ACUTE BIOLOGIC CRISIS f.

Neck – stiffness, masses

g. Breast – lumps, secretion, pain, tenderness
HIGH RISK PREGNANCY h. Respiratory – cough, wheezing, asthma, SOB
Definition: One in which a concurrent disorder, pregnancy- i. Cardiovascular – heart murmur, history of heart disease,
related complication, or external factor jeopardizes the health of HPN
the mother and/or fetus. j. G.I.T – pre-pregnant weight, diarrhea, constipation,
 Many factors enter into the categorization of high risk. hemorrhoids, ulcer
 No tool is perfect because the concept of high risk is a k. Genito-urinary – infection, STD’s
very individualized one l. Extremities – varicose veins, pain or stiffness of joints,
 The woman identified this way needs close fractures
observation during pregnancy to see that pregnancy is m. Skin – rashes, acne, psoriasis
progressing well
 The infant born of a woman identified this way needs
close observation in the neonatal period until it is I. Support Persons Role
confirmed that no anomalies exist  Questions asked to the support person : Current
 The failure to identify risk potential in pregnancy leads health status, feelings and concern about the
to increased perinatal mortality pregnancy, knowledge of pregnancy and childbirth
2. PHYSICAL EXAMINATION
ASSESSMENT FOR A FIRST PREGNANCY VISIT : A. Baseline Data : to establish a baseline for future
1. HEALTH HISTORY comparison
Purpose : - Weight, Height, BP, PR, RR
a. To establish rapport - FHR : 120-160 beats/min
b. To gain information about the woman’s physical and - 10-12 weeks (Doppler)
psychosocial health - 18-20 weeks (Stethoscope)
c. To obtain a basis for anticipatory guidance for the - Fundic height:
pregnancy 12-14 weeks – Symphysis pubis
20-22 weeks – Umbilicus
A. Demographic Data : Name, age, address, telephone 36 weeks - Xiphoid process
number, health insurance 40 weeks - Xiphoid process
B. Chief Concern – Reason why the woman has come to the
health care setting. B. System Assessment
1. Was the pregnancy planned? 1. General Appearance and Mental Status
2. Inquire date of last menstruation  Physical examination always begins with inspection of general
3. Ask if she has had a pregnancy test appearance to form a general impression of the woman’s health and
4. Elicit information about signs of early pregnancy well-being.
5. Observe for discomforts of pregnancy  A physical examination at a first prenatal visit typically includes
6. Has she been exposed to contagious diseases inspection of body systems, with emphasis on changes that occur
7. Has she taken any medicine that might be harmful to with pregnancy.
fetal growth  General appearance is important because it reveals how people
feel about themselves by the manner in which they dress, speak and
C. Family Profile – helps to know the woman earlier body posture they assume
1.Identify support persons, Family composition
2.What is her occupation, source of income, Nutrition, sleep 2. Head and Scalp
pattern, hobbies, living conditions  Examine head for symmetry, normal contour and tenderness
 Examine hair for distribution, thickness, excessive dryness or
D. Past Medical History – important because a past condition oiliness, cleanliness, or the use of hair dye.
may become active during or immediately following pregnancy.  Look for chloasma (extra pigment on the skin)
1. Any abdominal surgery, kidney, heart, etc.
3. Eyes
E. Gynecologic History – her past experience with her  Edema in the eyelids
reproductive system may have some influence on how well she  Spots before the eyes
accepts a pregnancy.  Diplopia (double vision)
1. When was her menarche - may indicate PIH
2. What is the length and duration of menstrual cycle 4. Nose
 Increased level of estrogen associated with pregnancy may
F. Obstetric History :
cause nasal congestion.
1. Review pregnancy briefly.
2. Determine woman’s status with respect to the number
5. Ears
of times she has been pregnant (gravida) and the
 The nasal stuffiness that accompanies pregnancy may lead to
number of children above the age of viability she has
blocked Eustachian tubes and therefore a feeling of fullness or
previously delivered (para).
dampening of sound during early pregnancy.
3. A more comprehensive system for classifying
pregnancy status (GTPAL or GTPALM) provides
6. Sinuses
greater detail on the pregnancy history. By this
system, the gravida classification remains the same,  Sinuses should feel nontender
but para is broken down into :
T : The # of full-term infants born (37 weeks or 7. Mouth, Teeth and Throat
after)  Pregnant woman is prone to vitamin deficiency because of the
P : The # of preterm infants born (infants born rapid growth of the fetus.
before 37 weeks)  Assess carefully for cracked corners of the mouth that would
A : The # of spontaneous or induced abortions reveal vitamin A deficiency.
L : The # of living children  Assess carefully for pinpoint lesions with an erythematous base
M : Multiple pregnancies on the lips; these suggest a herpes infection
 Gingival hypertrophy may result from estrogen stimulation
during pregnancy.
G. Typical Day History  Teach all women not to neglect good dental hygiene while
 Information about a woman’s current pregnant
nutrition, elimination, sleep, recreation and
interpersonal interactions can be elicited best by 8. Neck
asking the woman to describe a typical day of her  Slight thyroid hypertrophy may occur with pregnancy because
life. the overall metabolic rate is increased.
 Encourage a woman to continue to use iodized salt during
H. Review of Systems – Brief review of all body systems pregnancy and to eat seafood at least once weekly to supply enough
a. Head – Ask about headache, head injury, seizures, iodine for thyroxine production with this increased rate.
dizziness
b. Eyes – Inquire about vision, eyeglasses, eye diseases 9. Lymph Nodes
c. Ears – Infection, discharges, pain  No palpable lymph nodes should be present.
d. Nose – Bleeding, discharges, colds, allergy, sinuses
e. Mouth and pharynx –Dentures, teeth, toothache, 10. Breasts
bleeding, pain, surgery
  As pregnancy begins, the breast undergo the following :
Breast areola darkens; Montgomery’s tubercles become
prominent; Breast size increases; breast tone affirms; secondary
areola may develop surrounding the natural one; blue streaking
of veins becomes prominent; colostrums may be expelled as
early as the 16th week of pregnancy; any supernumerary nipple
also may become darker.
 All women should be instructed on monthly breast self
examination.
11. Heart
 Heart rate should range from 70 to 80 beats/minute.
 No accessory sounds or murmurs should be present.
 Because of the breast size , it may be difficult to hear the
woman’s heart beat during pregnancy
 Many women notice occasional palpitations (heart skipping
a beat) during pregnancy, especially when lying supine. Teach
pregnant woman to rest or sleep on their side (left side is best) to
avoid this problem.
12. Lungs
 Late in pregnancy, diaphragmatic excursion is lessened
because the diaphragm cannot descend as fully as usual
because of the distended uterus.
13. Back
 Assess the spine for any abnormal curve that would
suggest scoliosis.
14. Rectum
 Assess the pregnant woman’s rectum closely for
hemorrhoidal tissue, which commonly occurs from pelvic
pressure preventing venous return.
15. Extremities and Skin
 Assess the upper extremities. Many women develop palmar
erythema and itching early in pregnancy from a high estrogen
level and perhaps subclinical jaundice.
 Assess the lower extremities carefully for varicosities, filling
time of the toenails (should be under 5 seconds) and edema.
 Assess the gait of pregnant women to see that they are
keeping their pelvis tucked under the weight of their abdomen.
MEASUREMENT OF FUNDAL HEIGHT AND FETAL HEART
SOUNDS
 12-14 weeks of pregnancy – uterus is
palpable over the symphysis pubis as a firm
globular sphere
 20-22 weeks – reaches umbilicus
 36 weeks – xiphoid process
 40 weeks – often return to 4 about 4 cm
below the xiphoid due to lightening
 Auscultate for fetal heart sounds (120 to 160
beats/minute. These can be heard at 10 to 12
weeks if Doppler is used. 18 to 20 weeks if regular
stethoscope is used.
 Palpate for fetal outline and position after
the 28th week.
PELVIC EXAMINATION
> Reveals information on the health of both internal and
external reproductive organs
a. EXTERNAL GENITALIA – note for :
1. Signs of inflammation
2. Irritation
3. Infection
4. Herpes simplex II virus infection
5. Rectocele
6. Cystocele
b. INTERNAL GENITALIA
1. Cervix should be in the center and color should be almost
purple when pregnant.
 Retroverted Uterus – cervix positioned anteriorly
 Anteverted Uterus – cervix positioned posteriorly.
1. Nulligravida – woman who is not or never has been
pregnant, the cervical os is round and small.
2. A woman who has had a previous pregnancy, the cervical
os has a slitlike appearance.
3. If the woman had a cervical tear during a previous birth,
the cervical os may appear as a transverse crease.
4. If a cervical infection is present, a mucus discharge
maybe present. With infection, the epithelium of the
cervical canal often enlarges and spreads onto the area
surrounding the os. Giving the cervix a reddened
appearance called erosion. This area bleeds easily if
touched.
 Trichomoniasis – a protozoal infection, generally gives signs of
redness; a profuse, whitish, bubbly discharge; and petechial
spots on the vaginal walls.
 Candidal (Monilial) infection – presents with thick, white vaginal
patches that may bleed if scraped away.
 A gonorrheal infection – presents with a thick, greenish-yellow
discharge and extreme inflammation.
 Chlamydia infection – shows few symptoms.
 Carcinoma of the cervix appears as an irregular, granular
growth at the os.
 Cervical polyps (red, soft, pedunculated protrusions) also may
be seen occasionally at the os.
c. PAPANICOLAOU SMEAR
 Weapon for detecting cervical cancer
 American Cancer Society recommends a pap smear every 3
years in women who have had 2 consecutive negative tests.
 Recommended more frequently to women who were exposed
to diethylstilbestrol (DES) in utero, who have multiple sexual
partners, who have a history of human papillomavirus (HPV),
cigarette smokers, who were sexually active before age 21
d. VAGINAL INSPECTION
 A culture for gonorrhea, chlamydia or group B streptococcus
may be taken. All these organism can cause disease in the NB
so it is best if they can be eradicated during pregnancy
 Any areas of inflammation, ulceration, lesions or discharge
should be noted
 Vaginal examination is critical for a woman whose mother took
DES during her pregnancy. Female children of mothers who
took DES are prone to develop adenosis or overgrowth of
cervical endothelium (which is possibly associated with vaginal
cancer).
e. EXAMINATION OF PELVIC ORGANS
 A bimanual (two-handed) examination is performed to assess
the position, contour, consistency, and tenderness of pelvic
organs
 Abnormalities that can be noted by bimanual examination
include ovarian cysts, enlarged fallopian tubes (perhaps from
pelvic Inflammatory Disease) and an enlarged uterus.
 An early sign of pregnancy (Hegar’s sign) is elicited on
bimanual examination.
f. RECTOVAGINAL EXAMINATION
 To assess the strength and irregularity of the posterior vaginal
wall
e. ESTIMATING PELVIC SIZE
 It is hard to see from the outward appearance of a woman
whether her pelvis is adequate for the passage of a fetus.
 Pelvic measurements should be taken if the woman is pregnant
and if she has never given birth vaginally
 In sonogram, estimations may be made by a combination of
pelvic pelvimetry and fetal sonogram
 Estimation of pelvic adequacy must be done at least by the 24 th
week of pregnancy, because by this time, there is danger that
the fetal head will reach a size that will interfere with safe
passage and birth if the pelvic measurements are small
 Once a woman has given birth vaginally, her pelvis has been
approved adequate, and it is not necessary to take pelvic
measurements.
Types of Pelvis
> Categorized into 4 groups :
• Gynecoid : normal female pelvis
• Anthropoid : Ape-like pelvis
• Platypelloid : Flattened pelvis
• Android : Male pelvis
PELVIC MEASUREMENTS
 Internal pelvic measurements give the actual diameters of the
inlet and outlet through which the fetus must pass. The
following measurements are made most commonly :
1. The Diagonal Conjugate – The distance between the anterior
surface of the sacral prominence and the anterior surface of the
inferior margin of the symphysis pubis. The most useful
measurement for estimation of pelvic size, because it suggests the
anteroposterior diameter of the pelvic inlet.
2. The True Conjugate – Conjugate Vera.
The measurement between the anterior surface of the sacral
prominence and the posterior surface of the inferior margin of the
symphysis pubis.
3. The Ischial Tuberosity – The distance between the ischial
tuberosities, or the transverse diameter of the outlet. A diameter of
11 cm is considered adequate because it will allow the widest
diameter of the fetal head.
3. LABORATORY ASSESSMENT
• Blood Studies
• Urinalysis
• Tuberculosis Testing
• Ultrasound
IDENTIFYING THE HIGH-RISK PREGNANCY
 Some women enter pregnancy with a chronic illness that,
when superimposed on the pregnancy, makes it high risk.
 Other women enter pregnancy in good health but then
develop a complication of pregnancy that causes it to
become high risk.
 A combination of particular instances – poverty, lack of
support people, poor coping mechanisms, genetic
inheritance, or past history of pregnancy complications can
cause a pregnancy to be categorized as high risk.
FACTORS THAT CATEGORIZE A PREGNANCY AS HIGH
RISK
A. Infections During Pregnancy
• Maternal infections during pregnancy may
contribute significantly to fetal morbidity and
mortality.
• Infections in this category may be caused by
various viruses. Other organisms like bacteria,
spirochetes, protozoa, or yeast may also cause
maternal infections, which are harmful to the
developing fetus. Even though the infection in
the mother may be very mild, the effects on the
fetus may be catastrophic.
• Most organisms cross the placenta and infect the
fetus, causing birth anomalies. The fetus may
also acquire the organism as it travels the birth
canal during labor, causing illness after birth.
SEXUALLY TRANSMITTED DISEASES AND PREGNANCY
 Spread through sexual contact with an infected partner.
 All STD’s can be prevented to some extent by the use of
safer sex practices.
 Treatment begins with determining the causative organism
so the appropriate antibiotic or antifungal medication can be
prescribed.
Nursing Diagnosis : Pain related to vulvar irritation secondary to
existence of STD
1. THE WOMAN WITH CANDIDIASIS
 Candidiasis causes a vaginal infection spread by the fungus
Candida.
Assessment :
1. Thick, cream cheeselike vaginal discharge and extreme
pruritus.
2. Vagina appears red and irritated
Etiology :
1. Occurs more frequently during pregnancy because of the
increased estrogen level present during pregnancy.
2. Occurs frequently to women being treated with an antibiotic
for another infection.
3. Occurs frequently in women with gestational diabetes
4. Mostly seen in women with HIV infection
Dx : Diagnosed by microscopic analysis
Treatment : Local application of an antifungal cream such as
miconazole cream (Monistat) or oral fluconazole (Diflucan)
Complications :
1. If untreated during pregnancy, it may cause a candidal
infection, or thrush, in the NB.
2. THE WOMAN WITH TRICHOMONIASIS
 A single-cell protozoan spread by coitus.
Assessment :
1. A yellow-gray, frothy, odorous vaginal discharge.
2. Vulvar itching, edema, and redness
Dx: Diagnosed by examination of vaginal secretions on a wet
slide that has been treated with Potassium Hydoxide (KOH).
Treatment :
Topical clotrimazole instead of metronidazole because of its possible
teratogenic effects if used during the first trimester of pregnancy.
Etiology :
 Probably associated with preterm labor, premature rupture of
membranes and post cesarean section infection
3. THE WOMAN WITH BACTERIAL VAGINOSIS (GARDNERELLA
INFECTION)
 Local infection of the vagina by the invasion, most commonly, of
Gardnerella organisms.
Assessments :
1. Discharge is gray and has a fishlike odor
2. Intense pruritus
Treatment :
1. Metronidazole for non pregnant women.
2. Because Metronidazole is contraindicated during the first
trimester, women are usually treated with a topical cream
Complications :
1. Untreated bacterial infections are associated with amniotic fluid
infections, perhaps, preterm labor and premature rupture of
membranes.
4. CHLAMYDIA TRACHOMATIS
 One of the most common types of vaginal infections seen
during pregnancy.
> Infection is caused by a gram-negative intracellular parasite
Assessment :
1. Heavy gray-white vaginal discharge
Dx: Diagnosis is made by culture of the organism from vaginal
secretions using a specific chlamydia culture kit.
Treatment :
1. Therapy is usually with tetracyclines but contraindicated during
pregnancy because of possible long bone deformities; Erythromycin
and Amoxicillin are used instead.
 It is important that chlamydia infections be treated because they
are associated with PROM, preterm labor and endometritis in
the postpartal period.
 An infant who is born while a chlamydia infection is present in
the vagina can suffer from conjunctivitis or pneumonia after
birth.
5.SYPHILIS
 A systemic disease caused by the spirochete Treponema
pallidum.
Assessment :
1. The 1st stage results in a painless ulcer (chancre) on the
vulva or vagina.
2. Hepatic and splenic enlargement, headache, anorexia,
and maculopapular rash on the palms of the hand and the
soles of the feet ( secondary syphilis; occurring about two
months after initial infection
Complications :
1. Spontaneous Abortion
2. Preterm Labor
3. Stillbirth
4. Congenital anomalies in the NB
Dx: All pregnant women are screened for syphilis by VDRL, RPR or
FTA-ABS antibody reaction test.
Treatment :
1. One injection of Benzathine penicillin G is the drug of choice
during pregnancy
6.THE WOMAN WITH GONORRHEA
 A sexually transmitted disease caused by the gram-negative
coccus Neisseria gonorrhea.
Assessments :
1. May not produce symptoms in some women
2. A yellow-green vaginal discharge may be present
 Gonorrhea is associated with spontaneous abortion, preterm
birth, and endometritis in the postpartal period.
 Also a cause of pelvic infectious disease and infertility.
Dx : Diagnosis is made by culture of the organism from the vagina,
rectum or urethra
Treatment :
1. Traditionally treated with amoxicillin and probenecid but the
incidence of penicillinase-producing strains has made this
therapy ineffective.
2. Oral Cefixime and Ceftriaxone sodium IM are now the drug of
choice.
3. Sexual partner should also be treated to prevent infection.
Complications :
1. If untreated at time of birth, it can cause severe eye
infection that can lead to blindness in the NB
(Ophthalmia neonatorum).
2. Major cause of pelvic infectious disease and infertility
7.THE WOMAN WITH HUMAN PAPILLOMA VIRUS
INFECTION
 The Human papilloma virus (HPV) causes fibrous tissue
overgrowth on the external vulva (condyloma acuminatum)
Etiology :
1. Women who have multiple sexual partners
Assessments :
1. Discrete papillary structures at first which spreads, enlarges
and coalesce to form large, cauliflower-like lesions
2. Tend to increase in size during pregnancy because of the high
vascular flow in the pelvic area.
3. They may become secondarily ulcerated and infected; when
this occurs, a foul vulvar odor may develop
Treatment :
1. Aimed at dissolving the lesions and also ending any
secondary infection present.
2. Trichloroacetic acid (TCA) or Bichloroacetic acid (BCA)
applied to the lesions weekly
3. Large lesions may be removed by laser therapy, cryocautery
or knife excision.
4. If present at time of birth and obstruct birth canal, a CS maybe
performed
Complications :
1. Associated with the development of cervical cancer later in
life.
8.THE WOMAN WITH A GROUP B STREPTOCOCCI
INFECTION
Etiology :
1. Occurs at a higher incidence during pregnancy
Assessment :
1. Patient usually experiences no symptoms.
Complications :
1. Urinary Tract Infection (UTI)
2. Intra-amniotic Infection leading to preterm birth
3. Postpartal endometritis
4. 40 % to 70% of neonates whose mothers have an active
infection will become infected from placental transferal or from
direct contact with the organisms at birth.
5. Infected neonates may develop severe pneumonia, sepsis,
respiratory distress syndrome or meningitis
Dx: Women are screened at 35 to 38 weeks of pregnancy by a
vaginal culture.
Treatment :
1. Broad spectrum penicillin such as ampicillin
2. Women who experience rupture of membranes at less than 37
weeks of pregnancy are treated with Ampicillin IV
9.THE WOMAN WITH HUMAN IMMUNODEFICIENCY VIRUS
(HIV) INFECTION
 The HIV virus, which leads to AIDS, is the most serious of
the STD’s because it may be fatal to both mother and child.
Etiology :
1. Multiple sexual partners of the individual or sexual partner
2. Bisexual partners
3. IV drug use by the individual or sexual partner
4. Blood transfusions
Assessment :
1. Initial invasion of the virus, which may be accompanied by
mild, flu-like symptoms
2. Seroconversion in which the woman converts from having no
HIV antibodies in blood serum to having antibodies positive for
HIV.
3. Weight loss and fatigue (wasting syndrome)
4. Opportunistic infections and possible malignancies
Complications :
1. It may invade cerebral spinal fluid and cause extreme neurologic
involvement
2. Higher risk for the development of toxoplasmosis and
cytomegalovirus infections.
3. Tuberculosis occurs at a higher rate with HIV people and may
grow worse during pregnancy
Dx: ELISA antibody reaction. For confirmation a Western blot
analysis is required.
Complications :
1. HIV is associated with low birth weight and preterm birth.
2. If the mother is untreated, 20% to 50% of infants born to HIV-
positive women will develop AIDS in the first year of life.
Therapeutic Management :
1. If Pneumocystis carinii pneumonia develops, the woman is treated
with trimethoprim with sulfamethoxazole. Trimethoprim may be
teratogenic in early pregnancy; sulfamethoxazole may lead to
increased bilirubin in the newborn if administered late in pregnancy..
2. Pentamidine, the drug of choice for PCP in nonpregnant women,
maybe administered by aerosol.
3. Kaposi’s sarcoma, malignancy that tends to occur with AIDS, is
normally treated with chemotherapy. Chemotherapy is
contraindicated during early pregnancy because of the potential for
fetal injury but is used later in pregnancy to halt malignant growths.
4. Thrombocytopenia (lowered platelet count) may be present which
may make the woman a poor candidate for an epidural injection for
anesthesia during labor or for episiotomy. She may need a platelet
transfusion to restore coagulation ability
5. Newborns of HIV-positive mothers are treated with zidovudine for
the 1st 6 weeks of life to try to prevent seroconversion and
trimethroprim-sulfamethoxazole to prevent P. carinii pneumonia
Nursing Diagnosis: Risk for opportunistic infections
TORCH infections
The term TORCH was applied to perinatal infections (T,
toxoplasmosis; O, other; R, rubella; C, cytomagalovirus; H, herpes).
• Toxoplasmosis – caused by the protozoan organism
Toxoplasmosis gondii, which is contracted from oocytes in
cat feces or by eating uncooked meat. When primary
infection, which is generally asymptomatic, occurs just
before or during early pregnancy, congenital infection may
result. This can lead to the birth of a child who is mentally
and physically retarded, and who suffers from
chorioretinitis and microcephaly. Approximately 10% to
15% of these babies die, and most of the survivors are
severely compromised. Sulfamethoxazole may reduce the
fetal impact.
• Other – includes the STDs, hepatitis
• Rubella – although most concerns are for infection in the
first trimester, serious problem are known to occur when
the infection develops as late as the fifth month of
gestation, and later infections may be responsible for more
subtle problems. Infections in the first trimester may result
in abortion in more than 33% of cases.
• Cytomegalovirus – most common of perinatal infections.
Congenital defects include bone lesions, anemia, low birth
weight, hepatomegaly, splenomegaly, jaundice, petechiae,
heart disease, pneumonia, cataracts, chorioretinitis,
microcephaly, obstructive hydrocephaly, intracranial
calcifications, and encephalitis.
• Herpes (HERPES SIMPLEX VIRUS TYPE 2)
Genital herpes infection is a sexually transmitted disease
caused by the herpes simplex virus (HSV) type 2.
Herpes can be transmitted across the placenta to cause
congenital infection in the NB
Herpes can be transmitted at birth if active lesions are
present at that time in the vagina or vulva.
When infection in the NB occurs, Congenital Herpes can
result.
To avoid transmission, CS may be scheduled. If no lesions
are present, a vaginal birth is preferable.
Dx : Appearance of lesions, PAP smear, enzyme
Immunosorbent Assay (ELISA)
Treatment :
1. Drug of choice is acyclovir (Zovirax) in an ointment or oral
form
2. Women can reduce the pain of infection by sitz baths or
applying warm. Moist tea bags to the lesions.
Assessment :
Painful, small, pinpoint vesicles surrounded by erythema on
the vulva or in the vagina 3-7 days after exposure.

B.HEMATOLOGIC DISORDERS AND PREGNANCY
 Hematologic disorders during pregnancy involve either
blood formation or coagulation disorders.
Anemia And Pregnancy
 Because the blood volume expands during pregnancy,
most women have a pseudoanemia of early pregnancy.
This is normal and should not be confused with the true
anemia that can occur as a complication of pregnancy.
Nursing Diagnosis: Risk for altered tissue perfusion
1. THE WOMAN WITH IRON DEFICIENCY ANEMIA
 Most common anemia of pregnancy
 Iron deficiency anemia is characteristically a microcytic
(small-sized red blood cell), hypochromic (less Hgb than the
average red blood cell) anemia, because when an
adequate supply of iron is not ingested, iron is unavailable
for incorporation into red blood cells and so cells are not as
large or as rich in hemoglobin as normally. Both Hgb and
Hct will be reduced.
Therapeutic Management :
1. All women should take prenatal vitamins that contain an iron
supplement of 60 mg of elemental iron as prophylactic therapy.
2. Advise women to take iron supplements with orange juice or a
Vitamin C supplement.
3. They need to eat diet high in iron and vitamins
3. For severe iron deficiency anemia, and patient is
noncompliant with oral iron therapy, Iron Dextran IM or IV can be
administered.
Etiology :
1. Diet low in iron
2. Heavy menstrual periods
3. unwise weight-reducing programs
4. Low socio-economic status
Complications :
1. Low fetal birth weight
2. Preterm birth
Assessment :
1. Extreme fatigue and poor exercise tolerance.
2. THE WOMAN WITH FOLIC ACID DEFICIENCY ANEMIA
 Folic acid or Folacin is necessary for both the normal
formation of red blood cells in the mother.
 Associated with a decrease in neural tube defects in the
fetus.
Etiology :
1. Occurs most often in multiple pregnancies because of the
increased fetal demand.
2. In women with a secondary hemolytic illness in which there is
rapid destruction and production of red blood cells
3. In women who are taking hydantoin, a drug that interferes with
folate absorption.
4. Alcohol abuse – suppresses the metabolic effects of folic acid
Assessment:
The main symptom of folic acid deficiency anemia is a history of
severe, progressive fatigue. Associated findings include
shortness of breath, palpitations, diarrhea, nausea, anorexia,
headaches, forgetfulness, and irritability. The impaired oxygen-
carrying capacity of the blood from lowered hemoglobin levels
may produce complaints of weakness and light-headedness.
Megaloblastic anemia (enlarged red blood cells) – anemia that
develops.
 The mean corpuscular volume will be elevated.
 May be a factor in early abortion or abruptio placenta
Therapeutic Management :
1. Vitamin supplement of 400 ug of folic acid daily
2. assist with planning a well balanced diet that includes
meals and snacks that are high in folic acid (eg.
Asparagus, beef liver, brocolli, green and leafy
vegetables, mushrooms, oatmeal, peanut butter, red
beans, whole wheat bread)
3. Encourage to eat and drink a rich source of vitamin C
at each meal to enhance absorption of folic acid
3. THE WOMAN WITH SICKLE CELL ANEMIA
 Sickle cell anemia is a recessively inherited hemolytic
anemia caused by an abnormal amino acid in the beta
chain of hemoglobin. (The amino acid valine is substituted
for glutamic acid in the sixth position of the beta chain
causing the hemoglobin structure to change.) It is a
congenital hematologic disease that causes impaired
circulation, chronic ill health, and premature death. Patients
who suffer from this disease inherit the sickling gene from
both parents, although some parents may only be carriers
and don’t experience the symptoms. If both parents are
carriers, chances are that one in four of their children will be
affected.
 Infection, exposure to cold, high altitudes, overexertion or other
situations that cause cellular oxygen deprivation may trigger a
sickle cell crisis. The deoxygenated, sickle-shaped red blood
cells stick to the capillary wall and each other, blocking blood
flow and causing cellular hypoxia. The crisis worsens as tissue
hypoxia and acidic waste products cause more sickling and cell
damage.
Complications:
1. Increased incidence of asymptomatic bacteriuria, resulting in an
increased incidence of pyelonephritis.
2. In pregnancy, blockage to the placental circulation can lead to
direct fetal compromise with low birth weight and possibly death.
3. The anemia can threaten the pregnant woman’s life if vital blood
vessels as those to the liver, kidneys, heart, lungs, or brain become
blocked.
Assessment :
1. Hemolysis in a sickle cell crisis may occur so rapidly that a
woman’s hemoglobin level can fall to 5 or 6 mg/100 ml in a few
hours.
2. Rise in indirect bilirubin level
3. Susceptible to bacteriuria, preeclampsia and UTI’s
4. Assess for pooling of blood in the lower extremities
5. Severe abdominal pain, muscle spasms, leg pains, painful and
swollen joints, fever, vomiting, hematuria, seizures, stiff neck, coma
and paralysis.
Therapeutic Management :
1. Replace sickle cells with normal cells by exchange transfusion
periodically throughout the pregnancy.
2. If a crisis occurs, control pain, administer oxygen as needed
3. Increase fluid volume of the circulatory system to lower viscosity.
Fluid administered is often hypotonic(0,45 saline) to keep plasma
tension low
4. As a rule, women with sickle cell anemia should not be given iron
supplement because the woman’s cells can’t absorb iron in the usual
manner; taking supplements can lead to iron overload.
5. Keep woman well hydrated during labor.
COAGULATION DISORDERS AND PREGNANCY
 Most coagulation disorders are sex linked, or only occurs in
males, so have little effect on pregnancies.
 Von Willebrand’s disease is a coagulation disorder inherited as
an autosomal dominant trait that does occur in women.
Signs/Symptoms :
1. Menorrhagia
2. Frequent episodes of epistaxis
3. Prolonged bleeding time
IDIOPATHIC THROMBOCYTOPENIC PURPURA :
 A decrease number of platelets
Etiology:
- unknown but assumed to be autoimmune illness
Signs/Symptoms :
1. Miniature petechiae or large ecchymoses appear on the woman’s
body.
2. Frequent nose bleeds may occur
3. Marked thrombocytopenia
Therapeutic Management :
1. Platelet transfusion to temporarily increase platelet count
2. Oral prednisone is effective
C. RENAL AND URINARY DISORDERS AND PREGNANCY
 Adequate kidney function is important to successful pregnancy
outcome; any condition that interferes with kidney or urinary
function is therefore potentially serious.
1. THE WOMAN WITH A URINARY TRACT INFECTION
 The organism most commonly responsible for UTI is
Escherichia coli
Causes :
1. In pregnant woman, because of the dilated ureters from the effect
of progesterone, stasis of urine occurs.
2. .Minimal glucosuria that occurs with pregnancy contributes to the
growth of organisms.
3. Women with known vesicoureteral reflux often develop UTI or
pyelonephritis.
Complications :
1. Asymptomatic infections can flame into pyelonephritis.
2. Increased incidence of preterm labor, PROM and fetal loss may
be associated with pyelonephritis
Assessments :
1. Pain on urination
2. Frequency of urination
3. Hematuria
4. Bacterial count of more than 100,000 colonies per milliliter in a
clean-catch specimen
Therapeutic Management :
1. Urine for culture and sensitivity test to detect infection and to
determine which antibiotic to be used.
2. Amoxicillin, ampicillin and cephalosporins are effective against
most organisms causing UTI.
3. Sulfonamides can be used early in pregnancy but not near
term because they interfere with protein binding of bilirubin.
Nursing Diagnosis: Risk for infection
Common Measure to prevent UTI :
1. Voiding frequently (at least every two hours)
2. Wiping front to back after bowel movements
3. Wearing cotton, not synthetic fiber underwear
4. Voiding immediately after sexual intercourse
2. THE WOMAN WITH CHRONIC RENAL DISEASE
 Pregnancy increases the work load of the kidneys because
the woman’s kidneys must excrete waste products not only
for herself but for the fetus for 40 weeks.
 Many women with renal disease take a corticosteroid at a
maintenance level. An effect that may occur is that the
infant may be hyperglycemic at birth because of the
suppression of insulin activity by corticosteroid.
 Infants of women with renal disease tend to have
intrauterine growth restriction from lessened placental
perfusion.
 Women may develop severe anemia because their
diseased kidneys do not produce erythropoietin
 Many women with renal disease have elevated blood
pressure.
 Women with kidney disease who normally have an elevated
serum creatinine level more than 2.0 mg/dl may be advised
not to undertake a pregnancy or the increased strain on
already damaged kidneys could lead to kidney failure
 Women with kidney transplants should be considered
individually to determine whether they will be able to carry a
pregnancy to term before a pregnancy is initiated.
 Women with severe renal disease may require dialysis to
aid kidney function during pregnancy. This is associated
with a risk of preterm labor because progesterone is
removed with the dialysis. To prevent this complication
Progesterone IM may be administered before dialysis
D. RESPIRATORY DISORDERS AND PREGNANCY
 Chronic respiratory conditions may worsen in pregnancy
because the rising uterus compresses lung space.
 Any respiratory disorder can pose serious hazards to the
fetus if allowed to progress to the point where the mother’s
oxygen-carbon dioxide exchange is altered.
Nursing Diagnosis: Risk for ineffective breathing pattern
1. THE WOMAN WITH ACUTE NASOPHARYNGITIS
 Acute nasopharyngitis (common colds) tends to be more
severe during pregnancy because during this period
estrogen stimulation normally causes some degree of nasal
congestion.
2. THE WOMAN WITH INFLUENZA
 Influenza is caused by a virus that is identified as Type A, B
or C.
 Type A causes most infections.
Assessment :
1. Disease spreads in epidemic form
2. High fever
3. Extreme prostration
4. Aching pains in the back and extremities
5. A sore, raw throat.
 Correlate with preterm labor and abortion
 Treated with antipyretic to control fever and perhaps a
prophylactic antibiotic to prevent a secondary infection such
as pneumonia.
 Exposure to influenza while in utero was associated with
the development of schizophrenia in later life. Later studies
do not show this association.
3. THE WOMAN WITH PNEUMONIA
 Pneumonia is the bacterial or viral invasion of lung tissue.
 Pneumonia poses a serious complication of pregnancy because
fluid collects in alveolar spaces causing limited oxygen-carbon
dioxide exchange in the lungs.
 After the invasion, an acute inflammatory response occurs with
exudates of red blood cells, fibrin, and polymorphonuclear
leukocytes into the alveoli. This process confines the bacteria or
virus within segments of the lobes of the lungs.
Treatment :
1. Appropriate antibiotic
2. Oxygen administration
3. Ventilation support maybe necessary in severe cases.
 There is tendency of preterm labor late in pregnancy
4. THE WOMAN WITH ASTHMA
 Asthma is paroxysmal wheezing and dyspnea in response to an
inhaled allergen.
 With inhalation of allergen, there is an immediate histamine
release from IgE immunoglobulin interaction. This results in
constriction of the bronchial smooth muscle, marked mucosal
swelling, and the production of thick bronchial secretions.
These 3 processes reduce the lumen of air passages markedly.
Symptoms :
1. Difficulty with air exchange; on exhalation, she makes a high
pitched whistling sound (bronchial wheezing)
 Asthma has the potential of reducing oxygen supply to the fetus
if a major attack should occur.
 Many women find their asthma improved during pregnancy by
the high circulating levels of corticosteroid.
 Women with asthma have a higher rate of preterm birth
Treatment :
1. Beta-adrenergic agonists such as terbutaline and albuterol are the
drugs of choice. If ineffective, theophylline, a corticosteroid or
cromolyn sodium may be added to the regimen.
5. THE WOMAN WITH TUBERCULOSIS
 With TB, lung tissue is invaded by mycobacterium tuberculosis,
an acid-fast bacillus
Assessment:
1. Chronic cough
2. weight loss
3. Hemoptysis
4. Night sweats
5. Low-grade fever
6. Chronic fatigue
Therapeutic Management :
1. Isoniazid (INH) and ethambutol Hcl are drugs of choice. INH may
result in a peripheral neuritis if the woman does not take
supplemental pyridoxine (vitamin B6). Ethambutol may cause optic
nerve involvement in the mother.
2. Maintain an adequate level of calcium
3. A woman is advised to wait 1 to 2 years after the infection
becomes inactive before attempting to conceive.
TB lesions never really disappear but are only “closed off” and made
inactive.
 Recent inactive TB can become active during pregnancy,
because pressure on the diaphragm from below changes the
shape of the lungs, and a sealed pocket may be broken in this
process.
 Recent inactive TB may also become active during the post-
partal period, as the lung suddenly returns to its more vertical
pre-pregnant position and breaks open calcium deposits.
 Although TB can be spread by the placenta to the fetus, it is
usually spread to the infant after birth
 A woman should have at least 3 negative sputum cultures
before she holds/cares for her infant. If negative, there is no
need to isolate infant from mother; she can even breastfeed.
6. THE WOMAN WITH CYSTIC FIBROSIS
 Cystic Fibrosis is a recessively inherited disease in which there
is generalized dysfunction of the exocrine glands. This
dysfunction leads to mucus secretions, particularly in the
pancreas and lungs, so thick that normal secretion is blocked.
 Women may have lessened fertility from inability of sperm to
migrate through viscid cervical mucus.
Symptoms :
1. Chronic respiratory
2. Over inflation of lungs from the thickened mucus
3. Inability to digest fat and protein because the pancreas cannot F. GASTROINTESTINAL DISORDERS AND PREGNANCY
release amylase.  Minor gastrointestinal disorders are common in pregnancy
(nausea, heartburn, constipation). Acute abdominal pain or
Complications : vomiting are causes for concern
1. Increased risk for preterm labor  Women who have colostomies can complete pregnancy without
2. Risk for perinatal death difficulties.
3. High possibility of developing DM due to pancreas
involvement Nursing Diagnosis: Risk for altered nutrition, less than body
requirements

Treatment :
1. Pancrelipase – to supplement pancreatic enzymes 1. THE WOMAN WITH APPENDICITIS
2. Bronchodilator  Appendicitis is inflammation of the appendix.
3. Antibiotic
4. Postural drainage daily – to reduce a buildup of lung Assessment :
secretions 1. Nausea
5. Iron supplement – because panrelipase interferes with iron 2. Generalized abdominal discomfort
absorption 3. Vomiting
6. Monitor for serum glucose to detect development of 4.Sharp, peristaltic, lower right quadrant pain
gestational diabetes 5. Leukocytosis
6. Elevated temperature
 It is not usually recommended for postpartum women with 7. Ketones in the urine
cystic fibrosis to breastfeed because their breast milk  In the pregnant woman, the appendix is often displaced so far
contains more fatty acid. upward in the abdomen that the localized pain may be so high it
resembles pain of gallbladder disease.
E. RHEUMATIC DISORDERS AND PREGNANCY  Advise woman not to take food, liquid, or laxatives because
increasing peristalsis tends to cause an inflamed appendix to
Nursing Diagnosis : Pain related to rheumatic disorder during rupture.
pregnancy
Therapeutic Management :
1. THE WOMAN WITH JUVENILE RHEUMATOID ARTHRITIS 1. CS if fetus is near term, then remove appendix.
 Juvenile Rheumatoid Arthritis is a disease of connective 2. Laparoscopy – if condition occurs in early pregnancy
tissue with joint inflammation and contracture, probably the
result of an autoimmune response. 2. THE WOMAN WITH A HIATAL HERNIA
 Hiatal Hernia is a condition in which a portion of the stomach
Pathology : extends and protrudes up through the diaphragm into the chest
The disease pathology is synovial membrane destruction. cavity.
Inflammation with effusion, swelling, erythema, and painful
motionof the joints occurs. Overtime, formation of granulation Symptoms :
tissue can fill the joint space, resulting in permanent 1. Heartburn
disfigurement and loss of joint motion. 2. Gastric regurgitation
Treatment : 3. Indigestion
1. Corticosteroids and salicylate therapy – a danger of large 4. Dysphagia
amounts of salicylates is prolonged pregnancy (salicylates 5. Possible weight loss due to inability to eat
interferes with prostaglandin synthesis, so labor contractions are 6. Hematemesis in extreme cases
not initiated). The woman is asked to decrease salicylate intake
2 weeks before term to avoid the problem. Dx : Diagnosed by direct endoscopy or sonogram
2. THE WOMAN WITH SYSTEMIC LUPUS ERYTHEMATOSUS Therapeutic Management :
 SLE is a multisystem chronic disease of connective tissue 1. Antacids to relieve pain
that can occur in women of childbearing age. 2. Elevate head when sleeping
 Highest incidence is in women ages 20 to 40 years
 Widespread degeneration of connective tissue occurs with 3. THE WOMAN WITH CHOLECYSTITIS AND CHOLELITHIASIS
the onset of illness
Assessment : Etiology :
1. Marked skin change is erythematous “butterfly-shaped” rash 1. Associated with women older than 40 years
on the face. 2. Obesity
 Most serious of the kidney changes are fibrin deposits that 3. Multiparity
plug and block the glomeruli, leading to necrosis and 4. High fat diet
scarring. 5. Gallstones are formed from cholesterol
 The thickening of collagen tissue in the blood vessels
causes vessel obstruction, blood flow to the vital organs Symptoms :
become compromised and to the fetus if blood flow to the 1. Aching and pressure in the right epigastrium
placenta is obstructed 2. Jaundice
Treatment : Therapeutic Management :
1. Corticosteroid, NSAID’s and salicylate therapy to reduce 1. Lower fat intake. Low fat but fat free diet because of the
symptoms of joint pain and inflammation. importance of linoleic acid for fetal growth.
2. IVF for acute episodes to provide fluid and nutrients
Complication : 3. Analgesics
1. Acute nephritis with glomeruli destruction 4. Laparoscopy if cannot be controlled by conservative management
2. Higher incidence of abortion and preterm births.
3. Infants may be born with lupuslike rash, anemia and Dx : Sonogram
thrombocytopenia.
4. Congenital heart block can occur in the NB. 4. THE WOMAN WITH VIRAL HEPATITIS
 Hepatitis is liver disease that may occur from invasion of the A,
 With nephritis, BP will rise. Patient will develop hematuria B, C, or D virus.
and decreased urine output. Proteinuria and edema may  Hepatitis A is spread mainly by contact with another person or
begin. by ingestion of fecally contaminated water or shellfish
 Women will be monitored by frequent serum creatinine  Incubation period 2 to 6 weeks.
levels to assess kidney function. Dialysis or plasmapheresis  Prophylactic gamma globulin to prevent the disease after
may be necessary. exposure.
 Women are asked to reduce salicylate close to birth to  Hepatitis B (serum hepatitis) is spread by transfusion of
reduce possibility of bleeding in the NB contaminated blood or blood products; it can be spread by
 Hydrocortisone IV is administered during labor to help the semen or vaginal secretions and thus considered STD.
woman to adjust to the stress at this time.  Incubation period 6 weeks to 6 months
 Infants with woman who have SLE tends to be small for  Hepatitis B vaccine may be administered to those who are at
gestational age due to the decreased blood flow to high risk
placenta.
Assessment :
1.Nausea, vomiting  Woman is advised to inform health personnel that she has
2. Liver is tender to palpation recurrent seizures and the medications she is taking
3. Dark yellow urine
4. Light colored stools Nursing Diagnosis: Risk for altered parenting
5. Jaundice
6. On physical examination, liver is enlarged  A woman who has recurrent convulsions may worry that her
7. Elevated bilirubin child will have seizures as the child grows older.
8. Increased liver enzymes  If seizures are result of acquired disorder, assure the woman
that her child will have no tendency toward seizures.
Dx : Liver Biopsy
2. THE WOMAN WITH MYASTHENIA GRAVIS
 Myasthenia Gravis is an autoimmune disorder characterized by
Therapeutic Management : the presence of an IgG antibody against acetylcholine receptors
1. Bed rest in striated muscle.
2. High calorie diet  It produces sporadic but progressive weakness and abnormal
3. Contact precautions when giving care fatigue in striated (skeletal) muscles. This weakness and fatigue
are exacerbated by exercise and repeated movement but
improved by anticholinesterase drugs. Usually, myasthenia
Complications : gravis affects muscles innervated by the cranial nerves (face,
1. Abortion and preterm labor lips, tongue, neck, and throat), but it can affect any muscle
2. Infants with mothers who have HB Ag-positive will develop group.
chronic hepatitis
 Other common signs of myasthenia gravis include weak eye
 After birth, infant should be washed well to remove any closure, ptosis and diplopia, blank masklike facial expression,
maternal blood. difficulty chewing and swallowing, a hanging jaw, bobbing
 Hepatitis B immune globulin (HBIG) and Hepa B motion of the head, and symptoms of respiratory failure if
immunization should be administered to the NB respiratory muscles are involved
 Infants should be observed for infection
 Mother should not breastfeed because HB Ag antigens can Treatment :
be recovered from breast milk. 1. Administration of anti-cholinesterase drugs such as neostigmine
and pyridostigmine counteract fatigue and muscle weakness and
5. THE WOMAN WITH INFLAMMATORY BOWEL DISEASE enable about 80% of normal muscle function
 Crohn’s Disease (inflammation of the terminal ileus) and 2. Plasmapheresis (withdrawal and replacement of plasma) to
ulcerative colitis (inflammation of the distal colon) remove immune complexes from the bloodstream
Etiology :
1. Occurs most often in young adults Between ages 12 and 30 Interventions:
years 1. Help the woman plan daily activities to coincide with energy
2. Cause is unknown but an autoimmune process may be peaks.
responsible 2. Teach the client how to recognize adverse effects and signs of
toxicity of anticholinesterase drugs (headaches, sweating, abdominal
Symptoms : cramps, nausea, vomiting, diarrhea, excessive salivation,
1. Shallow ulcers bronchospasm). Warn her to avoid strenuous exercise, stress,
2. Chronic diarrhea infection, and unnecessary exposure to the sun or cold weather.
3. weight loss Caution her to avoid taking other medications without consulting her
4. Occult blood in stool primary care giver.
5.Nausea and vomiting 3. Magnesium sulfate should be avoided because it can diminish the
6. Obstruction and fistula formation with peritonitis can occur in acetylcholine effect and therefore increase disease symptoms.
extreme conditions
> Malabsorption particularly of Vit B12 occurs 3. THE WOMAN WITH MULTIPLE SCLEROSIS
Complications :  Nerve fibers become demyelinated and lose function. Pregnant
1. Interferes with fetal growth women with this disorder grow increasingly fatigued as
Therapy : pregnancy progresses.
1. Total rest for GI tract by total parenteral nutrition  Other signs and symptoms include visual disturbances such as
2. Sulfasalazine, an anti inflammatory. Close to birth, dosage is optic neuritis, diplopia and blurred vision, sensory impairment
reduced because it may interfere with bilirubin binding sited and such as paresthesia, urinary disturbances such as
can cause neonatal jaundice. incontinence, frequency, urgency, and infections, emotional
lability such as mood swings, irritability and euphoria and other
G. NEUROLOGIC DISORDERS AND PREGNANCY associated signs like poorly articulated speech and dysphagia
 Any neurologic disease with symptoms of seizures must be
carefully managed during pregnancy because anoxia Etiology :
caused by severe seizures could deprive the fetus with 1. exact cause is unclear; however, current theories suggest that it
oxygen, with serious outcomes. may be caused by an autoimmune response to a slow-acting or
latent viral infection or by environmental or genetic factors
Nursing Diagnosis : Risk for Injury (maternal) 2. Predominant in women between 20-40 years old (childbearing
1. THE WOMAN WITH A SEIZURE DISORDER age)

Etiology :
1. Head trauma
2. Meningitis
3. Cause of recurrent seizures are unknown (idiopathic)
Therapeutic Management :
1. “Do not take medication during pregnancy” rule does not apply
to seizure control medications. The risk of adverse maternal or
fetal outcome from seizures during pregnancy is greater than the
risk of teratogenicity from taking anticonvulsant drugs.
Complications :
1. Infants may have an increased danger of neural tube
disorders and childhood malignancies as a result of folic acid
displacement from maternal medication.
2. Infants are also prone to hemorrhagic disease because of
decreased Vit K coagulation factors at birth.
Nursing Diagnosis : Risk for altered placental perfusion
Tonic-clonic seizures (sustained full-body involvement) could
affect the fetus because of anoxia that can occur form spasms of
chest muscles.
 Administer oxygen by mask is good prophylaxis to ensure
adequate fetal oxygenation
Treatment :
1. ACTH or a corticosteroid to strengthen nerve conduction
2. Plasmapheresis (withdrawal and replacement of plasma)
Interventions:
⇒ Emphasize the need to avoid stress, infections, and
fatigue and to maintain independence by finding new ways
to perform daily activities.
⇒ Explain the value of a well balanced nutritious diet that
contains sufficient fiber.
⇒ Evaluate the need for bowel and bladder training
Complications :
1. UTI
2. Painless precipitous birth if quadriplegia is present
3. Dysreflexia from the pain of labor which leads to HPN, headache,
diaphoresis and bradycardia
H. MUSCULOSKELETAL DISORDERS AND PREGNANCY
1. THE WOMAN WITH SCOLIOSIS
 Scoliosis is lateral curvature of the spine
Etiology :
1. Often in women approximately 12 years of age 5. Poor fetal heart tone variability from poor tissue perfusion
6. Decreased amniotic fluid from intrauterine growth retardation
Complications : 7. Edema from poor venous return
1. Cosmetic deformity 8. Irregular pulse
2. Because of chest compression, interferes with respiration and 9. Chest pain on exertion
heart action
3. Pelvic distortion Diagnostic Assessment : Chest x-ray, ECG

Therapeutic Management : Fetal Assessment :

1. Stainless steel rods (Harrington rods) implanted on both sides 1. Low birth weights
of spinal vertebrae to strengthen and straighten the spine. 2. Severe fetal distress
2. CS, if pelvis is distorted.
Nursing Diagnosis : Knowledge deficit regarding the effects of
I. CARDIOVASCULAR DISORDERS AND PREGNANCY maternal cardiovascular disease

1. THE WOMAN WITH LEFT-SIDED HEART FAILURE Nursing Interventions :

 Occurs with conditions such as mitral stenosis, mitral
insufficiency and aortic coarctation.
 Occurs when the left ventricle is unable to move forward the
volume of blood received by the left atrium from the
pulmonary circulation
Clinical Manifestations :
1. Productive cough of blood-speckled sputum
2. Fatigue, weakness, dizziness
3. Orthopnea
4. Paroxysmal nocturnal dyspnea - suddenly waking at night
short of breath
Complications :
1. High risk for Abortion
2. preterm labor
3. Maternal death
Therapeutic Management :
1. Anti-hypertensives
2. Beta-blockers to decrease the force of myocardial
contractions
2. THE WOMAN WITH RIGHT-SIDED FAILURE
 Congenital heart defects such as pulmonary valve stenosis
and atrial and ventricular septal defects may result in right-
sided heart failure.
 Occurs when the output of the right ventricle is less than the
blood volume the heart receives at the right atrium from the
vena cava or venous circulation. Back pressure from this
results in congestion of the systemic venous circulation and
decreases cardiac output to the lungs.
 Blood pressure falls in the aorta because less blood is
reaching it ;
 Pressure is high in the vena cava
 Both jugular venous distention and increased portal
circulation occur.
 Both the liver and spleen become distended
 Distention of abdominal vessels can lead to exudates of
fluid from the vessels into the peritoneal cavity (ascites).
Fluid moves from the systemic circulation into interstitial
spaces (peripheral edema).
 Liver enlargement can cause extreme dyspnea and pain
because it will put extreme pressure on the diaphragm.
 Eisenmenger’s syndrome – congenital anomaly most apt to
cause right-sided failure (A right-to-left atrial or ventricular
septal defect with accompanying pulmonary stenosis). They
need oxygen administration and frequent arterial gases to
ensure fetal growth.
1. Promote rest
2. Promote healthy nutrition
3. Educate regarding medication
4. Educate regarding avoidance of Infection
4. THE WOMAN WITH AN ARTIFICIAL VALVE PROSTHESIS
 Many women with valve prosthesis take oral anticoagulants to
prevent formation of blood clots at valve site. However, these
medications increase the risk of congenital anomalies in infants
 Women are placed on heparin therapy before becoming
pregnant
 Observe for signs of premature separation of the placenta
during pregnancy and labor because anticoagulant in the
mother may cause placental dislodgement.
5. THE WOMAN WITH CHRONIC HYPERTENSIVE VASCULAR
DISEASE
 Women with chronic hypertensive vascular disease come into
pregnancy with elevated BP. This kind of HPN is usually
associated with arteriosclerosis or renal disease
 Fetal well-being is compromised by poor placental perfusion
during pregnancy
 Management is similar with PIH
6. THE WOMAN WITH VENOUS THROMBOEMBOLIC DISEASE
 Incidence increases during pregnancy due to acombination of
stasis of blood in the lower extremities from uterine pressure
and hypercoagulability (effect of increased estrogen)
Signs/symptoms :
1. Chest pain
2. Sudden onset of dyspnea
3. Cough with hemoptysis
4. Tachycardia or missed beats
5. Severe dizziness or fainting from lowered blood pressure
Therapeutic Management :
1. Avoid use of constrictive knee-high stockings,
2. Do not cross legs
3. Bed rest
4. Heparin IV administration
J. ENDOCRINE DISORDERS AND PREGNANCY
1. THE WOMAN WITH A THYROID DYSFUNCTION
 Thyroid gland enlarges slightly due to increased vascularity, as
a normal effect of pregnancy
Nursing Diagnosis: Risk for maternal and fetal injury

3. THE WOMAN WITH PERIPARTAL HEART DISEASE 2. THE WOMAN WITH HYPOTHYROIDISM
 A rare condition in pregnancy because women with symptoms
Peripartal cardiomyopathy – extremely rare condition that of untreated hypothyroidism are anovulatory and often unable
originate late in pregnancy. Due to the effect of pregnancy on the to conceive
circulatory system.
 Cause is unknown. May occur from previously undetected Signs/symptoms :
heart disease 1. Easy fatigability
Signs/symptoms : 2. Obese
1. Late in pregnancy, woman develops signs of myocardial 3. dry skin
failure : Shortness of breath, chest pain, and edema 4. Little tolerance for cold
2. Cardiomegaly (enlargement of the heart) 5. Extreme nausea and vomiting
Therapeutic Management :
1. Reduced activity Therapeutic Management :
2. Diuretic and digitalis therapy 1. Thyroxine – to supplement lack of thyroid hormone. As a rule, her
3. Low dose heparin to decrease the risk of thromboembolism. dose of thyroxine will be increased for the duration of pregnancy to
4. Immunosuppressive therapy simulate the effect that would normally occur in pregnancy

Assessment Of The Woman With Cardiac Disease : 3. THE WOMAN WITH HYPERTHYROIDISM
1.Fatigue
2. Cough Symptoms :
3. Increased respiratory rate 1. Rapid heart rate
4. tachycardia 2. Exophthalmos
3. Heat Intolerance
4. Nervousness
5. Heart palpitation
6. Weight loss
 If undiagnosed, woman may develop heart failure during
pregnancy because her rapid heart rate cannot adjust to the
increasing serum volume occurring with pregnancy.
Complications :
1. PIH
2. Fetal growth restriction
3. preterm labor
Therapeutic Management :
1. Thiomides to reduce thyroid activity. Unfortunately, these
drugs are teratogens and possibly enlarges thyroid gland of the
fetus. Woman should be regulated on the lowest dose possible
 Women on anti-thyroid drugs may be advised not to
breastfeed because these drugs are excreted in breast
milk.
4. THE WOMAN WITH DIABETES MELLITUS
 DM is an endocrine disorder in which the pancreas is
unable to produce adequate insulin to regulate body
glucose
Pathophysiology :
 The pancreas has both endocrine and exocrine types of
tissue. The Islets of Langerhans form the endocrine portion.
Alpha islet cells secrete glucagons; beta islet cells secrete
insulin.
 Insulin is essential for carbohydrate metabolism and is
important to the metabolism of fats and protein. The actual
amount of insulin produced is regulated by serum glucose
levels. When serum glucose exceeds 100 mg/dl, beta cells
immediately increase insulin production. When blood serum
levels are lowered, production decreases. Both the ability to
secrete additional insulin and the action to decrease
production are immediate responses.
The primary problem of any woman with DM is control of the
balance between insulin and blood glucose to prevent
hyperglycemia or hypoglycemia
 Glomerular filtration of glucose is increased causing slight
glycosuria. The rate of insulin secretion is increased, and
the fasting blood sugar is lowered.
 All women appear to develop insulin resistance as
pregnancy progresses, a phenomenon that is probably
caused by the presence of the hormone human placental
lactogen and high levels of cortisol, estrogen, progesterone
and catecholamines.
 If the pancreas cannot respond by producing additional
insulin, excess glucose moves across placenta to fetus
where fetal insulin metabolizes it, and acts as growth
hormone, promoting macrosomia
 The continued use of glucose by the fetus may lead to
hypoglycemia.
 There is a high incidence of congenital anomaly, abortion,
and stillbirth in infants.
 At birth, infants are more prone to hypoglycemia,
respiratory distress syndrome, hypocalcemia, and
hyperbilirubinemia.
Amanuel/Pslidasan/Ksjuliano
NCM 104
1st sem S.Y. 2006-2007
5. THE WOMAN WITH GESTATIONAL DIABETES
 Pregnant woman becomes diabetic usually at the midpoint
of pregnancy when insulin resistance become noticeable –
Gestational Diabetes Mellitus
Risk Factors for gestational diabetes :
1. Obesity
2. Age over 30 years
3. History of large babies
4. History of unexplained fetal loss
5. History of congenital anomalies in previous pregnancies
6. History of unexplained perinatal loss
7. Family history of diabetes
Pathophysiology
• In gestational diabetes mellitus, insulin antagonism by
placental hormones, human placental lactogen,
progesterone, cortisol, and prolactin leads to increased
blood glucose levels. The effect of these hormones
peaks at about 26 weeks gestation. This is called the
diabetogenic effect of pregnancy.
• The pancreatic beta cell functions are impaired in
response to the increased pancreatic stimulation and
induced insulin resistance.
• Pregnancy complicated by diabetes pits the mother at high
risk for the development of complications such as
spontaneous abortion, hypertensive disorders, preterm
labor, infection, and birth complications.
• The effects of diabetes on the fetus include hypoglycemia,
hyperglycemia, and ketoacidosis. Hyperglycemic effects
can include
a. congenital defects
b. macrosomia
c. intrauterine growth restriction
d. intrauterine fetal death
e. delayed lung maturity
f. neonatal hypoglycemia
g. neonatal hyperbilirubinemia
Assessment :
1. Dizziness
2. Confusion if hyperglycemic
3. Thirst
4. Increased risk of PIH
5. Congenital anomalies
6. Macrosomia
7. Poor fetal heart tone variability and rate from poor tissue perfusion
8. Hydramnios
9. Glycosuria, polyuria
10. Possibility of increased monilial infection
Nursing Interventions
• Teach the client the effects and interactions of diabetes
and pregnancy and signs of hyper and hypoglycemia
• Teach client how to control diabetes in pregnancy, advise
changes that need to be made in nutrition and activity
patterns to promote normal glucose levels and prevent
complications.
• Advise client of increased risk of infection and how to
avoid it.
• Observe and report any signs of pre-eclampsia.
• Monitor fetal status throughout pregnancy
• Assess status of mother and baby frequently
- carefully monitor fluid, calories, glucose and insulin during
labor and delivery
- continue careful observation in postdelivery period
6.HYPERGLYCEMIA
Nursing Diagnoses :
1. Risk for altered tissue perfusion
2. Altered nutrition less than body requirements r/t inability to use
glucose
3. Risk for ineffective individual coping
4. Risk for infection
5. Fluid volume deficit r/t polyuria accompanying disorder
6. Knowledge deficit r/t difficult and complex health problem
7. Health-seeking behaviors r/t to voiced need to learn home glucose
monitoring
8. Noncompliance r/t discouragement, misunderstanding or fear of
therapeutic measures
Nursing Interventions :
1. Education regarding nutrition
2. Education regarding exercise
Therapeutic Management :
1. Insulin
2. monitor fetal well-being
K. MENTAL ILLNESS AND PREGNANCY
 Mental illness may precede or occur with pregnancy.
Depression is the most common mental illness seen.
 Lithium, a mainstay of therapy for bipolar disorders is a known
teratogen.
L. TRAUMA AND PREGNANCY
 Trauma occurs at high incidence in childbearing years because
for this age group, automobile accidents, homicide, and suicide
are among the three leading causes of death.
 High incidence occurs during the last trimester due to
clumsiness, fainting and hyperventilation.
 Orthopedic injuries occur because the pregnant woman’s sense
of balance is altered
PHYSIOLOGIC CHANGES IN PREGNANCY THAT AFFECT
TRAUMA CARE
 After a traumatic injury, a woman’s body will maintain her own
homeostasis at the expense of the fetus.
 The woman’s total plasma volume increases during
pregnancy at term. This increase serves as a safeguard tot
the woman if trauma with bleeding should occur.
 Fluid replacement volume would be high in case of injury
because pregnant woman needs more fluid to restore fully
her circulatory volume.
 Peripheral venous pressure in pregnant woman is
unchanged, it tends to be higher in the lower extremities
because of the compression of the vena cava and back
pressure. This causes lacerations of the legs or perineum to
bleed much more profusely than usual.
 During pregnancy, leucocyte count rises so it is difficult to
use this determination as a sign of infection after an open
wound.
 Serum albumin level decreases during pregnancy, making
the large loss that normally occurs with burns a more
serious than usual response.
 Serum liver enzyme levels remain the same during
pregnancy, so if these are elevated during trauma, liver
trauma can be detected.
 Bleeding into the abdominal cavity with an abdominal injury
is apt to be forceful and extreme because of the increased
pressure in the pelvic vessels.
 Paracentesis is dangerous because the bowel, dislocated
from its usual position, can be easily punctured.
 Culdocentesis may be done
 Peritoneal lavage may reveal bleeding or bladder rupture
best.
 Bladder of pregnant woman is susceptible to rupture
because it is the most anterior organ and is elevated
abnormally.
 After abdominal trauma, an indwelling bladder catheter is
inserted to assess for blood in the urine.
Emotional Considerations :
 A feeling of guilt lowers self-esteem and increases the level
of stress.
 People under stress do not process well and so may not
perceive correctly the information given to them.
Initial Assessments After Trauma During Pregnancy
> With multiple trauma, a nasogastric tube is usually passed to
empty the stomach. A foley catheter is inserted to assess for
urine output and to rule out ruptured bladder.
 To prevent supine hypotension syndrome, be sure the
woman does not lie supine for an examination. If it is
necessary for her to lie supine, manually displace the
uterus from the vena cava by placing rolled towels or a
blanket under her right side to tip her body approximately
15o to the side
Nursing Diagnosis :
1. Fear related to threat of injury to the fetus
2. Risk for fetal injury
3. Altered tissue perfusion r/t to severed artery
4. Ineffective breathing pattern related to lung lacerated by
gunshot wound
5. Risk for infection
6. Situational low self-esteem r/t occurrence of accident
7. Powerlessness r/t seriousness of the injury sustained or
inability to prevent accident from occurring.
Therapeutic Management :
1. Immediate Care
 Interventions in emergency situations must be quick yet
always remember that the woman’s primary health
condition is that she is pregnant.
 Cardiopulmonary resuscitation (CPR)
 If there is blood loss, a central venous pressure line may be
inserted.
 If hypotension is present, it must be corrected quickly to
maintain a pressure gradient across the placenta. Epedrine
is the drug of choice for a pregnant woman because it has a
minimal peripheral vasoconstriction effect.
Nursing Diagnosis : Risk for altered tissue perfusion
OPEN WOUNDS:
1. LACERATIONS
 Bleeding should be halted by pressure on the edge of the
laceration
2. PUNCTURE WOUNDS
 If the woman has had tetanus immunization within the past
10 years, tetanus toxoid is administered.
 > If the woman did not have tetanus immunization within 10
years, tetanus toxoid plus immune tetanus globulin is
administered.
 Knife wounds cause deep penetration and are often directed
into the abdomen. Most stab wounds of the abdomen, however,
occur in the upper quadrants of the abdomen above the height
of the uterus.
 To determine the depth and extent of the wound, a fistulogram
may be done.
 If there is suspicion that there is bleeding in the abdomen, a
celiotomy or an exploratory surgical procedure into the
abdominal cavity may be performed
 After surgical repair of an injured diaphragm, CS may be
planned to avoid strain on a newly repaired diaphragm during
labor
3. ANIMAL BITES
 If the rabies immunization status of the dog is known, the
wound is washed and treated as a puncture wound.
 If the dog is questionable, the woman must be administered
rabies immune globulin vaccine.
 Pregnancy is not contraindicated to rabies immunization
because contracting the disease would be so much more
serious
4. BLUNT ABDOMINAL TRAUMA
 No visible break is present on the skin.
 After injury, underlying tissues becomes edematous; broken
underlying blood vessels may ooze and form ecchymosis or
hematoma at the site.
 To assess for abdominal bleeding, a diagnostic peritoneal
lavage may be done, UTZ may also be done.
 Traumatic blow to the abdomen could cause dislodgement of
the placenta (abruptio placentae) or preterm labor.
 Palpate the uterus for any bleeding and count fetal heart tones
using Doppler instrument.
 Sonogram may be used to show that the placenta and uterus
are intact
 A pelvic examination is performed to assess for vaginal
bleeding or seepage of clear water that would suggest the
amniotic membranes were ruptured from the force of an
abdominal blow.
 If there is a uterine contraction, a uterine and fetal monitor
should be placed to estimate the strength and effect on the fetal
heart rate and the possibility that preterm labor has begun.
 Magnesium sulfate is usually selected to halt preterm labor after
trauma.
 The possibility that placental blood will enter the maternal
circulation with uterine trauma is a threat to the Rh negative
woman. Rh (-) woman are therefore, administered Rh immune
globulin (RHIG) after trauma.
5. GUNSHOT WOUNDS
 Assessment of the wound includes inspection of the entry and
exit point of the bullet.
 Uterine wall is so thick that it may trap a bullet; thus there may
be no exit point if the uterus is punctured.
 Gunshot wounds are surgically cleaned and debrided, and is
treated with a high concentration of antibiotics
6. POISONING
 Syrup of Ipecac is the best emetic to cause vomiting and
discharge the poison from the body and is safe during
pregnancy.
 Remember, some poisons can be more harmful if vomited than
if allowed to remain in the body.
7. CHOKING
 It is difficult to use a Heimlich maneuver because of a lack of
space between the uterus and the sternum and because the
person can not reach from the rear around the woman’s
enlarged abdomen.
 Late in pregnancy, a rescuer must use successive chest
thrusts. P. 362 Nursing procedure 14.2
8. ORTHOPEDIC INJURIES
 A woman has poor balance late in pregnancy, she may trip
more readily than usual
 The extra weight pregnant woman carries puts a high
proportion of weight on the wrist, a serious wrist injury can
occur
 Applying ice to the area decreases swelling
 X-ray may be done to determine a fracture.
 Encourage high calcium intake if woman has fracture so both
she and the fetus can have adequate calcium for new bone
growth
9. BURNS
 Burns are dangerous to the pregnant woman because of 5. Knowledge deficit r/t signs and symptoms of possible
the thermal injury that occurs and the inhalation of carbon complications
monoxide gases which can lead to extreme fetal hypoxia as
carbon monoxide crosses the placenta in place of the BLEEDING DURING PREGNANCY
oxygen.  Vaginal bleeding is a deviation from the normal that may occur
 Smoke is irritating to the lung tissue and can result in at anytime during the pregnancy
extensive lung edema; this can cause additional fetal  Primary causes of bleeding during pregnancy
hypoxia due to the lack of oxygen-carbon dioxide exchange
space. 1. BLEEDING AND THE DEVELOPMENT OF SHOCK
 Because the fluid and electrolyte loss can be great with  A woman with any degree of bleeding needs to be evaluated for
burns, hypotension from hypovolemia or an electrolyte hypovolemic shock.
imbalance can occur.
 A body response to a harsh trauma such as burn is the Process of shock due to blood loss
production of prostaglandins, which may cause preterm
labor. Therapeutic Management
 Maternal and fetal prognosis are poor if burns cover more
than 50% of body surface area. Assessment :
 Interestingly, burn tissue heals more quickly than normal 1. Confusion
during pregnancy. This is probably related to the increased 2. Pallor
metabolism and to the increased corticosteroid serum level 3. Increased Pulse
that keeps inflammation and damage to tissue from the 4. Tachypnea
pressure of edema from occurring. 5. Decreased BP
6. Decreased cardiac output
THE BATTERED WOMAN 7. Fetal bradycardia
 Abused women may be pregnant because they were 8. Peripheral vasoconstriction
unable to resist sexual advances from their abusive partner. 9. Decreased urinary output
 Beatings may increase during pregnancy because stress is 10. Cold extremities
often a “trigger” to beatings, and pregnancy can increase Nursing Diagnosis : Risk for fluid volume deficit
the stress.
CONDITIONS ASSOCIATED WITH FIRST TRIMESTER
Assessment : BLEEDING
 A battered woman may come for care late in pregnancy
1. ABORTION
because her partner may control her transportation or
A. SPONTANEOUS ABORTION
money; she may fear that a health care provider will report
the abuse; pretending that the pregnancy does not exist to  Abortion-any interruption of a pregnancy before the fetus is
reduce stress in her home. viable. A non-viable fetus is usually defined as a fetus of 20 to
24 weeks’ gestation or weighing 500 gms. A fetus born at this
 She may be noticeable that she purchases no maternity
point would be considered a premature or immature birth
clothes.
1. Early abortion - occurs before week 16 of pregnancy
 She may decline laboratory tests if it involves transportation 2. Late abortion - occurs between weeks 16-24.
or money Causes:
 Battered woman may have difficulty following 1. Abnormal fetal formation due either to a teratogenic factor
recommended pregnancy nutrition. or to a chromosomal aberration.
 She may leave before health personnel sees her at prenatal 2. Immunologic factors
setting 3. Implantation abnormalities – placental circulation will not
 She may grow anxious if her prenatal appointment is be well established and fetal formation will be inadequate.
running late 4. Corpus luteum fails to produce enough progesterone to
 She may call and cancel appointments frequently. maintain the deciduas basalis
 She may dress inappropriately. 5. Infection
 Obvious bruises or lacerations, neck may reveal linear Assessment:
bruises from strangulation. 1. Vaginal spotting
 Battered woman may be anxious to hear baby’s heartbeat 2. History taking
because her partner recently punched or kicked her
abdomen and she is worried that fetus might have been B. THREATENED ABORTION
hurt. Minimal placental infarcts from blunt abdominal trauma S/Sx:
may lead to poor placental perfusion and low birth weight. - Vaginal bleeding, starts as scant bleeding usually bright red.
 A sonogram may be done for suspected abdominal trauma. - Slight cramping but no cervical dilatation
 Fetal heart tones and fundal height should be recorded. Intervention:
Nursing Diagnoses: - Limit activity to no strenuous activity for 24-48 hours is the
1. Powerlessness r/t perception that she is impossible to break key intervention.
away from abusing partner - Coitus is restricted for 2 weeks to prevent infection and to
2. Fear r/t constant threats of beatings avoid inducing further bleeding.
3. Social isolation r/t client’s need to hide evidence of abuse
3. Ineffective denial r/t inability to face the fact that spouse is C. IMMINENT (INEVITABLE) ABORTION
abusive  A threatened abortion becomes an imminent or inevitable
4. Ineffective family coping; compromised r/t dysfunctional abortion if uterine contractions and cervical dilatation occur.
relationship between client and abusive spouse. Symptoms :
1. Cramping or uterine contractions

Tasks the woman could accomplish to meet goals of care : Dx: UTZ
1. Client carries phone number for home for abused women with
her. Tx:
2. Client and abusive partner continue to attend counseling 1. D & C – to ensure all products of conception are removed.
sessions. 2. Suction Curettage
3. Client states she has filed restraining order against abusive 3. Any tissue fragments should be saved to be examined for possible
partner abnormalities such as gestational trophoblastic disease (H mole).
4. Client states she feels secure living at safe house
D. COMPLETE ABORTION
COMPLICATIONS OF PREGNANCY > Entire products of conception (fetus, membrane, and placenta) are
 Most women enter pregnancy in apparent good health and expelled spontaneously without any assistance.
achieve normal pregnancy and birth without complications.
In a few women, however, for reasons are usually unclear, E. INCOMPLETE ABORTION
unexpected deviations or complications from the course of  Part of the conception is expelled but the membranes or
pregnancy occurs. placenta is retained in the uterus.
 There is a danger of maternal hemorrhage as long as part of
Nursing Diagnosis : the conceptus is retained in the uterus.
1. Anxiety r/t guarded pregnancy outcome
2. Fluid volume deficit r/t third-trimester bleeding Treatment :
3. Risk for infection 1. Dilatation and Curettage
4. Altered tissue perfusion r/t hypertension of pregnancy 2. Suction Curettage
 1. Women with Rh(-) blood should receive Rho (D antigen) immune
F. MISSED ABORTION globulin (RHIG) to prevent the build up of antibodies in the event the
 Fetus dies in uterus but is not expelled. conceptus was Rh (+)

S/Sx: 5. POWERLESSNESS
1. no increase in fundic height > A feeling of grief and sadness over the loss or that they have lost
2. no fetal heart sounds heard control of their lives is to expected.
3. painless vaginal bleeding
2. ECTOPIC PREGNANCY
Dx: UTZ  Second most frequent cause of bleeding early in pregnancy.
 Implantation occurs outside the uterine cavity.
Treatment :  Fertilization occurs normally in the distal third of the fallopian
1. D & C tube.
2 .If beyond 14 weeks maybe induced by prostaglandin
suppository to dilate the cervix followed by oxytocin stimulation. Causes :
a. Obstructions
Cx: DIC (Disseminated Intravascular Coagulation) b. Congenital malformations
c. Scars from tubal surgery
G. RECURRENT ABORTION d. Tumors
 3 spontaneous abortion that occurred in same gestational e. Progestin-only Oral contraceptives, post conceptual estrogen,
age. ovarian induction drugs
f. IUD
Possible Causes :
1. defective spermatozoa or ova Signs & Symptoms :
2.endocrine factors a. Bleeding – growing zygote ruptures the site of implantation which
3.deviations of uterus results to tearing & destruction of blood vessels which results to
4.infection bleeding
5.autoimmune disorders b. Sharp, stabbing pain
COMPLICATION OF ABORTION c. Vaginal spotting – placental detachment, uterine deciduas sloughs
thus bleeding occurs
1. HEMORRHAGE d. Severe shock – evidenced by rapid pulse, rapid respirations and
 With complete spontaneous abortion, serious or fatal falling blood pressure
hemorrhage is rare. e. Leucocytosis due to trauma
 With an incomplete abortion or DIC, major hemorrhage is a f. Rigid abdomen due to peritoneal irritation
possibility. g. positive Cullen’s Sign
h. Pain in the shoulders from blood in the peritoneal cavity causing
Therapeutic Management : irritation to the phrenic nerve.
 Immediately position the woman flat on bed & massage the i. On vaginal examination, a tender mass is usually palpable in
uterine fundus to aid contraction Douglas’ cul-de-sac
 D&C j. Extensive or dull vaginal and abdominal pain
 Monitor VS to detect hypovolemic shock k. Excruciating pain on the cervix during pelvic examination
 Start blood transfusion
Therapeutic Management :
 Direct replacement of fibrinogen
1. Laboratories : Hgb, Blood typing and Xmatching, HCG level for
immediate pregnancy testing
2. INFECTION
2. IVF using a large gauge catheter to restore intravascular volume
 Observe for fever, abdominal pain, tenderness, foul vaginal 3. Blood Transfusion if necessary
discharges 4. Laparotomy – to ligate the bleeding vessels and to remove or
 Usually caused by E. Coli repair the damaged fallopian tube.
 Endometritis (Infection of the uterine lining) – is the infection 5. Women with Rh (-) blood should receive Rho (D) immune globulin
that usually occurs after abortion (RHIG)
6. Methotrexate – if tube is not yet ruptured
3. SEPTIC ABORTION 7. Leucovorin
> An abortion complicated by infection due to use of nonsterile
instruments Nursing Diagnosis: Powerlessness r/t early loss of pregnancy
S/S : Fever, crampy abdominal pain, uterine tenderness secondary to ectopic pregnancy.
Complications :
1. Toxic Shock Syndrome Abdominal Pregnancy
2. Septicemia > Very rarely after ectopic pregnancy, the product of conception is
3. Kidney Failure expelled into the pelvic cavity. The placenta continues to grow in the
4. Infertility fallopian tube, spreading perhaps into the uterus or it may escape
into the pelvic cavity and successfully implant on an organ such as
Laboratories : an intestine. The fetus will grow in the pelvic cavity (an abdominal
1. CBC, Serum Electrolytes, pregnancy).
2. BT, Xmatching
3. Cultures of vaginal, cervical & urine specimen History :
1. Previous uterine surgery
2. Sudden pain of ectopic pregnancy earlier in the pregnancy
Treatment :
1. Hydration Complications :
2. Antibiotic 1. Hemorrhage
3. D&C 2. Bowel perforation and Peritonitis
4. TT or HTIG for Tetanus

 A CVP or pulmonary artery catheter may be inserted to

monitor left atrial filling pressure and hemodynamic status.
 Dopamine and digitalis may be necessary to maintain
sufficient cardiac output.
 Oxygen and perhaps ventilatory support may be necessary
to maintain respiratory functions.
4. ISOIMMNUNIZATION
 Some blood from placental villi may enter maternal
circulation, either by spontaneous birth or by D&C. If the
woman is Rh (-), enough Rh (+) fetal blood may enter her
circulation to cause Isoimmunization.
 Isoimmunization – the production by her immunologic system
of antibodies against Rh(+) blood.
Treatment :
CONDITIONS ASSOCIATED WITH SECOND TRIMESTER
BLEEDING
1. GESTATIONAL TROPHOBLASTIC DISEASE (HYDATIDIFORM
MOLE)
> Proliferation and degeneration of the trophoblastic villi. As the cells
degenerate, they become filled with fluid, appearing as fluid-filled,
grape-sized vesicles. Embryo dies.
Etiology :
1. Occur most often in women from low socioeconomic groups who
have a low protein intake.
2. In young women (under age 18 years). In women older than 35
years
3. Women of Asian heritage
- cause essentially unknown 6. Monitor urine output frequently as an indicator of blood volume
adequacy
Assessment : 7. Monitor fetal heart sounds and uterine contraction
1. Uterus expands faster than normal; disproportionate to the 8. Hgb, Hct. PT,PTT, fibrinogen, platelet count, type and xmatch or
length of pregnancy antibody screen should be assessed to establish baselines, detect a
2. No fetal heart sounds nor palpable fetal parts possible clotting disorder
3. A blood or urine test of HCG for pregnancy will be strongly 9. Prepare BT if necessary
positive 10. Prepare oxygen equipment in case of fetal distress.
4. Excessive nausea and vomiting
5. A sonogram will show dense growth (a snowflake pattern) Complications :
6. Vaginal bleeding starting with spotting of dark brown blood or 1. Postpartal Hemorrhage – because the placental site is in the lower
as a profuse fresh flow, accompanied by discharge of the clear uterine segment which does not contract as efficiently as the upper
fluid-filled vesicles. segment
2. Endometritis – because the placental site is close to the cervix, the
Therapeutic Management : portal of entry for pathogens.
1. Suction curettage – to evacuate the mole
2. Every woman who had history of GTD should have a blood 2. PREMATURE SEPARATION OF THE PLACENTA (ABRUPTIO
test for HCG every 2 to 4 weeks along with pelvic examination PLACENTAE)
3. Thereafter, HCG levels and possibly chest xray are done once
a month for a full year. Predisposing Factors :
4. Instruct woman to use a reliable contraceptive method during 1. High parity
the year so that a positive pregnancy test will not be confused 2. Chronic hypertensive disease
with increasing levels and developing malignancy. 3. Hypertension of pregnancy
5. Prophylactic course of Methotrexate, the drug of choice for 4. Direct trauma
choriocarcinoma. Malignancy can be treated effectively with 5. Vasoconstriction from cocaine use
methotrexate. 6. Cigarette smoking

2. INCOMPETENT CERVIX Assessment :

> A cervix that dilates prematurely and therefore cannot hold a 1. Sharp, stabbing pain high in the uterine fundus
fetus until term. 2. Tenderness on uterine palpation
3. Heavy bleeding
Signs/Symptoms : 4. Hard, board-like uterus in cases of couvelaire uterus (Blood
1. A pink-stained vaginal discharged infiltrates uterine musculature
2. Increased pelvic pressure which maybe followed by rupture of 5. Signs of shock
the membranes and discharge of the amniotic fluid 6. Uterus becomes tense and rigid to the touch
3. Uterine contractions
Therapeutic Management :
Etiology : 1. Initial blood works – Hgb, typing and crossmatching
1. Associated with increased maternal age 2. Start IVF with a large-gauge catheter
2. Trauma to the cervix 3. Administer oxygen by mask to limit fetal anoxia.
3. Repeated D&C’s 4. Monitor fetal heart sounds
5. Monitor and record maternal vital signs every 5 to 15 minutes to
Therapeutic Management establish baselines
1. Cervical Cerclage – after one pregnancy loss due to an 6. Keep in lateral position to prevent pressure on the vena cava and
incompetent cervix to prevent from happening again additional compromising of fetal circulation.
2. McDonald or Shirodkar procedure – purse string sutures 7. Do not perform any vaginal or pelvic examination or give an
placed in the cervix to strengthen it and prevent from dilating. enema
3. Emergent cerclage – sutures placed in the cervix as
prophylaxis against pretem birth. DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
 Acquired disorder of blood clotting.
CONDITIONS ASSOCIATED WITH THIRD-TRIMESTER  Also known as consumptive coagulopathy
BLEEDING  A diffuse, pathologic form of clotting, secondary to underlying
disease/pathology
1. PLACENTA PREVIA: Low implantation of the placenta.  Occurs in critical maternity problems such as abruptio placenta,
intrauterine fetal death, amniotic fluid embolism, pre-
Occurs in 4 Degrees : eclampsia/eclampsia, hydatidiform mole and hemorrhagic
(1) Implantation in the lower rather than in the upper portion of shock
the uterus (Low-lying placenta)
(2) Marginal implantation (the placenta edge approaches that of Pathophysiology
the cervical os) - precoagulant substances released in the blood trigger
(3) Implantation that occludes a portion of the cervical os (partial microthrombosis in peripheral vessels and paradoxical
placenta previa) consumption of circulating clotting factors
(4) Implantation that totally obstructs the cervical os (total - fibrin-split products accumulate, further interfering with the
placenta previa) clotting process
- platelet and fibrinogen levels drop
Assessment :
1. Vaginal bleeding – abrupt, painless, bright red Symptoms :
1. Easy bruising or bleeding from an IV site. Bleeding may
Etiology : range from massive, unanticipated blood loss to localized
1. Increased parity bleeding.
2. Advanced maternal age 2. Presence of special maternity problems
3. Past cesarean births 3. Prolonged prothrombin and partial thromboplastin time
4. Past uterine curettage
5. Multiple gestation Therapeutic Management :
1. Prompt recognition and adequate management of the underlying
problem ( eg. delivery of the dead fetus and the placenta)
Therapeutic Management: 2. IV administration of heparin to halt the clotting
3. Institute nursing measures for severe bleeding/shock if needed.
Immediate Care Measures : BT maybe necessary to replace blood loss
1. Place woman immediately on bed rest in a side-lying position 4. Anti-thrombin III factor, fibrinogen, or cryoprecipitate can be used
to ensure an adequate blood supply to the woman and fetus. to restore blood clotting
2. Determine vaginal blood loss 5. Fresh frozen plasma can also aid in restoring clotting function
3. Never attempt a pelvic or rectal examination with painless
bleeding late in pregnancy because any agitation of the cervix PRETERM LABOR
may initiate a massive hemorrhage. > Labor that occurs before the end of week 37 of gestation
3. Obtain baseline vital signs to determine whether symptoms of
shock are present Etiology :
4. Monitor BP every 5 to 15 minutes 1. HPN, UTI
5. IVF therapy using a large gauge catheter 2. Occurs more frequently in adolescent
3. Dehydration
4. Urinary Tract Infection
5. Chorioamnionitis
6. Continuous strenuous jobs during pregnancy that leads to
fatigue
Signs/Symptoms :
1.Persistent, dull, low backache
2. Vaginal spotting
3. Feeling of pelvic pressure or abdominal tightening
4. Menstrual-like cramping
Therapeutic Management :
1. Bed rest – to relieve pressure of the fetus on the cervix
2. IVF therapy – hydration may have an influence on stopping
contractions
Drug Administration :
1.Corticosteroid to the fetus – to accelerate the formation of lung
surfactant
2. Tocolytic agent – drug used to halt labor
3. Magnesium sulfate – first drug used to halt contractions. Also
has CNS depressant action that slows and halts uterine
contractions.
Fetal Assessment :
To evaluate fetal movement the woman lies down on her left
side and times the number of minutes it takes for her to feel 10
fetal movements (about an hour) or counts the number of fetal
movements she feels in 1 hour (10 to 12). If the time it takes to
feel 10 fetal movements is twice what it was the day before or
she feels fewer than 5 movements during half an hour, she
monitors again for second hour. If at the end of this second hour
fetal activity has not increased, she should report it immediately
Labor That Cannot Be Halted
> Labor is too far advanced that it cannot be halted.
1. The rupturing of membranes is a point of no return in stopping
or delaying labor because of the increased risk of infection.
2. If the cervix is more than 50% effaced and 3-4 cm dilated
Management :
1. If the fetus is very immature, a CS maybe planned to reduce
pressure on the fetal head and reduce the possibility of subdural
or intraventricular hemorrhage
2. As a rule, artificial rupture of membranes should not be done
due to possibility of prolapse of the cord around a small head
until the fetal head is firmly engaged.
3. Administer analgesic agents with caution during preterm labor.
4. Monitor uterine contractions and fetal heart sounds during
labor
5. Explain to the patient that an episiotomy may be made larger
than usual, although the head of preterm maybe smaller it is
more fragile and excessive pressure might result in subdural or
intraventricular hemorrhage that could be fatal.
6. Forceps may be used at delivery to reduce pressure on the
fetal head.
7. Clamp cord immediately after birth, an immature infant has a
difficulty excreting large amount of bilirubin that will be formed if
this extra blood is added to the circulation. The extra amount of
blood may also burden the circulatory system.
PRETERM RUPTURE OF MEMBRANES (PROM)
 A spontaneous rupture of fetal membranes with loss of
amniotic fluid before onset of regular contractions that
results in progressive cervical dilation.
Etiology :
1. Although cause is unknown, malpresentation and a contracted
pelvis commonly accompany the rupture
2. Associated with infection of the membranes
(chorioamnionitis).
Complications :
1. Uterine and fetal infection
2. Increased pressure on the umbilical cord inhibiting the fetal
nutrient supply, or cord prolapse
3. Development of Potter – like syndrome of distorted facial
features and pulmonary hypoplasia
4. Preterm labor
Assessment :
1. A sudden gush of clear fluid from the vagina with continued
minimal leak
2. Sterile vaginal speculum examination is done to observe for
vaginal pooling of fluid. The fluid is tested with nitrazine paper
(appears blue). The fluid can also be tested for ferning.
3. A sonogram may be done to assess amniotic fluid index.
4. Cultures for Neisseria gonorrhea and Chlamydia are usually
taken.
5. Blood is drawn for white blood count and C – reactive protein.
Therapeutic Management :
1. Bed rest
2. Prophylactic administration of broad-spectrum antibiotics may
delay onset of labor and reduce infection in the newborn.
3. Women positive for streptococcus B need IV administration of
penicillin or ampicillin to reduce the possibility of this infection in the
newborn.
Health Education :
1. If at home, instruct to take temperature twice a day and to report a
fever, uterine tenderness, or odorous vaginal discharge.
2. Refrain from tub bathing, coitus, and douching because of the
danger of introducing infection.
White cell count needs to be assessed daily. A count of more than
18,000/mm3 to 20,000/mm3 is suggestive of infection.
PREGNANCY-INDUCED HYPERTENSION (PIH)
 A condition in which vasospasm occurs during pregnancy. The
vasospasm may be caused by the action of prostaglandins
(notably decreased prostacyclin and increased thromboxane).
Increased cardiac output may injure endothelial cells of the
arteries, leading to spasm. Normally, blood vessels during
pregnancy are resistant to the effects of pressor substances
such as angiotensin and norepinephrine so blood pressure
remains normal during pregnancy. With PIH, this reduced
responsiveness to BP changes appears to be lost.
Vasoconstriction occurs, and BP increases dramatically.
 The cardiac system is overwhelmed because the heart is forced
to pump against rising peripheral resistance. This reduces the
blood supply to organs esp. the kidney, pancreas, liver, brain
and placenta. Tissue hypoxia may follow in the maternal vital
organs; poor placental perfusion may reduce the fetal nutrient
and oxygen supply. Ischemia in the pancreas may result to
epigastric pain and an elevated amylase-creatinine ratio.
 Spasm of the arteries in the retina leads to vision changes.
 Vasospasm in the kidney increases blood flow resistance.
Degenerative changes develop in kidney glomeruli because of
the back pressure. This leads to increased permeability of the
glomerular membrane allowing the serum proteins, albumin and
globulin to escape into the urine (proteinuria). The degenerative
changes also result in decreased glomerular filtration so there is
lowered urine output and clearance of creatinine. Increased
tubular reabsorption of sodium occurs. Because sodium retains
fluid, edema results.
Changes associated with PIH:
Vasospasm
Effects on the vascular Effects on the renal Effects on the
system system intrstitial
Reduced glomerular filtration
Rate; Increased glomerular
membrane permeability
vasoconstriction Fluid diffusion from
vascular space into
interstitial space.
Increased serum blood
Impaired organ urea nitrogen
perfusion
Edema
Oliguria and proteinuria
Hypertension
Etiology :
1. Occurs more frequently in primiparas younger than age 20 years
or older than 40 years
2. Low socio-economic background
3. Five or more pregnancies
4. Women of color
5. Multiple pregnancies
6. Hx of hydramnios
7. Heart disease, DM with renal involvement
8. Essential hypertension
9. Associated with poor calcium or magnesium intake
Pathophysiologic Events
Assessment :
1. HPN, proteinuria and edema are classic signs of PIH
Symptoms of PIH :
GESTATIONAL HYPERTENSION
 An elevated blood pressure but has no proteinuria or edema.
MILD PREECLAMPSIA
 BP rises 30 mm Hg or more systolic or 15 mm Hg or more
diastolic above her prepregnancy level, taken on two
occasions at least 6 hours apart
 With proteinuria (1+ or 2+ on a reagent strip on a random
sample).
 Edema maybe present. This develops because of the protein
loss, sodium retention and lowered glomerular filtration rate.
Interventions:
- Promote bed rest as long as
signs of edema or proteinuria are minimal, preferably
left-side lying to promote uterine and placental perfusion
- Provide well balanced diet with adequate protein and
roughage, no sodium restriction
SEVERE PREECLAMPSIA
 Blood pressure has risen to 160 mm Hg systolic and 110 mm
Hg diastolic or above on at least two occasions 6 hours
apart at bed rest or her diastolic pressure is 30 mm Hg
above prepregnancy level.
Assessment :
1. Extreme edema is noticeable in the woman’s face and hands
as puffiness.
Nonpitting edema – If there is swelling or puffiness but the
swelling cannot be indented with finger pressure.
Slight indentation – 1+ pitting edema
Moderate indentation – 2+ pitting edema
Deep indentation – 3+ pitting edema
4+ pitting edema – indentation is so deep it remains after
removal of fingers
2. Severe epigastric pain and nausea and vomiting possibly due
to abdominal edema or ischemia to the pancreas and liver.
3. Pulmonary edema may cause them to feel short of breath
4. Cerebral edema will result in visual disturbances. May also
produce symptoms of severe headache and marked hyperflexia
and perhaps muscle clonus
Medical Management: Magnesium Sulfate
- Magnesium sulfate acts upon
the myoneural junction, diminishing neuromuscular
transmission
- It promotes maternal
vasodilation, better tissue perfusion, and has
anticonvulsant effect. Keep in mind that for magnesium
to be effective as an anticonvulsant, serum magnesium
levels should be between 5 and 8 mg/dl. Levels above
8 mg/dl indicate toxicity and place the patient at risk for
respiratory depression, cardiac arrhythmias, and cardiac
arrest.
- Monitor client’s respirations,
blood pressure, and reflexes, as well as urinary output
frequently.
- Assess the client’s patellar
reflex. If the client has received epidural anesthesia,
test the biceps or triceps reflex. Diminished or
hypoactive reflexes suggest magnesium toxicity.
- Assess for ankle clonus
( alternating contractions and relaxations of the
muscles) by rapidly dorsiflexing the client’s ankle three
times, then removing your hand and observing the foot’s
movement. If no further motion is noted, ankle clonus is
absent; if the foot continues to move involuntarily,
clonus is present. Moderate (3-5 movements) or severe
(6 or more movements) suggests possible magnesium
toxicity.
- Antidote for excess levels of
magnesium sulfate is calcium gluconate or calcium
chloride
Interventions
- promote complete bedrest, left
side lying
- carefully monitor maternal/fetal
vital signs
- monitor intake and output
- take daily weights
- institute seizure precautions
( restrict visitors, minimize all stimuli, monitor for
hyperreflexia, administer sedatives as ordered)
- instruct client about appropriate diet
- continue monitoring for up to 48
hours post delivery
- administer medications as ordered,
vasodilator of choice is usually hydralazine (apresoline)
ECLAMPSIA
 The most severe classification of hypertension of pregnancy
Assessment:
- increased hypertension precedes
convulsion followed by hypotension, seizure may recur
- coma may ensue
- labor may begin, putting fetus in
great jeopardy
Complications :
1. Cerebral hemorrhage
2. Circulatory collapse
3. Renal failure
Interventions
- minimize all stimuli
- monitor vital signs
- have airway, oxygen, and suction
equipment available
- administer medications as ordered
- prepare for caesarian section when
seizures stabilize
- continue observations 48 hours
post delivery
HELLP SYNDROME
 is a category of PIH that involves changes in blood components
and liver functions. It is an acronym that help identify the
underlying signs associated with the syndrome :
1. Hemolysis
2. Elevated Liver enzymes
3. Low Platelets
HELLP syndrome develops in 12% of women with PIH. It can
occur in primigravidas and multigravidas. When it occurs, maternal
and fetal mortality is high; approximately one-fourth of women and
one-third of infants die from this disorder. However, after birth,
laboratory results return to normal usually within 1 week and the
mother experiences no further problems.
Etiology
Although the exact cause of HELLP is unknown, theories have
been proposed about the development of its signs and symptoms.
Hemolysis is believed to result because RBCs are damaged by their
travel through small, impaired blood vessels. Elevated liver enzymes
are believed to result from obstruction in liver flow by fibrin deposits.
Low platelets are believed to be the result of vascular damage
secondary to vasospasm.
Intervention
- monitor maternal and fetal vital
signs
- maintain a quiet, calm, dimly lit
environment to reduce the risk of seizures
- institute bleeding precautions
- prepare patient for delivery
MULTIPLE PREGNANCY
 Considered a complication of pregnancy because the woman’s
body must adjust to the effects of more than one fetus.
 Incidence has increased dramatically due to use of fertility drugs
Assessment :
1. Uterus begins to increase in size faster than usual
2. Alpha-fetoprotein levels will be elevated
3. A sonogram will reveal multiple gestation sacs
4. At the time of quickening, flurries of action at different portions of
her abdomen are noted
5. On auscultation, multiple sets of fetal heart sounds may be heard
POLYHYDRAMNIOS
 An excessive amniotic fluid formation.
 Usually, amniotic fluid is between 500 and 1000 ml in amount at
term. An amount of more than 2000 ml or an amniotic fluid
index above 24 cm is considered hydramnios.
Complications :
1. Fetal malpresentation because of the extra uterine space
2. Premature rupture of membranes followed by preterm labor from
the increased pressure and possibly prostaglandin release
3. Preterm rupture of membranes adds additional risks of both
infection and prolapsed cord
Assessment :
1. Unusual rapid enlargement of uterus
2. Small parts of the fetus are difficult to palpate because the uterus
is unusually tense
3. Extreme shortness of breath because of the overly distended 3. Blood for coagulation studies to detect DIC
uterus that pushes up against her diaphragm.
4. Lower extremity varicosities and hemorrhoids because of poor Nursing Diagnosis : Powerlessness related to fetal death
venous return from the extensive uterine pressure
5. Increased weight gain

Nursing Intervention :
Therapeutic Management : A. Healthy process of grieving
1. Bed rest 1. Give woman opportunities to express feelings
2. Encourage to eat a high fiber diet to avoid constipation 2. Encourage support person to stay with the woman during labor
3. Assess vital signs and lower extremity edema 3. Present the baby if parents wished to in a manner like she were a
4. Amniocentesis – to give relief from the increasing pressure well newborn
5. A non steroidal anti inflammatory agent such as Indomethacin 4. Encourage parents to give name to the child to make him/her
therapy may be effective in reducing the amount of fluid formed more normal
6. If contractions begins, tocolysis with magnesium sulfate may 5. Explain how the anomaly affected the child
be begun to prevent or halt preterm labor 6. Explain hospital procedures regarding discharged
7. Ask about their desire for clergy or religious rites
POST-TERM PREGNANCY
A pregnancy that exceeds 42 weeks
HIGH RISK NEWBORN
Etiology :
1. Occurs in approximately 10% of all pregnancies  A neonate is considered to be high risk if he has an increased
2. Women who have long menstrual cycles (40 to 45 days) chance of dying during or shortly after birth or has a congenital
3. Women on high dose of salicylates interferes with the or perinatal problem that requires prompt intervention
synthesis of prostaglandins  Being able to predict that an infant is high risk allows for
4. Myometrial quiescence or a uterus that does not respond to advanced preparation
normal labor stimulation
Assessment :
Complications :  All infants should be assessed for obvious congenital anomalies
1. Macrosomia will create a delivery problem and gestational age. Assessments are made under prewarmed
2. Lack of growth radiant heat warmer to safeguard against heat loss.
3. Oligohydramnios leading to variable decelerations may occur  Assessment involves use of instrumentation such as cardiac,
4. Fetus may suffer from lack of oxygen, fluid and nutrients apnea and blood pressure monitoring.
Therapeutic Management : Nursing Diagnosis :
1. A nonstress test and/ or biophysical profile may be done to 1. Ineffective airway clearance r/t presence of mucus or amniotic
document the state of placental perfusion fluid in airway.
2. Prostaglandin gel applied to the cervix to initiate ripening or 2. Risk for fluid volume deficit 3. Ineffective thermoregulation r/t
stripping of membranes newborn status and stress from birth weight variation.
3. Oxytocin infusion is a common method to induce labor. 4. Risk for altered nutrition; less than body requirements
4. CS if oxytocin is ineffective 5. Risk for infection
6. Risk for altered parenting
7. Diversional activity deficit (lack of stimulation) r/t illness at birth
PSEUDOCYESIS Implementation :
 False pregnancy 1. Care should focus on conserving baby’s energy and providing a
thermoneutral environment to prevent exhaustion and chilling.
Assessment : 2. Painful procedures should be kept to a minimum
1. Nausea and vomiting 3. Parent teaching and participation with care such as bathing or
2. Amenorrhea feeding
3. Enlargement of the abdomen
Outcome Evaluation :
Etiology : 1. Infant maintains patent airway
1. Woman’s desire to be pregnant actually causes physiologic 2. Infant tolerates all procedures without accompanying apnea
changes 3. Infant demonstrates growth and development appropriate for
gestational age, birth weight, and condition
ISOIMMUNIZATION (RH INCOMPATIBILITY) 4. Infant maintains body temperature at 37oC in open crib with one
 Occurs when an Rh (-) mother is carrying a fetus with an Rh added blanket.
(+) blood 5. Parents visits at least once a week and make three telephone
calls to neonatal nursery weekly
Therapeutic Management : 6. Parents demonstrate positive coping skills and behaviors in
1. RHIG – administered to women at 28 weeks of pregnancy response to NB’s condition
2. Intrauterine transfusion – to restore fetal red blood cells. Done
by injecting red blood cells directly into a vessel in the fetal cord Neonatal Assessment
or depositing them in the fetal abdomen using amniocentesis
technique APGAR SCORE
During the initial examination of a neonate, expect to calculate an
FETAL DEATH Apgar score and make general observations about the neonate’s
 Obviously, one of the most severe complications of appearance and behavior. Developed by anesthesiologist Dr.
pregnancy. Virginia Apgar in 1952, Apgar scoring evaluates neonatal heart rate,
respiratory effort, muscle tone, reflex irritability, and color.
Causes : Evaluation of each category is performed 1 minute after birth and
1. Chromosomal Abnormalities again at 5 minutes after birth. Each item has a maximum score of 2
2. Congenital malformations and a minimum score of 0. The final Apgar score is the sum total of
3. Infections such as hepatitis B the five items; a maximum score is ten.
4. Immunologic causes Evaluation at 1 minute quickly indicates the neonate’s initial
5.Complications of maternal disease adaptation to extrauterine life and whether resuscitation is
necessary. The 5-minute score gives a more accurate picture of his
Symptoms : over-all status.
1. No fetal movements
2. No fetal heart tones Heart Rate. If the umbilical cord still pulsates, you can palpate the
3. Painless spotting neonate’s heart by placing your fingertips at the junction
4. Uterine contractions with cervical effacement and dilatation of the umbilical cord and the skin. The neonate’s cord
stump continues to pulsate for several hours and is a
Therapeutic Management : good, easy place to check heart rate. You can also place
1. Sonogram to confirm death of fetus to fingers or a stethoscope over the neonate’s chest at
2. If labor does not begin spontaneously, it will be induced the fifth intercostal space to obtain an apical pulse. For
through combination of prostaglandin gel application to the accuracy, the heart rate should be counted for 1 full
cervix to effect cervical ripening and oxytocin or prostaglandin minute.
administration to begin uterine contractions
Respiratory Effort. Assess the neonate’s cry, noting its volume
and vigor. Then auscultate his lungs, using a
stethoscope. Assess his respirations for depth and
regularity. If the neonate exhibits abnormal
respiratory responses, begin neonatal resuscitation
then use the Apgar score to judge the progress and
success of resuscitation efforts.
Muscle Tone. Determine by evaluating the degree of flexion in
the neonate’s arms and legs and their resistance to
straightening. This can be done by extending the
limbs and observing their rapid return to flexion – the
neonate’s normal state.
Reflex Irritability. Evaluate neonate’s cry. Initially, he may not
cry but you should be able to elicit a cry by flicking his
soles. The usual response is a loud, angry cry. A
high-pitched or shrill cry is abnormal. A newborn
whose mother was heavily sedated tend to have a
low score on this aspect.
Color. Observe skin color for cyanosis. A neonate usually has a
pink body and blue extremities. This condition called
acrocyanosis appears in about 85% of normal
neonates 1 minute after birth. Acrocyanosis results
from decreased peripheral oxygenation caused by
the transition from fetal to independent circulation.
Sign Apgar Score
0 1 2 shouldn’t bulge. Bulging fontanels require immediate attention
Heart Rate Absent Less than 100 More than 100
beats/min beats/min
Respiratory Absent Slow, irregular Good crying
Effort
Muscle tone Flaccid/Limp Some flexion and Active motion
resistance to
extension of
extremities
Reflex No response Grimace or weak Vigorous cry
Irritability cry
Color Pallor, Pink body, blue Completely
Cyanosis extremities pink
A total score of 7-10 indicates that the neonate is in good
condition; 4-6, fair condition (the neonate may have moderate
central nervous system depression, muscle flaccidity, cyanosis,
and poor respirations); 0-3, danger (the neonate needs
immediate resuscitation, as ordered).
HEAD TO TOE ASSESSMENT
The neonate should receive a thorough physical examination of
each body part. However, before each body part is examined,
assess the general appearance and posture of the neonate.
Neonates usually lie in a symmetrical, flexed position – the
characteristic “fetal position” – as a result of their position while
in utero.
Skin.
Common findings in a neonatal assessment may include:
Acrocyanosis – caused by vasomotor instability,
capillary stasis, and high hemoglobin level for the first 24
hours after birth.
Milia- clogged sebaceous glands on the nose or chin
Lanugo- fine, downy hair appearing after 20 weeks of
gestation on the entire body, except the palms and soles
vernix caseosa – a white cheesy protective coating
composed of desquamated epithelial cells and sebum
erythema toxicum neonatorum – a transient
maculopapular rash
telangiectasia – flat reddened vascular areas
appearing on the neck, upper eyelid or upper lip
port-wine stain (nevus flammeus) – a capillary
angioma located below the dermis and commonly found on
the face
strawberry hemangioma (nevus vasculosus) – a
capillary angioma located in the dermal and subdermal skin
layers indicated by a rough, raised, sharply demarcated
birthmark
sudamina or miliaria (distended sweat glands)- cause
minute vesicles on the skin surface, especially on the face
Mongolian spots – bluish black areas of pigmentation
more commonly noted on the back and buttocks of dark-
skinned neonates (regardless of race)
Make general observations about the appearance of the
neonate’s skin in relationship to his activity, position, and
temperature. Usually, the neonate is redder when crying or hot.
He may have transient episodes of cyanosis when crying. Cutis
marmorata is transient mottling when the neonate is exposed to
cooler temperatures.
Palpate the skin to assess skin turgor. To do this, roll a fold of skin
on the neonate’s abdomen between your thumb and forefinger.
Assess consistency, amount of subcutaneous tissue, and degree of
hydration. A well-hydrated infant’s skin returns to normal
immediately upon release.
Head.
The neonate’s head is about ¼ of its body size. Six bones make up
the cranium:
• the frontal bone
• the occipital bone
• two parietal bones
• two temporal bones
Bands of connective tissue, called sutures, lie between the junctures
of these bones. At the juncture of the sutures are wider spaces of
membranous tissues, called fontanels.
Fontanels.
The neonatal skull has two fontanels. The anterior fontanel is
diamond-shaped and located at the juncture of the frontal and
parietal bones. It measures 1 1/8 to 1 5/8” (3-4cm) long and ¾”
(2cm) to 1 1/8” wide. The anterior fontanel closes in about 18
months. The posterior fontanel is triangle-shaped. It is located at the
juncture of the occipital and parietal bones and measures about ¾”
across. The posterior fontanel closes in 8-12 weeks.
The fontanels should feel soft to touch but shouldn’t be depressed.
A depressed fontanel indicates dehydration. In addition, fontanels
because they may indicate increased intracranial pressure.
Pulsations in the fontanels reflect the peripheral pulse.
Molding refers to asymmetry of the cranial sutures due to difficulties
during vaginal delivery; it isn’t seen in neonates born by cesarean
delivery. There are two types of cranial abnormalities:
• Cephalhematoma occurs when blood collects between a
skull bone and the periosteum. It is caused by pressure
during delivery and tends to spontaneously resolve in 3-6
weeks. A cephalhematoma doesn’t cross cranial suture
lines.
• Caput succedaneum is a localized edematous area of the
presenting scalp. It is also caused by pressure during
delivery, but disappears spontaneously in 3-4 days and
can cross cranial suture lines
Craniotabes is localized softening of the cranial bones. It can be so
soft it can be indented by the pressure of the examining finger. The
bone returns to its normal contour when he pressure is removed.
This is probably caused by the pressure of the fetal skull against the
mother’s pelvic bone in utero.The condition corrects itself without
treatment after a matter of months
The degree of head control the neonate has should also be
evaluated during this part of the examination. If neonates are
placed down on a firm surface, they’ll turn their heads to the side to
maintain an open airway. They also attempt to keep their heads in
line with their body when raised by their arms. Although head lag is
normal in the neonate, marked head lag is seen in neonates with
Down syndrome or brain damage and hypoxic infants.
Eyes.
Neonates tend to keep their eyes tightly shut. Observe the lids for
edema, which is normally present for the first few days of life. The
eyes should also be assessed for symmetry in size and shape.
Here are some common findings of neonatal eye examination:
 The neonate’s eyes are usually blue or gray because of
scleral thinness. Permanent eye color is established
within 3-12 months.
 Lacrimal glands are immature at birth, resulting in
tearless crying for up to 2 months.
 Neonate may demonstrate transient strabismus.
 The Doll’s eye reflex (when the head is rotated laterally,
the eyes deviate in the opposite direction or remain
stationary) may persist for up to 10 days.
 Subconjunctival hemorrhages may appear from vascular
tension changes during birth.
 The corneal reflex is present but generally isn’t elicited
unless a problem is suspected.
Nose.
Observe the neonate’s nose for shape, placement, patency and
bridge configuration.
Because neonates are obligatory nose breathers for the first few
months of life, nasal passages must be kept clear to ensure
adequate respiration. Neonates instinctively sneeze to remove
obstruction. Test the patency of the nasal passages by occluding
each nares alternately while holding the neonate’s mouth closed.
Mouth and Pharynx.
The neonate’s mouth usually has scant saliva and pink lips.
Inspect the mouth for its existing structures. The palate is
usually narrow and highly arched. Inspect the hard and soft
palates for clefts.
Epstein pearls (pin-head sized, white or yellow, rounded
elevations) may be found on the gums or hard palate. These are
caused by retained secretions and disappear within a few weeks
or months. The frenulum of the upper lip may be quite thick.
Precocious teeth may also be apparent. The pharynx can be
best assessed when the neonate is crying. Tonsillar tissue
generally isn’t visible.
Ears.
Assess the neonate’s ears for placement on the head, amount of
cartilage, open auditory canal, and hearing.
The neonate’s ears are characterized by incurving of the pinna
and cartilage deposition. The pinna is usually flattened against
the side of the head from pressure in utero. The top of the ear
should be above or parallel to an imaginary line from the inner to
the outer canthus of the eye. Low-set ears are associated with
several syndromes, including chromosomal abnormalities.
Neck.
The neonate’s neck is typically short and weak with deep folds of
skin. Observe for range of motion, shape, and abnormal
masses. Also, palpate each clavicle and sternocleidomastoid
muscle. Note the position of the trachea. The thyroid gland
generally isn’t palpable.
Chest.
Inspect and palpate the chest, noting shape, clavicles, ribs,
nipples, breast tissue, respiratory movement, and amount of
cartilage in rib cage. The neonatal chest is characterized by a
cylindrical thorax (because the anteroposterior and lateral
diameters are equal) and flexible ribs. Slight intercostals
retractions are usually seen on inspiration. The sternum is
raised and slightly rounded, and the xiphoid process is usually
visible as a small protrusion at the end of the sternum.
Breast engorgement from maternal hormones may be apparent,
and the secretion of “witch’s milk” may occur. Supernumerary
nipples may be located below and medial to the true nipples.
Lungs.
Normal respirations of the neonate are abdominal with a rate
between 30 and 50 breaths/minute. After the first breaths to
initiate respiration, subsequent breaths should be easy and fairly
regular. Occasional irregularities may occur with crying,
sleeping, and feeding.
It’s easiest to auscultate the lung fields when the neonate is
quiet. Bilateral bronchial breath sounds should be heard.
Crackles soon after birth represent the transition of the lungs to
extrauterine life.
Heart.
The neonate’s heart rate is normally between 110 and 160
beats/minute. Because neonates have a fast heart rate, it’s
difficult to auscultate the specific components of the cardiac
cycle. Heart sounds during the neonatal period are generally of
higher pitch, shorter duration, and greater intensity than in later
life. The first sound is usually louder and duller than the second,
which is sharp in quality. Murmurs are commonly heard,
especially over the base of the heart or at the third or fourth
intercostals space at the left sternal border, due to incomplete
functional closure of the fetal shunts.
The apical impulse (point of maximal impulse) is at the fourth
intercostals space and to the left of the midclavicular line.
Abdomen.
The neonatal abdominal assessment should include:
 Inspection and palpation of the umbilical cord
 Evaluation of the size and contour of the abdomen
 Auscultation of bowel sounds
 Assessment of skin color
 Observation of movement with respirations
 Palpation of internal organs
The neonatal abdomen is usually cylindrical with some
protrusion. Bowel sounds are heard a few hours after birth. A
scaphoid (sunken anterior wall) appearance indicates a
diaphragmatic hernia. The umbilical cord is white and gelatinous
with two arteries and one vein and begins to dry within 1-2 hours
after delivery.
The liver is normally palpable 1” (2.5 cm) below the right costal
margin. Sometimes the tip of the spleen can be felt, but a
spleen that’s palpable more than 1/3” (1cm) below the left costal
margin warrants further investigation. Both kidneys should be
palpable; this is easiest done soon after delivery, when muscle
tone is lowest. The suprapubic area is palpated for a distended
urinary bladder. The neonate should void within the first 24 hours of
birth.
Femoral pulses should also be palpated at this point in the
examination. Inability to palpate femoral pulses should signify
coarctation of the aorta.
Anogenital Area.
The anus of the newborn must be inspected to be certain that it is
present, patent and is not covered by a membrane (imperforate
anus). The time after birth that the infant first passes meconium
should be noted. If the newborn does not do so in the first 24 hours,
the suspicion of imperforate anus or meconium ileus is aroused.
Characteristics of a male neonate’s genitalia include rugae on the
scrotum and testes descended into the scrotum. Scrotal edema may
be present for several days after birth due to the effects of maternal
hormones. It may be deeply pigmented in dark-skinned newborns.
Both testes should be present in the scrotum. Males with one or
both undescended testicles (cryptorchidism) need further referral to
establish the extent of the problem. It could be due to agenesis
( absence of an organ), ectopic testes (the testes cannot enter the
scrotum because the opening of the scrotal sac is closed), or
undescended testes (the vas deferens or artery is too short to allow
the testes to descend).
The urinary meatus is located in one of three places:
 At the penile tip (normal)
 On the dorsal surface (epispadias)
 On the ventral surface (hypospadias)
In the female neonate, the labia majora cover the labia minora and
clitoris. These structures may be prominent due to maternal
hormones. Mucoid vaginal discharge which may be blood-tinged
(pseudomenstruation) may also occur and the hymenal tag is
present.
Extremities.
The extremities should be assessed for range-of-motion, symmetry,
and signs of trauma. All neonates are bowlegged and have flat feet.
The hips should be assessed for dislocation. With the newborn in a
supine position, both legs can be flexed and abducted to such an
extent (180 degrees) that they touch or nearly touch the surface of
the bed. If the hip joints seem to lock short of this distance, hip
subluxation (a shallow and poorly formed acetabulum) is suggested.
If subluxation is present, when the infant’s leg is held with the fingers
on the greater and lesser trochanters and the hip then abducted, a
“clunk” of the femur head striking the shallow acetabulum can be
heard (Ortolani’s sign). If the hip can be felt to actually slip in the
socket, this is Barlow’s sign.
A neonate who was born in a frank breech position will tend to
straighten the legs at the knee and bring them up to the face.
The fingertips, when arms are held down by the sides, should cover
the proximal thigh. Unusually short arms may signify
achondroplastic dwarfism.
Hyperflexibility of joints is characteristic of Down syndrome.
Some neonates may have abnormal extremities. They may be
polydactyl (more than 5 digits on an extremity) or syndactyl (two or
more digits fused together).
The nailbeds should be pink, although they may appear slightly blue
due to acrocyanosis. Persistent cyanosis indicates hypoxia or
vasoconstriction.
The palms should have the usual creases. A single, tranverse
palmar crease in contrast to the three creases normally seen in a
palm, called a Simian crease, suggests Down syndrome.
Spine.
The neonatal spine should be straight and flat. The base of the
spine should be inspected carefully to e certain there is no pinpoint
opening or dimpling which may suggest spina bifida occulta.
The position of a baby presenting with a face presentation
sometimes simulates opisthotonos (back arched acutely with a deep
concave appearance, and the head is bent back on the neck.
NEUROLOGIC ASSESSMENT
An examination of the reflexes provides useful information about the
neonate’s nervous system and his state of neurologic maturation.
Some reflexive behaviors in the neonate are necessary for survival
whereas other reflexive behaviors act as safety mechanisms.
Normal neonates display several types of reflexes. Abnormalities
are indicated by absence, asymmetry, persistence, or weakness
in these reflexes:
 Sucking – begins when a nipple is placed in the neonate’s
mouth
 Moro reflex – when the neonate is lifted above the crib
and suddenly lowered; the arms and legs symmetrically
extend and then abduct while the fingers spread to form a
“C”.
 Rooting – when the neonate’s cheek is stroked, the
neonate turns the head in the direction of the stroke
 Tonic neck (fencing position) – when the neonate’s head
is turned while he is lying in a supine position, the
 extremities on the same side straighten and those on Assessment :
the opposite side flex A. Prenatal Assessment
 Babinski reflex – the sole on the side of the 1. Fundal height during pregnancy is less than what is expected.
neonate’s small toe is stroked and the toes fan upward Dx Procedures :
 Grasping - when a finger is placed in each of the 1. Sonogram
neonate’s hands, the neonates fingers grasp tightly 2. Biophysical profile including nonstress test, placental grading ,
enough to be pulled to a sitting position UTZ add information on placental function
 Stepping – when the neonate is held upright with the
feet touching a flat surface, he responds with dancing Appearance :
or stepping movements 1. Below average in weight, length, and head circumference
 Startle – a loud noise such as a hand clap elicits 2. May have a small liver
neonatal arm abduction and elbow flexion and the 3. Poor skin turgor
neonate’s hands stay clenched 4. Appears to have a large head because the rest of the body is
 Trunk incurvature – when a finger is run laterally small
down the neonate’s spine, the trunk flexes and the 5. Skull sutures widely separated
pelvis swings toward the stimulated side 6. Hair is dull and lusterless
7. Sunken abdomen
 Blinking – the neonate’s eyelids close in response to
8. Cord appears dry and may be stained yellow
bright light
- SGA neonates are prone to meconium aspiration because fetal
 Acoustic Blinking – both eyes of the neonate blink in hypoxia allows meconium to pass through a relaxed anal sphincter,
response to a loud noise thus causing the neonate to experience reflexive gasping
 Perez reflex – when the neonate is suspended prone
in one of the examiner’s hands and the thumb of the  In contrast, the child may have :
other hand is moved firmly up he neonate’s spine from 1. Better developed neurologic responses, sole creases, and ear
the sacrum, the neonate’s head and spine extend, the cartilage
knees flex, the neonate cries, and he may empty his 2. Skull may be firmer
bladder 3. Unusually active and alert for that weight that could be attributed
to prolonged prenatal hypoxia
Eight (8) Priorities In First Days Of Life :
1. Initiating and maintaining respirations
 SGA infant needs careful assessment for possible congenital
 Resuscitation anomalies
 Establishing an airway
 Expanding the lungs Laboratory Findings :
 Drug Therapy 1. High hematocrit level at birth
 Maintaining effective ventilation 2. Increase in total number of red blood cells
3. Decrease serum glucose
2. Establishing intrauterine circulation
3. Fluid and Electrolyte Balance Nursing Diagnosis : Ineffective breathing pattern related to
4. Thermometer Regulation underdeveloped body system
 Radiant heat sources
 Isolettes  Birth asphyxia is a common problem for SGA because they have
 Kangaroo Care underdeveloped chest muscles and because they are at risk for
developing meconium aspiration syndrome due to anoxia
during labor

5. Preventing Infection Nursing Diagnosis :

6. Establishing Parent-Infant Bonding Risk for ineffective thermoregulation
 Following High-Risk Infants At Home Risk for altered parenting
 High-Risk Infants and Child Abuse
 Providing for Growth and Development  Mental development may have been impaired because of lack of
7. Intake of adequate nourishment oxygen and nourishment in utero
8. Developmental care or care that balances physiologic  SGA infants may always be below normal on standard growths
needs and stimulation for mental development chart and this inability to reach normal levels of growth and
development may interfere with bonding because the child does
Whether they are preterm, term, or postterm, neonates are not meet the parents expectations and eventually affects the
classified by weight in three ways child’s self-esteem
 Large for gestational age (LGA)
neonates Nursing Intervention :
 Appropriate for gestational age 1. Discuss ways parents can promote the infants development once
(AGA) neonates they are at home
 Small for gestational age (SGA) 2. Adequate stimulation during the infant period to reach normal
neonates growth and development
3. Encourage parents to provide toys that are suitable for their child’s
THE SMALL-FOR-GESTATIONAL-AGE INFANT chronologic age
4. Play periods must be spaced with rest periods or hypoglycemia or
 Birth weight is below the 10th percentile on an intrauterine apnea may occur
growth curve for that age (based on a postnatal growth
chart). THE LARGE-FOR-GESTATIONAL-AGE INFANT
 Infant may be born preterm, post term or term.  An infant is large for gestational age (Macrosomia) if the birth
 They are small for their age because they have experienced weight is above the 90% percentile on an intrauterine growth
intrauterine growth restriction (IUGR) or failed to grow at the chart for that gestational age
expected rate in utero
Causes :
Causes : 1. Mothers with diabetes mellitus
1. Lack of adequate nutrition 2. Multiparous women
2. Pregnant adolescents 3. Transposition of the great vessels
3. Placental anomaly 4. Beckwith’s Syndrome, a rare condition characterized by
overgrowth
 Placenta is unable to obtain sufficient nutrients from the 5. Congenital anomalies such as omphalocele
uterine arteries or it is inefficient at transporting nutrients to
the fetus Assessment :
 Size of the uterus measures unusually large for the date of
4. Placental damage pregnancy. A sonogram can confirm suspicion.
5. Women with systemic diseases that decrease blood flow to  A nonstress test to assess the placenta’s ability to sustain the
the placenta large fetus during labor
6. Smoking or use of narcotics  Infant’s lung maturity may be assessed by amniocentesis
7. Infants with intrauterine infections such as rubella or  Baby is unable to descend through the pelvic rim during labor
toxoplasmosis
 CS may be necessary because of cephalopelvic disproportion or
8. Infants with chromosomal abnormalities
shoulder dystocia.

Appearance :
1. At birth, LGA infants may show immature reflexes and low
scores on gestational age examinations in relation to their size.
2. Infant may have extensive bruising or a birth injury such as
broken clavicle
3. Erb-Duchenne paralysis from trauma to the cervical nerves if
the infant was delivered vaginally
4. Prominent caput succedaneum, cephalohematoma, or
molding
Specific Criteria For Initial Or Continuing Assessment
CARDIOVASCULAR DYSFUNCTION
 Heart rate should be carefully observed.
 Cyanosis may be a sign of transposition of the great vessels,
a serious heart anomaly
 Polycythemia is caused by the infant’s system attempting to
fully oxygenate all body tissues
 Observe for signs of hyperbilirubinemia which may result
from bruising and polycythemia
HYPOGLYCEMIA
 Infants should be carefully assessed for hypoglycemia in the
early hours of life because the infants use up nutritional
stores readily to sustain weight.
 If mother has poor glucose control, the infant will have an
increased blood glucose level in utero, which causes the
infant to produce elevated levels of insulin.
 After birth, increased insulin levels will continue up to 24
hours of life, possibly causing rebound hypoglycemia
Nursing Diagnosis : Ineffective breathing pattern r/t possible birth
trauma
Outcome Identification : Newborn will initiate and maintain
respirations at birth
Outcome Evaluation : NB initiates breathing at birth; maintains
normal NB respiratory rate at 30 to 60 breaths per minute
 SGA infants have difficulty establishing respirations because
of birth trauma
 Increase intracranial pressure from birth may lead to
pressure on the respiratory center, in turn, causes a
decrease in respiratory function
 A diaphragmatic paralysis may occur due to cervical nerve
trauma as the head is bent laterally to allow for birth of the
large shoulders. This prevents active lung motion on the
affected side.
 During CS, transient fluid can remain in the lungs and
interfere with effective gas exchange
Nursing Diagnosis : Risk for altered nutrition; less than body
requirements r/t additional nutrients needed to maintain weight
and prevent hypoglycemia
Outcome Identification : Infant will ingest adequate fluid and
nutrients for growth during neonatal period
Outcome Evaluation : Infant’s weight loss follows percentile
growth curve; skin turgor is good; specific gravity of urine 1.003
to 1.030; serum glucose is above 45 mg/dl
 As a rule, the LGA infants need to be breastfeed immediately
to prevent hypoglycemia
 Infant may need supplemental feeding after breastfeeding to
supply enough fluid and glucose for the larger than normal
size for the first few days.
Nursing Diagnosis : Risk for altered parenting
Outcome Identification : Parents demonstrate adequate bonding
behavior during neonatal period
Outcome Evaluation : Parents hold infant; speak of the child in
positive terms; state accurately why the infant needs to be
closely observed in postnatal period
 Educate parents regarding status of infant
 Allow mother to express resentments or fear she may feel
toward the infant
 A LGA infant needs the same developmental care as normal
infants do. Infant stimulation are important for infant’s
development
 Encourage parents to treat their baby as a fragile NB who
needs warm nurturing
 Remind parents that infants birth weight is not a correlation of
the child’s projected adult size.
THE PRE TERM INFANT
 A preterm infant is usually defined as a live-born infant born
before the end of week 37 of gestation
 Weighs less than 2500 g (5 lb, 8 oz) at birth
 Infants born weighing 1500-2500g are considered low-birth
weight (LBW)
 Infants born weighing 1000-1500 g are considered very-low-birth
weight (VLBW)
 Infants born 500-1000 g are considered extremely-very-low-birth
weight (EVLBW)
 A lack of lung surfactant makes them extremely vulnerable to
respiratory disease syndrome
 Preterm babies of every weight need to be differentiated at birth
from small-for-gestational-age babies (who also may have low
birth weights)
 A preterm infant is immature and small but well proportioned for
age
DIFFERENTIATING CHARACTERISTICS OF SGA INFANTS AND
PRETERM INFANTS :
Causes :
1. Low socio-economic level
2. Inadequate nutrition before and during pregnancy
3. Lack of prenatal care
4. Multiple pregnancy
5. Prior previous early birth
6. Race ( nonwhites have higher percentage than whites)
7. Cigarette smoking
8. Age of mother (highest incidence is mothers younger than 20
years old)
9. Order of birth (early termination is highest in first pregnancies and
in those beyond the fourth)
10. Closely spaced pregnancies
11. Abnormalities of the reproductive system such as intrauterine
septum
12. Infections (esp. UTI)
13.Obstetric complications such as PROM or premature separation
of placenta
14. Early induction of labor
15.Elective CS
16.Chronic Diseases – DM, renal, cardiovascular, respiratory
Appearance :
1. Appears small and underdeveloped
2. Head is large (3 cm or more grater than chest size)
3. Skin is unusually ruddy because of little subcutaneous fat
4. Veins are noticeable
5. High degree of acrocyanosis may be present
6. Neonate is covered with vernix caseosa. However, very preterm
NB, less than 25 weeks gestation, vernix is absent
7. Lanugo is extensive
8. Anterior and posterior fontanels are small
9. There are few creases on the soles of the feet.
10. Small eyes. Pupillary reaction is present.
11. Ear cartilage is immature and allows the pinna to fall forward.
The ears appear large
12. Reflexes are absent if infant’s age is below 33 weeks
13. Much less active and rarely cries. Cry is weak and high pitched
14. (+) Scarf sign – elbow reaches midline
15. When the heel is drawn as near to the ear as possible, little
resistance is met
16. Barely visible areola and nipple
17. Males- testes are high in the inguinal canal with the presence of
minimal rugae on the scrotum
Female – prominent clitoris, small widely separated labia majora
Potential Complications :
1. Anemia or prematurity
2. Kernicterus (destruction of brain cells by invasion of indirect
bilirubin)
3. Persistent patent ductus arteriosus
4. Periventricular/Intraventricular Hemorrhage
5. Respiratory disease syndrome
6. Apnea
7. Retinopathy of prematurity
8. Necrotizing enterocolitis
Nursing Diagnosis : Impaired gas exchange related to immature
pulmonary functioning
 Preterm infants have difficulty initiating respirations at birth
because the pulmonary capillary bed is immature
 A fetus usually turns to a vertex position late in pregnancy, the
preterm infant may still be in a breech position at birth
Interventions :
1. Giving the mother oxygen by mask during birth will provide the
infant with optimal oxygen saturation at birth
2. Maternal analgesia and anesthesia to a minimum offers the
infant best chance of initiating effective respirations
3. CS has the advantage of reducing pressure on the immature
head but may lead to additional respiratory complications
because of retained lung fluid
4. Resuscitate infant within 2 minutes to avoid irreversible
acidosis.
5. Prepare preterm size laryngoscopes, endotracheal tubes,
suction catheters and synthetic surfactant
6. Infant must be kept warm during resuscitation
7. Continued oxygen administration
Nursing Diagnosis : Risk for fluid volume deficit
 Preterm babies have a high insensible loss due to the large
body surface as compared with total body weight.
 The infant is unable to concentrate urine well because of
immature kidney function and thus excretes a high
proportion of fluid from the body.
 It is important that the preterm baby receive up to 160 to 200
ml of fluid/kg of body weight daily
Interventions :
1. IVF administration within hours after birth to fulfill fluid
replacement and provide glucose to oprevent hypoglycemia
2. Monitor baby’s weight, specific gravity and amount of urine,
and serum electrolytes to ensure adequate fluid intake
3. Blood glucose determinations to help determine hypoglycemia
or hyperglycemia.
4. Record all blood drawn
5. Check for blood in the stools to determine bleeding from
intestinal tract.
Nursing Diagnosis : Risk for altered nutrition; less than body
requirement
 Nutrition problem arise with the preterm infant because the
body is attempting to continue to maintain the rapid rate of
intrauterine growth. Therefore, the NB requires a larger
amount of nutrients in the diet than the mature infant..
 If nutrients are not supplied, Hypocalcemia or azotemia
develops.
 Delayed feeding may also add to hyperbilirubinemia
 Nutrition problem is compounded with infant’s immature
reflexes, which makes swallowing and sucking difficult
 Small stomach capacity may affect nutrition, because a
distended stomach may cause respiratory distress
 Increased activity due to ineffective sucking may increase
metabolic rate and oxygen requirements, therefore,
increases caloric requirements even more
 Immature cardiac sphincter allows regurgitation to occur
readily.
 Lack of cough reflex may lead the infant to aspirate
regurgitated formula.
 Digestion and absorption of nutrients in the stomach and
intestine may also be immature.
Nursing Diagnosis : Ineffective thermoregulation r/t immaturity
 A preterm baby has difficulty maintaining body temperature
because of the large surface area per pound of body weight
 Rapid cooling from evaporation occurs due to extended
position
 The preterm infant has little subcutaneous fat for insulation
and because of poor muscular development the child does
not move actively to produce body heat.
 The preterm infant has limited amount of brown fat, the
special tissue present in NB’s to maintain body temperature
 Because of an immature central nervous system and
hypothalamic control, the child is unable to sweat thereby
reducing body temperature and unable to shiver , a useful
mechanism to increase body temperature
Nursing Management :
1.The infant must be kept under a radiant heat warmer
Nursing Diagnosis : Risk for infection
 The skin of preterm infant is easily traumatized therefore has
less resistance to infection
 Preterm infant has lowered resistance to infection
 The infant has difficulty producing phagocytes to localize
infection and has a deficiency of IgM antibodies
Nursing Management :
1. Linen and equipment used with the preterm infant must be
clean to reduce the chances of infection
2. Hospital staff must be free of infection, and hand washing and
gowning regulations must be strictly enforced
Nursing Diagnosis : Diversional activity deficit (lack of
stimulation) r/t preterm infant’s rest needs
 Preterm infant needs rest to conserve energy for growth and
respiratory function, to combat hypoglycemia and infection, to
stabilize temperature and to develop inner balance and
attentiveness
 Infant needs planned periods of pleasing sensory stimulation
THE POST TERM INFANT
 Infant born after the 42nd week of a pregnancy
 Infant who stays in utero past week 42 of pregnancy is at special
risk because a placenta appears to only function effectively for
40 weeks. Fetus may die or develop post term syndrome
Pathophysiology
- If the placenta continuous to function well, the fetus will continue
to grow, which results in an LGA infant who may manifest
problems such as birth trauma and hypoglycemia
- If placental function decreases, the fetus may not receive
adequate nutrition. The fetus will utilize its subcutaneous fat
stores for energy. Wasting of subcutaneous fat occurs, resulting
in fetal dysmaturity syndrome.
Stages of Fetal Dysmaturity Syndrome
1. Stage 1 – Chronic Placental Insufficiency
 Dry, cracked, peeling, loose, and
wrinkled skin
 Malnourished appearance
 Open-eyed and alert
2. Stage 2 – Acute Placental Insufficiency
 Dry, cracked, peeling, loose, and wrinkled skin
 Malnourished appearance
 Meconium staining
 Perinatal depression
3. Stage 3 – Subacute Placental Insufficiency
 Dry, cracked, peeling, loose, and wrinkled skin
 Malnourished appearance
 Meconium staining
 Green staining of skin, nails, cord, and placental
membrane
 A higher risk of intrapartum and neonatal death
-The newborn is at increased risk for developing complications
related to compromised uteroplacental perfusion and hypoxia (eg.
Meconium aspiration syndrome [MAS])
- Chronic intrauterine hypoxia causes increased fetal erythropoietin
and red blood cell production resulting in polycythemia
- Post-term infants are susceptible to hypoglycemia because of the
rapid use of glycogen stores
Nursing Management
1. Manage Meconium Aspiration Syndrome
- suction the infant’s mouth and
nares while the head is in the
perineum and before the first breath
is taken to prevent aspiration of
meconium that is in the airway
- once the infant is dry and in the
warmer, intubate and do direct
tracheal suctioning
- perform chest physiotherapy with
suctioning to remove excess
meconium and secretions
- provide supplemental oxygen and
respiratory support as needed.
2. Obtain serial blood glucose measurements
3. If not contraindicated by respiratory status, provide early
feeding to prevent hypoglycemia
4. Maintain skin integrity
- keep the skin clean and dry
- avoid the use of powders, creams
and lotions
-
ILLNESS IN THE NEWBORN
1. RESPIRATORY DISTRESS SYNDROME
 RDS most often occurs in preterm infants, infants of diabetic
mothers, infants born by CS, those who have decreased blood
perfusion of the lungs
Pathologic Feature: A hyaline-like (fibrous) membrane comprised of
products formed from an exudates of the infant’s blood that lines the
terminal bronchioles, alveolar ducts, and alveoli. This membrane
prevents exchange of oxygen and carbon dioxide at the alveolar-
capillary membrane.
Cause of RDS: A low level or absence of surfactant, the
phospholipid that normally lines the alveoli and resists surface
tension on expiration to keep alveoli from collapsing on
expiration.
Pathophysiology :
 High pressure is required to fill the lungs with air for the first
time and overcome the pressure of lung fluid. It takes a
pressure between 40 cm H2O and 70 cm H2O, to inspire a
first breath, but only 15 cm H2O to 20 cm H2O to maintain
quiet, continued breathing. If alveoli collapse with each
expiration, as happens when surfactant is deficient,
however, it continues to take forceful inspiration to inflate
them. With deficient surfactant, areas of hypoinflation occur
and pulmonary resistance is increased. Blood then shunts
through the foramen ovale and the ductus arteriosus. The
lungs are poorly perfused, thus affecting gas exchange. As
a result, the production of surfactant decrease even further.
The poor oxygen exchange leads to tissue hypoxia. Tissue
hypoxia causes the release of lactic acid. This, combined
with an increasing carbon dioxide level resulting from the
formation of the hyaline membrane on the alveolar surface,
leads to severe acidosis. Acidosis causes vasoconstriction,
and decreased pulmonary perfusion from vasoconstriction
further limits surfactant production. With decreased
surfactant production, the ability to stop alveoli from
collapsing with each expiration becomes impaired. This
vicious cycle continuous until the oxygen-carbon dioxide
exchange in the alveoli is no longer adequate to sustain life
without ventilator support.
Assessment :
1. Difficulty initiating respirations at birth
2. Low body temperature
3. Nasal flaring
4. Sternal and subcostal retractions
5. Tachypnea
6. Expiratory grunting
7. On auscultation, fine rales and diminished breath sounds
8.Seesaw respirations
9. Heart failure evidenced by decreased urine output and edema
of the extremities
10. Pale gray skin color
11. Periods of apnea
12. Bradycardia
Therapeutic Management :
1. Surfactant Replacement and Rescue
2. Oxygen administration
3. Ventilation
4. Use of muscle relaxants
5. Extracorpeal Membrane Oxygenation
6. Liquid ventilation
Prevention :
1. Preventing preterm labor by using tocolytic agents
2. Administer 2 injections of a glucocorticosteroid to the mother
at 12 and 24 hours before birth. Steroids quickens the formation
of lecithin production pathways
Nursing Diagnosis : Impaired gas exchange r/t immaturity of the
NB’s lungs and diminished surfactant
Interventions :
1. Assess NB’s status and note signs of increasing respiratory
distress
2. Maintain endotracheal tube, mechanical ventilation and
supplemental warm humidified oxygen
3. Prepare to administer surfactant rescue
4. Change the NB’s position during administration and refrain
from suctioning the ET tube for up to 1 hour following
administration
5. Anticipate administration of indomethacin and pancuronium
6. Maintain a neutral thermal environment and minimize physical
activity
7. Plan nursing care to allow for frequent rest periods and
attempt to anticipate the NB’s needs
2. TRANSIENT TACHYPNEA OF THE NEWBORN
Signs and Symptoms :
1. Mild retractions but not marked cyanosis
2. Mild hypoxia and hypercapnia
3. Feeding is difficult because infant cannot suck and breathe
this rapidly at the same time
4. Chest x-ray reveals fluid in the lungs
 Transient tachypnea results from slow absorption of lung fluid
Intervention :
1. Close observation is the priority
2. Oxygen administration
3. MECONIUM ASPIRATION SYNDROME
Meconium is a thick, sticky, greenish black substance that
constitutes the neonate’s first feces. It is present in the bowels of the
fetus as early as 10 weeks gestation. Meconium aspiration
syndrome results when the neonate inhales meconium that is mixed
with amniotic fluid. It typically occurs while the neonate is in utero or
with the neonate’s first breath. The meconium partially or completely
blocks the neonate’s airways so that air becomes trapped during
exhalation. Also, the meconium irritates the neonate’s airways,
making breathing difficult.
The severity of meconium aspiration syndrome depends on the
amount of meconium aspirated and the consistency of the
meconium. Thicker meconium generally causes more damage.
Neonates with meconium aspiration syndrome increase their
respiratory efforts to create greater negative intrathoracis pressures
and improve air flow to the lungs. Hyperinflation, hypoxemia, and
academia cause increased peripheral vascular resistance. Right to
left shunting often follows.
Pathophysiology:
Meconium aspiration syndrome is commonly related to fetal distress
during labor. When a neonate becomes hypoxic, peristalsis
increases and the anal sphincter relaxes. Occasionally, healthy
neonates pass meconium before birth. In either case, if the neonate
gasps or inhales the meconium, meconium aspiration can develop.
The resulting lack of oxygen may lead to brain damage.
Risk factors for meconium aspiration syndrome include:
 Maternal diabetes
 Maternal hypertension
 Difficult delivery
 Fetal distress
 Intrauterine hypoxia
 Advanced gestational age (greater than 40 weeks)
 Poor intrauterine growth
Signs and symptoms of meconium aspiration syndrome include:
 Dark greenish staining or streaking of the
amniotic fluid
 Obvious presence of meconium in the amniotic
fluid
 Skin with a greenish stain (if the meconium was
passed long before delivery)
 Limp appearance at birth
 Cyanosis
 Rapid and labored breathing. retractions
 Low heart rate before birth
 Low APGAR score
Nursing Interventions :
1. Infant should be suctioned with a bulb syringe while at the
perineum to avoid meconium aspiration
2. Infant should be intubated and meconium should be suctioned
from the trachea and bronchi as soon as the infant is born
Therapeutic Management :
1. Amniotransfusion may be used to dilute the amount of meconium
in amniotic fluid and reduce risk of aspiration
2. Oxygen adminitration
3. Antibiotic Therapy
4. Maintain a thermal neutral environment
5. Chest physiotherapy with clapping and vibration to facilitate
removal of remnants of meconium from the lungs
4. APNEA
 A pause in respirations longer than 20 seconds with
accompanying bradycardia
 Many preterm infants have periods of apnea as a result of fatigue
or the immaturity of their respiratory functions
 Babies with secondary stresses, such as infection,
hyperbilirubinemia, hypoglycemia or hypothermia tend to have
high incidence of apnea
Tx Management :
1. Gently shake or flick the sole of the foot to stimulate the baby
2. Apnea monitors to detect failing respiration
3. Ventilator to provide respiratory coordination
4. Maintain a neutral thermal environment
5. Always suction gently
6. Careful burping after feeding
7. Theophylline or caffeine sodium benzoate may be administered to
stimulate respirations
5. SUDDEN INFANT DEATH SYNDROME (SIDS)
 SID is the sudden unexplained death in infancy

Etiology :
 Occur usually in infants of adolescent mothers, infants of
closely spaced pregnancies and underweight and preterm
infants.
 Also prone to SIDS are infants with bronchopulmonary
dysplacia, twins, siblings of another child with SIDS
 Infants of narcotic-dependent mothers
 Peak ages of incidence are between 2 weeks and 1 year of
age
 Viral respiratory or botulism infection
 Distorted familial breathing patterns
 Possible lack of surfactant in alveoli
 Sleeping prone rather than on the side or back
Apparent Life-Threatening Event (ALTE)
 Infants discovered cyanotic and limp in their beds but have
survived after mouth-to-mouth resuscitation by parents
6. PERIVENTRICULAR LEUCOMALACIA (PVL)
 PVL is abnormal formation of the white matter of the brain
 Occurs most frequently in preterm infants who experience
cerebral ischemia
 Ischemic episode interferes with circulation to a portion of the
brain. Phagocytes and macrophages invade the area to
clear away necrotic tissue, what is left is an area in the
white matter of the brain that is revealed on sonogram as a
hollow space.
 No therapy is identified.
 Infants may die from the original insult; thay may be left with
long term effects such as learning disabilities.
7. HYPERBILIRUBINEMIA
Hyperbilirubinemia is an excess of bilirubin in the blood that
results in elevated serum bilirubin levels and mild jaundice.
Hyperbilirubinemia can be physiologic (with jaundice being the
only symptom) or pathologic (resulting from an underlying
disease).
Physiologic hyperbilirubinemia is self-limiting. It usually resolves
in 7-10 days. Prognosis for pathologic hyperbilirubinemia varies,
depending on the cause. If left untreated, hyperbilirubinemia
may result in kernicterus, a neurologic syndrome caused by
unconjugated bilirubin depositing in the brain cells. Survivors
may develop cerebral palsy, epilepsy, or mental retardation, or
they may have only minor effects, such as perceptual-motor
disabilities and learning disorders.
Pathophysiology:
As erythrocytes break down at the end of their neonatal life
cycle, hemoglobin separates into globin (protein) and heme (iron
and protoporphyrin) fragments.
Heme fragments (protoporphyrin component) form unconjugated
bilirubin. Unconjugated bilirubin is fat soluble and cannot be
excreted by the kidneys in this state. Instead unconjugated
bilirubin binds with albumin and is transported to the liver. In the
liver, it is converted by the liver enzyme glucuronyl transferase
into direct bilirubin, which is water soluble and is incorporated
into stool and then excreted in the feces.
Many newborns have such immature liver function that indirect
bilirubin can not be converted into direct form and, therefore,
remains indirect. Other factors include:
- certain drugs (such as aspirin, tranquilizers and
sulfonamides) or conditions ( such as hypothermia, anoxia,
hypoglycemia, and hypoalbuminemia) can disrupt conjugation
and usurp albumin-binding sites
-Increased erythrocyte production or breakdown (like in the
resolution of cephalhematoma), or Rh or ABO incompatibility
-Maternal enzymes and hormones (pregnanediol) present in
breast milk can inhibit the neonate’s glucuronyltransferase
conjugating activity
Manifestations:
The predominant sign of hyperbilirubinemia is jaundice in which
the usual pattern of progression is from head to feet. Blanch
skin over bony prominence or look at conjunctiva and buccal
membranes in dark-skinned infants. Jaundice doesn’t become
clinically apparent until serum bilirubin levels reach about
7mg/100ml. Around this serumlevel, unconjugated bilirubin
escape to the extravascular tissues.
Physiologic hyperbilirubinemia
- Typically develops within 2-3 days after birth in 50% of term
neonates and within 3-5 days after birth in 80% of preterm
neonates. It generally disappears by day 7 in term neonates and
by day 9 or 10 in preterm neonates. Throughout physiologic
jaundice, the serum unconjugated bilirubin level doesn’t exceed
12mg/100ml.
Pathologic hyperbilirubinemia
-May appear anytime after the first day of life and persists beyond 7
days with serum bilirubin levels greater than 12mg/100ml in a term
neonate, 15mg/100ml in a preterm neonate, or increasing more than
5mg/100ml in 24 hours.
Treatment:
Depending on the underlying cause, treatment may include:
*exchange transfusion – replaces the neonate’s blood with fresh
blood (blood that is less than 48 hours old), thus removing some of
the
unconjugated bilirubin in serum
*phototherapy - uses fluorescent light to decompose bilirubin
in the skin by oxidation. Implemented after the initial exchange
transfusion, phototherapy is usually
discontinued after bilirubin levels fll below 10mg/100ml and continue
to decrease for 24 hours and albumin infusion -(1g/kg of 25%
salt-poor albumin) which provides additional albumin for binding
unconjugated bilirubin.
Performing Phototherapy
 Set up the phototherapy unit about 18” above the
neonate’s crib and verify the placement of the light-bulb
shield. If the neonate is in the incubator, place the
phototherapy unit at least 3” above the incubator and turn
on the light. Place a photometer probe in the middle of
the crib to measure the energy emitted by the lights.
 Explain the procedure to the parents.
 Record the neonate’s initial bilirubin level and his axillary
temperature.
 Place the opaque eye mask over the neonate’s closed
eyes and fasten securely.
 Undress the neonate and place a diaper under him.
Cover male genitalia with a surgical mask or small diaper
to catch urine and prevent possible testicular damage
from the heat and light waves.
 Take the neonate’s axillary temperature every 2 hours
and provide additional warmth by adjusting the warming
unit’s thermostat
 Monitor elimination and weigh the neonate twice daily.
Watch for signs of dehydration (dry skin, poor turgor,
depressed fontanels) and check urine specific gravity with
a urinometer to gauge hydration status.
 Take the neonate out of the crib, turn off the phototherapy
lights, and unmask his eyes at least every 3-4 hours with
feedings. Assess his eyes for inflammation and injury.
 Reposition the neonate every 2 hours to expose all body
surfaces to the light and to prevent head molding and skin
breakdown from pressure.
 Check the bilirubin level at least once every 24 hours –
more often if levels rise significantly. Turn off the
phototherapy unit before drawing venous blood for testing
because the lights may degrade bilirubin in the blood.
Notify the doctor if the bilirubin level nears 20mg/dl in full-
term neonates or 15mg/dl in premature.
8. HEMOLYTIC DISEASE OF THE NEWBORN (Erythroblastosis
Fetalis)
A. General Information
- characterized by RBC destruction in
the newborn, with resultant anemia and hyperbilirubinemia
- possibly caused by Rh or ABO
incompatibility between the mother and the fetus (antigen-
antibody reaction)
- mechanisms of Rh incompatibility
sensitization of Rh-negative woman by transfusion of Rh-
positive blood
sensitization of Rh-negative woman by presence of Rh-
positive RBCs from her fetus conceived with Rh-positive man
approximately 65% of infants conceived by this
combination of parents will be Rh-positive
mother is sensitized by passage of fetal Rh-positive
RBCs through placenta either during pregnancy
(break/leak in the membrane) or at the time of separation
of placenta after delivery
this stimulates the mother’s immune response system to
produce anti-Rh positive antibodies that attack fetal RBCs
and cause hemolysis
if this sensitization occurs during pregnancy, the fetus is
affected in utero; if sensitization occurs at the time of
delivery, subsequent pregnancies may be affected.
- ABO incompatibility
same underlying mechanism
mother is blood type O; infant A, B, or AB
reaction in ABO incompatibility is less severe compared
to Rh-incompatibility
B. Rh- Incompatibility
first pregnancy, mother may become sensitized, baby
rarely affected
Indirect Coomb’s test (tests for anti-Rh positive
antibodies in mother’s circulation) performed during
pregnancy at first visit and again at 28 weeks
gestation. If indirect Coomb’s test is negative at 28
weeks, a small dose (Mic Rhogam) is given
prophylactically to prevent sensitization in the third
trimester ( Rhogam may also be given after the 2nd
trimester amniocentesis)
If positive, levels are titrated to determine extent of
maternal sensitization and potential effect on the
fetus
Direct Coomb’s test is done on cord blood at delivery
to determine presence of anti-Rh positive antibodies
on fetal RBCs.
If both direct and indirect Coomb’s tests are negative
(no formation of anti-Rh positive antibodies) and
infant is Rh-positive, then Rh-negative mother can be
given Rhogam (Rho human immune globulin) to
prevent development of anti-positive antibodies as
the result of sensitization from present pregnancy
In each pregnancy, an Rh-negative mother who
carries an Rh-positive fetus can receive Rhogam to
protect future pregnancies if the mother has had
negative indirect Coomb’s test and the infant has had
a negative direct Coomb’s test
If the mother has been sensitized (produced anti Rh-
positve antibodies), Rhogam is not indicated. She
may be given high doses of gamma globulin to help
reduce fetal involvement, hoping to interfere with the
rapid destruction of fetal RBCs. The fetus may
receive a blood transfusion in utero via an injection of
RBCs directly into a vessel in the fetal cord or
instillation in the fetal abdomen via amniocentesis.
After birth, the neonate may receive an axchange
transfusion to remove hemolyzed RBCs and replace
them with healthy blood cells.
Rhogam may be injected (IM in the gluteal area) into
unsensitized mother’s system within 72 hours of
delivery of Rh-positive infant.
C. ABO Incompatibility
Reaction less severe than with RH incompatibility
First born may be affected because type O mother
may have anti-A and anti-B antibodies even before
pregnancy
Fetal RBCs with A, B, or AB antigens evoke less
severe reaction on part of mother, thus fewer anti-A,
anti-B, or anti-AB antibodies are produced
Clinical manifestations of ABO incompatibility are
milder and of shorter duration than those of Rh compatibility
D. Assessment Findings
jaundice and pallor within the first 24-36 hours
anemia and hyperbilirubinemia – due to RBC
destruction
erythropoiesis
enlarged placenta and enlarged fetal liver and spleen
– due to the attempt to produce and supply new red blood
cells
edema and ascites – resulting from fluid shift because
the blood in the intravacular space is hypotonic relative to
the interstitial
* Hydrops fetalis – “fatal edema”, old term for the
appearance of a severely involved infant at birth
E. Nursing Interventions
determine blood type and Rh early in pregnancy
determine results of indirect Coomb’s test early in
pregnancy and again at 28-32 weeks
determine results of direct Coomb’s test on cord blood
administer Rhogam IM to mother as ordered
do careful monitoring
implement phototherapy or exchange transfusion for
any hyperbilirubinemia
9. HEMORRHAGIC DISEASE OF THE NEWBORN
 Results from a deficiency of Vit. K
 Vit K is essential for the formation of prothrombin by the liver
 Babies born to mothers on anticonvulsive medication are at
high risk
Symptoms :
1. Petechiae from superficial bleeding into the skin
2. Conjuntival, mucous membrane or retinal hemorrhage
3. May vomit fresh blood or pass black, tarry stools because of
bleeding into the GIT
Therapeutic Management :
1. Hemorrhagic disease of the NB can be prevented by Vit K 1 mg
IM immediately after birth
2. Blood transfusion of fresh whole blood in severe bleeding to
increase the prothrombin level
10. TWIN-TO-TWIN TRANSFUSION
 A phenomenon that can occur if twins are monozygotic (identical;
share the same placenta) and if abnormal arteriovenous shunts
occur that direct more blood to one twin than the other
 Can be identified through sonogram
 One twin is larger than the other
11. NECROTIZING ENTEROCOLITIS
A. General Information
- an ischemic attack to the intestines resulting in thrombosis and
infarction of affected bowel, mucosal ulcerations,,
pseudomembrane formation, and inflammation
- bacterial actions (E. coli, Klebsiella) complicates the process,
producing sepsis
- may be precipitated by any event in which blood is shunted away
from the intestines to more vital organs like the heart and brain (e.g.
fetal distress, low APGAR score, RDS, prematurity, neonatal shock,
and asphyxia).
- average age of onset is 4 days
- now that severely ill infants are surviving, NEC is encountered more
frequently
- may ultimately cause bowel perforation and death
B. Medical Management
- parenteral antibiotics
- gastric decompression
- correction of acidosis and fluid and electrolyte imbalance
- surgical removal of the diseased intestine
C. Assessment Findings
-history indicating high-risk group
-findings related to sepsis (temperature instability, apnea and
labored respiration, cardiovascular collapse, lethargy or irritability)
-gastrointestinal symptoms (abdominal distention and tenderness,
vomiting and poor feeding, hematest positive stools, x-rays showing
air in the bowel wall, adynamic ileus, and bowel wall thickening)
D. Nursing Interventions
-carefully assess infants at risk for early recognition of symptoms
-discontinue oral feedings, insert nasogastric tube
-prevent trauma to abdomen by avoiding diapers and planning care
for minimal handling
-maintain acid base balance by administering fluid and electrolytes
as ordered
-administer antibiotics as ordered
-inform parents of progress and support them in expressing their
fears and concerns
THE NEWBORN AT RISK BECAUSE OF MATERNAL INFECTION
OR ILLNESS
1. BETA-HEMOLYTIC, GROUP B STREPTOCOCCAL INFECTION
 Beta-hemolytic, group B streptococcal organism is the major
cause of infection in NB infants
Assessment :
1. Tachypnea
2. Apnea
3. Symptoms of shock such as decreased urine output, extreme
paleness, or hypotonia
4. Lethargy
5. Fever
6. Loss of appetite
7. Bulging fontannels
Therapeutic Management :
1. Antibiotics. Gentamicin, ampicillin and penicillin.
2. Immunization of all childbearing age women against streptococcal
organisms
2. CONGENITAL RUBELLA
 Rubella virus is capable of causing extensive congenital fetal
malformations if the mother is infected during the first trimester
of pregnancy
 The greatest risk to an embryo from rubella virus is during weeks
2 to 6 of intrauterine life.
Assessment : Therapeutic Management :
1. Thrombocytopenia 1. Drugs that inhibit viral deoxyribonucleic acid synthesis (acyclovir
2. Cataracts and vidaribine) are effective in combating this infection
3. Heart Disease 2. Women with active herpetic vulvar lesions are often delivered by
4. Deafness caesarian to minimize the NB’s exposure
5. Microcephaly 3. Infants with this infection are separated from other infants
6. Motor and cognitive impairment 4. Women with lesions on their face should not feed or hold their
NB’s until lesions are crusted and no longer contagious
Therapeutic Management :
1. Treatment is symptomatic, depending on the congenital 6. THE INFANT OF A DIABETIC MOTHER
defects present
2. Contact precautions Assessment :
3. Susceptible pregnant women should avoid contacts with the 1. Infants of a diabetic mother whose illness was poorly controlled
NB still having the virus during pregnancy is typically longer and weighs more thatn other
4. Women with low rubella titers should be given rubella vaccine babies (macrosomia)
to ensure that rubella infection does not occur in future 2. Infant has a greater chance of having congenital anomaly
pregnancies 3. Caudal regression syndrome or hypoplasia of the lower
extremities is a syndrome that occurs almost exclusively in such
3. OPHTHALMIA NEONATORUM infants
 Ophthalmia neonatorum is eye infection at birth or during the 4. Cushingoid (fat and puffy) appearance
first month 5. Lethargic or limp in the first days of life, effects of hyperglycemia
 Most common causative organisms include Neisseria 6. Lungs may be immature
gonorrhea or Chlamydia trachomatis 7. RDS occurs frequently
 N. gonorrhea if left untreated could progress to corneal
ulceration and destruction, resulting in opacity of the cornea Complications :
and severe vision impairment 1.Greater chance of birth injury if infant is macrosomic
Assessment : 2. Infants tend to be hyperglycemic immediately after birth
1. Ophthalmia neonatorum is generally bilateral 3. Hyperbilirubinemia
2. Eye conjunctivae become fiery red, there is thick pus and the 4. Hypocalcemia
eyelids are edematous 5. Infants will be small for gestational age (SGA) because of poor
placental perfusion
Prevention :
1. Prophylactic instillation of erythromycin ointment into the eyes Therapeutic Management :
of NB’s 1. To prevent hypoglycemia, infants are fed early with formula or
administered a continuous infusion of glucose
Therapeutic Management : 2. It is important not to give bolus of glucose to avoid rebound
1. Therapy is individualized depending on the organism cultured hypoglycemia
from the exudate
2. If gonococci is identified, Ceftriaxone and penicillin IV are 7. THE INFANT OF A DRUG-DEPENDENT MOTHER
effective drugs
3. If chlamydia is identified, Erythromycin ophthalmic solution is Assessment :
used 1. Infants tend to be small for gestational age
4. The eyes are irrigated with sterile saline solution to clear the 2. Irritability
copious discharge 3. Disturbed sleep patterns
5. The mother of the infected infant needs treatment for Constant movement possibly leading to abrasions on their elbows,
gonorrhea or chlamydia knees or nose
4. Tremors
4. HEPATITIS B VIRUS INFECTION 5. Frequent sneezing
 The hepatitis B virus can be transmitted to the NB through 6. Shrill, high –pitched cry
contact with infected vaginal blood at birth 7. Possible hyperplasia and clonus (neuromuscular irritability)
 70 to 90% of infected infants become chronic carriers of the 8. Convulsions
virus. 9. Tachypnea
10. Vomiting and diarrhea leading to large fluid losses and
 A number of these NB’s will develop liver cancer later in life
secondary hydration
Prevention :
Therapeutic Management :
1. Routine vaccination of infants at birth
1. Infants are most comfortable when firmly swaddled.
2. If mother is identified as HbsAg+. The infant is administered
2. Infants should be kept in an environment free from excessive
immune serum globulin (HBIG) within 12 hours of birth to
stimuli
decrease possibility of infection
3. Infants must be gavage fed if infants have poor sucking ability and
3. The infant should be bathed immediately after birth to remove
may have difficulty getting enough fluid intake
HBV-infected blood and secretions
4. Maintenance of electrolyte and fluid balance is essential
4. Suctioning should be with gentle technique to avoid possible
5. IVF administration is necessary if infant has vomiting or diarrhea
trauma to the mucous membrane which could allow HBV
6. Drugs used to counteract withdrawal symptoms include paregoric,
invasion
Phenobarbital, methadone, chlorpromazine and diazepam
7. Infants should not be breastfeed to avoid passing narcotics to the
5. GENERALIZED HERPESVIRUS INFECTION
child
 A herpes simplex virus type 2 (HSV-2) infections can be
contracted by a fetus across the placenta if the mother has 8. THE INFANT WITH FETAL ALCOHOL SYNDROME (FAS)
a primary infection during pregnancy. - A cluster of birth defects that are caused by in utero exposure to
 Most often, the virus is contracted from the vaginal secretions alcohol referred to as FAS.
from the mother who has active herpetic vulvovaginitis at - Although prenatal alcohol exposure doesn’t always result in FAS,
the time of birth the safe level of alcohol consumption during pregnancy isn’t known.
- Alcohol crosses through the placenta and enters fetal blood supply,
Assessment : and it can interfere with the healthy development of the fetus. In fact,
1. Vesicles covering the skin if the infection was acquired during birth defects associated with prenatal alcohol exposure can occur in
pregnancy the first 3-8 weeks of pregnancy, before a woman even knows she is
2. Loss of appetite pregnant.
3. Low-grade fever Variables that affect the extent of damage caused by the fetus by
4. Lethargy alcohol include the amount of alcohol consumed, the timing of
5. Stomatitis (ulcers of the mouth) or a few vesicles in the skin consumption, and the pattern of alcohol use.
6. Herpes vesicles are always clustered, pinpoint in size and Characteristics :
surrounded by a reddened base 1. Pre and postnatal growth restriction
7. After vesicles appear, infants become extremely ill. They 2. Central nervous system involvement such as cognitive
develop dyspnea, jaundice, purpura, convulsions, and shock impairment, microcephaly and cerebral palsy
3. Facial features such as short palpebral fissures, thin upper lip,
Complications : strabismus, low nasal bridge, flat midface, flat or absent groove in
1. Death may occur within hours or days the upper lip, short nose and receding jaw
2. Some who survived the infection may have permanent central 4. Infant may be tremulous, fidgety, irritable, and may have a weak
nervous system sequelae sucking reflex during neonatal period
5. Sleep disturbances are common
6. Behavior problems such as hyperactivity may occur in school-
age children
7. Growth deficiencies may remain through life
Supportive treatment is implemented.
Emphasis on management of respiratory problems, nutrition, and
maternal-neonate bonding should be made.
HIGH RISK ADULT
RESPIRATORY DISORDERS
ACUTE RESPIRATORY DISTRESS SYNDROME
 A clinical syndrome characterized by a sudden and
progressive pulmonary edema, increasing bilateral
infiltrates, hypoxemia refractory to oxygen supplementation
and reduced lung compliance
Etiologic Factors Related to ARDS :
1. Aspiration (gastric secretions, drowning, hydrocarbons)
2. Drug ingestion and overdose
3. Hematologic disorders
4. Prolonged inhalation of high concentrations of oxygen, smoke,
or corrosive substances
5. Localized infection (bacterial, fungal, viral pneumonia)
6. Metabolic disorders ( pancreatitis, uremia)
7. Shock (any cause)
8. Trauma ( pulmonary contusion, multiple fractures, head injury)
9. Fat or air embolism
10. Systemic sepsis
Pathophysiology
Clinical Manifestations :
1. Rapid onset of severe dyspnea
2. Anxiety
3. Labored breathing and tachypnea
Assessment : Intercostal retractions and crackles
Medical Management :
1. Primary focus of management includes identification and
treatment of the condition.
2. Supportive Therapy : Intubation and mechanical ventilation
3. Circulatory support, adequate fluid volume and nutritional
support
4. Supplemental oxygen is used as the patient begins the initial
spiral of hypoxemia
5. Positive end-expiratory pressure (PEEP)
6. Hypovolemia must be carefully treated
7. Intravenous crystalloid solutions are administered
8. Pulmonary artery pressure catheters are used to monitor
patients fluid status
Nursing Management :
1. Positioning is important. Nurse should turn the patient
frequently to improve ventilation and perfusion in the lungs and
enhance secretion drainage
2. Nurse must closely monitor rapid changes in oxygenation with
changes in position
3. The nurse should explain all procedures and deliver care in a
calm, reassuring manner
4. Rest is essential to reduce oxygen consumption
Nursing Diagnosis : Impaired gas exchange r/t inadequate
respiratory center activity, chest wall movement, airway
obstruction, fluids in the lungs
ACUTE RESPIRATORY FAILURE (ARF)
 Defined as a fall in arterial oxygen tension and a rise in
arterial carbon dioxide tension.
 The ventilation and/or perfusion mechanisms in the lung are
impaired.
 Respiratory system mechanisms leading to ARF include:
1. Alveolar hypoventilation
2. Diffusion abnormalities
3. Ventilation-perfusion mismatching
4. Shunting
Pathophysiology:
Common Causes of Acute Respiratory Failure :
Decreased Respiratory Drive
 May occur with severe brain injury, large lesions of the brain
stem (multiple sclerosis), use of sedative medications, and
metabolic disorders such as hyperthyroidism. This
disorders impair the normal response of chemoreceptors in
the brain to normal respiratory stimulation
Dysfunction Of The Chest Wall
 The impulses arising in the respiratory center travel through
nerves that extend from the brain stem down the spinal cord to
receptors in the muscles of respiration. Thus, any disease of
the nerves, spinal cord, muscles or neuromuscular junction
involved in respiration seriously affects ventilation and may lead
to ARF
Dysfunction Of Lung Parenchyma
 Pleural effusion, hemothorax, pneumothorax, and upper airway
obstruction are conditions that interfere with ventilation by
preventing expansion of the lung. These conditions, which may
cause respiratory failure, usually are produced by an underlying
lung disease, pleural disease, trauma and injury.
 Other diseases and conditions of the lung that lead to ARF
include pneumonia, status asthmaticus, lobar atelectasis,
pulmonary embolism and pulmonary edema
Other Factors
 In the postoperative period, esp. after major thoracic or
abdominal surgery, inadequate ventilation and respiratory
failure may occur. Causes of ARF during this period include the
effects of anesthetic agents, analgesics, and sedatives; they
may depress respiration and lead to hypoventilation
Clinical Manifestations:
 Early signs are those associated with impaired oxygenation
 Restlessness, fatigue, headache, dyspnea, air hunger,
tachycardia, tachypnea, central cyanosis, diaphoresis and
finally, respiratory arrest
 Physical findings : use of accessory muscles, decreased breath
sounds
Medical Management:
 Objectives of treatment are to correct the underlying cause and
to restore adequate gas exchange in the lung
 Intubation and mechanical ventilation
Nursing Management:
 Assist with intubation
 Assess respiratory status by monitoring patient’s level of
response, arterial blood gases, pulse oximetry and vital signs
 Implement strategies to prevent complications : turning schedule,
mouth care, skin care, ROM
CHRONIC RESPIRATORY FAILURE
 Defined as a deterioration in the gas exchange function of the
lung that has developed insidiously or has persisted for a long
period after an episode of ARF
 Patients develop a tolerance to the worsening hypoxemia and
hypercapnia
 Patient with chronic respiratory failure may develop Acute
respiratory failure – seen in COPD patients who develops an
exacerbation or infection that causes additional deterioration of
the gas exchange mechanism
2 Causes of Chronic Respiratory Failure:
1. COPD
2. Neuromuscular Diseases
RESPIRATORY FAILURE
 Respiratory failure is a sudden and life-threatening deterioration
of the gas exchange function of the lung.
 Exists when the exchange of oxygen for carbon dioxide in the
lungs can not keep up with the rate of oxygen consumption and
carbon dioxide production by the cells of the body.
ENDOCRINE/METABOLIC DISORDERS
DIABETIC KETOACIDOSIS
 DKA is caused by an absence or markedly inadequate amount of
insulin
Three Main Clinical Features of DKA :
1. Hyperglycemia
2. Dehydration and electrolyte loss
3. Acidosis
Pathophysiology
Three Main Causes of DKA :
1. Decreased or missed dose of insulin
2. Illness or infection
3. Undiagnosed and untreated diabetes
Clinical Manifestations :
1. Acetone breath
2. Poor appetite or anorexia
3. Nausea and vomiting
4. Abdominal pain
5. Blurred vision
6. Weakness
7. Headache
8. Dehydration
9. Thirst or polydipsia
10. Orthostatic hypotension
11. Hyperventilation
12. Mental status changes in DKA vary from patient to patient
Assessment and Diagnostic Findings :
1. Blood glucose levels may vary from300 to 800 mg/dl
2. The severity of DKA is not necessarily related to the blood
glucose level
3. Evidence of DKA is reflected in low serum bicarbonate and
low pH values
Prevention :
1. Patients must be taught “sick day “rules for maintaining their
diabetes when ill.
2. The most important issue is not to eliminate insulin doses
when nausea and vomiting occur and then attempt to consume
frequent small portions of carbohydrates
3. Drinking fluids every hour is important to prevent dehydration
4. Patients are taught to have available foods for use on sick
days.
5. Supply of urine test strips and blood glucose test strips should
be available. Patients must know how to contact their physician
Medical Management :
1. Rehydration is important for maintaining tissue perfusion and
enhancing the excretion of excessive glucose by the kidneys
2. The major electrolyte of concern during treatment of DKA is
potassium. Potassium replacement is vital to avoid dysrhythmias
that may occur with hypokalemia
3. Insulin is usually infused IV at a slow, continuous rate
4. Dextrose is added to IVF, such as normal saline solution when
blood glucose level reach 250 to 300 mg/dl to avoid too rapid
drop in the blood glucose level
Nursing Management :
1. Nursing care focuses on monitoring fluid and electrolyte
status, blood glucose levels, administering fluids, insulin and
other medications and preventing complications such as fluid
overload.
2. Urine output is monitored to ensure adequate renal function
3. ECG is monitored for dysrhythmias
4. VS, arterial blood gases and other clinical findings are
recorded on a flow sheet
THYROTOXIC CRISIS (THYROID STORM)
 A severe form of hyperthyroidism marked by sudden release
of thyroid hormone into the blood stream
Precipitating Factors :
1. Stress such as injury, infection, thyroidal and non-thyroid
surgery, tooth extraction, insulin reaction, diabetic acidosis,
pregnancy, digitalis intoxication, abrupt withdrawal of anti-thyroid
medications, extreme emotional stress, or vigorous palpation of
the thyroid.
Clinical Manifestations :
1. High fever
2. Diaphoresis
3. Cardiopulmonary symptoms : extreme tachycardia, HPN,
arrhythmias, CHF, pulmonary edema
4. CNS symptoms : increasing feeling of tremulousness to
severe agitation, psychosis with developing apathy, irritability,
coma , heat intolerance
5. GI disturbance : weight loss, diarrhea, abdominal pain
6. Increased T3T4 and elevated BUN
Medical Management :
1. Immediate objectives are to reduced body temperature and
heart rate and to prevent vascular collapse
2. Humidified oxygen is administered to improve tissue
oxygenation and meet metabolic demands
3. Monitor respiratory status by arterial blood gas or pulse
oximetry
4. PTU or methimazole is administered to impede formation of
thyroid hormone and block conversion of T4 to T3, the more
active form of thyroid hormone
5. Hydrocortisone is prescribed to treat shock or adrenal
insufficiency.
6. Iodine is administered to decrease output of T4 from the
thyroid gland
7. For cardiac problems, Sympatholytic agents may be
administered. Propranolol in combination with digitalis, has been
effective in reducing severe cardiac problems
ADRENAL CRISIS
Pheochromocytoma
 A tumor that originates from the chromaffin cells of the
adrenal medulla
 Peak incidence is between ages 20 and 50 years old
 The cause of high BP in 0.9% to 2.2% of patients with HPN
 One form of HPN that is usually cured by surgery
Clinical Manifestations:
 Typical triad of symptoms : Headache, Diaphoresis, Palpitations
 HPN may be intermittent or persistent
 Tremor, flushing and anxiety
 Hyperglycemia may result from conversion of liver and muscle
glycogen to glucose
 Clinical picture is usually characterized by :
1. Acute, unpredictable attacks, lasting seconds or several
hours
2. Patient is anxious, tremulous and weak
3. Headache, vertigo, blurring of vision, tinnitus, air hunger,
and dyspnea
4. Polyuria, nausea, vomiting, diarrhea, abdominal pain
5. Feeling of impending doom
6. Palpitations and tachycardia
7. BP as high as 350/200 mm Hg
Assessment/Diagnostic Findings:
 Signs of sympathetic nervous system over activity : 5 H’s (HPN,
headache, hyperhidorsis (excessive sweating),
hypermetabolism, and hyperglycemia
Medical Management:
Pharmacologic Therapy
 Close monitoring of ECG changes and careful administration of
alpha-adrenergic blocking agents, muscle relaxants – to lower
BP quickly
 Long-acting alpha blocker to prepare patient for surgery
 Beta-adrenergic blocking agents for patients with cardiac
dysrhythmias
Surgical Management:
 Adrenalectomy- surgical removal of the tumor
HEPATIC FAILURE (Hepatic Coma)
 An end stage of liver disease, usually arises as a complication of
conditions that cause liver dysfunction although it can be
idiopathic
 Also called Hepatic coma because the patient’s neurologic
status gradually deteriorates
 Represents the most advanced stage of hepatic encephalopathy
 A life threatening crisis may occur if the serum ammonia level
rises, causing cerebral ammonia intoxication
Causes :
1. Cirrhosis
2. Hepatitis
3. Drug or toxin-induced damage
4. Fatty liver
5. Portal HPN
6. Surgically-created portal systemic shunts that bypass the liver and
allow toxins into the blood
Pathophysiology :
Liver disease alters liver structure and compromises essential
functions. This leads to impaired protein, fat and carbohydrate
metabolism, fluid and electrolyte imbalance, poor lymphatic
drainage, reduced coagulation and impaired detoxification of
ammonia and of the metabolites. Ammonia accumulation and
intoxication is the primary pathogenesis of hepatic failure and the
ensuing encephalopathy. Ammonia accumulates because liver cells
can not detoxify and convert to urea the ammonia that is in constant
supply in GI tract blood. Remaining liver functions may become
impaired and may be difficult to treat or control. Hepatic failure may
progress insidiously to a comatose state from which the patient
rarely recovers.
Clinical Findings :
Stage 1
 Slight personality and mood changes, disorientation,
forgetfulness, slurred speech, slight tremors, periods of lethargy
and euphoria, mild confusion, inability to concentrate,
hyperactive reflexes, sleep-wake patterns, handwriting starts to
decline and mild asterixis (flapping tremors of the hand) may
appear
Stage 2
 The patient grows more disoriented and drowsy. He may display
inappropriate behavior, mood swings, agitation, apraxia. His
hand writing becomes illegible and asterixes may become
pronounced
Stage 3
The patient becomes severely confused and may become
combative, incoherent and hard to arouse. Sleeps most of the time.
You may detect hyperactive deep tendon reflexes and rigid
extremities
Stage 4
The pupil is comatose and does not react to stimuli. Pupils are
dilated and lack corneal and deep tendon reflexes. Extremities
are flaccid and may assume flexion or extension posturing,
decebrate rigidity. The EEG is markedly abnormal.
Assessment and Diagnostic Findings :
1. Elevated arterial ammonia blood levels
2. The encephalogram shows generalized slowing and an
increase in amplitude of brain waves and the appearance of
characteristic triphasic waves
3. Occasionally, fetor hepaticus, a characteristic breath odor like
freshly mowed grass, acetone, or old wine, may be noticed.
4. In a more advanced stage, there are gross disturbances of
consciousness and the patient is completely disoriented with
respect to time and place
5. With further progression of the disorder, the patient lapses into
frank coma and may have seizures.
Intervention :
1. Anti-infective agents – to decrease bacterial action in the
colon.
2. Ammonia detoxicants – to reduce ammonia. Lactulose
(Duphulac) is administered
3. Cleansing enemas with diluted acetic acid or neomycin
4. Discontinuation of any precipitating substance : Dietary
proteins, sedatives, diuretic therapy, analgesics
5. IV administration of glucose to minimize protein breakdown
6. Oxygen administration
7. Correction of any electrolyte imbalance
8. Promote rest, comfort and quiet environment
Nursing Diagnosis :
1. Altered thought process
2. Potential impaired skin integrity
3. Impaired skin integrity
RENAL DISORDER
RENAL FAILURE
 Renal Failure is a systemic disease and is a final common
pathway of many different kidney and urinary tract
diseases.
 Results when the kidneys are unable to remove the body’s
metabolic wastes or perform their regulatory functions
 The substances normally eliminated in the urine accumulate
in the body fluids as a result of impaired renal excretion and
lead to a disruption in endocrine and metabolic functions
and fluid and electrolyte, an acid-base disturbances.
ACUTE RENAL FAILURE
 Acute renal failure is a sudden and almost complete loss of
kidney function over a period of hours to days.
Categories of Acute Renal Failure :
1. Prerenal Condition (hypoperfusion of kidney). Occurs as a
result of impaired blood flow that leads to hypoperfusion of the
kidney and a drop in the GFR. Common clinical situations are
volume-depletion states(hemorrhage or gastrointestinal losses),
impaired cardiac performance and vasodilation (sepsis or
anaphylaxis)
2. Intrarenal. Intrarenal causes of acute renal failure are the
result of actual parenchymal damage to the glomeruli or kidney
tubules. Conditions such as burns crush injuries, and infections,
as well as nephrotoxic agents, may lead to acute tubular
necrosis and cessation of renal function. Severe transfusion
reaction may also cause intrarenal failure. Medications may also
predispose a patient to intrarenal damage, esp. nonsteroidal
anti-inflammatory drugs and ACE inhibitors
3. Post renal conditions. Postrenal causes of acute renal
failure are usually the result of an obstruction somewhere distal
to the kidney.
PHASES OF ACUTE RENAL FAILURE :
1. Initiation period – begins with the initial insult and ends when
oliguria develops.
2. Period of Oliguria – accompanied by a rise in the serum
concentration of substances usually excreted by the kidney
(urea, creatinine, uric acid, organic acids and the intracellular
cations – potassium and magnesium
3. Period of diuresis – The patient experiences a gradual
increase in urinary output, which signals that glomerular filtration
has started to recover. Laboratory values start rising and
eventually begin a downward trend.Uremic symptoms may still
be present. The patient must be closely monitored for
dehydration during this phase; if dehydration occurs, the uremic
symptoms are likely to increase.
4. Period of Recovery – signals the improvement of renal function.
Laboratory values return to the patient’s normal level.
Clinical Manifestations :
1. May appear critically ill and lethargic
2. Persistent nausea, vomiting and diarrhea
3. The skin and mucous membranes are dry due to dehydration
4. Uremic fetor – breath have the odor of urine
5. CNS manifestations : drowsiness, headache, muscle twitching,
and seizures
Assessment and Diagnostic Findings :
1. Changes in urine. The urinary output varies (from scanty to normal
volume). Hematuria may be present and urine has low-specific
gravity. Patients with prerenal azotemia have a decreased amount of
sodium. Those patients with intrarenal azotemia usually have urinary
sodium levels greater than 40 mEq/L.
2. Increased blood urea nitrogen and creatinine levels (Azotemia)
3. Hyperkalemia
4. Metabolic acidosis
5. Calcium and Phosphorus Abnormalities
6. Anemia – due to reduced erythropoietin production, uremic
gastrointestinal lesions, reduced Rbc lifespan, and blood loss
Prevention:
1. Renal function must be monitored closely if patient has been
taking nephrotoxic antibiotic agents or has been exposed to
environmental toxins. Blood should be drawn for determining
baseline and monitoring serum BUN and creatinine levels by 24
hours after initiation of medication therapy
Medical Management:
1. Prerenal azotemia is treated by optimizing renal perfusion.
2. Postrenal failure is treated by relieving the obstruction
3. Overall, medical management includes maintaining fluid balance,
avoiding fluid excesses, or performing dialysis
4. The elevated potassium levels may be reduced by administering
ion-exchange resins ( sodium polystyrene sulfonate “kayexalate”)
5. Diuretics are used for management of volume status
6. Low-dose dopamine is often used to dilate the renal arteries
7. Atrial natriuretic peptide – inhibits sodium and water absorption
and dilates the afferent arteriole, thus improving blood flow to the
glomerulus
8. Correction of acidosis and elevated phosphate levels. When
severe acidosis is present, the arterial blood gases or serum
bicarbonate levels must be monitored because patient may require
sodium bicarbonate therapy or dialysis. Patient’s elevated phosphate
level may be controlled with phophate-binding agents (aluminum
hydroxide).
9. Nutritional Therapy. Dietary proteins are limited to about 1 g/kg
during the oliguric phase. High-carbohydrate meals to meet caloric
requirements. Foods and fluids containing potassium and
phosphorus are restricted.
Nursing Management :
1. Monitoring fluid and electrolyte balance. Hyperkalemia is the most
immediate life-threatening imbalance seen in acute renal failure.
2. Reducing metabolic rate. To reduce catabolism and the
subsequent release of potassium and accumulation of endogenous
waste products. Bed rest is indicated and fever and infection are
prevented or treated promptly.
3. Promoting pulmonary function. Patient is assisted to turn, cough
and take deep breaths frequently to prevent atelectasis and
respiratory infection.
4. Preventing Infection. Asepsis is essential with invasive lines and
catheters
5. Providing skin care. Meticulous skin care is important. Massaging
bony prominences, turning the patient frequently, and bathing the
patient with cool water are comforting and prevent skin breakdown
6. Providing support. The patient and family will need assistance,
explanation and support during this time.
CHRONIC RENAL FAILURE (End-Stage Renal Disease) ESRD
 CRF is a progressive, irreversible deterioration in renal function in
which the body’s ability to maintain metabolic and fluid and
electrolyte balance fails, resulting in uremia or azotemia
(retention of urea and other nitrogenous wastes in the blood)
Pathophysiology:
As renal function declines, the end products of protein metabolism
(which are normally excreted in urine) accumulate in the blood.
Uremia develops and adversely affects every system in the body.
3 Stages of Chronic Renal Disease :
Stage 1
Reduced renal reserve. Characterized by a 40 to 75% loss of
nephron function. The patient usually does not have symptoms
because the remaining nephrons are able to carry out the normal
functions of the kidney.
Stage 2
Renal Insufficiency. Occurs when 75 to 90% of nephron function
is lost. At this point, the serum creatinine and blood urea
nitrogen rise, the kidney loses its ability to concentrate urine and
anemia develops. The patient may report polyuria and nocturia.
Stage 3
End-stage renal Disease (ESRD). The final stage of CRF occurs
when there is less than 10% nephron function remaining. All of
the normal regulatory, excretory, and hormonal functions of the
kidney are severely impaired. ESRD is evidenced by elevated
creatinine and blood urea nitrogen levels as well as electrolyte
imbalances. Once the patient reaches this point, dialysis is
usually indicated.
Signs And Symptoms Of CRF :
1. Neurologic
Weakness and fatigue; confusion; inability to concentrate;
disorientation; tremors; seizures; asterixis; restlessness of legs;
burning of soles of feet; behavior changes.
2. Integumentary
Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis;
purpura; thin, brittle nails; coarse, thinning hair
3. Cardiovascular
HPN; pitting edema(feet , hands, sacrum), periorbital edema;
pericardial friction rub; engorged neck veins; pericarditis;
pericardial effusion; pericardial tamponade; hyperkalemia;
hyperlipidemia
4. Pulmonary
Crackles; thick, tenacious sputum; depressed cough reflex;
pleuritic pain; shortness of breath; tachypnea; kussmaul-type
respirations; uremic pneumonitis; “ uremic lung
5. Gastrointestinal
Ammonia odor to breath (uremic fetor); metallic taste; mouth
ulcerations and bleeding; anorexia; nausea and vomiting;
hiccups; constipation or diarrhea; bleeding from GIT
6. Hematologic
Anemia; thrombocytopenia
7. Reproductive
Amenorrhea; testicular atrophy; infertility; decreased libido
8. Musculoskeletal
Muscle cramps; loss of muscle strength; renal osteodystrophy;
bone pain; bone fractures; foot drop
Assessment And Diagnostic Findings :
1. Glomerular Filtration Rate. Decreased GFR can be detected
by obtaining a 24-hour urine analysis for creatinine clearance. As
GFR decreases, the creatinine clearance value decreases,
whereas the serum creatinine and BUN levels increase.
2. Sodium and Water Retention. The kidney is unable to
concentrate or dilute the urine normally in ESRD. Some patients
retain sodium and water, increasing the risk for edema, CHF,
and HPN.
3. Acidosis. With advanced renal disease, metabolic acidosis
occurs because the kidney is unable to excrete increased loads
of acid.
4. Anemia. Anemia develops as a result of inadequate
erythoropoietin production, the shortened life span of RBC’s,
nutritional deficiencies, and the patient’s tendency to bleed,
particularly from GIT
5. Calcium and Phosphorus Imbalance. The body’s serum
calcium and phosphate levels have a reciprocal relationship in
the body; as one rises, the other decreases.
Complications:
1. Hyperkalemia. Due to decreased excretion, metabolic
acidosis, catabolism, and excessive intake (diet, medications,
fluids)
2. Pericarditis. Due to retention of uremic waste products and
inadequate analysis
3. Hypertension. Due to sodium and water retention and
malfunction of the rennin-angiotensin-aldosterone system
4. Anemia. Due to decrease erythropoietin, decreased RBC life
span, GIT bleeding and blood loss during dialysis.
5. Bone disease and metastatic calcifications. Due to retention of
phosphorus, low serum calcium levels, abnormal vitamin D
metabolism, and elevated aluminum levels
Medical Management:
1. Pharmacologic Therapy
a. Antacids. Hyperphosphatemia and hypocalcemia are treated with
aluminum based antacids that bind dietary
phophorus in the GIT
b. Antihypertensive and Cardiovascular agents. HPN is managed by
intravascular control and a variety of hypertensive medications. CHF
and pulmonary edema may require treatment with fluid restriction,
low sodium diets, diuretics, inotropic agents such as digitalis, or
dobutamine, and dialysis.
c. Anticonvulsants. If seizures occurs. The onset of seizure is
recorded along with the type, duration and general effect on the
patient. Intravenous Diazepam or phenytoin is usually administered
to control seizures. The side rails must be padded to protect the
patient
d. Erythropoietin. Anemia associated with CRF is treated with
recombinant human erythropoietin (Epogen)
2. Nutritional Therapy
> Includes careful regulation of protein intake, fluid intake to balance
fluid losses, sodium intake to balance sodium losses and some
restriction of potassium
3. Dialysis
> Hyperkalemia is usually prevented by ensuring adequate dialysis
treatments with potassium removal and careful monitoring of all
medications for their potassium intake
Nursing Management
Nursing Diagnoses :
1. Fluid volume excess r/t decreased urine output, dietary excesses,
and retention of sodium and water
2. Altered nutrition; less than body requirements r/t anorexia, nausea
and vomiting, dietary restrictions, and altered oral mucous
membranes
3. Knowledge deficit regarding condition and treatment regimen
4. Activity intolerance r/t fatigue, anemia, retention of waste products,
and dialysis procedure
5. Self-esteem disturbance r/t dependency, role changes, changes in
body image, and sexual dysfunction
Nursing Care :
1. Directed toward assessing fluid status and identifying potential
sources of imbalance
2. Implementing a dietary program to ensure proper nutritional intake
within the limits of the treatment regimen
3. Promoting positive feelings by encouraging increased self-care
and greater independence
CARDIOVASCULAR DISORDERS
CARDIAC FAILURE
CONGESTIVE HEART FAILURE (CHF)
 Often referred to as cardiac failure, is the inability of the heart to
pump sufficient blood to meet the needs of the tissues for
oxygenation and nutrients.
 CHF is most commonly used when referring to left-sided and
right-sided failure
 The incidence of CHF increases with age
Pathophysiology:
Cardiac failure most commonly occurs with disorders of cardiac
muscles that result in decreased contractile properties of the heart.
Common underlying conditions that lead to decreased myocardial
contractility include myocardial dysfunction, arterial hypertension,
and valvular dysfunction.
Myocardial dysfunction may be due to coronary artery disease,
dilated cardiomyopathy, or inflammatory and degenerative diseases
of the myocardium. Atherosclerosis of the coronary arteries is the
primary cause of heart failure. Ischemia causes myocardial
dysfunction because of resulting hypoxia and acidosis (from
accumulation of lactic acid). Myocardial infarction causes focal
myocellular necrosis, the death of myocardial cells, and a loss of
contractility; the extent of the infarction is prognostic of the severity of
CHF.
Dilated cardiomyopathy causes diffuse cellular necrosis, leading to
decreased contractility. Inflammatory and degenerative diseases of
the myocardium, such as myocarditis, may also damage myocardial
fibers, with a resultant decrease in contractility.
Systemic or pulmonary HPN increases afterload which increases the
workload of the heart and in turn leads to hypertrophy of myocardial
muscle fibers; this can be considered a compensatory
mechanism because it increases contractility.
Valvular heart disease is also a cause of cardiac failure. The
valves ensure that blood flows in one direction. With valvular
dysfunction, valve has increasing difficulty moving forward. This
decreases the amount of blood being ejected, increases
pressure within the heart, and eventually leads to pulmonary and
venous congestion.
Etiologic Factors :
1. Increased metabolic rate (eg. fever, thyrotoxicosis)
2. Hypoxia
3. Anemia
VENTRICULAR FAILURE
LEFT-SIDED CARDIAC FAILURE
 Pulmonary congestion occurs when the left ventricle cannot
pump the blood out of the chamber. This increases
pressure in the left ventricle and decreases the blood flow
from the left atrium. The pressure in the left atrium
increases, which decreases the blood flow coming from the
pulmonary vessels. The resultant increase in pressure in
the pulmonary circulation forces fluid into the pulmonary
tissues and alveoli; which impairs gas exchange
Clinical Manifestations :
1. Dyspnea on exertion
2. Cough
3. Adventitious breath sounds
4. Restless and anxious
5. Skin appears pale and ashen and feels cool and clammy
6. Tachycardia and palpitations
7. Weak, thready pulse
8. Easy fatigability and decreased activity tolerance
RIGHT-SIDED CARDIAC FAILURE
 When the right ventricle fails, congestion of the viscera and
the peripheral tissues predominates. This occurs because
the right side of the heart cannot eject blood and thus
cannot accommodate all the blood that normally returns to it
from the venous circulation.
Clinical Manifestations :
1. Edema of the lower extremities (dependent edema)
2. Weight gain
3. Hepatomegaly (enlargement of the liver)
4. Distended neck veins
5. Ascites (accumulation of fluid in the peritoneal cavity)
6. Anorexia and nausea
7. Nocturia (need to urinate at night)
8. Weakness
Medical Management
The basic objectives in CHF management are the following :
1. Reducing the workload on the heart
2. Increasing the force and efficiency of myocardial contraction
3. Eliminating the excessive accumulation of body water by
avoiding excess fluid, controlling the diet, and monitoring diuretic
and angiotensin-converting enzyme (ACE) inhibitor therapy
Pharmacologic Therapy:
If the patient is in mild failure, usually an ACE inhibitor is
prescribed. A diuretic is added if there is no improvement or if
there are signs of fluid overload. Next, digitalis is added if the
symptoms continue. If symptoms are severe, all three
medications are usually started immediately.
ACE Inhibitors. Promote vasodilation and diuresis by decreasing
afterload and preload eventually decreasing the workload of the
heart.
Diuretic Therapy. A diuretic is one of the first medications
prescribed to a patient with CHF. Diuretics promote the excretion
of sodium and water through the kidneys.
Digitalis. This medication increases the force of myocardial
contraction and slows conduction through the AV node. It
improves contractility thus, increasing left ventricular output.
Dobutamine.(Dobutrex) is an intravenous medication given to
patients with significant left ventricular dysfunction. A
catecholamine, it stimulates the beta1-adrenergic receptors. Its
major action is to increase cardiac contractility.
Milrinone (Primacor). A phosphodiesterase inhibitor that prolongs
the release and prevents the uptake of calcium. This in turn,
promotes vasodilation, causing a decrease in preload and afterload
and decreasing the workload of the heart.
Other medications. Anticoagulants may be prescribed. Beta-
adrenergic blockers maybe indicated in patients with mild or
moderate failure.
Nutritional Therapy:
1. A low-sodium diet
2. Avoidance of excessive amount of fluids
Nursing Management:
1. Record intake and output to identify a negative balance (more
output than input)
2. Weigh patient daily at the same time
3. Auscultate lung sounds daily to detect a decrease or an absence
of pulmonary crackles
4. Determine the degree of jugular distention
5. Identify and evaluate severity of dependent edema
6. Monitor pulse rate and BP, and make sure the patient does not
become hypotensive from dehydration
7. Examine skin turgor and mucous membranes for signs of
dehydration
8. Assess for symptoms of fluid overload (orthopnea, paroxysmal
nocturnal dyspnea, and dyspnea on exertion)
Nursing Process : The Patient With Cardiac Failure
Assessment
 The focus of the nursing assessment for the patient with cardiac
failure is directed toward observing for signs and symptoms of
pulmonary and systemic fluid overload.
Health History
 The nurse explores sleep disturbances, particularly sleep
suddenly interrupted by shortness of breath.
 The nurse finds out about the number of pillows needed for sleep
(indication of dyspnea)
 Find out also the activities of daily living and the activities that
causes shortness of breath
Physical Examination
 The lungs are auscultated at frequent intervals to detect crackles
and wheezes or their absence. The rate and depth of
respiration are also noted.
 The heart is auscultated for an S3 heart sound, a sign that the
heart pump is beginning to fail and that increased blood volume
remains in the ventricle with each beat. HR and rhythm are also
noted.
 Jugular vein distention is also assessed. Distention greater than
3 cm above the sternal angle is considered abnormal.
 Sensorium and level of consciousness must be evaluated
 Dependent parts of the patient’s body are assessed for perfusion
and edema.
 The liver is examined for hepatojugular reflux.
 Output is measured carefully to establish a baseline against
which to measure the effectiveness of diuretic therapy. Intake
and output record are maintained
Nursing Diagnoses :
1. Activity intolerance r/t imbalance between oxygen supply and
demand secondary to decreased CO
2. Excess fluid volume r/t excess fluid/sodium intake or retention
secondary to CHF and its medical therapy
3. Anxiety r/t breathlessness and restlessness secondary to
inadequate oxygenation
4. Non-compliance r/t to lack of knowledge
5. Powerlessness r/t inability to perform role responsibilities
secondary to chronic illness and hospitalization.
Potential Complications :
1. Cardiogenic shock
2. Dysrhythmias
3. Thromboembolism
4. Pericardial effusion and pericardial tamponade
Planning And Goals :
1. Promoting activity while maintaining vital signs within identified
range
2. Reducing fatigue
3. Relieving fluid overload symptoms
4. Decreasing the incidence of anxiety or increasing patient’s ability
to manage anxiety
5. Teaching the patient about the self-care program.
6. Encouraging the patient to verbalize his ability to make decisions
and influence outcomes.
Nursing Interventions :
1. Promoting Activity Tolerance
 The patient is encouraged to perform an activity more slowly
than usual, for a shorter duration, or with assistance initially.
 Barriers that could limit abilities to perform an activity are
identified
 Pacing and prioritizing activities will maintain the patient’s
energy to allow participation in regular exercise.
 Vital signs should be taken before, during and immediately
after an activity to identify whether they are within the
predetermined range.
2. Reducing Fatigue
 The nurse and patient can collaborate to develop a schedule
that promotes pacing and prioritization of activities. The
schedule should alternate activities with periods of rest and
avoid having two significant energy-consuming activities
occur on the same day or in immediate succession.
3. Managing Fluid Volume
 The nurse monitors the patient’s fluid status closely.
Auscultating the lungs, comparing daily body weights,
monitoring intake and output and assisting the patient to
adhere to a low-sodium diet.
 The nurse needs to position the patient or teach the patient
how to assume a position that shifts fluid away from the
heart.
 The nurse needs to assess for skin breakdown and institute
preventive measures
4. Controlling Anxiety
 The nurse should take steps to promote physical comfort and
psychological support. A family member’s presence
provides reassurance. Speaking in a slow, calm, and
confident manner is helpful. Stating specific, brief directions
for an activity is helpful in decreasing anxiety.
5. Minimizing Powerlessness
 Patients need to recognize that they are not helpless and that
they can influence their direction, their lives, and their
outcomes.
 The nurse needs to assess for factors contributing to a
perception of powerlessness and intervene accordingly.
Contributing factors may include lack of knowledge, hospital
policies, and lack of opportunities to make decisions.
 Taking time to listen to patient encourages them to express
their concerns and questions
 Provide the patient with decision-making opportunities
 Provide encouragement and praise
Expected Outcomes :
1. Demonstrates tolerance for increased activity
2. Has less fatigue and dyspnea
3. Maintains fluid balance
4. Is less anxious
5. Adheres to self-care regimen
6. Makes decisions regarding care and treatment
7. Absence of complications
CARDIOGENIC SHOCK
 Occurs when the heart cannot pump enough blood to supply
the amount of oxygen needed by the tissues.
Pathophysiology:
The heart muscle loses its contractile power, resulting in a
marked reduction in SV and CO, sometimes called “forward
failure”. The damage to myocardium results in a decrease in CO,
which in turn reduces arterial blood pressure and tissue
perfusion in the vital organs (heart, brain, kidneys). Flow to the
coronary artery is reduced, resulting in decreased oxygen supply
to the myocardium, which in turn increases ischemia and further
reduces the heart’s ability to pump. The inadequate emptying of
the ventricle also leads to increased pulmonary pressures,
pulmonary congestion, and pulmonary edema, exacerbating the
hypoxia and resulting ischemia of vital organs.
Clinical Manifestations :
1. Tissue hypoperfusion – classic signs of cardiogenic shock
manifested as cerebral hypoxia (restlessness, confusion,
agitation), low blood pressure, rapid and weak pulse, cold and
clammy skin, increased respiratory crackles, hypoactive bowel
sounds, and decreased urinary output.
2. Initially, arterial blood gas analysis may show respiratory
alkalosis.
3. Dysrhythmias are common
Assessment and Diagnostic Findings :
1. The use of a Pulmonary Artery catheter to measure left
ventricular pressures and CO is important in assessing the
severity of the problem and planning management. The PA
wedge pressure is elevated and the CO is decreased as the left
ventricle loses its ability to pump.
2. The systemic vascular resistance is elevated due to the
sympathetic nervous system stimulation that occurs as a
compensatory response to the decrease in blood pressure.
3. The decreased blood flow to the kidneys causes a hormonal
response that causes fluid retention and further vasoconstriction.
4. The increases in HR, circulating volume, and vasoconstriction
occur to maintain circulation to the brain, heart and lungs, however,
the workload of the heart is increased.
5. Continued cellular hypoperfusion eventually results in organ
failure. The patient becomes unresponsive, severe hypotension
occurs, and the patient develops shallow respirations, cold, cyanotic
or mottled skin, and absent bowel sounds.
6. Arterial blood gas analysis shows metabolic acidosis
7. All laboratory results indicate organ dysfunction.
Medical Management :
1. Reduce any further demand on the heart
2. Improve oxygenation and restore tissue perfusion
3. Diuretics, vasodilators, and mechanical devices (filtration and
dialysis)
4. Intravenous volume expanders (normal saline, lactated Ringer’s
solution, and albumin) are given for hypovolemia or low intravascular
volume.
5. Strict bed rest to conserve energy
6. Oxygen administration is increased for hypoxemia
7. Intubation and sedation may be necessary to maintain
oxygenation balance.
Pharmacologic Therapy:
 Most medication are administered IV because of the decreased
perfusion to the gastrointestinal system
1. Pressor agents are medications used to raise BP and increase
CO. Many pressor medications are catecholamines ( norepinephrine
and high-dose dopamine) to promote perfusion to the heart and
brain.
2. Diuretics and vasodilators may be administered to reduce the
workload of the heart.
3. Positive inotropic medications are given to increase myocardial
contractility
4. Circulatory assist devices: Intra-aortic balloon pump – to augment
the pumping action of the heart. The device inflates during diastole,
increasing the pressure in the aorta and therefore increasing
perfusion. It deflates just before systole, lessening the pressure
within the aorta before ventricular contraction, decreasing the
amount of resistance the heart has to overcome to eject blood and
therefore decreasing the amount of work the heart must complete to
eject blood.
Nursing Management:
1. Nurse must carefully assess the patient, observe the cardiac
rhythm, measure hemodynamic parameters, and record fluid intake
and urinary output.
2. The patient must be closely monitored for responses to the
medical interventions and for the development of complications
3. The patient is always treated in intensive care environment
because of the frequency of nursing interventions and the technology
required for effective medical management.
THROMBOEMBOLISM
 The decreased mobility of the patient with cardiac diseases and
the impaired circulation that accompany these disorders
contribute to the development of intracardiac and intravascular
thrombosis.
Intracardiac Thrombus
 Detected by an echocardiogram and treated with anticoagulants,
such as warfarin.
 A part of the thrombus may become detached and may be
carried to the brain, kidneys, intestines, or lungs
 The most common problem is pulmonary embolism. The
symptoms of pulmonary embolism include chest pain, cyanosis,
and shortness of breath, rapid respirations and hemoptysis.
 The pulmonary embolus may block the circulation to a part of the
lung, producing an area of pulmonary infarction
 Systemic embolism may present as cerebral, mesenteric, or renal
infarction
 An embolism can also compromise the blood supply to an
extremity
PERICARDIAL EFFUSION AND CARDIAC TAMPONADE
Pathophysiology:
Pericardial effusion refers to the escape of fluid into the
pericardial sac. Normally, the pericardial sac contains less than
50 ml of fluid, which the heart needs to decrease friction for the
beating heart. An increase in pericardial fluid raises the pressure
within the pericardial sac and compresses the heart. This results
in :
 Increased right and left ventricular-end diastolic pressures
 Decreased venous return
 Inability of the ventricles to distend adequately
Pericardial fluid may accumulate slowly without causing
noticeable symptoms. A rapidly developing effusion, however,
can stretch the pericardium to its maximum size and, because of
increased pericardial pressure, and reduce venous return to the
heart, and decrease cardiac output. The result is cardiac
tamponade.
Clinical Manifestations :
1. The patient may complain of a feeling of fullness within the
chest. The feeling of pressure may result from stretching of the
pericardial sac
2. Engorged neck veins
3. Shortness of breath
4. A drop and fluctuation in BP
Assessment and Diagnostic Findings :
1. Pericardial effusion is detected by percussing the chest and
noting an extension of flatness across the anterior aspect of the
chest
2. Echocardiogram to confirm diagnosis
Medical Management :
1. Pericardial Fluid Aspiration (pericardiocentesis) – performed to
remove fluid from the pericardial sac
2. Pericardiotomy. A portion of pericardium is sliced to permit the
pericardial fluid to drain into the lymphatic system.
CARDIAC ARREST
 Occurs when the heart ceases to produce an effective pulse
and blood circulation. It may be due to a cardiac electrical
event, as when the HR is too fast or too slow or when there
is no heart rate at all.
Clinical Manifestations :
1. Loss of consciousness, pulse and BP
2. Ineffective respiratory gasping
3. The pupils of the eyes dilate within 45 seconds.
4. Seizures may or may not occur
Emergency Management :
Cardiopulmonary Resuscitation
1. Airway – maintain open airway
2. Breathing – provide artificial circulation by rescue breathing
3. Circulation – promoting artificial circulation by external cardiac
compression
4. Defibrillation – restoring the heart beat
Maintaining Airway and Breathing
 The first step in CPR is to obtain an open airway. Any
obvious material in the mouth and throat should be
removed. The chin is directed up and back or the jaw
(mandible) is lifted forward. The rescuer “looks, listen. and
feels” for air movement. An oropharyngeal airway is
inserted if available. Two rescue ventilations over 3 to 4
seconds are provided using a bag or mouth-mask device. If
the first rescue ventilation entered easily, then the patient is
ventilated with 12 breaths per minute and the open airway
is maintained. Endotracheal intubation is performed to
ensure an adequate airway and ventilation.
Restoring Circulation
 After performing ventilation, the carotid pulse is assessed
and external cardiac compressions are provided when no
pulse is detected.
 1. Compressions are performed with the patient on a firm
surface (Cardiac board, floor)
 2. The rescuer (facing the patient’s head) places the heel of
one hand on the lower half of the sternum, two fingerwidths
from the tip of the xiphoid and positions the other hand on
top of the first hand. The fingers should not touch the chest
wall.
 3. Using the body weight while keeping the elbows straight,
the rescuer presses quickly downward from the shoulder
area to deliver a forceful compression to the victim’s lower
sternum toward the spine.
 4. The chest compression rate is 80 to 100 times/minute
Follow-up Monitoring
1. After successful resuscitation, the patient is transferred to an
intensive care unit for close monitoring. Continuous
electrocardiographic monitoring and frequent BP assessment are
essential until hemodynamic stability is reestablished.
DYSRHYTHMIAS
 Disorders of the formation and/or conduction of the electrical
impulse within the heart. This can cause disturbances of the
heart rate, the heart rhythm, or both.
Normal Electrical Conduction
The electrical impulse that stimulates and paces the cardiac muscle
normally originates in the sinus node, located near the vena cava in
the right atrium. Normally, the impulse occurs at a rate between 60
and 100 times a minute in the adult. The impulse quickly travels from
the sinus node through the atria to the atrioventricular (AV) node
causing the atria to contract. The structure of the AV node slows the
impulse, which allows time for the atria to contract and the ventricles
to fill with blood. From the AV node, the impulse travels quickly along
the right and left bundle branches and the Purkinje fibers, located in
the ventricular muscle. The electrical stimulation of the ventricles, in
turn, causes the ventricles to contract (systole). Then the
electromechanical impulse completes the circuit and the cycle begins
again. In this way, sinus rhythm promotes cardiovascular circulation.
The electrical stimulus causes the mechanical event of the heart.
 Depolarization. The electrical stimulation: the mechanical
contraction is called systole.
 Repolarization. The electrical relaxation and mechanical
relaxation is called diastole.
Influences on Heart Rate and Contractility
 Heart rate is influenced by the autonomic nervous system, which
consists of sympathetic and parasympathetic fibers.
 Stimulation of the sympathetic system increases heart rate.
 Sympathetic stimulation also causes the constriction of peripheral
blood vessels and, therefore, an increase in BP
 Parasympathetic stimulation slows the heart rate
 Manipulation of the autonomic nervous system may increase or
decrease the incidence of dysrhythmias
Types of Dysrhythmias
1. Sinus Node Dysrhythmias
A. Sinus Bradycardia
 Occurs when the sinus node creates an impulse at a slower –
than-normal rate.
Etiology :
1. Slower metabolic needs (sleep, athletic training, hypothyroidism)
2. Vagal stimulation (vomiting, suctioning, severe pain, extreme
emotions)
3. Medications
4. Increased intracranial pressure and MI
Treatment :
1. Atropine 0.5 to 1.0 mg given quickly and IV as bolus – medication
of choice
2. Catecholamines and emergency transcutaneous pacing
B. Sinus Tachycardia
 Occurs when the sinus node creates an impulse at a faster-than-
normal rate.
 It may be caused by acute blood loss, anemia shock,
hypovolemia, hypervolemia, CHF, pain, hypermetabolic state,
fever, exercise, anxiety or sympathomimetic medications.
Treatment :
1. Calcium channel blockers (ex. Diltiazem)
2. Beta-blockers (ex. Propranolol)
C. Sinus Arrhythmia
 Occurs when the sinus node creates an impulse at an irregular
rhythm; the rate increases with inspiration and decreases with
expiration
2. Atrial Dysrhythmias
A. Premature Atrial Complex (PAC)
 This is a single ECG complex that occurs when an electrical
impulse starts in the atrium before the next normal impulse of
the SA node.
 The PAC may be caused by caffeine, alcohol, nicotine, stretched
atrial myocardium
 PAC’s are common in normal hearts. The patient may say “My
heart skipped a beat.” A pulse deficit may exist.
 If PAC’s are infrequent, no treatment is necessary.

B. Paroxysmal Atrial Tachycardia
 A term used to indicate a tachycardia characterized by abrupt
onset and abrupt cessation and a QRS of normal duration.
 Now called AV nodal reentry tachycardia
C. Atrial Flutter
 Occurs in the atrium and creates impulses at an atrial rate
between 250 and 400 times per minute
 May cause serious signs and symptoms: chest pain,
shortness of breath, and low blood pressure.
Treatment :
1. If patient is unstable, electrical cardioversion is indicated
2. If patient is stable, diltiazem, verapamil, beta-blockers or
digitalis may be administered IV to slow the ventricular rate.
D. Atrial Fibrillation
 Causes a rapid, disorganized, and uncoordinated twitching of
atrial musculature.
 The most common dysrhythmias
 Usually associated with advanced age, valvular heart
disease, cardiomyopathy, hyperthyroidism, pulmonary
disease, moderate to heavy ingestion of alcohol and the
aftermath of open heart surgery
Treatment :
 Treatment depends on its cause and duration and the
patient’s symptoms and instability
 In some cases, AF converts to sinus rhythm within 24 hours
without treatment
 Both stable and unstable AF of short duration are treated the
same as stable and unstable atrial flutter
 To prevent recurrence and to promote heart rate control over
a long period, quinidine, procainnamide, flecainide, sotalol,
or amiodatone may be prescribed
 Anti-coagulation therapy is indicated if patient is elderly or
has hypertension, heart failure or a history of stroke.
 Pacemaker or surgery is sometimes indicated for patients
who are unresponsive to medications
3. Junctional Dysrhythmias
A. Premature Junctional Complex
 An impulse that starts in the AV nodal area before the next
normal sinus impulse.
 Causes include : digitalis toxicity, congestive heart failure,
and coronary artery disease
 Rarely produce any significant symptoms
 Treatment is the same as for frequent PAC’s
B. Junctional Rhythm
 Occurs when the AV node, instead of the SA node, becomes
the pacemaker of the heart.
 Junctional rhythm may produce signs and symptoms of
reduced cardiac output. If so, the treatment is the same as
for sinus bradycardia.
C. AV Nodal Reentry Tachycardia
 Occurs when an impulse is conducted to an area in the AV
node that causes the impulse to be rerouted back into the
same area over and over again at a very fast rate.
 Factors associated with the development of AV nodal reentry
tachycardia include caffeine, nicotine, hypoxemia, and
stress
 Signs and symptoms vary with the rate and duration of the
tachycardia and the patient’s underlying condition. Usually
of short duration, resulting only in palpitations. A fast rate
may reduce cardiac output, resulting in significant signs and
symptoms such as restlessness, chest pain, shortness of
breath, pallor, hypotension and loss of consciousness
Treatment :
 Treatment is aimed at breaking the reentry of the impulse.
1. Vagal maneuvers, such as carotid sinus massage, gag reflex,
breath holding, and immersing the face in ice water – increase
parasympathetic stimulation, causing slower conduction through
the AV node and blocking the reentry of the rerouted impulse.
 Because of the risk of a cerebral embolic event, carotid sinus
massage is contraindicated in patients with carotid bruits.
2. If vagal maneuvers are ineffective, the patient may then
receive a bolus of adenosine, verapamil, or diltiazem.
3. Cardioversion is the treatment of choice if the patient is
unstable or does not respond to the medications.
4. Intravenous adenosine may be prescribed to cause a conversion
to sinus rhythm.
4. Ventricular Dysrhythmias
A. Premature Ventricular Complex (PVC)
 PVC is an impulse that starts in a ventricle before the next normal
sinus impulse.
 PVC’s can occur in healthy people, esp. with the use of caffeine,
nicotine, and alcohol.
 Also caused by cardiac ischemia or infarction, increased
workload on the heart (ex. Exercise, fever. Hypervolemia, CHF,
and tachycardia), digitalis toxicity, hypoxia, acidosis, and
electrolyte imbalances, esp. hypokalemia
 In the absence of disease, PVC’s are not serious. In the patient
with acute MI, PVC’s may indicate the need for more
aggressive therapy.
 The following are warning or complex PVC’s (precursors of
ventricular tachycardia) : (1) more than 6/minute (2) multifocal
(having different shapes), (3) two in a row (pair), and (4)
occurring on the T wave (the vulnerable period of ventricular
depolarization)
Treatment :
1. Lidocaine is the medication most commonly used for immediate
short-term therapy
B. Ventricular Tachycardia
 Defined as three or more PVC’s in a row, occurring at a rate
exceeding 100 beats/minute.
 Ventricular tachycardia is usually associated with coronary artery
disease and may precede ventricular fibrillation.
 Ventricular tachycardia is an emergency because the patient is
usually unresponsive and pulseless.
Treatment :
1. Lidocaine is the initial choice
2. Cardioversion maybe indicated if the medications are ineffective or
if the patient becomes unstable
3. Immediate defibrillation
 Ventricular tachycardia in a patient who is unconscious and
without pulse is treated in the same manner as ventricular
fibrillation.
C. Ventricular Fibrillation
 A rapid but disorganized ventricular rhythm that causes
ineffective quivering of the ventricles.
 This dysrhythmias is always characterized by the absence of an
audible heartbeat, a palpable pulse, and respirations.
 Cardiac arrest and death are imminent if VF is uncorrected
Treatment :
1. Immediate defibrillation and activation of emergency services.
Placing a call for emergency assistance takes precedence over
initiating CPR
2. After a successful defibrillation, eradicating causes and
administering anti dysrhythmics medication are treatments to prevent
the recurrence of VF.
D. Idioventricular Rhythm
 Also called ventricular rhythm, occurs when the impulse starts in
the conduction system below the AV node
 Commonly causes the patient to lose consciousness and
experience other signs and symptoms of reduced cardiac
output. In such cases, treatment is the same as for any
bradycardia, including identifying the underlying etiology,
administering IV atropine, and initiating emergency
transcutaneous pacing.
 Bed rest is prescribed so as not to increase cardiac workload
E. Ventricular Asystole
 Commonly called flatline, ventricular asystole is characterized by
absent QRS complexes, although P waves may be apparent for
a short duration.
 There is no heart beat, no palpable pulse, and no respiration.
 Without treatment, ventricular asystole is fatal.
Treatment :
1. CPR
2. Rapid assessment to identify possible causes
3. Intubation and establishment of IV access are the first
recommended actions
4. Bolus of IV epinephrine and to be repeated at 3-5 minutes
intervals
5. Sodium bicarbonate maybe administered IV
Nursing Process: The Patient With A Dysrhythmia
Assessment
 Major areas of assessment include possible causes of the
dysrhythmias and the dysrhythmia’s effect on the heart’s
ability to pump an adequate blood volume
 When cardiac output is reduced, the amount of oxygen
reaching the tissues and vital organs is diminished. This
diminished oxygen produces the signs and symptoms
associated with dysrhythmias.
 A health history is obtained to identify possible causes and
past incidences of syncope (fainting), lightheadedness,
dizziness, fatigue, chest discomfort, and palpitations.
 Psychosocial assessment is also performed to identify the
possible effects of dysrhythmia
 Physical assessment is conducted to confirm the data
obtained from the history and to observe for signs of
diminished cardiac output during the dysrhythmic event,
esp. changes in level of consciousness. Skin may be pale
and cool. Signs of fluid retention, such as neck vein
distention, crackles and wheezes in the lungs may be
detected during auscultation.
 The rate and rhythm of apical and peripheral pulses are
assessed and any pulse deficit is noted.
 The chest is auscultated for extra heart sounds, esp. S3 and
S4, measures BP and determines pulse pressures. A
declining pulse pressure indicates reduced cardiac output.
Diagnosis:
1. Potential/actual decrease in cardiac output
2. Anxiety related to fear of the unknown
3. Lack of knowledge about the dysrhythmias and its treatment.
Potential Complications : Ischemic Heart Disease
Nursing Interventions :
1. Monitoring and Managing the Dysrhythmias
 Controlling the incidence or effect of dysrhythmias is often
achieved by the use of ant-idysrhythmic medications
 A constant serum blood level of the medication is maintained
to maximize beneficial effects and minimize adverse effects
 If the patient is hospitalized, an ECG is initiated and rhythm
strips are analyzed to track dysrhythmias
 BP, rate and depth of respirations, pulse rate and rhythm are
evaluated regularly to determine the hemodynamic effect of
the dysrhythmias
2. Minimizing Anxiety
 Nurse must maintain a calm and reassuring attitude
 Maximize the patient’s control and to make the unknown less
threatening
Evaluation
Expected Outcomes :
1. Cardiac output is maintained
2. Anxiety is minimized
3. The patient knows about dysrhythmias and its treatment
Adjunctive Modalities and Management
1. Cardioversion and Defibrillation
 Treatment for tachydysrhythmias.
 Used to deliver an electrical current to stimulate a critical
mass of myocardial cells. This allows the sinus node to
recapture its role as the heart’s pacemaker.
 One major difference between cardioversion and defibrillation
has to do with the timing of the delivery of electrical current.
 Defibrillation is usually performed as an emergency
treatment, whereas cardioversion is usually a planned
procedure
 Cardioversion involves the delivery of a “timed” electrical
current to terminate a tachydysrhythmia.
 Defibrillation is the treatment of choice for ventricular
fibrillation and pulseless ventricular tachycardia.
2. Pacemaker Therapy
 An electronic device that provides electrical stimuli to the
heart muscle.
 Usually used when a patient has a slower-than-normal
impulse formation
 May also be used to control tachydysrhythmias that do not
respond to medication therapy
Complications of Pacemakers :
1. Local infection at the entry site of the leads or at the
subcutaneous site
2. Bleeding and hematoma at the lead-entry sites or at the
subcutaneous sites for permanent generator placement
3. Hemothorax from puncture of the subclavian vein or internal
mammary artery
4. Ventricular ectopy and tachycardia from irritation of the ventricular
wall by the endocardial electrode
5. Movement or dislocation of the lead placed transvenously
(perforation of the myocardium)
6. Phrenic nerve, diaphragmatic (hiccupping) or skeletal muscle
stimulation may occur if the lead is dislocated or if the delivered
energy is set high
7. Rarely, cardiac tamponade occurs after removal of epicardial
wires
8. Dislodgement of the pacing electrode – most common
complication. Minimizing patient activities can help to prevent this
complication.
BURNS
There are 4 major goals relating to burns :
1. Prevention
2. Institution of lifesaving measures for the severely burned person
3. Prevention of disability and disfigurement through early,
specialized, individual treatment
4. Rehabilitation through reconstructive surgery and rehabilitative
programs
Pathophysiology:
Burns are caused by a transfer of energy from a heat source to the
body. Heat maybe transferred through conduction or electromagnetic
radiation. Burns are categorized as thermal (including electrical
burns), radiation or chemical. Tissue destruction results from
coagulation, protein denaturation, or ionization of cellular contents.
The skin and the mucosa of the upper airways are the sires of tissue
destruction. Deep tissues, including the viscera, can be damaged by
electrical burns or through prolonged contact.
The depth of the injury depends on the temperature of the burning
agent and the duration of contact with the agent.
Classification of Burns
 Burn injuries are described according to the depth of the injury
and the extent of body surface area (BSA) injured.
Characteristics of Burns according to Depth
Factors to consider in the determination of depth :
1. History of how the injury occurred
2. Causative agent, such as flame or scalding liquid
3. Temperature of the burning agent
4. Duration of contact with the agent
5. Thickness of the skin
Extent of Body Surface Area Injured
Rule of Nines
 An estimation of the total BSA involved in a burn is simplified
using the rule of nines
Lund and Browder Method
 A more precise method of estimating the extent of a burn
 Recognizes that the percentage of BSA of various anatomic
parts, especially the head and legs, changes with growth.
 By dividing the body into very small areas and providing an
estimate of the proportion of BSA accounted for by such body
parts, one can obtain a reliable estimate of the total BSA
burned.
 The initial evaluation is made on the patient’s arrival at the
hospital.
Palm Method
 A method to estimate the percentage of scattered burns.
 The size of the patient’s palm is approximately 1% of BSA. The
size of the palm can be used to assess the extent of burn injury.
Local and Systemic Responses to Burns
 Burns that do not exceed 25% of the total BSA produce a
primarily local response
 Burns that exceed 25% BSA may produce both a local and a
systemic response, which is considered a major burn injury.
Overview of physiologic changes after a major burn injury
Cardiovascular Response
 Cardiac output decreases before any significant change in blood
volume is evident. As fluid loss continuous and vascular volume
decreases, cardiac output continuous to fall and blood pressure
drops. This is the onset of burn shock. In response, the
sympathetic nervous system releases catecholamines, resulting
in an increase in peripheral resistance (vasoconstriction) and an
 increase in pulse rate. Peripheral vasoconstriction further
decreases cardiac output.
 Prompt fluid resuscitation maintains the blood pressure in the
low-normal range and improves cardiac output. Despite
adequate fluid resuscitation, cardiac filling pressures remain
low during the burn-shock period. If inadequate fluid
resuscitation occurs, distributive shock will occur.
 Generally, the greatest volume of fluid leak occurs in the first
24 to 36 hours after the burn, peaking by 6 to 8 hours.
 As the capillaries begin to regain their integrity, burn shock
resolves and fluid returns to the vascular compartment.
 As fluid is reabsorbed from the interstitial tissue into the
vascular compartment, blood volume increases.
 If renal and cardiac function is adequate, urinary output
increases.
 Patients with severe burns develop massive systemic
edema. As edema increases in circumferential burns,
pressure on small blood vessels and nerves in distal
extremities causes an obstruction of blood flow and
consequent ischemia. This complication is known as
compartment syndrome. The physician may need to
perform an esharotomy, a surgical incision into the eschar
(devitalized tissue resulting from a burn), to relieve the
constricting effect of the burned tissue.
Effects on Fluids, Electrolytes, and Blood Volume
 Circulating blood volume decreases dramatically during burn
shock. Evaporative fluid loss through the burn may reach 3
to 5 L or more over a period of 24 hours until the burn
surfaces are covered.
 During the shock, serum sodium levels vary in response to
fluid resuscitation. Usually hyponatremia (sodium depletion)
is present, as water shifts from the interstitial to the vascular
space.
 Immediately after burn injury, hyperkalemia (excessive K)
results from massive cell destruction. Hypokalemia may
occur later with fluid shifts and inadequate potassium
intake.
 At the time of burn injury, some red blood cells may be
destroyed and/or damaged resulting in anemia. Despite
this, patient’s hematocrit may be elevated due to plasma
loss
 Blood transfusions are required periodically to maintain
adequate hemoglobin levels for oxygen delivery.
 Abnormalities in coagulation, including a decrease in
platelets (thrombocytopenia) and prolonged clotting and
prothrombin time, also occur with burn injury.
Pulmonary Response
 Inhalation injury is the leading cause of death in fire victims.
 One third of all burn injuries have a pulmonary problem
related to the burn injury.
 Even without pulmonary injury, hypoxemia may be present.
Early in the post burn period, catecholamine release in
response to the stress of the burn injury alters peripheral
blood flow, thereby reducing oxygen delivery to the
periphery. Later, hypermetabolism and continued
catecholamine release lead to increased tissue oxygen
consumption, which can lead to hypoxemia.
Categories of Pulmonary Injury :
1. Upper Airway Injury
 Results from direct heat or edema.
 Manifested by mechanical obstruction of the upper airway,
including the pharynx and larynx
 Because of the cooling effect of rapid vaporization in the
pulmonary tract, direct heat injury does not normally occur
below the level of the bronchus.
 Treated by early nasotracheal or endotracheal intubation.
2. Inhalation below the glottis
 Results from inhaling the products of incomplete combustion
or noxious gases. These products include carbon
monoside, sulfur oxides, nitrogen oxides, aldehydes,
cyanide, ammonia, chlorine, phosgene, benzene, and
halogens.
 The injury results directly from chemical irritation of the
pulmonary tissues at the alveolar level.
 Inhalation injuries below the glottis cause loss of ciliary
action, hypersecretion, severe mucosal edema, and
possibly bronchospasm.
 The pulmonary surfactant is reduced, resulting in atelectasis
(collapse of alveoli). Expectoration of carbon particles in the
sputum is the cardinal sign of this injury.
 Carbon monoxide is the most common cause of inhalation
injury because it is a byproduct of the combustion of
organic materials and is therefore present in smoke.
 Treatment usually consists of early intubation and mechanical
ventilation with 100% oxygen. Using 100% oxygen is essential
to accelerate the removal of carbon monoxide from the
hemoglobin molecule.
Indicators of possible pulmonary damage :
1. History indicating hat the burn occurred in an enclosed area
2. Burns of the face or neck
3. Singed nasal hair
4. Hoarseness, voice change, dry cough, stridor, sooty sputum
5. Bloody sputum
6. Labored breathing or tachypnea (rapid breathing) and other signs
of reduced oxygen levels (hypoxemia).
7. Erythema and blistering of the oral or pharyngeal mucosa
Pulmonary Complications secondary to Inhalation Injury :
1. Acute respiratory failure
 Occurs when impairment of ventilation and gas exchange is life-
threatening.
 The immediate intervention is intubation and mechanical
ventilation.
 If ventilation is impaired by restricted chest excursion, immediate
escharotomy is needed.
2. Acute respiratory distress syndrome
> May develop in the first few days after injury secondary to systemic
and pulmonary responses to the burn and inhalation injury.
Other Systemic Responses
 Renal function may be altered as a result of decreased blood
volume. If there is inadequate blood flow through the kidney,
the hemoglobin and myoglobin occlude the renal tubules,
resulting in acute tubular necrosis and renal failure.
 The immunologic defenses of the body are greatly altered by
burn injury. The loss of skin integrity is compounded by the
release of abnormal inflammatory factors. Immunosuppression
places the patient at high risk for sepsis.
 Loss of skin also results in an inability to regulate body
temperature. Burn patients may therefore exhibit low body
temperature in the early hours after burn injury, but as
hypermetabolism resets core temperatures, burn patients
becomes hyperthermic for most of the postburn period, even in
the absence of infection.
 Two potential gastrointestinal complications may occur: paralytic
ileus (absence of intestinal peristalsis) and Curling’s ulcer.
Decreased peristalsis and bowel sounds are manifestations of
paralytic ileus resulting from burn trauma. Gastric distention and
nausea may lead to vomiting unless gastric decompression is
initiated.
Management Of The Patient With A Burn Injury
A. Emergent/Resuscitative Phase of Burn Care
 The first priority in on-the-scene care for a burn victim is to
prevent injury to the rescuer.
Airway, Breathing, Circulation
 It is important to remember the ABC’s of all trauma care because
the systemic effects pose a greater threat to life.
1. Airway
2. Breathing
3. Circulation; Cervical spine immobilization for all high voltage
electrical injury; Cardiac monitoring for all electrical injuries for at
least 24 hours after cessation of dysrhythmias.
 Breathing must be assessed and a patent airway established
immediately during the initial minutes of emergency care.
Immediate therapy is directed toward establishing an airway
and administering humidified 100% oxygen.
 The circulatory system must also be assessed quickly. Apical
pulse and blood pressure are monitored frequently
Management of Fluid Loss and Shock
 Next to respiratory difficulties, the most important is preventing
irreversible shock by replacing lost fluids and electrolytes.
Survival of burn victims depends on adequate fluid
resuscitation.
1. Fluid Replacement
 Some combination of fluid categories may be used : Colloids
( whole blood, plasma, and plasma expanders) and
crystalloids/electrolytes (physiologic sodium chloride or lactated
Ringer’s solution)
 Formulas have been developed for estimating fluid loss based on
the estimated percentage of burns BSA and the weight of the
 patient. Length of time is also very important in calculating
estimated fluid needs.
 The formulas are individualized to meet the requirements of
each patient
 The NIH Consensus Development Conference on Supportive
Therapy in Burn Care established that salt and water are
required in burn patients, but that colloid may or may not be
useful during the first 24 to 48 postburn hours
 The consensus formula provides for the volume of balanced
saline solution to be administered in the first 24 hours in a
range of 2 to 4 mL/kg per percent burn.
 Generally, 2 mL/kg/ percent burn of lactated Ringer’s solution
may be used initially for adults. This is the most common
fluid replacement in use today.
 Studies show that with large burn, there is a failure of the
sodium-potassium pump at the cellular level. Thus, patients
with very large burns may need proportionately more
milliliters of fluid per percent of burn than those with smaller
burns
 Most fluid replacement formulas use isotonic electrolyte
solutions.
 Another fluid replacement method requires hypertonic
electrolyte solutions. This method uses concentrated
solutions of sodium chloride and lactate (a balanced salt
solution). The rationale for this replacement method is that
by increasing serum osmolality, fluid will be pulled back into
the vascular space from the interstitial space. Reduced
systemic and pulmonary edema results from administering
hypertonic solutions.
Goals of Fluid Replacement Therapy: A systolic blood pressure
exceeding 100 mm Hg, pulse rate less than 110/minute, and
urine output of 30 to 50 ml/hour.
 Another gauge for fluid requirements and response to fluid
resuscitation include hematocrit and hemoglobin and serum
sodium levels.
Nursing Process : Care during the Emergent/Resuscitative
Phase
 Nursing assessment in the emergent phase of burn injury
focuses on the major priorities for any trauma patient; the
burn wound is a secondary consideration.
 Aseptic management of the burn wounds and invasive line
continues.
 The nurse checks vital signs frequently. Respiratory status is
monitored closely. Apical, carotid, and femoral pulses are
evaluated
 Cardiac monitoring for patients with cardiac problems,
electrical injury or respiratory problems or if the pulse is
dysrhythmic or the rate is abnormally slow or rapid.
 Determining BP is a problem if all extremities are burned. A
sterile dressing under the BP cuff will protect the wound
from contamination. A Doppler UTZ or a non-invasive
electronic BP may be helpful.
 In severe burns, an arterial catheter is used for BP
measurement and for collecting blood specimen
 Peripheral pulses of burned extremities are checked hourly.
Doppler is used.
 Elevation of burned extremities is crucial to decrease edema.
 Elevation of the lower extremities on pillows and of the upper
extremities on pillows or by suspension using intravenous
poles may be helpful.
 Large-bore IV lines and Indwelling urinary catheter are
inserted.
 Assessment includes monitoring of fluid intake and output.
 Urine output, an excellent indicator of circulatory status, is
monitored carefully.
 The amount of urine first recorded may assist in determining
the extent of preburn renal function and fluid status.
 Burgundy-colored urine suggests the presence of
hemochromogen and myoglobin resulting from muscle
damage. This is associated with deep burns caused by
electrical injury.
 Glucosuria results from the release of stored glucose from
the liver in response to stress.
 Infusion pumps and rate controllers are used to deliver a
prescribed IV fluids
 Monitoring IV therapy is a major nursing responsibility.
 Body temperature, body weight, preburn weight, and history
of allergies, tetanus immunization, past medical and
surgical problems, current illnesses, and use of medication
are assessed.
 A head-to-toe assessment is performed, focusing on
signs/symptoms of concomitant illness, injury, or developing
complications.
 Patients with facial burns should have eye examination for
potential injuries to the cornea
 Assessment should include the time of injury, mechanism of
burn, whether the burn occurred in closed space.
 The neurologic assessment focuses on the client’s level of
consciousness, psychological status, pain and anxiety levels,
and behavior
Acute or Intermediate Phase of Burn Care
 Begins 48 to 72 hours after the burn injury.
 Attention is directed toward continued assessment and
maintenance of respiratory and circulatory status, fluid and
electrolyte balance, and gastrointestinal function.
 Airway obstruction caused by upper airway edema can take as
long as 48 hours to develop. Changes may occur as the effects
of resuscitative fluid and the chemical reaction of smoke
ingredients with lung tissues become apparent. The patient’s
arterial blood gas values and other parameters determine the
need for intubation and mechanical ventilation.
 If cardiac or renal function is inadequate, fluid overload occurs
and symptoms of congestive heart failure may result.
Vasoactive medications, diuretics, and fluid restriction may be
used to support circulatory function and prevent congestive
heart failure and pulmonary edema
 Cautious administration of fluids and electrolytes continuous
because of the shifts in fluid from the interstitial to intravascular
compartments. Blood components are administered as needed
to treat blood loss and anemia
 A resetting of the core body temperature in severely burned
patients results in a body temperature slightly higher than
normal for several weeks after the burn injury. Bacteremia and
septicemia also causes fever in many patients.. Acetaminophen
and hypothermia blankets may be required to maintain body
temperature to reduce metabolic stress and tissue oxygen
demand.
 Central venous, peripheral arterial or pulmonary artery
thermodilution catheters may be required for monitoring venous
and arterial pressures. However, invasive vascular lines are
avoided because they provide an additional port for infection.
 Infection progressing to septic shock is the major cause of death
in patients who have survived the first few days after a major
burn injury. The immunosuppression place the patient at high
risk for sepsis. The infection that begins within the burn site
may spread to the bloodstream.
Infection Prevention
 Burn wound is an excellent medium for bacterial growth and
proliferation.
 Bacteria such as Staphylococcus, Proteus, Pseudomonas,
Escherichia coli, and Klebsiella find optimal conditions for
growth within the burn wound. The burn eschar is a non-viable
crust, no blood supply; therefore, neither polymorphonuclear
leucocytes or antibodies nor systemic antibiotics can reach the
area.
 Phenominal numbers of bacteria- 1 billion per gram of tissue-
may appear and spread to the blood stream or release their
toxins, which reach distant sites.
 Fungi such as Candida albicans also grow easily in burn wounds
 The primary source of bacterial infection appears to be the
patient’s intestinal tract.
 Major secondary source is the environment.
 Cap, gown, mask and gloves are worn while caring for patient’s
with open burn wounds. Clean technique is used when caring
directly for burn wounds.
 Antibiotics are seldom given prophylactically because of the risk
of promoting resistant strains of bacteria.
 Tissue specimens are taken for culture regularly to monitor
colonization of the wound by microbial organisms.
 Systemic antibiotics are administered when there is
documentation of burn wound sepsis or other positive cultures
such as urine, sputum, or blood.
Wound Cleaning
 Hydrotherapy in the form of shower carts, individual showers and
bed baths.
 Because of the high risk of infection and sepsis, the use of plastic
liners and thorough decontamination of hydrotherapy
equipment and wound care areas are necessary to prevent
cross-contamination.
 Tap water alone can be used for burn wound cleansing.
 Hydrotherapy in any form should be limited to 20 to 30 minute
period to prevent chilling and additional metabolic stress.
 Hydrotherapy provides an excellent opportunity for exercising the
extremities and cleaning the entire body.
 At the time of wound cleaning, all skin is inspected for any hints
of redness, breakdown, or local infection.
 Hair in and around burn area, except the eyebrows, should be
clipped short.
 Intact blisters may be left, but the fluid should be aspirated with a
needle and syringe
 Wound cleaning is usually performed daily.
 When the eschar begins to separate from the viable tissue
beneath, more frequent cleaning and debridement may be
necessary
 After burn wounds are cleaned, they are gently patted with
towel and the prescribed method of wound care is
performed.
 Whatever is the method of wound care, the goal is to protect
the wound from overwhelming proliferation of pathogenic
organisms. Patient comfort and ability to participate are also
important considerations.
Topical Antibacterial Therapy
 Topical antibacterial therapy does not sterilize the burn
wound; it simply reduces the number of bacteria so that the
overall microbial population can be controlled by the body’s
host defense mechanisms
 The three most commonly used topical agents are Silver
sulfadiazine (Silvadene), silver nitrate, and Mafenide
acetate (Sulfamylon)
 No single agent is universally effective. Using different
agents at different times in the postburn period may be
necessary. Prudent use and alternation of antimicrobial
agents results in less-resistant strains of bacteria, greater
effectiveness of the agents.
 Before a topical agent is applied, the previously applied
topical agent must be thoroughly removed.
Wound Dressing
 After the wound is cleaned, patted dry and applied topical
agent; the wound is then covered with several layers of
dressings.
 A light dressing is used over joints to allow for motion, light
dressing is also applied over areas for which a splint has
been designed to conform to the body contour for proper
positioning
 Circumferential dressings should be applied distally to
proximal.
 If the hand or foot is burned, the fingers and toes should be
individually wrapped to promote adequate healing.
Exposure Method
 Occasionally, a wound is treated by exposing it to air. Wound
care proceeds in the same manner and a topical agent is
applied, but no dressings are applied.
 The success of exposure method depends on keeping the
immediate environment free of organisms. Everything
coming in contact with the patient must be sterile. Those
who come in direct contact must wear masks, caps, sterile
gowns and gloves; visitors are instructed to wear protective
garb and not to touch the bed or hand anything to the
patient.
 The room must be maintained at warm temperature with 40
to 50% humidity to prevent excessive evaporative fluid
losses.
 A cradle may be placed over the patient to prevent sheets
from coming in contact with the burn area, to minimize the
effects of air currents (to which burn patient is sensitive)
Occlusive Method
 An occlusive dressing is a thin gauze that is either
impregnated with a topical antimicrobial or that is applied
after topical antimicrobial application
 Occlusive dressing are most often used over areas with new
skin grafts. These are applied under sterile conditions in the
operating room.
 Their purpose is to protect the graft, promoting an optimal
condition for its adherence to the recipient site.
 Ideally, these dressings remain in place for 3 to 5 days.
 Precautions are taken to prevent two body surfaces from
touching, such as fingers or toes, ear and scalp, areas
under the breasts, any point of flexion, or between the
genital folds.
Dressing Changes
> Dressings are changed approximately 20 minutes after an
analgesic is administered.
> A mask, hair cover, disposable plastic apron or cover gown,
and gloves are worn by health care personnel.
 Dressings that adhere to the wound can be removed more
easily if they are moistened with saline solution or if the
patient is allowed to soak for a few moments in the tub.
 The patient may participate, providing some degree of control
over this painful procedure.
Wound Debridement
Debridement has two goals :
1. To remove contaminated tissue, thereby protecting the
patient from invasion of bacteria
2. To remove devitalized tissue or burn eschar in preparation
for grafting and wound healing.
Natural Debridement
 The dead tissue separates from the underlying viable tissue
spontaneously. After partial and full- thickness burns occur,
bacteria that are present at the interface of the burned tissue
and the viable tissue underneath gradually liquefy the fibrils of
collagen that hold the eschar in place for the first or second
postburn week.
 Using antibacterial topical agents tends to slow down this natural
process of eschar separation
Mechanical Debridement
 Involves using surgical scissors and forceps to separate and
remove the eschar.
 This is carried out to the point of pain and bleeding
 Dressings are also helpful debriding agents. Coarse-mesh
dressings applied dry or wet-to-dry (applied wet and allowed to
dry) will slowly debride the wound of exudates and eschar when
they are removed.
Surgical Debridement
 An operative procedure involving either primary excision (surgical
removal of tissue) of the full thickness of the skin or shaving the
burned skin layers gradually down to freely bleeding, viable
tissue.
 Surgical excision is initiated early in burn wound management.
This may be performed a few days after or as soon as the
patient is hemodynamically stable and edema has decreased.
 Ideally, the wound is then covered immediately with a skin graft
and an occlusive dressing.
 The use of surgical excision carries with it risks and
complications, especially with large burns. The procedure
creates a high risk for extensive bleeding (as much as 100 to
125 ml of blood per percent BSA excised).
Grafting the Burn Wound
 If wounds are deep (full thickness) reepitheliazation is not
possible. Therefore coverage of the burn wound is necessary
until coverage with a graft of the patient’s own skin (autograft) is
possible.
 The purpose of wound coverage is to decrease the risk for
infection; prevent loss of protein, fluid, and electrolytes through
the wound; and minimize heat loss through evaporation.
 The main areas for skin grafting include the face, for cosmetic
and psychological reasons; the hands and other functional
areas such as the feet; and areas that involve joints.
 Grafting permits earlier functional ability and reduces
contractures (shrinkage of burn scar through collagen
maturation).
 When burns are extensive, the chest and abdomen maybe
grafted first to reduce the burn surface.
 During wound healing, granulation tissue develops. It fills the
space created by the wound, creates a barrier to bacteria, and
serves as a bed for epithelial cell growth.
 Richly vascular tissue is pink, firm, shiny, and free of exudates
and debris. It should have a bacterial count of less than
100,000 per gram of tissue to optimize graft take.
 A preoperative culture is mandatory before grafting, because
enzymes of bacteria can dissolve a graft and lead to its failure.
Beta hemolytic streptococci are a major factor in graft failure.
Biologic Dressings (Homografts And Heterografts)
 In extensive burns, biologic dressings can be lifesaving by
providing temporary wound closure and protecting the
granulation tissue until autografting is possible.
 Biologic dressing may also be used to debride untidy wounds
after eschar separation.
 With each biologic dressing change, debridement occurs.
 Once the biologic dressing appears to be taking or adhering to
the granulating surface with minimal underlying exudation, the
patient is ready for an autograft.
 Biologic dressing also provides immediate coverage for clean,
superficial burns and decreases the wound’s evaporative water
and protein loss.
 Biologic dressing decrease pain by protecting nerve endings and
are an effective barrier against water loss and entry of bacteria.
 When applied to superficial partial-thickness wounds, they seem
to speed healing.
 Biologic dressings consist of homografts (or allografts) and
heterografts(or xenografts).
 Homografts are skin obtained from living or recently
deceased humans. The amniotic membrane (amnion) from
the human placenta may also be used as a biologic
dressing.
 Heterografts consist of skin taken from animals (usually
pigs).
 Most biologic dressings are used as temporary coverings of
burn wounds and are eventually rejected because of the
body’s immune reaction to them as foreign.
 Homografts tend to be the most expensive biologic
dressings. They are available from skin banks in fresh and
cryopreserved (frozen) forms.
 Homografts are thought to provide the best infection control.
Of all the biologic and bio synthetic dressings available.
Revascularization occurs within 48 hours, and the graft may
be left place for several weeks.
 Amnion is low in cost, however, amnion grafts do not become
vascularized by the patient’s vessels and can be left in
place only briefly.
 Pigskin is available from commercial suppliers. Pigskin
impregnated with a topical antibacterial such as silver
nitrate is also available.
 One new biologic dressing that has shown promise for
permanent burn wound coverage is Alloderm.
 Alloderm is processed dermis from human cadaver skin.
When a donor site is taken for an autologous skin graft,
both the epidermal and dermal layers of skin are removed
from the donor site. However, Alloderm provides a
permanent dermal layer replacement.
 Use of alloderm allows the surgeon to take a thinner skin
graft consisting of the epidermal layer only. The patient’s
epidermal layer is placed directly over the dermal base
(Alloderm).
 Use of Alloderm has resulted in less scarring and
contractures with healed grafts; donor sites heal much more
quickly than conventional donor sites because only the
epidermal layer has been taken.
Biosynthetic And Synthetic Dressings
 Currently, the most widely used synthetic dressing is
Biobrane, which is composed of nylon. Silastic membrane
combined with a collagen derivative.
 Less costly than homograft or pigskin.
 Biobrane dressings adhere to donor sites and meticulously
clean debrided partial-thickness wounds; they will remain
until spontaneous epitheliazation and wound healing occur.
 Like biologic dressing, Biobrane protects the wound from
fluid loss and bacterial invasion.
 Biobrane is also useful for intermediate or long-term closure
of a surgically excised wound until an autograft becomes
available.
 Like Biologic dressing, Biobrane should not be used over
grossly contaminated or necrotic wounds.
 Several other synthetic dressings are available: Op-site, a
thin, transparent, polyurethane elastic film, can be used to
cover clean partial-thickness wounds and donor sites. This
dressing is occlusive and waterproof but permeable to
water vapor and air; this permeability provides protection
from microbial contamination and allows for the exchange
of gases. Other synthetic dressings are Tegaderm, N-
Terface, and Duoderm.
 Artificial skin (Integra) is the newest type of synthetic
dressing. A dermal analogue, Integra is composed of two
main layers. The epidermal layer, consisting of Silastic, acts
as a bacterial barrier and prevents water loss from the
dermis. The dermal layer is composed of animal collagen. It
interfaces with the open wound surface and allows
migration of fibroblasts and capillaries into the material.
Autografts
 The ideal means of covering burn wounds because they
come from the patient’s own skin and thus are not rejected
by the patient’s immune system.
 They can be split-thickness, full-thickness, pedicle flaps, or
cultured epithelium. Full-thickness and pedicle flaps are
commonly used for reconstructive surgery, months or years
after the initial injury.
 Split-thickness autografts can be applied in sheets or in
postage stamp-like pieces, or they can be expanded by
meshing so that they can cover 1.5 to 9 times more than a
given donor site area. Skin meshers enable the surgeon to
cut tiny slits into a sheet of donor skin, making it possible to
cover large areas with smaller amounts of donor skin.
These expanded grafts cling to the recipient site more
easily than sheet grafts and prevent the accumulation of
blood, serum, air, or purulent material under the graft.
 Using expanded grafts may be necessary in large wounds but
should be viewed as a compromise in terms of cosmetics.
Care of the Patient with an Autograft
 Occlusive dressings are commonly used initially after grafting to
immobilize the graft.
 Occupational therapists may be helpful in constructing splints to
immobilize newly grafted areas to prevent dislodging the graft
 If the graft is dislodged, sterile saline compresses will help
prevent drying of the graft until the physician reapplies it.
 The patient is positioned and turned carefully to avoid disturbing
the graft or putting pressure on the graft site.
 If an extremity has been grafted, it is elevated to minimize
edema.
 The patient begins exercising the area 5 to 7 days after grafting.
Care of Donor site
 Moist gauze is applied at the time of surgery to maintain pressure
and to stop any oozing.
 A thrombostatic agent such as thrombin or epinephrine may be
applied directly to the site.
 The donor site may be applied with a single-layer gauze
impregnated with petrolatum, scarlet red, or bismuth to new
biosynthetic dressings such as Biobrane.
 Donor site must remain clean, dry, and free from pressure.
 Because a donor site is usually a partial-thickness wound, it will
heal spontaneously within 7 to 14 days with proper care
Pain Management
 Pain management is the most difficult challenges facing the burn
team.
 Many factors contribute to the patient’s burn pain experience:
severity of the pain, health provider’s pain assessment, the
appropriateness and adequacy of pharmacologic treatment of
pain, the multiple procedures involved and assessment of the
effectiveness of pain relief measures.
 The outstanding features of burn pain are its intensity and long
duration.
 Wound care carries with it anticipation of pain and anxiety.
 In partial-thickness burn, the nerve endings are exposed,
resulting to excruciating pain with exposure to air currents.
 Although, nerve endings are destroyed in full-thickness burns,
there is deep pain and pain in adjacent structures.
 The primary pain is intense in the initial acute post burn phase.
This pain gradually subsides. However, until the skin heals or
graft are applied and taken, the pain level remains high
because of treatment-induced pain. Wound cleaning, dressing
changes, debridement, and physical therapy inflict intense pain.
Discomforts related to tissue healing, such as itching, tingling,
and tightness of contracting skin and joints adds to the duration
and intensity of pain.
 Because pain can not be eliminated short of anesthesia, the goal
is to minimize the pain with analgesics before the patien faces
wound care procedures.
 Bolus doses of opioids, usually morphine, are often provided.
Ketamine anesthesia administered IV are also used.
 Sedation with anti-anxiety agents such as lorazepam (Ativan) or
midazolam(Versed) may be indicated in addition to analgesia.
 Patient-controlled analgesia, using both continuous and bolus
morphine infusions, and sustained release oral morphine, given
every 12 hours have helped burn patients.
 Self-administered nitrous oxide also helps to make dressing
changes tolerable to those patients who have sufficient hand
function to hold a mask to their faces intermittently during
dressing changes.
 Early surgical excision with grafting under anesthesia may be the
best way to reduce the overall pain experience for burn
patients.
Nutritional Support
 Hypermetabolism persist after burn injury until wounds are
closed, thereby increasing the basal metabolic need by as
much as 100%.
 The goal of nutritional support is to promote a state of positive
nitrogen balance.
 The nutritional support required is based on the patient’s preburn
status and the extent of total BSA burned.
 Several formulas exist for estimating the daily metabolic
expenditure and caloric requirements of burn patients.
 Protein requirements may range from 1.5 to 4 g of protein per kg
of body weight every 24 hours
 Lipids are included in the nutritional support because of their
importance for wound healing, cellular integrity, and absorption
of fat-soluble vitamins.
 Carbohydrates are included to meet caloric requirements as high
as 5,000 cal per day
 Adequate vitamins and minerals are also needed.
 The proportions of fat, protein, and carbohydrate are planned
for maximal use.
 Overfeeding can be detrimental. Therefore, a dietitian familiar
with current concepts in nutrition for burn patients is
necessary.
 As soon as GIT function resumes, nutritional support begins.
The enteral route is preferred. In patients with extensive
burns, tube feedings may be indicated to ensure daily
calories needed.
 Indications for Total parenteral nutrition (TPN) include weight
loss greater than 10% of normal body weight, inadequate
intake of enteral nutrition prolonged wound exposure, and
malnutrition or debilitated condition before injury.
DISORDERS OF WOUND HEALING
SCARS
 Results from excessive abnormal healing or inadequate new
tissue formation.
 Hypertrophic scars and wound contractures are more likely to
occur if the initial burn injury extends below the level of the
deep dermis. Healing of such deep wounds result in the
replacement of normal integument
 Compression measures are instituted early in the burn
wound treatment to prevent scar formation. Ace wraps are
used to promote adequate circulation, used as the first form
of compression.
 Scar management occurs mainly in the rehabilitative phase,
after the wounds are closed.
KELOIDS
 A large, heaped-up mass of scar tissue.
 Keloids tend to be found in darkly pigmented people, grow
outside of wound margins, and recur after surgical excision.
FAILURE TO HEAL
 Failure to heal may be due to many factors, including
infection and inadequate nutrition
 A serum albumin level of less than 2g/dL is a usual factor
CONTRACTURES
 The burn wound tissue shortens because of the force exerted
by the fibroblasts and the flexion in natural wound healing.
 An opposing force provided by splints, traction, and
purposeful movement and positioning must be used to
counteract deformity in burns affecting joints.
Nursing Process : Burn Care During The Acute Phase
Assessment
 Continued assessment focuses on hemodynamic alterations,
wound healing, pain and psychosocial responses, and early
detection of complications.
 Nurse assess VS frequently
 Continued assessment of peripheral pulses is essential for
the first few post burn days while edema continuous to
increase, potentially damaging peripheral nerves and
restricting blood flow.
 Observation of the electrocardiogram may give clues to
cardiac dysrhythmias resulting from potassium imbalance,
preexisting cardiac disease, or the effects of electrical injury
or burn shock
 Assessment focuses on hemodynamic alterations, wound
healing, pain and psychosocial responses, and early
detection of complications.
 Assessment of respiratory and fluid status is the highest
priority for detection of complications.
 Assess VS
 Assessment of peripheral pulses while edema continuous to
increase, damaging peripheral nerves and restricting blood
flow
 ECG may give clues to cardiac dysrhythmias resulting from
potassium imbalance, preexisting cardiac disease, or the
effects of electrical injury or burn shock
 Assessment of residual gastric volumes and pH in the patient
with a NGT- gives clues to early sepsis or the need for
antacid therapy. Blood in the gastric fluid or stools must
also be reported
 Important wound assessment include size, color, odor,
eschar, exudates, abscess formation under the eschar,
epithelial buds (small pearl-like clusters of cells on the
wound surface), bleeding, granulation tissue appearance,
progress of grafts and donor sites, and quality of
surrounding skin
 Assessment on pain and psychosocial responses, daily body
weights, caloric intake, general hydration, and serum electrolyte
and hemoglobin levels and hematocrit
 Assessment for excessive bleeding from blood vessels adjacent
to areas of surgical site and debridement
Potential Complications :
1. Congestive heart failure and pulmonary edema
2. Sepsis
3. Acute Respiratory Failure
4. Visceral Damage
Planning and Goals :
The major goals :
 restoration of normal fluid balance,
 absence of infection,
 attainment of anabolic state and normal weight,
 improved skin integrity,
 reduction of pain and discomfort
 optimal physical mobility
 adequate patient and family coping
 adequate patient and family knowledge of burn treatment
 absence of complications
Nursing Interventions:
Restoring Normal Fluid Balance
 Monitor IV and oral intake to reduce risk for fluid overload and
consequent CHF
1. Use IV infusion pumps
2. Daily weights are obtained
 Low-dose dopamine to increase renal perfusion
 Diuretics to increase urine output
Preventing Infection
 A clean and safe environment
 Detect early signs of infection – culture results and WBC counts
are monitored
 Aseptic technique for wound care procedures. Hand washing
before and after each patient contact
 Fresh flowers, plants or fresh fruit baskets should not be allowed
inside the room because of the risk of microorganism growth
 Visitors are screened to avoid exposing the immunocompromised
patient to pathogens
Maintaining Adequate Nutrition
 Oral fluids should be initiated slowly when bowel sounds
resumes. If vomiting and abdominal distention do not occur,
fluids may be gradually increased
 The nurse collaborates with the dietitian to plan a protein-and
calorie-rich diet
 If caloric goals can not be met by oral feeding, a feeding tube is
inserted
Promoting Skin Integrity
 Assess and record changes or progress in wound healing
 Wound care
 Topical antibacterial agents
Relieving Pain and Discomfort
 Pain is more severe in partial-thickness burns than in full-
thickness burns because the nerve endings are not destroyed.
Cover exposed nerve endings to help reduce pain
 Analgesics and anti-anxiety medications
 Teach relaxation techniques
 Give patient control over wound care
 Pain-relieving distractions : video programs/games, hypnosis
 Complete treatments and dressings quickly. Analgesics before
any painful procedures
 Oral anti-pruritic agents, cool environment, frequent lubrication of
skin with water or silica-based lotion – to reduce discomfort in
itching
 Exercise and splinting to prevent skin contracture
Promoting Physical Mobility
 Early priority is to prevent complications resulting from immobility
 Deep breathing, turning, and proper positioning to prevent
atelectasis and pneumonia, control edema and to prevent
pressure ulcers and contractures.
 Early sitting and ambulation
 When lower extremities are burned elastic bandage are applied
before the patient is placed in an upright position. This
bandages promote venous return and minimize swelling
 Passive and active ROM to prevent contracture
 Splints or other functional devices are used for contracture
control. Monitor splinted areas for signs of vascular insufficiency
and nerve compression
Strengthening Coping Strategies Choice of Article 5pts
 The patient is facing the reality of burn trauma and is grieving Comprehensiveness 10pts
over obvious loss. Depression, regression and manipulative Neatness & organization 5pts
disorders are common problems ================================
 Develop effective coping strategies by : Total 20pts for each reading
1. Setting specific expectations for behavior
2. Promoting truthful communications to build trust REFERENCE MATERIALS:
 Patient always ventilates feelings of anger – enlist someone 1. Books
to whom patient can vent feelings without fear of retaliation a. The Lippincott Manual of Nursing Practice, 7th edition,
2001.
Monitoring and Managing Potential Complications : b. Luckmann and Sorensen Medical and Surgical Nursing:
A Psychophysiologic Approach, 4th edition, 1992
Congestive Heart Failure and Pulmonary Edema c. Maternal and Child Health Nursing: Care of the
 Patient is assessed for pulmonary overload – may occur as Childbearing and Childrearing Family. Adele Pilliteri.1999.
fluid is mobilized from the interstitial compartment back into d. Maternal and Child Health Nursing. Koniak.
the intravascular compartment. If the cardiac and renal e. Maternal and Neonatal Nursing Made Incredibly Easy.
system cannot compensate for the excess vascular volume, 2004
CHF and pulmonary edema may result. f. Medical-Surgical Nursing books
 Crackles in the lungs and increased difficulty with respiration
may indicate a fluid buildup in the lungs. 2. Websites
1. Patient is positioned comfortably with the head of the a. google.com
bed raised to promote lung expansion and gas b. eMedicines.com
exchange c. yahoo.com
2. Provide supplemental oxygen
3. Administer IV diuretics

Sepsis
 Early signs are increased in temperature, increased pulse
rate, flushed dry skin, increased pulse rate, widened pulse
pressure, and flushed dry skin in unburned areas
 Wound and blood cultures
 Antibiotics

Acute Respiratory Failure and Acute Respiratory Distress

Syndrome
 Patient is assessed for increased difficulty in breathing,
change in respiratory pattern, onset of adventitious
(abnormal) sounds
 Signs of hypoxia (decreased O2 to the tissues), decreased
breath sounds, wheezing, tachypnea, stridor
 Patients receiving mechanical ventilation must be assessed
for a decrease in tidal volume and lung compliance
 Key sign of ARDS is hypoxemia while receiving 100%
oxygen, decreased lung compliance and significant
shunting
 Management includes intubation and mechanical ventilation

Visceral Damage
 Assess for signs of necrosis of visceral organs due to
electrical injury. Tissues affected are usually between the
entrance and exit wounds of the electrical burn
 All patients with electrical burns should undergo
electrocardiographic monitoring
 Assess for pain relate to deep muscle ischemia
 Fasciotomies are performed to relieve the swelling and
ischemia in the muscles

Rehabilitation Phase Of Burn Care

 Rehabilitation begins immediately after the burn has occurred
 Wound healing, psychosocial support, and restoring maximal
functional activity remain priorities
 Continued focus on maintaining fluid and electrolyte balance
and improving nutritional status
 Reconstructive surgery to improve body appearance and
function
 Psychological and vocational counseling and referral to
support groups

COURSE REQUIREMENTS:
1. Quizzes – after each topic, a quiz will be
administered.
2. Readings – current issues (2003-present) on High
risk pregnancy, High risk newborn and High risk adult.
One reading for each of the High risk conditions.
Provide cover sheet, photocopy or print out of the
issue, one page summary, and one page reaction
(staple the pages properly). Include the date and
reference (book, article, website). Computer
encoded/typewritten (short size coupon bond, 1.5 line
spacing, and font size 12). Deadline of submission will
be on the first day of class.

GRADING POLICY:
Reguirement (3 Readings - High risk pregnancy,
newborn and adult):