-standing disease
H Heart murmur in all patients except those with early
acute endocarditis and I.V. drug users with tricuspid
valve infection
H Murmur that changes suddenly or new murmur that
develops with a fever (classic physical sign)
H Oslers nodes
H Roths spots
H Janeway lesions
H Splenomegaly in long-standing disease
H Dyspnea, tachycardia, and bibasilar crackles possible
with left-sided heart failure
H Splenic infarction causing pain in the upper left
quadrant, radiating to the left shoulder, and abdominal rigidity
H Renal infarction causing hematuria, pyuria, flank
pain, and decreased urine output
H Cerebral infarction causing hemiparesis, aphasia,
and other neurologic deficits
H Pulmonary infarction causing cough, pleuritic pain,
pleural friction rub, dyspnea, and hemoptysis
H Peripheral vascular occlusion causing numbness and
tingling in arm, leg, finger, or toe or signs of impending peripheral gangrene

Test results
Laboratory
H Three or more blood cultures over 24 to 48 hours
identify the causative organism in up to 90% of patients.
H White blood cell count with differential are normal
or elevated.

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H Complete blood count shows normocytic, normo-

chromic anemia in subacute infective endocarditis.


H Erythrocyte sedimentation rate and serum creatinine
levels are elevated.
H Serum rheumatoid factor is positive in about half of
patients after the disease is present for 6 weeks.
H Urinalysis shows proteinuria and microscopic hematuria.
Imaging
H Echocardiography may identify valvular damage in up
to 80% of patients with native valve disease.
Diagnostic procedures
H Electrocardiography may show atrial fibrillation and
other arrhythmias that accompany valvular disease.

Degenerative changes in endocarditis


This illustration shows typical vegetations on the endocardium produced by fibrin and platelet deposits on infection sites.

Treatment
General
H Prompt therapy that continues for several weeks
H Selection of anti-infective drug based on type of in-

fecting organism and sensitivity studies


H If blood cultures negative (10% to 20% of subacute

cases), possible I.V. antibiotic therapy (usually for 4


to 6 weeks) against probable infecting organism
H Sufficient fluid intake
H Bed rest

Medications
H Antiplatelets or antipyretics such as aspirin
H Antibiotics, according to isolated organism

Surgery
H With severe valvular damage, especially aortic insuffi-

ciency or infection of a cardiac prosthesis, possible


corrective surgery if refractory heart failure develops
or if an infected prosthetic valve must be replaced

Monitoring
H Vital signs
H Cardiac rhythm and cardiovascular status
H Respiratory status, including pulse oximetry
H Neurologic status
H Intake and output
H Renal status
H Arterial blood gas analysis, as needed

ALERT
Watch for signs of embolization, a common occurrence during the first 3 months of treatment. Tell
the patient to watch for and report these signs.

Nursing considerations

Patient teaching

Key outcomes

Be sure to cover:
H the disorder, diagnosis, and treatment
H anti-infectives the patient needs to continue taking
H the need to watch closely for fever, anorexia, and
other signs of relapse about 2 weeks after treatment
stops
H the need for prophylactic antibiotics before dental
work and some surgical procedures
H proper dental hygiene and avoiding flossing the teeth
H how to recognize symptoms of endocarditis and to
notify the practitioner immediately if such symptoms
occur.

The patient will:


H carry out activities of daily living without weakness or
fatigue
H maintain hemodynamic stability with adequate cardiac output
H exhibit no arrhythmias
H maintain adequate ventilation
H express feelings about diminished capacity to perform usual roles.

Nursing interventions
H Stress the importance of bed rest.
H Provide a bedside commode.
H Allow the patient to express his concerns.
H Obtain a history of allergies.
H Administer antibiotics, as prescribed.
H Administer oxygen.
H Elevate the head of the bed at least 30 degrees.

Discharge planning
H Encourage follow-up care with a cardiologist.

Endocarditis

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Endometriosis
Overview
Description
H Poorly understood gynecologic condition character-

ized by pain that occurs with menstruation


H Endometrial tissue appears outside uterine cavity

lining
H Ectopic tissue generally confined to the pelvic
area, but can appear anywhere in the body

Pathophysiology
H Endometrial cells respond to estrogen and proges-

terone with proliferation and secretion.


H During menstruation, ectopic tissue bleeds and caus-

es inflammation of the surrounding tissues.


H Inflammation leads to fibrosis.
H Fibrosis leads to adhesions that produce pain and in-

fertility.

Assessment
History
H Cyclic pelvic pain that peaks 5 to 7 days before

menses and lasts 2 to 3 days


H Infertility
H Acquired dysmenorrhea
H Pain in lower abdomen, vagina, posterior pelvis and

back; often radiates down legs


H Additional symptoms depending on site of involve-

ment:
Hypermenorrhea (oviducts and ovaries)
Deep-thrust dyspareunia (ovaries and cul-de-sac)
Suprapubic pain, dysuria, and hematuria (bladder)
Dyschezia, rectal bleeding with menses, and pain
in the coccyx or sacrum (rectovaginal septum and
colon)
Nausea and vomiting that worsen before menses
(small bowel and appendix)
Abdominal cramps (small bowel and appendix)

Causes

Physical findings

H Direct cause unknown


H Familial susceptibility
H Direct implantation
H Transportation (retrograde menstruation)
H Formation in situ
H Induction of labor
H Immune system defects
H Lymphatic spread theory
H Inflammatory influence
H Environmental contaminants

H Multiple tender nodules on uterosacral ligaments or

Incidence
H Usually occurs between ages 20 and 40; uncommon

before age 20
H More common in females who postpone childbear-

ing
H More common in white females

Common characteristics
H Early menarche
H Menstrual flow lasting longer than 7 days
H Cycles lasting longer than 27 days
H Family history of endometriosis
H Multiparity
H Cyclic pelvic pain
H Severe dysmenorrhea

Complications
H Infertility
H Spontaneous abortion
H Anemia secondary to excessive bleeding
H Emotional problems secondary to infertility
H Pelvic adhesions
H Severe dysmenorrhea
H Ovarian cyst
H Ovarian cancer

rectovaginal septum
H Enlarged nodules (tender during menses)
H Ovarian enlargement with endometrial cysts on the

ovaries
H Thickened, nodular adnexa

Test results
Diagnostic procedures
H A scoring and staging system created by the American
Fertility Society quantifies endometrial implants according to size, character, and location:
Stage I indicates minimal disease (1 to 5 points).
Stage II indicates mild disease (6 to 15 points).
Stage III indicates moderate disease (16 to 40
points).
Stage IV indicates severe disease (more than 40
points).
H Laparoscopy confirms the diagnosis and identifies
the disease stage.
H Ultrasonography helps confirm the diagnosis.

Treatment
General
H Determined by stage of disease, patients age, and de-

sire to have children


H Pregnancy, if possible (provides temporary relief)
H Activity, as tolerated

Medications
H Progestins such as medroxyprogesterone
H Hormonal contraceptives such as norethindrone
H Gonadotropin-releasing hormone, such as goserelin

and leuprolide
H Analgesics such as ibuprofen

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Surgery
H Laparoscopy to lyse adhesions, remove small im-

plants, and cauterize implants; for laser vaporization


of implants; usually followed by hormonal therapy to
suppress return of endometrial implants
H Total abdominal hysterectomy with bilateral
salpingo-oophorectomy in stages III and IV

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H exhibit no signs of infection
H express understanding of the disorder and treatment
H develop adequate coping behaviors.

Nursing interventions
H Encourage the patient to express her feelings about

the disorder.
H Offer emotional support.
H Encourage using open communication before and

during intercourse.
H Help the patient develop effective coping strategies.

Monitoring
H Effect of treatment
H Complications
H Adverse drug reactions
H Coping ability
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H associated complications
H avoiding minor gynecologic procedures immediately
before and during menstruation
H not postponing childbearing due to potential for infertility
H annual pelvic examination and Papanicolaou test.

Discharge planning
H Refer the patient and her partner to a mental health

professional for additional counseling, if necessary.


H Refer the patient to a support group such as the En-

dometriosis Association.

Endometriosis

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Enterobacteriaceae
infections
Overview
Description

Assessment
History
H Recent travel to another country
H Ingestion of contaminated food or water
H Recent close contact with a person who has diarrhea
H Abrupt onset of watery diarrhea

H Variety of infections caused by a family of mostly aer-

Physical findings

obic, gram-negative bacilli


H Cause local and systemic infections, including invasive diarrhea resembling shigellosis and noninvasive,
toxin-mediated diarrhea resembling cholera
H Escherichia coli: the cause of most nosocomial infections

H Cramping abdominal pain with hyperactive bowel

Pathophysiology
H When infected, incubation takes 12 to 72 hours.
H Noninvasive diarrhea results from two toxins pro-

duced by enterotoxigenic or enteropathogenic strains


of E. coli.
H Toxins interact with intestinal juices and promote excessive loss of chloride and water.
H The invasive form directly attacks the intestinal mucosa without producing enterotoxins, causing local
irritation, inflammation, and diarrhea. This form
produces sporadic and outbreak-associated bloody
diarrhea due to hemorrhagic colitis, which can be
life-threatening at age extremes.

Causes

sounds
H Blood and pus in infected stools
H Vomiting and anorexia
H Low-grade fever
H Signs of dehydration, especially in children
H Signs and symptoms of hyponatremia, hypokalemia,

hypomagnesemia, and hypocalcemia from electrolyte


losses
H Orthostatic hypotension
H Rapid, thready pulse
H Initially in infants, loose, watery stools that change
from yellow to green and contain little mucus or
blood
H Listlessness and irritability in infants

Test results
Laboratory
H Cultures growth of E. coli in a normally sterile location, including the bloodstream, cerebrospinal fluid, biliary tract, pleural fluid, or peritoneal cavity
suggest E. coli infection at that site.

H Some strains of E. coli that are part of normal GI flo-

ra but cause infection in immunocompromised patients


H Infection usually from nonindigenous strains
H Transmission directly from an infected person
H Ingestion of contaminated food or water or contact
with contaminated utensils
H Enterotoxigenic E. coli (major cause of diarrhea
among those who travel from industrialized to developing regions)
H Most common food source: ground beef

Treatment

Incidence

H Activity, as tolerated

H May be major cause of diarrheal illness in children

in United States
H Incidence highest among travelers returning from

abroad, especially Mexico (noninvasive form),


Southeast Asia (noninvasive form), and South America (invasive form)

General
H Contact enteric precautions
H Correction of fluid and electrolyte imbalances
H Initially, nothing by mouth
H Increased fluid intake (if appropriate)
H Avoidance of foods that cause diarrhea
H Small frequent meals until bowel function returns to

normal

Medications
H I.V. antibiotics such as cotrimoxazole

Nursing considerations

Common characteristics

Key outcomes

H Diarrhea (cardinal symptom)

The patient will:


H regain or maintain normal fluid and electrolyte balance
H have an elimination pattern that returns to normal
H show no further evidence of weight loss
H maintain normal cardiac output.

Complications
H Bacteremia
H Severe dehydration and life-threatening electrolyte

disturbances
H Acidosis
H Shock

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Nursing interventions
H Institute contact enteric precautions and use proper

hand-washing technique.
H Replace fluids and electrolytes, as needed.
H Clean the perianal area after each episode of diar-

rhea and apply skin protectant, as needed.


H Administer prescribed antibiotics.
H During epidemics, screen all facility personnel and

visitors for diarrhea, and prevent people with the disorder from having direct patient contact.

Monitoring
H Intake and output
H Stool volume measurement and presence of blood

and pus
H Serum electrolyte results
H Signs and symptoms of gram-negative septic shock
H Signs and symptoms of dehydration
H Vital signs
H GI status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H the need to avoid unbottled water, ice, unpeeled fruit,
and uncooked vegetables in other countries
H signs of dehydration and seeking prompt medical attention if these occur (if the patient will be cared for
at home).

Enterobacteriaceae infections

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Epididymitis
Overview
Description
H Infection of the epididymis (cordlike excretory duct

of the testis)
H One of most common infections of the male repro-

ductive tract

Pathophysiology
H Organisms enter the epididymis by the vas deferens

or lymphatics.
H Inflammation occurs.
H Other organs, such as the testes and prostate, may be

Incidence
H Usually affects males ages 19 to 40 or older than 60
H Affects 1 in 1,000 males anually
H Rare before puberty

Common characteristics
H Dull, aching groin pain
H Fever

Complications
H Orchitis (see Understanding orchitis)
H Sterility
H Abscess
H Atrophy
H Pyocele
H Infarction
H Sepsis

affected.

Causes
H Pyogenic organisms, such as staphylococci, Es-

cherichia coli, streptococci, chlamydia, Neisseria


gonorrhoeae, and Treponema pallidum
H Tuberculosis
H Sarcoidosis
H Brucellosis
H Leprosy
H Trauma
H Certain drugs such as amiodarone
H Obstruction

Risk factors
H Urinary tract infection
H Unprotected sex
H Prostatitis
H Trauma

Assessment
History
H Chills
H Fever
H Unilateral, dull, aching pain
H Pain radiating to spermatic cord, lower abdomen,

and flank
H Scrotal pain
H Dysuria, frequency, urgency, and urine retention
H Mild scrotal cellulitis
H Scrotal edema

Physical findings
H Erythema
H High fever
H Characteristic waddle (attempt to protect groin and

scrotum while walking)

Understanding orchitis
Orchitis, an infection of the testes, is a serious complication of epididymitis. It may also result from mumps,
which can lead to sterility or, less commonly, another systemic infection.

Signs and symptoms


Typical effects of orchitis include unilateral or bilateral tenderness and redness, sudden onset of pain, and swelling
of the scrotum and testes. Nausea and vomiting also occur. Sudden cessation of pain indicates testicular ischemia, which can cause permanent damage to one or
both testes. Hydrocele may also be present.

Treatment
Appropriate treatment consists of immediate antibiotic
therapy in bacterial infection or, in mumps orchitis, injection of 20 ml of lidocaine near the spermatic cord of the
affected testis, which may relieve swelling and pain. Severe orchitis may require surgery to incise and drain the
hydrocele and to improve testicular circulation. Other
treatments are similar to those for epididymitis.
To prevent mumps orchitis, suggest that prepubertal
males receive the mumps vaccine (or gamma globulin injection after contracting mumps).

266

Epididymitis

H Urethral discharge
H Prehn sign: elevation of hemiscrotum relieves pain
H Scrotal abscess

Test results
Laboratory
H Urinalysis shows an increased white blood cell
(WBC) count, indicating infection.
H Urine culture and sensitivity tests may show the
causative organism.
H Serum WBC count is greater than 10,000/l, indicating infection.
Imaging
H Ultrasonography shows an enlarged epididymis
(larger than 17 mm) and can rule out testicular torsion.

Treatment
General
H Scrotal elevation
H Ice bag to groin

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H Increased oral fluids


H Bed rest until condition improves
H Use of an athletic supporter until recovered

Medications
H Broad-spectrum antibiotics such as cefazolin
H Analgesics such as ibuprofen
H Antipyretics such as acetaminophen

Surgery
H Scrotal exploration for complications of acute epi-

didymitis
H Epididymectomy under local anesthesia, if disease is

refractory to antibiotic therapy

Nursing considerations
Key outcomes
The patient will:
H avoid or have minimal complications
H express feelings of increased comfort
H express concern about self-concept and body image
H express feelings about potential or actual changes in
sexual activity.

Nursing interventions
H Administer prescribed drugs.
H Apply ice packs for comfort.

Monitoring
H Signs of abscess formation
H Vital signs
H Pain control
H Intake and output

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible adverse effects
H the use of a scrotal support while sitting, standing, or
walking
H safer sex practices.

Epididymitis

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Life-threatening disorder

Epidural hematoma
Overview

Assessment
History
H Injury to head
H Headache
H Nausea, vomiting
H Change in mental status

Description

Physical findings

H Acceleration-deceleration or coup-contrecoup in-

H Head wound
H Neurologic signs based on the extent of bleeding

juries that disrupt normal nerve functions in bruised


area and cause intracranial bleeding

Pathophysiology
H Injury is directly beneath the site of impact when the

brain rebounds against the skull from the force of a


blow (a beating with a blunt instrument, for example), when the force of the blow drives the brain
against the opposite side of the skull, or when the
head is hurled forward and stopped abruptly (as in
an automobile accident when a drivers head strikes
the windshield).
H Brain continues moving and slaps against the skull
(acceleration), then rebounds (deceleration). Brain
may strike bony prominences inside the skull (especially the sphenoidal ridges), causing intracranial
hemorrhage or hematoma that may result in tentorial
herniation.

Causes
H Trauma
H Anticoagulation
H Thrombolysis
H Lumbar puncture
H Epidural anesthesia
H Coagulopathy or bleeding diathesis
H Hepatic disease with portal hypertension
H Vascular malformation
H Disk herniation
H Paget disease of bone
H Valsalvas maneuver
H Hypertension
H Intracerebral lesion

Incidence
H Rare in people younger than age 2 and older than

age 60
H Four times more common in males than in females

dilated pupils, weakness, sensory deficits, alterations


in reflexes, alterations in bladder or anal sphincter
tone
H Bradycardia and hypertension (with increased ICP)

Test results
Laboratory
H Coagulation studies show clotting abnormalities (if
cause is anticoagulation).
Imaging
H Computed tomography scan or magnetic resonance
imaging identifies abnormal masses or structural
shifts within the cranium.

Treatment
General
H Supportive: airway, breathing, circulation
H Wound care
H Head of the bed elevated 30 degrees with intracere-

bral injury
H Diet based on extent of injury
H Nothing by mouth if surgery is necessary
H Bed rest initially, then activity, as tolerated

Medications
H Vitamin K, fresh frozen plasma, platelets, or clotting

products (if coagulation studies are abnormal)


H Analgesics such as codeine
H Osmotic diuretics such as mannitol
H Anticonvulsants such as phenytoin
H Prophylactic antibiotics
H Corticosteroids such as dexamethasone

Surgery

Common characteristics

H Placement of burr holes


H Evacuation of the hematoma
H Craniotomy

H Brief loss of consciousness


H Headache
H Deteriorating mental status

Nursing considerations

Complications

Key outcomes

H Increased intracranial pressure (ICP)


H Seizures
H Respiratory depression and failure

The patient will:


H be hemodynamically stable
H recover or be rehabilitated from physical injuries to
the greatest extent possible

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H use support systems to assist with coping


H express a feeling of increased comfort and pain

relief.

Nursing interventions
H Provide appropriate wound care.
H Administer prescribed drugs.
H Provide emotional support.
H Institute seizure precautions.

Monitoring
H Vital signs
H Neurologic status
H Wound healing
H Seizure activity
H Respiratory status
H Cardiovascular status, including cardiac rhythm

Patient teaching
Be sure to cover:
H reporting changes in neurologic status
H avoiding aspirin as a pain treatment
H observing for cerebrospinal fluid drainage and signs
of infection.

Discharge planning
H Refer the patient to physical, occupational, and

speech therapy, as appropriate.


H Refer the patient to social service for extended ser-

vices, as appropriate.

Epidural hematoma

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Life-threatening disorder

Epiglottiditis
Overview
Description
H Acute inflammation of the epiglottis and surrounding

area
H Life-threatening emergency that rapidly causes edema and induration
H If untreated, results in complete airway obstruction
H Mortality 8% to 12%, typically in children

Pathophysiology

H Apprehension
H Irritability

Complications
H Airway obstruction
H Death
H Sepsis
H Vocal cord paralysis

Assessment
History
H Recent upper respiratory tract infection
H Sore throat
H Dysphagia
H Sudden onset of high fever

H An infection of the epiglottis and surrounding area

Physical findings

leads to intense inflammation of the supraglottic region.


H Swelling of the epiglottis, aryepiglottic folds, arytenoid cartilage, and ventricular bands leads to acute
airway obstruction.

H Stridor
H Red and inflamed throat
H Fever
H Drooling
H Pale or cyanotic skin
H Restlessness and irritability
H Nasal flaring
H Tendency to sit in tripod position with mouth open

Causes
H Viral infection, usually Haemophilus influenzae

type B

and tongue protruding

H Pneumococci or group A streptococci

Incidence
H Higher incidence in Blacks and Hispanics
H Most common in children ages 2 to 6 years
H Occurs in any season
H More common in males than females

Common characteristics
H Sore throat
H Dysphagia

Airway crisis
Epiglottiditis can progress to complete airway obstruction
within minutes. To prepare for this medical emergency,
keep these tips in mind:
H Watch for the inability to speak; weak, ineffective
cough; high-pitched sounds or no sounds while inhaling; increased difficulty breathing; and possible
cyanosis. These are warning signs of total airway obstruction and the need for an emergency tracheotomy.
H Keep the following equipment available at the patients
bedside in case of sudden, complete airway obstruction: a tracheotomy tray, endotracheal tubes, a handheld resuscitation bag, oxygen equipment, and a laryngoscope with blades of various sizes.
H Remember that using a tongue blade or throat culture
swab can initiate sudden, complete airway obstruction.
H Before examining the patients throat, request trained
personnel, such as an anesthesiologist, to stand by if
emergency airway insertion is needed.

270

Epiglottiditis

H Thick and muffled voice sounds


H Subcostal, suprasternal, and intercostal retractions

Test results
Laboratory
H Arterial blood gas (ABG) analysis may show hypoxia.
H Blood studies reveal elevated white blood cell count.
Imaging
H Lateral neck X-rays show an enlarged epiglottis and
distended hypopharynx.
Diagnostic procedures
H Direct laryngoscopy shows swollen, beefy-red
epiglottis.
Other
H Pulse oximetry may show decreased oxygen saturation.

Treatment
General
H Emergency hospitalization
H Humidification of airway
H Parenteral fluids
H Activity, as tolerated
H Endotracheal intubation and mechanical ventilation

Medications
H Parenteral antibiotics according to infective organism
H Corticosteroids such as hydrocortisone
H Oxygen therapy

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Surgery
H Possible tracheotomy

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain adequate fluid volume
H maintain a patent airway (see Airway crisis)
H use alternate means of communication.

Nursing interventions
H Administer prescribed drugs.
H Place the patient in a sitting position.
H Place the patient in a cool-mist tent.
H Encourage the parents to remain with their child.
H Offer reassurance and support.
H Ensure adequate fluid intake.
H Minimize external stimuli.
H Maintain a patent airway.

Monitoring
H Swallowing
H Vital signs
H Intake and output
H Respiratory status
H ABG results
H Pulse oximetry
H Signs and symptoms of secondary infection
H Signs and symptoms of dehydration
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prescribed medications and possible adverse effects
H when to call the practitioner
H humidification
H signs and symptoms of respiratory distress
H signs and symptoms of dehydration.

Discharge planning
H Refer the patient for H. influenzae b conjugate vac-

cine, preferably at age 2 months, if indicated.

Epiglottiditis

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Epilepsy

H Also known as seizure disorder

H Headache
H Mood changes
H Lethargy
H Myoclonic jerking
H Description of an aura
H Pungent smell
H GI distress
H Rising or sinking feeling in the stomach
H Dreamy feeling
H Unusual taste in the mouth
H Vision disturbance
H Incontinence

Pathophysiology

Physical findings

H Seizures are paroxysmal events involving abnormal

H Findings possibly normal while patient isnt having a

Overview
Description
H Neurologic condition characterized by recurrent

seizures
H Good seizure control in about 80% of patients with

strict adherence to prescribed treatment

electrical discharges of neurons in the brain and cell


membrane potential.
H On stimulation, the neuron fires, the discharge
spreads to surrounding cells, and stimulation continues to one side or both sides of the brain, resulting
in seizure activity.

Causes
H Idiopathic in half of cases

Nonidiopathic epilepsy
H Birth trauma
H Anoxia
H Perinatal infection
H Genetic abnormalities (tuberous sclerosis and
phenylketonuria)
H Perinatal injuries
H Metabolic abnormalities (hypoglycemia, pyridoxine
deficiency, hypoparathyroidism)
H Brain tumors or other space-occupying lesions
H Meningitis, encephalitis, or brain abscess
H Traumatic injury
H Ingestion of toxins, such as mercury, lead, or carbon
monoxide
H Stroke
H Apparent familial incidence in some seizure disorders

seizure and when the cause is idiopathic


H Findings related to underlying cause of the seizure

Test results
Laboratory
H Serum glucose and calcium study results rule out
other diagnoses.
Imaging
H Computed tomography scan and magnetic resonance
imaging may indicate abnormalities in internal structures.
H Skull radiography may show certain neoplasms within the brain substance or skull fractures.
H Brain scan may show malignant lesions when X-ray
findings are normal or questionable.
H Cerebral angiography may show cerebrovascular abnormalities, such as aneurysm or tumor.
Other
H EEG shows paroxysmal abnormalities. (A negative
EEG doesnt rule out epilepsy because paroxysmal
abnormalities occur intermittently.)

Treatment
General

Incidence

H Airway protection during seizure


H Vagus nerve stimulation by pacemaker (see Vagus

H Patients usually younger than age 20


H Affects both sexes
H First seizure usually during childhood or after age 50

H A detailed presurgical evaluation to characterize

nerve stimulation)

Complications

seizure type, frequency, site of onset, psychological


functioning, and degree of disability to select candidates for surgery in medically intractable patients
H No dietary restrictions
H Safety measures
H Activity, as tolerated

H Anoxia
H Traumatic injury

Medications

Common characteristics
H Recurring seizures

Assessment
History
H Seizure occurrence unpredictable and unrelated to

activities
H Precipitating factors or events possibly reported

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Epilepsy

H Anticonvulsants such as phenytoin


H Benzodiazepines such as lorazepam

Surgery
H Removal of a demonstrated focal lesion
H Correction of the underlying problem

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Vagus nerve stimulation


The vagus nerve stimulator is a Food and Drug Administrationapproved method to treat medically refractory
epilepsy. The stimulator device is about the size of a pacemaker and is surgically placed in a pocket under the skin
in the upper chest. Leadwires from the stimulator are tunneled under the skin to a neck incision where the vagus
nerve has been exposed. The electrode coils are then
placed around the nerve. The treating practitioner has a
computer, which can be used to alter the stimulation
parameters, thereby optimizing the treatment of seizures.
The device stimulates the vagus nerve for 30 seconds
every 5 minutes to prevent seizure occurrence. A magnet
over the area can activate the device to give extra, ondemand stimulation if the patient feels a seizure coming
on. Adverse effects are voice change, throat discomfort,
shortness of breath, and coughing and are usually experienced only when the device is on.

Discharge planning
H Refer the patient to the Epilepsy Foundation of Amer-

ica.
H Refer the patient to his states motor vehicle depart-

ment for information about a drivers license.

Nursing considerations
Key outcomes
The patient will:
H remain free from injury
H communicate understanding of the condition and
treatment regimen
H use support systems and develop adequate coping
H maintain usual participation in social situations and
activities.

Nursing interventions
H Institute seizure precautions.
H Prepare the patient for surgery, if indicated.
H Administer prescribed anticonvulsants.

Monitoring
H Neurologic status
H Response to anticonvulsants
H Vital signs
H Seizure activity
H Respiratory status
H Adverse drug reactions
H Associated injuries

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H maintaining a normal lifestyle
H compliance with the prescribed drug schedule
H adverse drug effects
H care during a seizure
H the importance of regular meals and checking with
the practitioner before dieting
H the importance of carrying a medical identification
card or wearing medical identification jewelry.

Epilepsy

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Erectile dysfunction
Overview
Description
H Inability to attain or maintain penile erection long

enough to complete intercourse


H Classified as primary or secondary:

Assessment
History
H Long-standing inability to achieve erection
H Sudden loss of erectile function
H Gradual decline in sexual function
H Medical disorders, drug therapy, or psychological

trauma
H Achievement of erection through masturbation but

Primary impotence: never achieving sufficient


erection
Secondary impotence: patient has achieved erection and completed intercourse in the past
H Also called impotence

Physical findings

Pathophysiology

DSM-IV-TR criteria

H A lack of autonomic signal or impairment of perfu-

H Diagnosis confirmed when patient meets criteria:

sion may interfere with arteriolar dilation due to inappropriate adrenergic stimulation.
H Premature collapse of the sacs of the corpus cavernosum occurs.
H Pelvic steal syndrome can cause loss of erection before ejaculation due to increased blood flow to pelvic
muscles.

Causes

not with a partner


H Anxious appearance
H Signs of depression

Persistent or recurrent partial or complete failure


to attain or maintain erection until completion of
sexual activity
Marked distress or interpersonal difficulty as a result of erectile dysfunction
Erectile dysfunction not better accounted for by
another Axis I disorder and not caused by a drug
or medical condition

H 80% of cases believed to have an organic cause, such

Test results

as vascular insufficiency and veno-occlusive dysfunction


H 20% of cases believed to be psychogenic in origin

Laboratory
H Hormone levels may be decreased.
Imaging
H Ultrasonography evaluates vascular function.
Diagnostic procedures
H Angiography evaluates vaso-occlusive disease.
Other
H Direct injection of prostaglandin E1 (alprostadil)
into the corpora evaluates the quality of erection.
H Nocturnal penile tumescence testing helps distinguish psychogenic impotence from organic impotence.

Risk factors
H Medication
H Pelvic injury or surgery
H Alcohol use
H Increasing age
H Smoking
H Obesity
H Hypertension
H Diabetes mellitus
H Scleroderma
H Renal failure
H Cancer treatment
H Stroke
H Multiple sclerosis
H Alzheimers disease
H Depression

Incidence
H Affects males of all age-groups, but incidence in-

creases with age

Common characteristics
H Depression
H Inability to obtain or maintain an erection

Complications
H Serious disruption of marital or other sexual rela-

tionships

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Erectile dysfunction

Treatment
General
H Sex therapy for psychogenic impotence
H Treatment of cause for organic impotence
H Psychological counseling
H Avoidance of alcohol
H External vacuum device

Medications
H Intracavernosal injection therapy
H Medicated Urethral System for Erections

intraurethral suppository
H Hormone replacement such as testosterone
H Phosphodiesterase type-5 inhibitors, such as silde-

nafil and vardenafil

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Surgery
H Surgically inserted inflatable or semirigid penile

prosthesis

Nursing considerations
Key outcomes
The patient will:
H acknowledge a problem in sexual function
H discuss feelings and perceptions about changes in
sexual performance
H develop and maintain a positive attitude toward sexuality and sexual performance.

Nursing interventions
H Encourage verbalization and provide support.
H As needed, refer the patient to a physician, nurse,

psychologist, social worker, or counselor trained in


sex therapy.
After penile prosthesis surgery
H Apply ice packs to the penis for 24 hours.
H Empty the drainage device when its full.
H If the patient has an inflatable prosthesis, provide instructions for use.

Monitoring
H Response to treatment
H Adverse effects of medication
H Complications
H Postoperative bleeding
H Postoperative infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the anatomy and physiology of the reproductive system and the human sexual response cycle
H the need to avoid intercourse until the incision heals,
usually 6 weeks after penile implant surgery
H signs of infection.

Discharge planning
H Refer the patient to support services.

Erectile dysfunction

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Life-threatening disorder

Erythroblastosis fetalis
Overview
Description
H Hemolytic disease of the fetus and neonate
H Stems from an incompatibility of fetal and maternal

blood
H Also known as hemolytic disease of the newborn

Pathophysiology
ABO incompatibility
H Each blood group has specific antigens on red blood
cells (RBCs) and specific antibodies in the serum.
H The maternal immune system forms antibodies
against fetal cells when blood groups differ.

What happens in Rh isoimmunization


Rh-negative woman before pregnancy

H This can cause hemolytic disease even if fetal ery-

throcytes dont escape into the maternal circulation


during pregnancy.
Rh incompatibility
H During her first pregnancy, an Rh-negative female becomes sensitized (during delivery or abortion) by exposure to Rh-positive fetal blood antigens inherited
from the father.
H A female may also become sensitized from receiving
blood transfusions with alien Rh antigens; from inadequate doses of Rh0(D) (RhoGAM); or from failure
to receive Rh0(D) after significant fetal-maternal
leakage during abruptio placentae (premature detachment of the placenta).
H A subsequent pregnancy with an Rh-positive fetus
provokes maternal production of agglutinating antibodies, which cross the placental barrier, attach to
Rh-positive cells in the fetus, and cause hemolysis
and anemia.
H To compensate, the fetal blood-forming organs step
up the production of RBCs, and erythroblasts (immature RBCs) appear in the fetal circulation.
H Extensive hemolysis releases more unconjugated
bilirubin than the liver can conjugate and excrete,
causing hyperbilirubinemia and hemolytic anemia.

Causes
H ABO incompatibility
H Rh isoimmunization (see What happens in Rh

isoimmunization)

Incidence
H Rh negativity 15% of Whites, 5% to7% of Blacks,
Pregnancy with Rh-positive fetus

rare in Asians
H About 4,000 cases per year
H ABO incompatibility frequently occurs during first

pregnancy; present in about 12% of pregnancies


Placental separation

Maternal sensitization to Rh-positive blood

Common characteristics
H Jaundice
H Anemia
H Hepatosplenomegaly
H Hydrops fetalis

Complications
Next pregnancy with Rh-positive fetus

Maternal anti-Rh antibodies enter fetal circulation

H Fetal death in utero


H Severe anemia
H Heart failure
H Kernicterus

Assessment
History

Anti-Rh antibody to fetal Rh-positive red blood cells (RBCs)

H Mother Rh-positive; father Rh-negative


H Antigen-antibody response developed during previ-

ous pregnancy
Hemolysis of fetal RBCs

H Blood transfusion
H Maternal history (for erythroblastotic stillbirths,

abortions, previously affected children, previous antiRh titers)

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Physical findings
H Pallor
H Edema
H Petechiae
H Bile-stained umbilical cord
H Yellow- or meconium-stained amniotic fluid
H Mild to moderate hepatosplenomegaly
H Pulmonary crackles
H Heart murmur
H Jaundice

Test results
Laboratory
H Paternal blood is typed for ABO and Rh.
H Amniotic fluid analysis shows increased bilirubin and
anti-Rh titers.
H Direct Coombs test of umbilical cord blood measures RBC (Rh-positive) antibodies in the neonate
(positive only when the mother is Rh negative and
the fetus is Rh positive).
H Cord hemoglobin level in neonate is less than 10 g,
indicating severe disease.
H Many nucleated peripheral RBCs are present.
Imaging
H Radiologic studies show edema and, in hydrops fetalis, the halo sign (edematous, elevated, subcutaneous
fat layers) and the Buddha position (fetuss legs are
crossed).

H maintain fluid balance within normal limits


H maintain normal temperature.

Nursing interventions
H Encourage expression of fears by parents concerning

possible complications of treatment.


H Promote normal parental bonding.
H Administer Rho(D) I.M., as ordered.

Monitoring
H Vital signs
H Cardiac rhythm and rate
H Temperature
H Respiratory status
H Transfusion complications
H Intake and output

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications, drug routes, and administration
H preventive measures for reoccurrence.

Discharge planning
H Encourage follow-up appointments.

Treatment
General
H Phototherapy (exposure to ultraviolet light to reduce

bilirubin levels)
H Intubation of neonate
H Removal of excess fluid
H Maintenance of body temperature

Medications
H Intrauterine-intraperitoneal transfusion (if amniotic

fluid analysis suggests the fetus is severely affected


and not mature enough to deliver)
H Exchange transfusion
H Albumin infusion
H Gamma globulin containing anti-Rh antibody
(Rho[D])

Surgery
H Planned delivery (usually 2 to 4 weeks before term

date, depending on maternal history, serologic test


results, and amniocentesis)

Nursing considerations
Key outcomes
The patient will:
H exhibit adequate ventilation
H remain hemodynamically stable

Erythroblastosis fetalis

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Esophageal cancer
Overview
Description
H Esophageal tumors usually fungating and infiltrating

and nearly always fatal


H Common sites of metastasis are liver and lungs
H Includes two types of malignant tumors: squamous
cell carcinoma and adenocarcinoma
H Grim prognosis (5-year survival rates occur in less
than 5% of cases; most patients die within 6 months
of diagnosis)

Pathophysiology
H Most esophageal cancers are poorly differentiated

squamous cell carcinomas, with 50% occurring in


the lower portion of the esophagus, 40% in the middle portion, and 10% in the upper or cervical esophagus.
H Adenocarcinomas occur less frequently and are contained to the lower third of the esophagus.
H The tumor partially constricts the lumen of the
esophagus.
H Regional metastasis occurs early by way of submucosal lymphatics, often fatally invading adjacent vital
intrathoracic organs. (If the patient survives primary
extension, the liver and lungs are the usual sites of
distant metastases; unusual metastasis sites include
the bone, kidneys, and adrenal glands.)

Causes
H Unknown

Risk factors
H Human papillomavirus
H Chronic irritation from heavy smoking
H Excessive use of alcohol
H Stasis-induced inflammation, as in achalasia or stric-

ture
H Previous head and neck tumors
H Nutritional deficiency, such as in untreated sprue and

Complications
H Direct invasion of adjoining structures
H Inability to control secretions
H Obstruction of the esophagus
H Loss of lower esophageal sphincter control (may re-

sult in aspiration pneumonia)

Assessment
History
H Feeling of fullness, pressure, indigestion, or subster-

nal burning
H Dysphagia and weight loss; the degree of dysphagia

varies, depending on the extent of disease


H Hoarseness
H Pain on swallowing or pain that radiates to the back
H Anorexia, vomiting, and regurgitation of food

Physical findings
H Chronic cough (possibly from aspiration)
H Cachexia and dehydration

Test results
Laboratory
H Complete blood count reveals anemia.
H Bleeding time may be prolonged.
Imaging
H X-rays of the esophagus, with barium swallow and
motility studies, are used to delineate structural and
filling defects and reduced peristalsis.
H Computed tomography scan may help to diagnose
and monitor esophageal lesions.
H Esophagogastroduodenoscopy shows tumor and permits biopsy.
Diagnostic procedures
H Esophagoscopy, punch and brush biopsies, and exfoliative cytologic tests confirm esophageal tumors.
H Bronchoscopy (usually performed after an esophagoscopy) may reveal tumor growth in the tracheobronchial tree.
H Endoscopic ultrasonography of the esophagus combines endoscopy and ultrasound technology to measure the depth of penetration of the tumor.

Plummer-Vinson syndrome
H Exposure to nitrosamines

Incidence
H Most common in males older than age 60
H Occurs worldwide, but most common in Japan, Rus-

sia, China, the Middle East, and the Transkei region


of South Africa

Common characteristics
H Dysphagia
H Weight loss
H Esophageal obstruction
H Acute pain
H Hoarseness, coughing
H Cachexia

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Esophageal cancer

Treatment
General
H Surgery and other treatments to relieve disease ef-

fects
H Palliative therapy used to keep esophagus open:

Dilatation of the esophagus


Laser therapy
Radiation therapy
Installation of prosthetic tubes (such as Celestins
tube)
H Liquid to soft diet, as tolerated
H High-calorie supplements

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Medications
H Chemotherapy such as fluorouracil
H Analgesics such as morphine

Surgery
H Radical surgery to excise tumor and resect esopha-

gus or stomach and esophagus


H Gastrostomy or jejunostomy

Other
H Endoscopic laser treatment and bipolar electrocoag-

ulation

Nursing considerations
Key outcomes
The patient will:
H maintain weight
H maintain fluid volumes within the normal range
H not aspirate
H express feelings of increased comfort and decreased
pain.

Nursing interventions
H Provide support and encourage verbalization.
H Position the patient with the head of the bed elevated

at least 30 degrees to prevent aspiration.


H Provide tube feedings, as ordered.
H Administer prescribed drugs.
H Encourage incentive spirometer use.

Monitoring
H Vital signs
H Hydration and nutritional status
H Electrolyte levels
H Intake and output
H Postoperative complications
H Swallowing ability
H Pain control
H Respiratory status

Patient teaching
Be sure to cover:
H the disease process, treatment, and postoperative
course
H dietary needs
H the need for rest between activities.

Discharge planning
H Arrange for home care follow-up after discharge.
H Refer the patient to the American Cancer Society.

Esophageal cancer

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Exophthalmos
Overview
Description

Assessment
History
H Vision changes
H Eye trauma

H Unilateral or bilateral bulging or protrusion of the

Physical findings

eyeballs or their apparent forward displacement


(with lid retraction)
H Also called proptosis

H Eye protrusion (see Detecting unilateral exophthal-

Pathophysiology
H Increase in volume within the fixed bony orbital con-

fines displaces the globular orbit anteriorly.

Causes
H Ophthalmic Graves disease
H Trauma
H Hemorrhage
H Varicosities
H Thrombosis
H Edema
H Infection
H Orbital cellulitis
H Panophthalmitis
H Tumors and neoplastic diseases
H Vasculitis

Incidence
H Occurs more often in females than in males
H Can occur at any age, but more common between

ages 30 and 50

Common characteristics
H Bulging eyeball (see Recognizing exophthalmos)
H Diplopia

Complications
H Vision changes

mos)
H Visible rim of the sclera
H Infrequent blinking
H Limited ocular movement
H Ocular tenderness

Test results
Laboratory
H Culture of discharge determines the infecting organism.
H Sensitivity testing indicates appropriate antibiotic
therapy.
Imaging
H Computed tomography scan detects swollen extraocular muscles or lesions within the orbit.
Diagnostic procedures
H Exophthalmometer readings confirm diagnosis by
showing the degree of anterior projection and asymmetry between the eyes. (Normal bar readings range
from 12 to 20 mm.)

Treatment
General
H Cold and warm compresses (trauma)
H Activity, as tolerated

Medications
H Antibiotics such as cefazolin to treat infection
H Antithyroid therapy such as propylthyrouracil for

Graves disease
H Corticosteroids such as dexamethasone to treat optic

neuropathy
H Eye lubricants

Surgery
Recognizing exophthalmos
This photo shows the characteristic forward protrusion of
the eyes from the orbit associated with exophthalmos.

H Orbital decompression (removal of the superior and

lateral orbital walls) if vision threatened, followed by


lid (blepharoplasty) and muscle surgery
H Surgical exploration of the orbit and excision of the
tumor

Nursing considerations
Key outcomes
The patient will:
H maintain functional eyesight
H understand cause and treatment of exopthalmus
H experience normal eye movement.

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Detecting unilateral exophthalmos


If one of the patients eyes seems more prominent than
the other, examine both eyes from above the patients
head. Look down across his face, gently draw his lids up,
and compare the relationship of the corneas to the lower
lids. Abnormal protrusion of one eye suggests unilateral
exophthalmos.
Dont perform this test if you suspect eye trauma.

Nursing interventions
H Administer prescribed drugs.
H Apply cold and warm compresses, as ordered, for

fracture or other trauma.


H Provide postoperative care.
H Provide emotional support.
H Protect the exposed cornea with lubricants to prevent

corneal drying.

Monitoring
H Response to therapy
H Visual acuity

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H eye care
H prescribed medications and possible adverse effects
H proper administration of eyedrops.

Discharge planning
H Encourage follow-up care.

Exophthalmos

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Failure to thrive
Overview

H Young or single mother without social supports


H Parents who are overly focused on career
H Caregivers with inadequate adaptive and social skills
H Depression (in parent or in adult patient with failure

to thrive)

Description

Incidence

H Failure to maintain weight (and sometimes height)

H Exact figures unknown


H 1% to 5% of children younger than age 2 years who

above the fifth percentile


H Deviation from established growth curve
H Three types
Organic
Nonorganic
Mixed
H Occurs in infants, children, adolescents, and adults

Pathophysiology

are admitted to hospitals


H An estimated 10% of children in primary care set-

tings
H Higher in children from families with medical and

psychosocial problems, those of low socioeconomic


status, and undeveloped countries
H Nonorganic form slightly higher in females

H Organic

Common characteristics

Calorie intake is less than required for nutritional


needs due to the presence of a physiologic disorder.
H Nonorganic
A complex dynamic exists between the caregiver
and the patient, including a decreased emotional
attachment.
Sufficient food is available, but the patient may be
fed an unusual or overly restricted diet.
H Mixed
This is a combination of organic and nonorganic
explanations.

H Absence of weight gain or weight loss


H Altered body posture
H Thin appearance
H Muscle wasting

Causes

Assessment

H Organic

Complications
H Disease susceptibility
H Growth retardation
H Developmental delays
H Impaired bonding
H Altered family relationships

Acute or chronic illness


Defects in major organ systems
Malabsorption syndrome
Endocrine deficiencies
Congenital heart defects
Fetal alcohol syndrome
Cystic fibrosis
Feeding difficulties
Long-term gastroenteritis
Premature birth
Dementia (in adults)
H Nonorganic
Psychological problem between patient and primary caregiver
Failure to bond
Dysfunctional parenting behaviors
Economic problems
Poor eating habits
Neglect or abuse
Parental ignorance about appropriate child care
H Mixed
Combination of organic and nonorganic causes

History

Risk factors

Physical findings

H Untreated medical conditions


H Low-birth-weight or premature infant
H Domestic violence
H Poverty

H Short stature
H Weight below fifth percentile
H Small head circumference
H Decreased skin-fold thickness

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Failure to thrive

H Prenatal

Use of drugs, alcohol, cigarettes


Diseases
H Labor and delivery
H Family medical and social history, including genetic
disorders
H Early neonatal
Birth weight
Initial weight loss
Birth defects
H Feeding
Nursing patterns of breast-fed infant; frequency
and time spent nursing
Maternal diet
Formula; type, amount, and frequency
Current eating patterns
H Psychosocial family problems
H Age at which the problem was first observed
H Previous growth information
H Medications
H Caregivers knowledge of appropriate care

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H Delayed motor function


H Developmental delays
H Neuromuscular weakness
H Gaze avoidance
H Minimal smiling
H Signs and symptoms of underlying disease
H Caregiver-patient interactions

Test results
Laboratory
H Complete blood count shows anemia.
H Stool analysis shows abnormal absorption or blood
indicating possible underlying disorder.
H Erythrocyte sedimentation rate is elevated, indicating
possible underlying disorder.
H Decreased electrolyte levels show poor nutritional intake.
H Blood lead level indicates lead poisoning.
H Thyroid test results indicate a hyperthyroid state.
H Elevated liver function study results point to an underlying disorder.
H Sweat-chloride test is done to rule out cystic fibrosis.
H Elevated glucose or glycosylated hemoglobin level indicates diabetes.
H Elevated blood urea nitrogen and creatinine levels indicate a kidney disorder.
X-rays
H GI studies may detect an organic cause.
H Bone X-rays establish bone age.
Other
H Short-term hospitalization determines whether disorder is nonorganic (child will gain weight).
H Developmental testing shows delays.

Nursing interventions
H Plot the childs growth and weight, as ordered.
H Assess for signs and symptoms of organic disease.
H Provide supportive environment.
H Encourage positive parenting.

Monitoring
H Signs and symptoms of complications
H Nutritional status
H Caregiver compliance with patients nutritional needs
H Weight

Patient teaching
Be sure to cover:
H the disorder and its treatment
H importance of maintaining the feeding schedule
H normal growth and development
H where and how to obtain help during crisis situations
H the proper care of infants and children.

Discharge planning
H Refer the patient to social worker and nutrition spe-

cialist, as appropriate.
H Refer the patient to community agencies, education

programs, stress management training, and support


groups, as indicated.

Treatment
General
H Underlying medical condition
H Liquid nutritional supplements
H High-calorie balanced diet

Medications
H Vitamins

Nursing considerations
Key outcomes
The patient will:
H receive appropriate medical care
H display age-appropriate nutrient intake
H demonstrate normal growth and development.
The caregiver will:
H verbalize understanding of the need for adequate nutrition
H demonstrate appropriate feeding techniques
H participate in developing a plan to promote parenting
skills, as appropriate
H seek psychological care and social assistance, as
needed.

Failure to thrive

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Fibrocystic breast
disease

Complications
H Benign condition usually not leading to breast cancer
H Makes it more challenging to do breast self-examina-

tions
H May make mammography more difficult to interpret;

Overview

early cancerous lesions possibly being overlooked

Description

Assessment

H Common, benign breast condition


H Changes in breast tissue related to hormonal cycles
H Typically resolves after menopause

History

Pathophysiology
H Hormonal variations during the menstrual cycle are

normal.
H Estrogen and progesterone cause breast tissue cells

to grow and multiply.


H Prolactin, growth factor, insulin, and thyroid hor-

mone also affect breast tissue.


H They stimulate growth of breast glandular tissue and
increase the activity of blood vessels, cell metabolism, and supporting tissue.
H Secretions produced by glandular cells may not be
completely reabsorbed, causing fibrosis.
H Secretions become trapped in glandular cells, forming cysts.

Causes
H Fluctuations in hormone levels during menstrual

cycle
H Changes typically right before menstruation
H Dietary factors, including consumption of caffeine,
excessive saturated fats, and salts
H Estradiol excess (can occur from taking oral contraceptives or other synthetic forms of estrogen)
H Diabetes or thyroid dysfunction

Risk factors

H Premenstrual breast tenderness and swelling that im-

proves after menstrual period


H Dull, heavy pain and tenderness
H Feeling of fullness in breasts
H Nipple sensation changes; possibly itching

Physical findings
H Dense, irregular, and bumpy cobblestone consis-

tency in breast tissue


H Usually found in outer upper quadrants and under-

side of the breast


H Can occur as an isolated lump, in clusters, or wide-

spread
H Free movement of lumps in breast tissue
H Lumps usually smooth, round, fluid-filled, and slight-

ly elastic; varying in texture and size


H Possibly severe breast tenderness and pain
H Non-bloody nipple discharge; varying from clear and

watery to sticky

Test results
Imaging
H Mammography, ultrasonography, or magnetic resonance imaging rule out malignancy.
Diagnostic procedures
H Needle aspiration and biopsy confirm benign condition.

H Hormone replacement therapy


H Nullipara
H Irregular menstrual cycles
H Family history of fibrocystic breast disease or breast

Treatment

cancer
H Dietary factors

H Dietary changes such as:

Incidence
H Present in about 30% of females in United States
H Most common between the ages of 30 and 50
H Estimated to affect over 60% of all females
H Rare in postmenopausal females

Common characteristics
H Tends to be symmetrical but can occur in only one

breast
H Lumps that move freely in the breast tissue and vary

in texture and size


H Breast tenderness and pain ranging from mild to se-

vere

284

Fibrocystic breast disease

General
Reducing or eliminating caffeine consumption
(controversial); includes chocolate, sodas, coffee,
and tea
Reducing sugar and salt intake
Limiting consumption of saturated fats
Avoiding commercially raised meats containing
hormones
Eating a high-fiber diet, including many plantbased foods, fruits and vegetables, beans and peas,
raw seeds and nuts, and whole grains
Increasing seafood consumption, such as salmon,
trout, and mackerel (high in omega-3 fatty acids
and iodine)
H Increased vitamin and mineral intake
Vitamin A to reduce the pain symptoms and the
size of the breast lesions

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Vitamin E to reduce pain and tenderness as well as


size of cysts
Magnesium supplement to help relieve cyclic
breast pain
Evening primrose oil, a source of the essential fatty acid, linoleic acid, and its chemical derivative,
gamma linolenic acid, to relieve symptoms and
possibly aid in correction of hormonal irregularities
H Application of heat to relieve pain
H Use of bra with good support to restrict motion
H Avoidance of estrogen supplementation

Medications
H Diuretics, such as furosemide, hydrochlorothiazide,

and triamterene
H Drugs that alter hormone levels, such as bromocrip-

tine, tamoxifen, and danazol


H Acetaminophen or nonsteroidal anti-inflammatory

drugs, such as ibuprofen and naproxen

Surgery
H Removal of lumps in the most severe cases

Nursing considerations
Key outcomes
The patient will:
H express feelings of comfort and reduced pain
H verbalize understanding of the disease and its treatment
H demonstrate correct procedure for performing
breast self-examination
H acknowledge need to contact practitioner if changes
occur in breasts.

Nursing interventions
H Provide pain medication, as ordered.
H Assist with breast examination.

Monitoring
H Pain signs and symptoms
H Changes in breast lumps

Patient teaching
Be sure to cover:
H the disease and its treatment
H the correct method of breast self-examination
H dietary modifications
H when to contact the practitioner.

Fibrocystic breast disease

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Fibromyalgia syndrome

H Sleep disturbances with frequent arousal and frag-

Overview

mented sleep or frequent waking throughout night


(patient unaware of arousals)
H Possible report of irritable bowel syndrome, tension
headaches, puffy hands, and paresthesia

Description

Physical findings

H A diffuse chronic pain syndrome


H Referred to as FMS
H Previously called fibrositis

H Tender points are elicited by applying a moderate

Pathophysiology

Test results

H Several theories describe FMS:

H Diagnostic testing in FMS not associated with an un-

Blood flow to the muscle is decreased (due to


poor muscle aerobic conditioning, rather than
other physiologic abnormalities).
Blood flow in the thalamus and caudate nucleus is
decreased, leading to a lowered pain threshold.
Endocrine dysfunction such as abnormal
pituitary-adrenal axis responses or abnormal
levels of the neurotransmitter serotonin in brain
centers affects pain and sleep.
The functioning of other pain-processing pathways
is abnormal.

Causes
H Unknown
H May be primary disorder or associated with underly-

ing disease
H Possible association with infection
H May be multifactorial and influenced by stress, physical conditioning, abnormal-quality sleep, neuroendocrine factors, psychiatric factors and, possibly,
hormonal factors (due to predominance in females)

Incidence
H Observed in up to 15% of patients seen in general

rheumatology practice and 5% of general medicine


clinic patients
H More common in females than in males
H May occur at almost any age; peak incidence among
those ages 20 to 60

Common characteristics
H Widespread pain and fatigue

Complications
H Pain
H Depression
H Sleep deprivation

Assessment
History

amount of pressure to a specific location. (See Tender points of fibromyalgia.)

derlying disease is generally negative for significant


abnormalities.

Treatment
General
H Massage therapy
H Ultrasound treatments
H Regular, low-impact aerobic exercise program such

as water aerobics
H Preexercise and postexercise stretching to minimize

injury

Medications
H Serotonin reuptake inhibitors such as paroxetine
H Tricyclic antidepressants, such as amitriptyline and

nortriptyline
H Nonsteroidal anti-inflammatory drugs such as

ibuprofen
H Magnesium supplements
H Lidocaine injections

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H attain the highest degree of mobility possible within
the confines of the disease
H express feelings about limitations
H express an increased sense of well-being.

Nursing interventions
H Administer prescribed drugs.
H Provide emotional support.
H Encourage the patient to perform regular stretching

exercises safely and effectively.


H Provide reassurance that FMS can be treated.

H Diffuse, dull, aching pain across neck and shoulders

Monitoring

and in lower back and proximal limbs


H Pain typically worse in morning, sometimes with stiffness; can be exacerbated by stress, lack of sleep,
weather changes, and inactivity

H Sensory disturbances
H Pain control
H Response to treatment
H Fatigue
H Depression

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Tender points of fibromyalgia


The patient with fibromyalgia syndrome may complain of specific areas of tenderness, which are shown in the
illustrations below.
Occiput:
Suboccipital muscle
insertions
Trapezius:
Midpoint of the upper
border
Supraspinatus:
Above the scapular spine
near the medial border

Gluteal:
Upper outer quadrants
of buttocks
Greater trochanter:
Posterior to the
trochanteric prominence

Low cervical:
Anterior aspects of the intertransverse spaces at C5 to C7

Second rib:
Second costochondral
junctions

Lateral epicondyle:
2 cm distal to the
epicondyles
Knee:
Medial fat pad proximal
to the joint line

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of exercise in maintaining muscle
conditioning, improving energy and, possibly, improving sleep quality
H the importance of taking the tricyclic antidepressant
dose 1 to 2 hours before bedtime, which can improve sleep benefits while reducing the morningafter effect
H the avoidance of decongestants and caffeine before
bedtime
H the need for a low-fat diet, high in complex carbohydrates, to decrease symptoms.

Discharge planning
H Refer the patient to appropriate counseling, as

needed.

Fibromyalgia syndrome

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Folliculitis,
furunculosis, and
carbunculosis

Carbunculosis
H Abscess of adjacent furuncles
H Develops more slowly

Pathophysiology
H The infecting organism invades the hair follicle.
H An inflammatory reaction within the hair follicle re-

sults. (See Hair follicles and bacterial infection.)

Overview

Causes

Description

H Bacterial infection, typically coagulase-positive

Folliculitis
H Superficial bacterial infection of hair follicles that
usually heals without scarring
H Characterized by the formation of pustules
H Typically a localized eruption
H Predilection for perifollicular (hairy) areas and flexural surfaces
H May occur in the beard region (sycosis barbae)
H May occur in the scalp or on extremities (follicular
impetigo)
H May lead to the development of furuncles (furunculosis) or carbuncles
H Prognosis depending on severity, patients physical
condition, and ability to resist infection
Furunculosis
H Deeper infections characterized by deeper, more tender, and erythematous nodules or boils
H Worsened by irritation, friction, or perspiration

Hair follicles and bacterial infection


The degree of hair follicle involvement in bacterial skin infection ranges from superficial folliculitis (erythema and a
pustule in a single follicle) to deep folliculitis (extensive
follicle involvement), to furunculosis (red, tender nodules
that surround follicles with a single draining point) and, finally, to carbunculosis (deep abscesses that involve several follicles with multiple draining points).
Superficial folliculitis
Deep folliculitis

Staphylococcus aureus
H Contamination from an infected wound elsewhere on

the body

Risk factors
H Poor personal hygiene
H Debilitation
H Immunosuppression
H Diabetes mellitus
H Occlusive agents or chemicals such as cosmetics
H Tight-fitting clothing
H Improper shaving technique
H Occlusive therapy, using steroids
H Obesity
H Chronic colonization of S. aureus in nares or per-

ineum

Incidence
Folliculitis
H Common infection
H Affects all ages
H Affects males more commonly than females
Furunculosis
H Uncommon in children unless immunocompromised
H Increased frequency after puberty
H More common in adolescents and young adults
H Affects males and females equally
Carbunculosis
H Not uncommon for several family members to be affected at the same time
H More common in patients with diabetes and in patients who are immunocompromised
H Affects males more commonly than females

Common characteristics

Furunculosis
Carbunculosis

H Pustules
H Pain
H Erythema

Complications
H Cellulitis
H Septicemia
H Hematogenous seeding to heart valves, joints, and

other organs
H Residual scarring

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Assessment
History
H Presence of risk factors
H Pain and erythema for several days or longer
H Malaise

Physical findings
Folliculitis
H Localized pustules, usually on the scalp or extremities
H Pustules possibly also in beard area or on eyelids
(styes)
Furunculosis
H Hard, painful, or fluctuant nodules usually on neck,
face, axillae, or buttocks
H If nodules enlarge and rupture, pus and necrotic material on the skin surface
H Erythema that may persist for days or weeks after
nodule rupture
Carbunculosis
H Fever
H Extremely painful, deep abscesses
H Abscesses drain through multiple openings onto the
skin surface
H Pain, tenderness, and edema around pustule sites
H Hard or fluctuant nodules under skin surface
H Localized lymphadenopathy

Test results
Laboratory
H Wound culture and sensitivity results show the infecting organism.
H Complete blood count may reveal leukocytosis.

H report feelings of increased comfort


H demonstrate understanding of proper skin care regi-

men.

Nursing interventions
H Perform wound care.
H Properly dispose of contaminated dressings.
H Follow standard precautions.
H Apply warm, moist compresses.
H Assist with general hygiene and comfort measures, as

needed.
H Administer prescribed pain medications and antibi-

otics.

Monitoring
H Adverse drug reactions
H Response to treatment
H Level of comfort
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H meticulous hand-washing technique
H good personal hygiene
H how to prevent the spread of the infection
H lesion care
H the prescribed medication and possible adverse effects.

Discharge planning
H Refer patients with recurrent furunculosis for a phys-

ical examination to assess for underlying diseases.

Treatment
General
H Thorough cleaning of infected area with soap and

water
H Avoidance of occlusive agents
H Application of warm, moist compresses

Medications
H Topical or systemic antibiotics, according to the iso-

lated organism

Surgery
H Possible incision and drainage in patients with furun-

culosis or carbunculosis

Nursing considerations
Key outcomes
The patient will:
H avoid or minimize complications
H exhibit improved or healed wounds or lesions

Folliculitis, furunculosis, and carbunculosis

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Fragile X syndrome
Overview
Description
H Most common inherited cause of mental retardation;

average IQ about 30 to 70
H Signs and symptoms of the syndrome apparent in

about 85% of males and 50% of females who inherit


the fragile X mental retardation-1 (FMR1) gene
H Distinct physical features, behavioral difficulties, and
cognitive impairment often found in postpubescent
males with syndrome
H More subtle symptoms usually found in females with
syndrome

Pathophysiology
H This X-linked condition doesnt follow a simple

X-linked inheritance pattern.


H Full mutation typically causes abnormal methylation

(methyl groups attach to components of the gene) of


FMR1.
H Methylation inhibits gene transcription and, thus,
protein production.
H The reduced or absent protein production leads to
the clinical features of fragile X syndrome.

Assessment
History
H Hyperactivity, speech difficulties, language delay, and

autistic-like behaviors
H Excessive shyness or social anxiety

Physical findings
H A prominent jaw and forehead
H Head circumference exceeding the 90th percentile
H Long, narrow face with long or large ears that may be

posteriorly rotated
H Hyperextension of the fingers
H Severe pectus excavatum
H Unusually large testes after puberty

Test results
Laboratory
H Positive genetic test, preferably deoxyribonucleic
acid analysis of blood or buccal samples, detects the
size of the cytosine-guanine-guanine repeat and the
methylation status of FMR1.
Imaging
H Echocardiography reveals a floppy mitral valve.

Treatment

Causes

General

H Genetic defect of the X-chromosome


H Well-defined mutation at a specific location on the

H Early intervention during preschool years


H Special education tailored to the childs needs
H Activity, as tolerated

FMR1 gene

Incidence

Medications

H Estimated to occur in about 1 in 1,500 males and

1 in 2,500 females
H Occurs in almost all races and ethnic populations

H Anticonvulsants such as phenytoin


H Antidepressants such as clomipramine
H Sedatives such as diazepam

Common characteristics

Surgery

Males
H Physical manifestations
H Hyperactivity, speech difficulties, language delay, and
autistic-like behaviors
Females
H Some degree of cognitive impairment, most commonly learning disabilities (math difficulties, language deficits, and attentional problems)
H Autistic-like features (rare)
H Excessive shyness or social anxiety

H Mitral valve repair

Complications

Nursing interventions

H Behavioral or learning difficulties


H Cognitive impairment
H Connective tissue abnormalities

H Administer prescribed drugs.


H Provide emotional support to the patient and his

Nursing considerations
Key outcomes
The patient will:
H function at the highest level possible
H be free from signs and symptoms of infection
H demonstrate effective learning related to potential.

family.
H Encourage appropriate activities for the patients

ability.
H Encourage the family to follow a routine schedule.

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Monitoring
H Language development
H Seizures
H Hyperactivity

Patient teaching
Be sure to cover:
H medication administration and possible adverse effects.

Discharge planning
H Refer the patient and family for genetic counseling.
H Refer the family to a support group.
H Advocate for special education services and individu-

alized speech, language, and occupational therapy


services during the patients schooling.

Fragile X syndrome

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Frostbite
Overview
Description
H Damage to skin and other tissues caused by freezing
H Caused by sustained exposure to cold temperatures

or to certain chemicals without proper protection


H Signs or symptoms persisting longer than 30 minutes

after start of rewarming


H Classified by degree of injury as first-, second-,

third-, or fourth-degree
H Frost nip: less severe cold exposure with complete

resolution within 30 minutes of starting to rewarm

Pathophysiology
H Loss of body heat causes a fall in tissue temperature.
H Tissue hypoxia and acidosis occurs as blood vessels

narrow in response to cold.


H Tissues begin to freeze; ice crystals form and force

water out of cells, causing cell death.


H Blood no longer flows through the capillaries, and

Common characteristics
H First-degree frostbite characterized by white or blue

skin, edema, waxy appearance, spongy texture of the


tissue, and sensory deficits
H Second-degree frostbite characterized by white,
blotchy, or blue skin; edema; and formation of vesicles filled with clear or milky fluid (form within 24
hours of injury)
H Third-degree frostbite characterized by presence of
blood-filled vesicles, which progress to a black eschar
H Fourth-degree frostbite characterized by fullthickness damage affecting muscles, tendons, and
bone, with resultant tissue loss

Complications
H Wound-related sepsis
H Gangrene
H Compartment syndrome
H Loss of affected part; amputation
H Increased sensitivity to cold
H Pain with use of the affected area
H Altered sensation in the affected area, possibly lasting

throughout life

clots form in the arterioles and venules from increased blood viscosity.
H Inflammatory mediators are released, causing further
damage.
H Extent of permanent injury depends on duration of
frozen tissue.

H Tetanus
H Osteoporosis
H Muscle atrophy
H Phantom pain of amputated extremities
H Death, when associated with hypothermia or sepsis

Causes

Assessment

H Exposure to cold temperatures, without proper pro-

tection
H Time for this to occur affected by air temperature,

wind speed, and moisture (in the air as well as wet


clothing and skin)
H Chemical exposure, such as to dry ice or highly compressed gases

Risk factors
H Outdoor winter activities
H Workers in cold environments
H Homelessness
H Alcohol consumption and smoking
H Fatigue
H Inadequate, tight, or wet clothing
H Previous cold injury
H Young children and older adults
H Diseases, including diabetes, atherosclerosis, and

thyroid disease
H Infections
H Medications such as beta-adrenergic blockers

Incidence
H Hands or feet affected in 90% of injuries
H Ears, nose, chin, cheeks, or penis affected in remain-

ing 10% of injuries


H Males affected more often than females

292

Frostbite

History
H Prolonged exposure to cold or exposure without ad-

equate protection
H Numbness in affected part
H Feeling of clumsiness and confusion
H Possible shivering
H Pain, burning, or throbbing on rewarming

Physical findings
H Skin

Color: White, blotchy, or blue; purple in large affected area


Waxy appearance
Stiff to touch
H Spongy feeling to underlying tissue
H Edema
H Vesicles filled with clear or milky fluid or blood
H Joint stiffness and pain
H Sweating

Test results
Laboratory
H Complete blood count may show hemoconcentration.
Imaging
H X-rays determine bone involvement.
H Angiography determines extent of blood vessel damage.

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H Thermography measures blood flow.


H Technetium-99 pertechnetate scintigraphy deter-

mines extent of deep-tissue injury and assesses the


response of damaged tissue to therapy.

Treatment
General
H Replacement of wet or tight clothing with dry, loose

clothing
H Protection of injured area
H Rewarming affected part for 20 to 40 minutes in wa-

ter at 100 to 108 F (37.8 to 42.2 C) to halt ice


crystal formation and dilate blood vessels
H Hydration with warm fluids
H High-protein, high-calorie diet
H Physical therapy
H Acupuncture and homeopathic and botanical therapies
H Hyperbaric therapy

Medications
H Tetanus toxoid immunization and appropriate antibi-

otics, if needed, with open injuries


H Nonsteroidal anti-inflammatory drugs, such as

ibuprofen and naproxen, for inflammation and pain


H Opioids, such as morphine, meperidine, and
propoxyphene, for severe pain
H Vasodilators, such as nifedipine, to increase perfusion
H Aloe vera cream to debride blisters and prevent further trauma
H Anticlotting agent, tissue plasminogen activator, to reduce the risk of amputation (experimental)

H Assist with rewarming and other treatments, as or-

dered.
H Maintain aseptic technique when changing dressings.
H Provide pain medication, as ordered.

Monitoring
H Wound condition
H Pain level
H Capillary refill time
H Sensation
H Peripheral pulses
H Hydration status

Patient teaching
Be sure to cover:
H the disorder and its treatment
H possible long-term effects
H need for smoking or alcohol cessation, if indicated
H increased susceptibility to cold
H how to prevent future cold injuries. (See Preventing
frostbite.)

Discharge planning
H Refer the patient to a social service agency, if indi-

cated.

Surgery
H Debridement or fasciotomy, if indicated
H Amputation, as needed (necessity usually unknown

for at least 1 month)

Nursing considerations
Key outcomes
The patient will:
H express understanding of the injury and how to prevent future occurrences
H experience no further injury from frostbite
H remain free from infection
H express feelings of increased comfort and reduced
pain
H show progressive wound healing
H maintain optimal perfusion to affected areas
H demonstrate effective coping.

Nursing interventions
H Provide a bed cradle to keep covers off lower ex-

tremities, if indicated.

Prevention

Preventing frostbite
H Anticipate poor weather, and dress appropriately.
H Be aware that wet and windy conditions worsen the
chill factor and increase the risk of cold injury.
H Limit exposure time.
H Wear layers of loose-fitting clothing. Mittens provide
more warmth than gloves.
H Wear head, face, and ear coverings at all times.
H Wear two pairs of socks. An outer layer of wool socks
worn over synthetic socks that wick moisture away
from the skin provides the best insulation.
H Wear waterproof shoes or boots.
H Avoid smoking cigarettes and drinking alcohol, which
impair circulation.
H Remove metal jewelry, which conducts cold.

Frostbite

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Gas gangrene

H Most common in extremities and abdominal wounds;

less common in uterus

Common characteristics

Overview

H Sudden, severe pain at wound site

Description

Complications

H Rare condition caused by local infection with anaero-

H Renal failure
H Hypotension and shock
H Hemolytic anemia
H Tissue death requiring amputation of the affected

bic, spore-forming, gram-positive, rod-shaped bacillus Clostridium perfringens or another clostridial


species
H Occurs in devitalized tissues and results from compromised arterial circulation

body part

Assessment

Pathophysiology
H Incubation is 1 to 4 days but can vary from 3 hours

to 6 weeks or longer.
H C. perfringens invades soft tissues, producing

thrombosis of regional blood vessels, tissue necrosis,


and localized edema. (See Effects of Clostridium
perfringens.)
H Necrosis releases carbon dioxide and hydrogen subcutaneously, producing interstitial gas bubbles.

History
H Recent surgery (within 72 hours)
H Traumatic injury
H Septic abortion
H Delivery

Physical findings
H Normothermia, followed by a moderate increase,

Causes

usually not above 101 F (38.3 C)

H C. perfringens
H Transmission when the organism enters the body

during trauma or surgery

H Toxemia (hypotension, tachycardia, tachypnea)


H Localized swelling and discoloration (often dusky

brown or reddish)
H Bullae and tissue necrosis
H Dark red or black necrotic muscle
H Foul-smelling, watery, or frothy discharge
H Subcutaneous emphysema (hallmark of gas gan-

Risk factors
H Diabetes mellitus

Incidence

grene)

H Rare, although more than 30% of deep wounds in-

fected with clostridia

H In later stages, altered level of consciousness that

may deteriorate to delirium and coma

H Most common in deep wounds, especially when tis-

sue necrosis further reduces oxygen supply

Effects of Clostridium perfringens


As C. perfringens grows in a closed wound, it destroys
cell walls and causes hemolysis, local tissue death, and
increasing edema.

C. perfringens
and necrotic
muscle in
closed wound

Test results
Laboratory
H Anaerobic cultures of wound drainage disclose
C. perfringens.
H Gram stain of wound drainage shows large,
gram-positive, rod-shaped bacteria.
H Blood studies show leukocytosis and, later,
hemolysis.
Imaging
H X-rays reveal gas in tissues.

Treatment

Increased
edema

General
Destruction
of cell walls

Edema

H Hyperbaric oxygen therapy


H Adequate hydration
H Nothing by mouth if surgery is planned
H Bed rest until recovery begins

Medications
Local
tissue
death

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Gas gangrene

Hemolysis

H I.V. antibiotics such as vancomycin


H Analgesics such as morphine

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Surgery
H Immediate wide surgical excision of all affected tis-

sues and necrotic muscle in myositis


H Amputation of the affected part

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H have skin that remains warm, dry, and intact
H maintain collateral circulation
H express feelings of increased comfort and relief from
pain.

Nursing interventions
H Administer prescribed analgesics.
H Prepare for surgery, if indicated.
H Provide adequate fluid replacement.
H Maintain the airway and ventilation.
H Provide appropriate skin care and meticulous wound

care; place the patient on an air mattress or an


air-fluidized bed.
H Encourage verbalization and provide support.

Monitoring
H Vital signs
H Intake and output
H Pulmonary and cardiac status
H Wound site
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to report severe pain at the wound site immediately
H the need to report foul odor or drainage from the
wound site.

Discharge planning
H After recovery, refer the patient for physical rehabili-

tation, as necessary.
H After extensive surgery, such as amputation, refer the

patient for psychological support, as necessary.

Gas gangrene

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Gastric cancer

H Vague feeling of fullness, heaviness, and moderate

abdominal distention after meals

Overview

H Weight loss, nausea, vomiting


H Weakness and fatigue
H Dysphagia

Description

Physical findings

H Cancer of the GI tract classified according to gross

H Abdominal distention
H Palpable mass
H Palpable lymph nodes, especially the supraclavicular

appearance (polypoid, ulcerating, ulcerating and infiltrating, or diffuse)


H Prognosis depending on stage of disease at time of
diagnosis (5-year survival rate about 15%)

Pathophysiology

and axillary nodes


H Other assessment findings that depend on extent of

disease and location of metastasis

H The most commonly affected areas of the stomach

Test results

are the pylorus and antrum.


H The remaining areas affected in order of descending
frequency are the lesser curvature of the stomach,
the cardia, the body of the stomach, and the greater
curvature of the stomach.
H Rapid metastasis occurs to the regional lymph nodes,
omentum, liver, and lungs.

Laboratory
H Complete blood count may show iron deficiency anemia.
H Liver function studies may be elevated with metastatic
spread of tumor to liver.
H Carcinoembryonic antigen radioimmunoassay may
be elevated.
Imaging
H Barium X-rays of the GI tract with fluoroscopy show
changes that suggest gastric cancer, including a tumor or filling defect in the outline of the stomach,
loss of flexibility and distensibility, and abnormal gastric mucosa with or without ulceration.
Diagnostic procedures
H Gastroscopy with fiber-optic endoscope helps rule
out other diffuse gastric mucosal abnormalities by allowing direct visualization.
H Gastroscopic biopsy permits evaluation of gastric
mucosal lesions.
Other
H Gastric acid stimulation test discloses whether the
stomach secretes acid properly.

Causes
H Unknown

Risk factors
H Gastritis with gastric atrophy
H Type A blood (10% increased risk)
H Family history of gastric cancer
H Smoked foods, pickled vegetables, and salted fish

and meat
H High alcohol consumption
H Smoking
H Helicobacter pylori infection

Incidence
H Common worldwide in all races
H Incidence greater in males older than age 40
H Mortality high in Japan, Iceland, Chile, and Austria
H Incidence decreased 50% over the past 25 years;

death rate now one-third that of 30 years ago

Common characteristics
H Feeling of fullness
H Abdominal distention
H Back, epigastric, or retrosternal pain

Complications
H Malnutrition
H GI obstruction
H Iron deficiency anemia
H Metastasis

Assessment
History
H Back, epigastric, or retrosternal pain not relieved

with nonprescription medications

296

Gastric cancer

Treatment
General
H Radiation therapy combined with chemotherapy (not

indicated preoperatively because it may damage viscera and impede healing)


H Diet based on the extent of the disorder and clinical
condition
H Parenteral feeding with an inability to consume adequate calories

Medications
H Chemotherapy, such as fluorouracil and doxorubicin
H Antiemetics, such as aprepitant and dolasetron
H Opioid analgesics such as morphine
H Antibiotics such as tetracycline

Surgery
H Excision of lesion with appropriate margins (in more

than one-third of patients)


H Gastroduodenostomy
H Gastrojejunostomy

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H Partial gastric resection


H Total gastrectomy (If metastasis has occurred, omen-

tum and spleen may have to be removed.)

Nursing considerations
Key outcomes
The patient will:
H maintain weight
H express feelings of increased energy
H report feeling less tension and pain
H maintain skin integrity.

Nursing interventions
H Encourage coughing, deep breathing, and incentive

spirometer use.
H Provide a high-protein, high-calorie diet with dietary

supplements.
H Administer prescribed drugs.
H Provide parenteral nutrition, as appropriate.
H After surgery, provide supportive care.
H Elevate the head of the bed at least 30 degrees.

Monitoring
H Pain control
H Vital signs
H Nutritional status
H Nasogastric tube function and drainage
H Wound site
H Postoperative complications
H Effects of medication
H Intake and output
H Cardiovascular status
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the dietary plan
H effective pulmonary toileting
H avoidance of crowds and people with known infection
H relaxation techniques
H medication administration, dosage, and possible adverse effects.

Discharge planning
H Refer the patient and his family to support services.
H Refer the patient for home services, as necessary.
H Refer the patient for physical or occupational thera-

py, as necessary.

Gastric cancer

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Gastritis
Overview
Description
H Inflammation of the gastric mucosa
H May be acute or chronic
H Most common stomach disorder (acute)

Pathophysiology
Acute gastritis
H The protective mucosal layer is altered.
H Acid secretion produces mucosal reddening, edema,
and superficial surface erosion.
Chronic gastritis
H Progressive thinning and degeneration of gastric mucosa occur.

Causes
Acute gastritis
H Chronic ingestion of irritating foods and alcohol
H Drugs, such as aspirin and other nonsteroidal
anti-inflammatory drugs (in large doses), cytotoxic
agents, caffeine, corticosteroids, antimetabolites,
phenylbutazone, and indomethacin
H Ingested poisons, especially dichloro-diphenyltrichloroethane (DDT), ammonia, mercury, carbon
tetrachloride, or corrosive substances
H Endotoxins released from infecting bacteria, such as
staphylococci, Escherichia coli, and salmonella
H Complication of acute illness
Chronic gastritis
H Recurring exposure to irritating substances, such as
drugs, alcohol, cigarette smoke, and environmental
agents
H Pernicious anemia, renal disease, or diabetes mellitus
H Helicobacter pylori infection (common cause of
nonerosive gastritis)

Risk factors
H Age older than 60
H Exposure to toxic substances
H Hemodynamic disorder

Incidence
H May occur at any age; increased incidence of H. py-

lori in people older than age 60


H Occurs equally in both sexes
H Acute gastritis in 8 of 1,000 people; chronic gastritis

in 2 of 10,000 people

Common characteristics
H Abdominal pain
H Indigestion

Complications
H Hemorrhage
H Obstruction

298

Gastritis

H Perforation
H Peritonitis
H Gastric cancer

Assessment
History
H Exposure to one or more causative agents
H Rapid onset of symptoms (acute gastritis)
H Epigastric discomfort
H Indigestion
H Cramping
H Anorexia
H Nausea, hematemesis, and vomiting
H Coffee-ground emesis or melena (if GI bleeding is

present)

Physical findings
H Possible normal appearance
H Grimacing
H Restlessness
H Pallor
H Tachycardia
H Hypotension
H Abdominal distention, tenderness, and guarding
H Normoactive to hyperactive bowel sounds

Test results
Laboratory
H Occult blood is found in vomitus or stools (or both)
if the patient has gastric bleeding.
H Hemoglobin (Hb) level and hematocrit are decreased.
H Urea breath test shows H. pylori.
Diagnostic procedures
H Upper GI endoscopy reveals gastritis when its performed within 24 hours of bleeding.
H Biopsy reveals inflammatory process.

Treatment
General
H Elimination of cause
H For massive bleeding:

Blood transfusion
Iced saline lavage
Angiography with vasopressin
H Nothing by mouth if bleeding occurs
H Elimination of irritating foods
H Activity, as tolerated (encourage mobilization)

Medications
H Histamine antagonists, such as famotidine, ranitidine,

and cimetidine
H Proton pump inhibitors such as pantoprazole
H Prostaglandins such as misoprostol
H Vitamin B12
H Antibiotic therapy, according to infective agent

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Surgery
H When conservative treatment fails
H Vagotomy, pyloroplasty
H Partial or total gastrectomy (rarely)

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H maintain normal fluid volume
H maintain weight
H express concerns about current condition
H verbalize understanding of the disorder and treatment regimen.

Nursing interventions
H Provide physical and emotional support.
H Administer prescribed drugs and I.V. fluids.
H Assist the patient with diet modification.
H If surgery is necessary, prepare the patient preopera-

tively and provide appropriate postoperative care.


H Consult a dietitian, as necessary.

Monitoring
H Vital signs
H Fluid intake and output
H Electrolyte and Hb levels
H Returning symptoms as food is reintroduced
H Response to medication
H Pain control
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H lifestyle and diet modifications
H preoperative teaching if surgery is necessary
H stress-reduction techniques
H medication administration and possible adverse effects.

Discharge planning
H Refer the patient to a smoking-cessation program, if

indicated.
H Refer the patient to an alcohol treatment program, if

indicated.

Gastritis

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Gastroenteritis

H Viruses, such as adenoviruses, echoviruses, and cox-

sackieviruses
H Ingestion of toxins, such as poisonous plants and

Overview
Description
H Self-limiting inflammation of the stomach and small

intestine
H Intestinal flu, travelers diarrhea, viral enteritis, and

food poisoning

Pathophysiology

toadstools
H Drug reactions from antibiotics
H Food allergens
H Enzyme deficiencies

Risk factors
H Consumption of improperly prepared food or conta-

minated water
H Travel or residence in areas of poor sanitation

H The bowel reacts to the various causes of gastroen-

Incidence

teritis with increased luminal fluid that cant be absorbed.


H This results in abdominal pain, vomiting, severe diarrhea (primarily), and secondary depletion of intracellular fluid.
H Dehydration and electrolyte loss occur.

H Occurs at any age


H Major cause of morbidity and mortality in underde-

Causes

H Can be life-threatening in elderly and debilitated pa-

veloped nations
H Ranks second to common cold as cause of lost work

time in the United States


H Fifth most common cause of death among young

children

H Bacteria, such as Staphylococcus aureus, Salmonel-

la, Shigella, Clostridium botulinum, Clostridium


perfringens, and Escherichia coli
H Amoebas, especially Entamoeba histolytica
H Parasites, such as Ascaris, Enterobius, and
Trichinella spiralis
Prevention

Preventing travelers diarrhea


If the patient travels, especially to developing nations, discuss precautions that he can take to reduce his chances
of getting travelers diarrhea. Explain that travelers diarrhea is caused by inadequate sanitation and occurs after
bacteria-contaminated food or water is ingested. These
organisms attach to the lining of the small intestine,
where they release a toxin that causes diarrhea and
cramps. To minimize this risk, advise him to:
H drink water (or brush his teeth with water) only if its
chlorinated or bottled (Chlorination protects the water
supply from bacterial contaminants such as Escherichia coli.)
H avoid beverages in glasses that may have been washed
in contaminated water
H refuse ice cubes that may have been made from contaminated water
H drink only beverages made with boiled water, such as
coffee and tea, or those in bottles or cans
H sanitize impure water by adding 2% tincture of iodine
(5 drops/L of clear water, 10 drops/L of cloudy water)
or by adding liquid laundry bleach (about 2 drops/L of
clear water; 4 drops/L of cloudy water)
H avoid uncooked vegetables, unpeeled fresh fruits, salads, unpasteurized milk, and other dairy products
H beware of foods offered by street vendors.
If travelers diarrhea occurs despite precautions, bismuth subsalicylate, diphenoxylate with atropine, or loperamide can be used to relieve symptoms.

tients

Common characteristics
H Diarrhea
H Nausea and vomiting

Complications
H Severe dehydration
H Electrolyte imbalance

Assessment
History
H Acute onset of diarrhea
H Abdominal pain and discomfort
H Nausea, vomiting
H Malaise and fatigue
H Exposure to contaminated food
H Recent travel (see Preventing travelers diarrhea)

Physical findings
H Slight abdominal distention
H Poor skin turgor (with dehydration)
H Hyperactive bowel sounds
H Decreased blood pressure

Test results
Laboratory
H Gram stain, stool culture (by direct rectal swab), or
blood culture shows the causative bacteria.

Treatment
General
H Supportive treatment for nausea, vomiting, and diar-

rhea

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Gastroenteritis

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H Antidiarrheals generally not given; they can prolong

the infection
H Rehydration
H Initially, clear liquids as tolerated
H Electrolyte solutions
H Avoidance of milk products
H Activity, as tolerated (encourage mobilization)

Medications
H Antiemetics such as prochlorperazine
H Antibiotics, according to the infective organism
H I.V. fluids

Nursing considerations
Key outcomes
The patient will:
H maintain weight without further loss
H express feelings of increased comfort
H maintain adequate fluid volume
H maintain normal vital signs.

Nursing interventions
H Allow uninterrupted rest periods.
H Replace lost fluids and electrolytes through diet or

I.V. fluids.
H Administer prescribed drugs.

Monitoring
H Intake and output
H Vital signs
H Signs of dehydration
H Electrolytes
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary modifications
H medication administration, dosage, and possible adverse effects
H preventive measures
H how to perform warm sitz baths three times per day
to relieve anal irritation.

Gastroenteritis

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Gastroesophageal reflux
disease
Overview
Description

Assessment
History
H Minimal or no symptoms in one-third of patients
H Heartburn that typically occurs 112 to 2 hours after

eating
H Heartburn that worsens with vigorous exercise,

into the esophagus and past the lower esophageal


sphincter (LES), without associated belching or vomiting
H Reflux of gastric acid, causing acute epigastric pain,
usually after a meal
H Popularly called heartburn
H Also called GERD

bending, lying down, wearing tight clothing, coughing, constipation, and obesity
H Reported relief by using antacids or sitting upright
H Regurgitation without associated nausea or belching
H Feeling of fluid accumulation in the throat with a
sour or bitter taste
H Chronic pain radiating to the neck, jaws, and arms
that may mimic angina pectoris
H Nocturnal hypersalivation and wheezing

Pathophysiology

Physical findings

H Reflux occurs when LES pressure is deficient or pres-

H Odynophagia (sharp substernal pain on swallowing),

H Backflow of gastric or duodenal contents, or both,

sure in the stomach exceeds LES pressure. The LES


relaxes, and gastric contents regurgitate into the
esophagus.
H The degree of mucosal injury is based on the amount
and concentration of refluxed gastric acid, proteolytic enzymes, and bile acids.

Causes
H Pyloric surgery (alteration or removal of the py-

lorus), which allows reflux of bile or pancreatic juice


H Hiatal hernia with incompetent sphincter
H Condition or position that increases intra-abdominal

pressure

Risk factors
H Any agent that lowers LES pressure: acidic and fatty

food, alcohol, cigarettes, anticholinergics (atropine,


belladonna, propantheline) or other drugs (morphine, diazepam, calcium channel blockers, meperidine)
H Nasogastric (NG) intubation for longer than 4 days

possibly followed by a dull substernal ache


H Bright red or dark brown blood in vomitus
H Laryngitis and morning hoarseness
H Chronic cough

Test results
Imaging
H Barium swallow with fluoroscopy shows evidence of
recurrent reflux.
Diagnostic procedures
H Esophageal acidity test reveals degree of gastroesophageal reflux.
H Gastroesophageal scintillation testing shows reflux.
H Esophageal manometry reveals abnormal LES pressure and sphincter incompetence.
H Acid perfusion (Bernstein) test confirms esophagitis.
H Esophagoscopy and biopsy confirm pathologic
changes in the mucosa.

Treatment

Incidence

General

H Affects about 7 million U.S. residents


H Affects all ethnic groups and socioeconomic classes
H Most common in people ages 45 to 64

H Modification of lifestyle
H Positional therapy
H Removal of cause
H Weight reduction, if appropriate
H Avoidance of dietary causes
H Avoidance of eating 2 hours before sleep (see Fac-

Common characteristics
H Epigastric pain, usually after a meal or when lying

down

Complications
H Reflux esophagitis
H Esophageal stricture
H Esophageal ulcer
H Barretts esophagus (metaplasia and possible in-

creased risk of neoplasm)


H Anemia from esophageal bleeding
H Reflux aspiration leading to chronic pulmonary disease

302

Gastroesophageal reflux disease

tors affecting LES pressure)


H Parenteral nutrition or tube feedings
H No activity restrictions for medical treatment
H Lifting restrictions for surgical treatment

Medications
H Histamine-2 receptor antagonists, such as cimeta-

dine, ranitidine, and famotidine


H Proton pump inhibitors, such as esomeprazole, lan-

soprazole, pantoprazole, and rabeprazole

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Factors affecting LES pressure


Various dietary and lifestyle elements can increase or decrease lower esophageal sphincter (LES) pressure. Take
these into account as you plan the patients treatment program.

What increases LES pressure


H Protein
H Carbohydrates
H Nonfat milk
H Low-dose ethanol

What decreases LES pressure


H Fat
H Whole milk
H Orange juice
H Tomatoes
H Antiflatulent (simethicone)
H Chocolate
H High-dose ethanol
H Cigarette smoking
H Lying on right or left side
H Sitting

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H causes of gastroesophageal reflux
H prescribed antireflux regimen of medication, diet,
and positional therapy
H developing a dietary plan
H the need to identify situations or activities that increase intra-abdominal pressure
H the need to refrain from using substances that reduce
sphincter control
H signs and symptoms to watch for and report.

Discharge planning
H Refer the patient to a dietitian, as appropriate.

Surgery
H Hiatal hernia repair
H Vagotomy or pyloroplasty
H Esophagectomy

Nursing considerations
Key outcomes
The patient will:
H state and demonstrate understanding of the disorder
and its treatment
H express feelings of increased comfort
H show no signs of aspiration
H have minimal or no complications.

Nursing interventions
H Administer prescribed drugs.
H Offer emotional and psychological support.
H Assist with diet modification.
H Perform chest physiotherapy.
H Use semi-Fowlers position for the patient with an NG

tube.
H Elevate the head of the bed at least 30 degrees.

Monitoring
H Response to therapy
H Adverse effects of medication

After surgery
H Respiratory status
H Pain control
H Intake and output
H Vital signs
H Chest tube drainage
H GI status

Gastroesophageal reflux disease

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Generalized anxiety
disorder
Overview
Description

H Anger
H Difficulty concentrating, eating, and sleeping

Physical findings
H Trembling
H Shortness of breath
H Tachycardia
H Sweating

H Feeling of apprehension sometimes described as an

DSM-IV-TR criteria

exaggerated feeling of impending doom, dread, or


uneasiness
H Reaction to an internal threat
H Uncontrollable, unreasonable worry that persists for
at least 6 months and narrows perceptions or interferes with normal functioning

A diagnosis is confirmed when the patients symptoms


match the following criteria:
H Excessive anxiety and worry about a number of
events or activities occur more days than not for at
least 6 months.
H The person finds it difficult to control the worry.
H The anxiety and worry are associated with at least
three of the following six symptoms:
restlessness or feeling keyed up or on edge
being easily fatigued
difficulty concentrating or mind going blank
irritability
muscle tension
sleep disturbances (difficulty falling or staying
asleep, or restless, unsatisfying sleep).
H The focus of the anxiety and worry isnt confined to
features of an axis disorder.
H The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
H The disturbance isnt due to the direct physiologic effects of a substance or a general medical condition
and doesnt occur exclusively during a mood disorder, a psychotic disorder, or a pervasive, developmental disorder.

Pathophysiology
H Aberration in benzodiazepine receptor regulation oc-

curs.

Causes
H Unknown
H Roles played by biologic and physiologic factors

Risk factors
H Stressful life situations
H Learned maladaptive behaviors

Incidence
H Can begin at any age but typically begins between

ages 20 and 40
H Twice as common in females as in males

Common characteristics
Mild anxiety
H Psychological symptoms
H Unusually self-aware and alert to surroundings
Moderate anxiety
H Selective inattention, but can concentrate on a single
task
Severe anxiety
H Inability to concentrate on more than scattered details of a task
H Panic state with acute anxiety causing complete loss
of concentration, typically with unintelligible speech

Complications

Test results
Laboratory
H Tests, such as cardiac enzymes, troponin level, and
thyroid studies, rule out organic causes of symptoms.
Diagnostic procedures
H Electrocardiography excludes myocardial ischemia.
Other
H Psychiatric evaluation helps confirm the diagnosis.

Treatment

H Impaired social or occupational functioning


H Substance abuse

General

Assessment

Medications

History

H Benzodiazepines, such as diazepam and lorazepam


H Tricyclic antidepressants such as doxepin
H Serotonin receptor reuptake inhibitors, such as ser-

H Muscle aches and spasms


H Headaches
H Inability to relax
H Apprehension
H Fear

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Generalized anxiety disorder

H Psychotherapy
H Relaxation techniques

traline, paroxetine, and escitalopram

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Nursing considerations
Key outcomes
The patient will:
H develop effective coping strategies
H identify anxiety triggers
H experience reduced anxiety.

Nursing interventions
H Administer prescribed drugs.
H Reduce environmental stimuli.
H Help identify triggers to anxiety.
H Provide emotional support.

Monitoring
H Response to therapy

Patient teaching
Be sure to cover:
H prescribed drugs
H relaxation techniques
H effective coping strategies.

Discharge planning
H Refer the patient for psychological counseling.

Generalized anxiety disorder

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Genital herpes

Common characteristics

Overview

H Fever
H Malaise
H Dysuria

H Fluid-filled vesicles that develop into shallow, painful

ulcers with yellow, oozing centers

Description
H Acute inflammatory disease of the genitalia
H Usually self-limiting but able to cause painful local or

systemic disease (see Understanding the genital


herpes cycle)

Pathophysiology
H Virus invades and replicates in neurons and epider-

mal and dermal cells.


H Virions travel to sensory dorsal root ganglion.
H Replication in the sensory ganglia leads to recurrent

Complications
H Herpetic keratitis, which may lead to blindness
H Herpetic encephalitis

Assessment
History

Causes

H Intimate contact with an infected person


H Fever
H Malaise
H Dysuria
H Leukorrhea (females)

H Herpes simplex virus (HSV), type 1 or type 2


H Typically transmitted through sexual intercourse,

Physical findings

clinical outbreaks.

orogenital sexual activity, kissing, hand-to-body contact, and vaginal delivery

Risk factors
H Unprotected sexual activity

Incidence
H One in five adults in the United States serologically

H Shallow, reddened, painful ulcers with yellow, oozing

centers usually on the cervix (the primary infection


site) and possibly on the labia, perianal skin, vulva,
or vagina and on the glans penis, foreskin, or penis
H Extragenital lesions, possibly on the mouth or anus
H Marked edema
H Tender inguinal lymph nodes

HSV-positive

Test results

Understanding the genital herpes cycle

Laboratory
H Vesicular fluid reveals HSV.
H Antigen testing identifies specific antigens.

After a patient is infected with genital herpes, a latency period follows. The virus takes up permanent residence in
the nerve cells surrounding the lesions, and intermittent
viral shedding may take place.
Repeated outbreaks may develop at any time, again followed by a latent stage during which the lesions heal
completely. Outbreaks may recur as often as three to eight
times yearly.
Although the cycle continues indefinitely, some people
remain symptom-free for years.
INITIAL INFECTION
Highly infectious period marked by fever, aches, adenopathy, pain,
and ulcerated skin and mucous membranes

LATENCY
Intermittently infectious period marked by viral dormancy or viral
shedding and no disease symptoms

RECURRENT INFECTION
Highly infectious period similar to initial infection with milder
symptoms that resolve faster

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Genital herpes

Treatment
General
H Adequate rest periods

Medications
H Antivirals, such as acyclovir, famciclovir, and valacy-

clovir

Nursing considerations
Key outcomes
The patient will:
H express an understanding of the disorder and its
treatment
H practice safe sex
H report feelings of increased comfort
H demonstrate improved skin integrity.

Nursing interventions
H Encourage expression of feelings and concerns.
H Keep lesions dry.

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Monitoring
H Response to treatment
H Skin integrity
H Wound healing

Patient teaching
Be sure to cover:
H avoiding sexual intercourse during the active stage of
this disease (while lesions are present)
H using condoms during all sexual encounters
H urging sexual partners to seek medical examination
H having a Papanicolaou test every 6 months (females).

Discharge planning
H Refer the patient to the Herpes Resource Center for

support.

Genital herpes

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Genital warts

H Genital tract dysplasia


H Cervical and vulvar cancer in females, penile cancer

in males, and some rectal carcinomas in both sexes

Overview
Description

Assessment

H Papillomas that consist of fibrous tissue overgrowth

History

from the dermis and thickened epithelial coverings


H Also known as venereal warts and condylomata
acuminata

H Unprotected sexual contact with a partner with a

Pathophysiology

H Warts on moist genital surfaces (subpreputial sac,

H Infection is transmitted by sexual contact and incu-

known infection, a new partner, or many partners

Physical findings

bates for 1 to 6 months (2 months, average) before


warts erupt.
H Infection of the basal cells occurs, with proliferation
of all epidermal layers, producing acanthosis, parakeratosis, and hyperkeratosis.

urethral meatus, penile shaft, scrotum, vulva, vaginal


and cervical walls) and around the anus and inside
the rectum
H Tiny red or pink swellings that may grow as large as
10 cm and that may be pedunculated
H Infected lesions that become malodorous

Causes

Test results

H Infection with one of more than 60 strains of human

Laboratory
H Dark-field microscopy of wart-cell scrapings shows
marked epidermal cell vascularization.
H Application of 5% acetic acid (white vinegar) turns
warts white if theyre papillomas.

papillomavirus (HPV)

Risk factors
H Unprotected sexual activity

Incidence
H One of the most common sexually transmitted dis-

eases (STDs) in the United States

Common characteristics
H Appearance of small, pink to red, moist warts with ir-

regular surfaces (see Recognizing genital warts)

Treatment
General
H Good hygiene practices
H Contact precautions

H Usually located around the external genitalia and

Medications

possibly inside the urethra or vagina or on the cervix


H No symptoms in most patients

H Topical interferon alfa 2-b


H Vaccine preparations such as HPV recombinant vac-

Complications

H Immune response modifier such as imiquimod

H During pregnancy, genital warts in the vaginal and

cervical walls that grow large enough to impede vaginal delivery

Recognizing genital warts


Genital warts are marked by clusters of flesh-colored papillary growths that may be barely visible or several inches
in diameter.

cine

Surgery
H Cryosurgery
H Electrodesiccation
H Surgical excision
H Laser ablation
H Circumcision to prevent recurrence

Nursing considerations
Key outcomes
The patient will:
H remain free from all signs and symptoms of infection
H exhibit improved or healed lesions or wounds
H acknowledge the change in body image
H voice feelings about potential or actual changes in
sexuality
H express feelings of increased comfort and decreased
pain.

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Nursing interventions
H Provide a nonthreatening, nonjudgmental atmos-

phere that encourages verbalization, and provide


support.
H Institute contact precautions to avoid transmission.

Monitoring
H Response to treatment
H Adverse effects of medication
H Signs and symptoms of infection (postoperative)
H Concomitant STDs or infections
H Papanicolaou (Pap) test results

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need for sexual abstinence or condom use during
intercourse until healing is complete
H evaluation of the patients sexual partners
H the importance of testing for human immunodeficiency virus infection and other STDs
H the emphasis that genital warts can recur and that the
virus can mutate, causing infection with warts of a
different strain
H recommendation that female patients have a Pap test
every 6 months.

Genital warts

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Life-threatening disorder

H Roughly 5% incidence of preeclampsia progressing

to eclampsia

Gestational
hypertension

Common characteristics

Overview

Complications

Description

H Abruptio placentae
H HELLP syndrome: hemolysis, elevated liver enzyme

H Hypertension
H Sudden weight gain
H Irritability
H Emotional tension

H High blood pressure, most commonly occurring after

levels, low platelet count

the 20th week of gestation in a nulliparous woman


H Carries a high risk for fetal mortality because of the
increased incidence of premature delivery
H Among the most common causes of maternal death
in developed countries (especially when complications occur)
H Nonconvulsive form (also called preeclampsia) occurring after the 20th week of gestation; may be mild
or severe
H Convulsive form (also called eclampsia) occurring
between the 24th week of gestation and the end of
the first postpartum week

H Coagulopathy
H Stillbirth
H Seizures
H Coma
H Premature labor
H Renal failure
H Maternal hepatic damage

Pathophysiology
H Generalized arteriolar vasoconstriction is thought to

cause decreased blood flow through the placenta and


maternal organs.
H This leads to intrauterine growth retardation or restriction, placental infarcts, and abruptio placentae.

Causes
H Unknown
H Contributing factors:

Geographic, ethnic, racial, nutritional, immunologic, and familial factors


Preexisting vascular disease
Maternal age
Autolysis of placental infarcts
Autointoxication
Uremia
Maternal sensitization to total proteins
Pyelonephritis
Diabetes

Special populations
Adolescents and primiparas older than age 35 are
at higher risk for preeclampsia.

Risk factors
H First-time pregnancy
H Multiple fetuses
H History of vascular disease

Incidence
H Occurs in about 7% of pregnancies; more common

in females from lower socioeconomic groups

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Gestational hypertension

Assessment
History
H Sudden weight gain
H Irritability
H Emotional tension
H Severe frontal headache
H Blurred vision
H Epigastric pain or heartburn

Physical findings
H Preeclampsia: blood pressure of 160/110 mm Hg or

higher
H Eclampsia: systolic blood pressure of 180 or

200 mm Hg or higher
H Generalized edema, especially of the face
H Pitting edema of the legs and feet
H Hyperreflexia
H Oliguria
H Vascular spasm, papilledema, retinal edema or de-

tachment, and arteriovenous nicking or hemorrhage


(seen on ophthalmoscopy)
H Seizures

Test results
Laboratory
H In preeclampsia: proteinuria is more than
300 mg/24 hours [1+].
H In severe eclampsia: proteinuria is 5 g/24 hours
[5+] or more.
H In HELLP syndrome: hemolysis, elevated liver enzymes and decreased platelet count are evident.
Imaging
H Ultrasonography aids evaluation of fetal well-being.
Diagnostic procedures
H Stress and nonstress tests and biophysical profiles
help evaluate fetal well-being.

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Treatment
General
H Measures to halt progression of the disorder and en-

sure fetal survival


H Prompt labor induction, especially if the patient is

near term (advocated by some clinicians)


H Adequate nutrition
H Low-sodium diet, if indicated
H Limited caffeine
H Complete bed rest
H Left lateral lying position

Medications
H Antihypertensives
H Magnesium sulfate
H Oxytocin
H Oxygen

Surgery

Emergency interventions for gestational


hypertension
When caring for a patient with gestational hypertension,
be prepared to perform the following interventions:
H Observe for signs of fetal distress by closely monitoring results of stress and nonstress tests.
H Keep emergency resuscitative equipment and anticonvulsants at hand in case of seizures and cardiac or respiratory arrest.
H Carefully monitor magnesium sulfate administration.
Signs of drug toxicity include absence of patellar reflexes, flushing, muscle flaccidity, decreased urinary
output, significant blood pressure drop (> 15 mm Hg),
and a respiratory rate below 12 per minute. Keep calcium gluconate at the bedside to counteract the toxic
effects of magnesium sulfate.
H Prepare for emergency cesarean delivery, if indicated.
Alert the anesthesiologist and pediatrician.
H To protect the patient from injury, maintain seizure precautions. Dont leave an unstable patient unattended.
Maintain a patent airway, and have supplemental oxygen readily available.

H Possible cesarean delivery

Nursing considerations

Patient teaching

Key outcomes

Be sure to cover:
H the disorder, diagnosis, and treatment
H signs and symptoms of preeclampsia and eclampsia
H importance of bed rest in the left lateral position, as
ordered
H adequate nutrition and a low-sodium diet
H good prenatal care
H control of preexisting hypertension
H early recognition and prompt treatment of
preeclampsia
H likelihood that the neonate will be small for gestational age, with the probability that hell do better
than other premature neonates of the same weight.

The patient will:


H maintain normal vital signs
H maintain adequate fluid volume
H avoid complications
H remain oriented to the environment.

Nursing interventions
H Administer prescribed drugs.
H Elevate edematous arms or legs.
H Eliminate constricting hose, slippers, and bed linens.
H Assist with or insert an indwelling urinary catheter, if

necessary.
H Provide a quiet, darkened room.
H Enforce absolute bed rest.
H Provide emotional support.
H Encourage the patient to express feelings.
H Help the patient develop effective coping strategies.

Discharge planning
H Refer the patient for professional counseling, as indi-

cated.

(See Emergency interventions for gestational


hypertension.)

Monitoring
H Vital signs
H Fetal heart rate
H Vision
H Edema
H Daily weight
H Intake and output
H Level of consciousness
H Deep tendon reflexes
H Headache unrelieved by medication
H Complications

Gestational hypertension

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Giardiasis
Overview
Description
H Infection of the small bowel by Giardia lamblia, a

symmetrical flagellate protozoan


H Reinfection possible because infection doesnt confer

H Drinking of suspect water


H Institutionalization

Physical findings
H Possibly, no intestinal symptoms in mild infection
H Abdominal cramps, bloating
H Belching, flatus
H Nausea, vomiting
H Explosive pale, loose, greasy, malodorous, frequent

stools (occurring 2 to 10 times daily)

immunity
H Also called G. enteritis and lambliasis

H Fatigue, weight loss


H Hyperactive bowel sounds in the right upper and left

Pathophysiology

H General upper and right lower quadrant discomfort

H Cysts enter the small bowel and release trophozoites,

which attach to the bowels epithelial surface.


H Attachment causes superficial mucosal invasion and
destruction, inflammation, and irritation.
H Trophozoites become encysted again, travel down the
colon, and are excreted. (Unformed stool may contain trophozoites as well as cysts.)

Causes

lower quadrants just before bowel movements


and guarding

Test results
Laboratory
H Examination of a fresh stool specimen shows cysts or
examination of duodenal aspirate or biopsy shows
trophozoites.

H Ingestion of G. lamblia cysts in stool-contaminated

Treatment

water
H Fecal-oral transfer of cysts from an infected person

General

Incidence
H Occurs worldwide but most common in developing

countries and other areas where sanitation and hygiene are poor (G. lamblia has been found in municipal water sources, nursing homes, and day-care
centers.)
H Children generally more likely to develop giardiasis
than adults
H In the United States, most common in travelers recently returned from endemic areas, campers who
drink water from contaminated streams, male homosexuals, patients with congenital immunoglobulin A
deficiency, and children in day-care centers

Common characteristics
H Diarrhea
H Abdominal pain
H Bloating
H Belching
H Flatus
H Nausea and vomiting

Complications
H Malabsorption
H Dehydration
H Lactose intolerance
H Possible death, in hypogammaglobulinemia

H Examination for possible testing and treatment for

people living with an infected person or those having


had sexual contact with an infected person
H Parenteral fluid replacement to prevent dehydration

Medications
H Antiprotozoals, such as nitazoxanide and tinidazole

Nursing considerations
Key outcomes
The patient will:
H avoid skin breakdown or infection
H maintain stable vital signs
H maintain normal electrolyte levels
H have an elimination pattern that returns to normal
H express feelings of increased comfort and relief from
pain.

Nursing interventions
H Institute enteric contact precautions, and quickly dis-

pose of all fecal material.


H Place a child or an incontinent adult in a private

room.
H Keep the perianal area clean, especially after each

bowel movement.

Assessment

H Administer I.V. fluid therapy, as needed.


H Provide nutritionally adequate foods.
H Administer prescribed drugs.
H Report to public health authorities.

History

Monitoring

H Recent travel to an area with poor sanitation


H Sexual practices that involve oral-anal contact

H Frequency and characteristics of bowel movements


H Nutritional intake (to prevent malnutrition)

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H Adverse drug effects


H Skin integrity
H Signs and symptoms of dehydration
H Intake and output

Patient teaching
Be sure to cover:
H prescribed medications, including precautions and
adverse effects
H need for the patient whos taking metronidazole or
furazolidone to avoid alcohol while taking the drug
and for 3 days after completing treatment
H need for the family and others in contact with the patient to have their stools tested for G. lamblia cysts
H need for good personal hygiene, especially proper
hand washing as well as correct handling of infectious material by the patient and his family
H importance of safer s