NCM 109 NURSING CARE MANAGEMENT 109
MON & WED ::: 2:00 PM - 5:00 PM
March 02, 2022
INTRODUCTION
Lesson 1: Programs, Trends, and Issues in Maternal Health
Introduction
In 1990s
● Every minute, a woman dies in childbirth or from
complications of pregnancy
● 500,000 women die each year; almost all (95%)
occur in developing countries
● For every woman who dies as many as 30 others
suffer chronic illness or disability
● Maternal mortality is the health indicator with
the most disparity between developed and
developing countries
- The cumulative lifetime risk of dying as a
result of pregnancy is 1:2800 in developed
versus 1:16 in developing countries
● Maternal mortality trends are unacceptable, but
not insurmountable because the major causes
are known and avoidable.
● Nearly 2/3 of maternal deaths are due:
- Hemorrhage
- Obstructed labor
- Pregnancy-induced hypertension
- Sepsis/infection
- Complications of unsafe abortion
● Interventions can be made available even in
resource-poor settings
Different agencies around the world, either within or
outside of the United Nations, have included maternal
survival as one of their most pressing agenda
1987 Safe Motherhood Initiative 1990-
World Summit for Children
1994 International Conference on
Populations and Development
1995 4th World Conference on Women
2000-Millennium
Summit/Declaration (MDGs)
2015 Sustainable Development Goals
(SDGs)
Why aim for maternal survival?
1. Moral imperative
● The death of a woman during pregnancy or
childbirth is a violation of her rights to life and
health
● Governments must promote dignity and equity
for women within the health-care system
2. Social implications
● Maternal death or disability can plunge families
into poverty and deeper despair; surviving
children esp. those < 5 years old are at risk of
dying since no one will attend to their needs
● The loss may reverberate throughout an entire
community
Maternal death
The death of a woman while pregnant or within 42 days
of termination of pregnancy, irrespective of the duration
and site of the pregnancy, from any cause related to or
aggravated by the pregnancy or its management but not
from accidental or incidental causes.
- ICD-10, 1992
➔ Philippines maternal mortality rate for 2013 was
121.00, a 3.97% decline from 2012.
➔ Philippines maternal mortality rate for 2012 was
126.00, a 0.79% decline from 2011.

Methodological issues in measuring maternal mortality

1. It is a rare event and therefore its number may not be

large enough to detect statistically significant changes
over time

2. Underreporting - especially if most occur outside of

health facilities (in the absence of health personnel to
report them)

Lessons learned
3. Misreporting because of the complicated definition
requiring also its cause and timing OR sometimes done
Most maternal deaths and disabilities would be averted
intentionally to avoid legal action
if…
- All pregnancies are wanted and planned - All
PHILIPPINES COUNTRY PROFILE
pregnancies are adequately managed
Philippines Maternal Mortality Rate 1990-2015
throughout its course
- All births are attended by skilled health
MATERNAL MORTALITY RATIO (MMR) - number of
professionals (ideally facility-based)
women who die from pregnancy-related causes while
- All complications are managed in adequately
pregnant or within 42 days of pregnancy termination per
staffed and equipped facilities offering
100,000 live births.
emergency obstetric care
➔ Philippines maternal mortality rate for 2015 was
114.00, a 2.56% decline from 2014.
Strategies to reduce maternal mortality
➔ Philippines maternal mortality rate for 2014 was
1. Universal access to contraceptive services to reduce
117.00, a 3.31% decline from 2013.
unintended pregnancies
2. Skilled attendance at all births
 Lesson 2:
GENETIC ASSESSMENT AND COUNSELING
GENETIC DISORDERS
● Disorders that can be passed from one
generation to the next
● Result from some disorder in gene or
chromosome structure
GENES
● Are basic units of heredity that determine both
the physical and cognitive characteristic of
people
● Composed of segments of DNA
● Woven into strands in the nucleus of all body
cells to form chromosomes
PHENOTYPE
● Refers to the person's outward appearance or
the expression of the genes
GENOTYPE
● Refers to the person's actual gene composition
GENOME
● Complete set of genes present Normal genome -
46XX or 46XY
MENDELIAN INHERITANCE: DOMINANT AND RECESSIVE
PATTERNS
MENDELIAN INHERITANCE
● Discovered and described by Gregor Mendel in
1800's
● A person who has two like genes for a trait - two
healthy genes for example (one from the mother
and one from the father) --is said to be
HOMOZYGOUS for a trait
● lf the genes differ (a healthy gene from the
mother and an unhealthy gene from the father,
or vice versa), the person is said to be
HETEROZYGOUS for that trait.
DOMINANT GENES
● Dominant in action when paired with other
genes
● Visibly expressed
RECESSIVE GENES
● Gene that is not dominant Masked and does not
show
HOMOZYGOUS DOMINANT
● Individual with two homozygous genes for a
dominant trait
HOMOZYGOUS RECESSIVE
● Individual with two genes for a recessive trait
GENETIC COUNSELLING
AIMS OF GENETIC COUNSELING:
● To provide accurate information
● To provide reassurance
● To assist individual/couple to make informed
choices
● To educate individual/couple about the effects
of genetic disorders
● A couple who has a child with a congenital
disorder or an inborn error of metabolism
WHO MAY BENEFIT FROM GENETIC COUNSELLING?
● A couple who has a child with a congenital
disorder or an inborn error of metabolism
● A couple whose close relatives have a child with
a genetic disorder
● Any individual who is known balanced
translocation carrier
● Any individual who has an inborn error of
metabolism or chromosomal disorder
● A consanguineous (closely related) couple
● Any woman older than 35 years of age and any
man older than 45 years of age
 ● Couples of ethnic backgrounds in which specific ● Elevated level: spinal cord disease Decreased:
illnesses are known to occur trisomy 21

ASSESSMENT FOR GENETIC DISORDERS CHORIONIC VILLI SAMPLING

ASSESSMENT ● Involves retrieval and analysis of chorionic villi

● Careful assessment of the pattern of inheritance ● Commonly done at 8-10 weeks, earliest at weeK
● History 5
● Physical assessment ● Reveals genetic abnormalities like
● Diagnostic testing Retinoblastoma, myotonic dystrophy (muscle
problems), sickle cell anemia, thalassemia
Family Genogram: X-linked Inheritance
AMNIOCENTESIS

● Withdrawal of amniotic fluid through the

abdominal wall at 14th-16th wk
● Needle is inserted, aspirate 20ml

PERCUTANEOUS UMBILICAL BLOOD SAMPLING

● Removal of blood from fetal umbilical cord at

about 17 weeks using amniocentesis technique

LEGAL AND ETHICAL ASPECTS OF GENETIC SCREENING

AND COUNSELLING

● Participation by couples or individuals in genetic

screening must be elective
DIAGNOSTIC TEST ● People desiring genetic screening must sign an
informed consent
KARYOTYPING ● Results must be interpreted
● Visual presentation of the chromosome pattern ● Results must not be withheld, and given only to
of an individual the people directly involved
● Specimen: venous blood/cells from buccal ● After genetic counselling, persons must not be
membrane coerced to have abortion or sterilization
● Metaphase (stage of mitosis)
● Stained, place under microscope and
photographed COMMON CHROMOSOMAL DISORDERS RESULTING IN
PHYSICAL OR COGNITIVE DEVELOPMENTAL DISORDERS
MATERNAL SERUM SCREENING
TRISOMY 13 SYNDROME (47XY13+ or 47XX13+)
● Alpha fetoprotein-glycoprotein produced by the ● PATAU Syndrome
fetal liver ● Extra chromosome 13
● Peaked in maternal serum between 13th and ● Severely cognitively challenged Midline
32nd week disorders: cleft lip and palate, heart disorders,
● Usually done at the 15th week of pregnancy abnormal genitalia
 ● Do not survive beyond early childhood
A. Cleft lip and palate
B. Supernumerary digits (polydactyly)
TRISOMY 18 SYNDROME (47XY18+ or 47XX18+)
● EDWARDS Syndrome
● Three copies of chromosome 18 Severely
cognitively challenged
● Small for gestational age, low-set ears, small jaw,
congenital heart defects, misshapen fingers and
toes, rounded soles of the feet .
● Do not survive beyond infancy
CRI-DU-CHAT SYNDROME (46XX5P- or 46XY5P-)
● Missing portion of chromosome 5
● Abnormal cry (sound of a cat)
● Small head, wide-set eyes, downward slant to
the palpebral fissure of the eye, recessed
mandible
● Severely cognitively challenged
TURNER SYNDROME (45X0)
● GONADAL DYSGENESIS
● One functional chromosome
● Short in stature
● Small & nonfunctional ovaries
● Webbed & short neck/ wide neck folds
● Congenital anomalies- coarctation of the aorta,
kidney disorders
● Severely cognitively challenged
KLINEFELTER SYNDROME (47XXY)
● Males with an extra X chromosome
● At puberty, secondary sex characteristics do not
develop
● Testes remain small & produce ineffective sperm
● Gynecomastia (Increased breast size) High risk of
male breast cancer
FRAGILE X SYNDROME (46XY230)
● Common cause of cognitive challenge in males
● X-linked disorder- one long arm of an X
● chromosome is defective
● Hyperactivity, aggression, autism
● Deficits in speech & arithmetic
● Large head, face with a high forehead,
prominent lower jaw, large protruding ears,
obese
● After puberty, enlarged testicles may become
evident
● Fertile & can reproduce
● Carrier females- may show physical & cognitive
characteristics
DOWN SYNDROME (TRISOMY 21) (47XY21+ or
47XX21+)
● Most common chromosomal disorder
● High risk - women more 35 yrs. old
● Nose is broad & flat
● Eyelids have extra fold of tissue at the inner
canthus (Epicanthal fold)
● Palpebral fissure (opening between the eyelids)
tends to slant laterally upward
 ● Iris of the eye have white specks (Brushfield
spots) CHILD WITH DOWN SYNDROME
● Protruding tongue (due to small oral cavity)
● Back of the head is flat Typical facial features of a child with Down syndrome
● Neck is short
● Low set ears
● Poor muscle tone - rag doll appearance
● Short & thick fingers
● Palm of the hand shows peculiar crease (Simian
line)- a single horizontal crease
● IQ less than 20
● Congenital heart disease
● Prone to Upper Respiratory Tract Infection
(URTI), Acute Lymphocytic Leukemia (ALL)
Simian Line, a horizontal crease seen in children with
● Life span is 50-60 years
Down Syndrome

Karyotype of Trisomy 21
MARCH 07, 2022
LESSON 3:
NURSING CARE OF THE HIGH RISK PREGNANT CLIENT – PART 1

HIGH RISK PREGNANCY

CARING FOR A WOMAN WHO DEVELOPS A
One in which a concurrent disorder, pregnancy-related COMPLICATION OF PREGNANCY:
complications or external factor jeopardize the health of ASSESSMENT
the woman, the fetus or both
● Provide enough time for thorough health
RISK FACTORS history.
● Problems such as headache, blurred vision,
● Physiological vaginal spotting should be discovered and
● Socio demographic investigated thoroughly
● Psychological
● Environmental COMMON NURSING DIAGNOSIS

PHYSIOLOGIC ● Anxiety related to guarded pregnancy outcome

● Risk for infection related to incomplete
● Concurrent illness miscarriage
● Malnutrition ● Deficient knowledge related to signs and
● Physically challenged symptoms of possible complications.
● Frequent pregnancies ● Risk for ineffective tissue perfusion related to
pregnancy-induced hypertension.
SOCIO DEMOGRAPHIC ● Ineffective role performance related to
increasing level of daily restrictions secondary to
● Poverty chronic illness and pregnancy
● Unemployment
● Lack of education
● Age
● Poor access to transportation for care IMPLEMENTATION
● Lack of support people
● oInterventions for woman experiencing a
PSYCHOLOGICAL FACTOR complication of pregnancy include measures to
maintain number of different areas:
● Cognitively challenge ● Continued healthy fetal growth
● Single /Separated mothers ● A woman's and family's psychological health
● Victims of Abuse, domestic violence, rape, incest ● Continuation of the pregnancy as long as
● Mental Retardation possible

EVALUATION
ENVIRONMENTAL FACTORS
● Exposure to Teratogens due to employment ● Client's BP is maintained within acceptable
● Environmental contaminants at home parameters
● Poor Housing
 ● Couple state they feel able to cope with anxiety Missed Vaginal
associated with the pregnancy complication miscarriage spotting,
perhaps
● Client accurately verbalizes crucial signs and slight,
cramping
symptoms to report to the health care provider
no
immediately. apparent
loss of
pregnancy

Incomplete Vaginal
SUDDEN PREGNANCY COMPLICATIONS miscarriage spotting,
cramping,
cervical
● Bleeding during pregnancy dilations,
● Ectopic pregnancy but
incomplete
● Gestational trophoblastic disease expulsion
of uterine
● Premature cervical dilatation contents
● Placenta previa Abruptio placenta
Complete Complete
● Disseminated intravascular coagulation miscarriage expulsion
● Preterm labor of uterine
contents
● Preterm rupture of membranes
● Pregnancy induced hypertension 2nd Ectopic Implantati Sudden May have
Trimester pregnancy on of unilateral repeat
● HELLP Syndrome zygote at lower ectopic
● Multiple pregnancy site other abdominal pregnancy
than the quadrant in future
● Abnormal amniotic fluid volume uterus pain, tubal
minimal scarring in
● lsoimmunization vaginal bilateral
bleeding,
possible
Bleeding during pregnancy signs of
● Always deviation from the normal shock or
hemmorrh
age

Hydatidati Abnormal Overgrowt

on form proliferatio h
mole (H- n of
Mole) trophoblas
t cells,
fertilization
SUMMARY OF PRIMARY CAUSES OF BLEEDING DURING or division
PREGNANCY defect

Premature Cervix Painless Can have

cervical begins to bleeding cervical
TIME TYPE CAUSE ASSESSME CAUTIONS
dilation dilate and leading to sutures
NT
pregnancy expulsion placed to
is lost at of fetus. ensure a
1st Threatene Unknown, Vaginal Disseminat about 20 second
Trimester miscarriage possibly spotting ed intra weeks. pregnancy.
chromoso perhaps vascular
mal uterine slight coagulatio
3rd Placenta Low Painless No vaginal
abnormaliti cramping n
Trimester previa implantatio bleeding at examinatio
es associated
n of beginning ns.
with
placenta of cervical
missed
possibly dilation.
miscarriage
because of
uterine
Imminent Vaginal abnormalit
miscarriage spotting, y.
cramping,
cervical
Abruptio Unknown Sharp Disseminat
dilation
placenta cause, abdominal ed
placenta pain intravascul
 separates followed ar ● Avoid strenuous activity
from by uterine coagulatio ● Coitus usually restricted for 2 weeks
uterus tenderness n.
, vaginal ● Spotting usually stops within 24-48 hours
bleeding.

Preterm Trauma, Show Preterm IMMINENT (INEVITABLE) MISCARRIAGE

Labor substance accompani labor may
abuse, PIH, ed by be halted if
● Uterine contractions and cervical dilatation
cervicitis, uterine the cervix occurs
increased contraction is less than
chance in s becoming 4 cm ● Loss of product of conception cannot be halted
multiple regular and dilated and ● lf no FHT and UTZ reveals empty uterus-
gestations, effective. the
maternal membrane dilatation and evacuation may be performed
illness. s are
impact.
COMPLETE MISCARRIAGE
SHOW - Cervix is Less than 4cm dilated and the
membranes are still intact
Entire products of conception are expelled
spontaneously without assistance
ABORTION
INCOMPLETE MISCARRIAGE
Medical term for any interruption of a pregnancy before
a fetus is viable
● Part of the conceptus is expelled, but the
membrane or placenta is retained
SPONTANEOUS MISCARRIAGE
MANAGEMENT:
Early miscarriage if it occurs before 16th week
● Dilatation and curettage or suction curettage
Late between 16-24 weeks
RECURRENT PREGNANCY LOSS
CAUSES:
● Terratogenic factor
● Women who had 3 spontaneous miscarriages
● Chromosomal abberations/abnormal fetal
● Defective spermatozoa or ova
development
● Endocrine factors
● Implantation abnormalities
● Deviations of the uterus
● Failure to produce enough progesterone
● Uterine infections
● Infection
● Autoimmune disorders

PRESENTING SYMPTOM
COMPLICATIONS OF MISCARRIAGE
● Vaginal bleeding/spotting o Should consult
● Hemorrhage
attending Obstetrician so that instructions may
● Infection
be given
● Risk for isoimmunization

THREATENED MISCARRIAGE
PROCESS OF SHOCK BECAUSE OF BLOOD LOSS
● Vaginal bleeding, scant, bright red usually, slight
cramping
● No cervical dilatation

MANAGEMENT:
● Fetal heart assessment
● Utz
● hCG determination
 ● Due to fallopian scarring that slow the travel of
the zygote
● Woman still experience the signs of pregnancy
● Missed period
● Signs and symptoms of pregnancy is experienced
by the woman
● (+) Pregnancy test

6. Lethargy, coma, decreased renal outputrenal failure-

maternal and fetal death

SIGNS AND SYMPTOMS OF HYPOVOLEMIC SHOCK

Assessment Significance

Increased pulse rate Heart is attempting to

compensate to increase
Blood Volume

Decreased BP Less peripheral

resistance

Increased RR Increase gas exchange

Ruptured Ectopic Pregnancy
to oxygenate decreased
RBC volume
Cold, clammy skin Vasoconstriction occurs
to maintain blood
volume in central body
core
Decreased urine output Decrease blood supply
in the kidney
● Sharp stabbing pain in lower abdominal
quadrant
● Vaginal spotting
● Amount of bleeding not evident
● May lead to shock
● Falling hcg level
● Utz – providers clear cut picture

Dizziness Inadequate blood is

reaching the cerebrum

Decreased CVP Decreased venous

return

Ectopic Pregnancy - Included in quiz

● Implantation occurs outside the uterine cavity If the woman does not seek help at once
● Ovary or cervix ● Cullen’s sign (umbilicus may develop a bluish
● Most common is fallopian tube tinge)
 ● Dull, vaginal abdominal pain
● Movement of cervix cause excruciating pain
● Pain in shoulder
Management
● Unruptured – methotrexate followed by
leucovorin, mifepristone (abortifacient)
● Ruptured – emergency situation
● Laparoscopy – ligate the bleeding vessels and
remove/ repair fallopian tube
● CBC
● Administration of fluids
Abdominal Pregnancy
● Woman may report sudden lower quadrant pain
● Fetal outline is easily palpable
● Danger is infiltration of large blood vessel, bowel
perforation, poor nutrient supply to the fetus
● Infant must be born through laparotomy
Rate of Survival
● 60%
Gestational Trophoblastic Disease (Hydatidiform Mole)
● Abnormal proliferation and then degeneration
of the trophoblastic villi
● Cells become filled with fluid and appears as fluid
filled grape sized vesicles
● 1 in every 1500 pregnancy
● Two types:
● Complete mole – all trophoblastic villi
swell and become cystic.
● Partial mole – some of the villiform
normally.
Assessment
● Uterus tends to expand faster
● Strong (+) result of hCG-1 to 2 M IU compared to
a normal of 400, 000 IU)
● Symptoms of pregnancy induced hypertensio
may appear before 20th week
● Ultrasound – no fetal growth and fetal heart
sound.
● Marked nausea and vomiting
● Dark brown blood, profuse flesh flow (16 weeks)
with clear fluid filled vesicles.
Therapeutic Management
● Suction curettage
● Post surgery:
● Pelvic examination, chest radiography, hCG level
● hCG monitoring
● Half of woman positive at 3 weeks
● ¼ positive result at 40 days
● Assess every 2 weeks until normal
● Every 4 weeks for the next 6 to 12 months
● Should use reliable contraceptive method
● Plan pregnancy at 12 months if hcg is normal.
Prophylaxis
● Methotrexate
● Dactinomycin
Premature Cervical Dilation
● Old name – Incompetent cervix
● Cervix that dilate prematurely, cannot hold a
fetus until term
● Painless
● Pink – stained vaginal discharge (1st symptom)
 ● Followed by rupture of membrane, discharge of
amniotic fluid Mc Donald Procedure
● Uterine contractions – birth of the fetus ● Nylon suture are placed vertically and
horizontally across the cervix and pulled tight to
Associated with: reduce the cervical canal.
● Increased maternal age ● Shirodkar
● Congenital structured defect ● Sterile tape is threaded in a purse string manner
● Trauma to cervix under the submucous layer of the cervix.

Management:
● Cervical cerclage – purse – string sutures are
placed in the cervix by vaginal route.
 March 09, 2022
LESSON 4:
NURSING CARE OF THE HIGH RISK PREGNANT CLIENT – PART 2

abnormal position of placenta

Placenta Previa -
● Past CS
● Placenta is implanted abnormally in the uterus. ● Past uterine curettage
● Most common cause of painless
-
bleeding in the ● Multiple gestation
0third trimester of pregnancy. ● Male fetus

ASSESS:
● Duration of pregnancy
● Time the bleeding began
● Estimate amount of blood loss
● Accompanying pain
cervix
● Color of the blood
-wasa ● What has she done
● Prior episodes of bleeding
● Prior cervical surgery

THERAPEUTIC MANAGEMENT
● Never attempt a pelvic or rectal examination
with painless bleeding late in pregnancy
● Obtain baseline VS vital sign
-

● lVE therapy Intravenous

-

● I and O monitoring
● External monitoring equipment
● Complete blood count
OCCURS IN 4 DEGREES ● Blood typing and crossmatching
gilid ● Low lying- implantation in the lower rather than
in the upper portion of the uterus HOW IS THE FETUS DELIVERED!
edge
● Marginal -the placenta edge approaches that of ● Depends on the percentage of previa and the
the cervical os condition of the pregnancy
half of ● Partial-implantation that partially obstructs the
cervix
cervical os PREMATURE SEPARATION OF THE PLACENTA/
● Total placenta previa - totally obstructs the
cervix
-
cervical os -separation of placenta touterus
ABRUPTIO PLACENTA
● Placenta appears to be implanted correctly
ASSESSMENT ● Begins to separate and bleeding results
● Bleeding is abrupt, painless , bright red and ● Cause is unknown
sudden
● Immediate care measures:
● Place the woman immediately on bedrest in a
- side lying position

ASSOCIATED WITH:
● Increased parity
● Advanced maternal age
 O
after birth

1 -
Minimal separation, but enough to
-

cause vaginal bleeding and changes in

maternal VS,-no fetal distress

2 -
Moderate separation, there is evidence
-

of fetal distress, uterus tense and

painful

PREDISPOSING FACTORS: 3 Extreme separation, maternal shock and

● High parity fetal death may occur
● Advanced maternal age DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
● Short umbilical cord ● Acquired disorder of blood clotting, fibrinogen
-
● Chronic hypertensive disease (plasma protein produced in the liver and is
● Pregnancy induced hypertension converted into fibrin during blood clot
● Direct trauma formation) level falls to below effective limits
● Vasoconstriction ● Conditions associated with its development:
● Autoimmune antibodies ● Premature separation of placenta
● Chorioamnionitis ● PIH Pregnancy Induced Hypertension
-

● Amniotic fluid embolism (obstruction of blood

ASSESSMENT: vessel)
● Sharp stabbing pain high in the uterine fundus
- ● Placental retention retained placenta
-

● If labor begins, each contraction will be ● Septic abortion

accompanied by pain over and above the pain of ● Retention of dead fetus -
retained dead fetus
contraction ●
● Heavy bleeding - evident if separation occurs at ● Test tube-clemature separation of placenta
the edges ● PIH
● Couvelaire uterus (uteroplacental apoplexy) - ● Amniotic fluid embolism (obstruction of blood
hard board like uterus with no apparent or vessel)
minimally apparent bleedingDisseminated ● Placental retention
Intravascular Coagulation (DIC) may occur ● Septic abortion
● Retention of dead fetus
THERAPEUTIC MANAGEMENT: DIC
● Emergency situation ● Extreme bleeding causes many platelets and
-
● Large gauge IV catheter fibrin from the general circulation rush to the
● Oxygen by mask site, not enough are left for the rest of the body
● FHT and maternal VS monitoring
● Lateral position Di
TEST CLOTTING -

● No abdominal, pelvic or vaginal examination ● Test tube-clot must form

● Unless separation is minimal, pregnancy must be ● Platelet assessment - less than or equal to
TERMINATED 100,000/uL /uL
● Prothrombin -low
DEGREES OF PREMATURE PLACENTAL SEPARATION ● Thrombin-elevated
Grade Criteria ● Fibrinogen -less than 150
● mg/dL
0 No symptoms apparent, diagnosis made
MANAGEMENT:
 nawawala/ decreasing
↑

● Halt the underlying insult ● If contractions are halt. oral terbutaline may be
● IV administration of given
● Heparin
7
DRUG ADMINISTRATION: -after 24h days -
● Blood or platelet transfusion
● Steroid (betamethasone) - to hasten lung
PRETERM LABOR maturity
● Labor that occurs before the end of the 37 weeks ● Effects after-
24 hours and lasts 7 days
of gestation cannotbe
stopped
● Persistent uterine contractions, cervical LABOR THAT CANNOT BE- HALTED
-

effacement over 80% and dilation over 1cm

-
● Membranes have ruptured
- -

● Unknown cause than lam ● Cervix more than0 50% 50%

-

3-4cm-

Conditions associated: ● effaced andO 3-4 cm dilated

and inflammation of ques
delivery
↑infection
● Dehydration ● If fetus is very immature - CS cesarean
-

● UTI
● Periodontal disease METHOD OF DELIVERY:
● Chorioamnionitis ● If very immature - CS delivery to reduce pressure
● Inadequate prenatal care on the fetal head
● Cord is clamped immediately extra amount of
ASSESSMENT: blood could overburden the circulatory system
● Persistent , dull, low backache
● Vaginal spotting
● Pelvic pressure or abdominal tightening
● Menstrual like cramping PRETERM RUPTURE OF THE MEMBRANES
● Rupture of fetal membranes with loss of
WAYS TO PREDICT WHICH PREGNANCY WILL END amniotic fluid during pregnancy before 37 weeks
EARLY:
● Analyze change in vaginal mucus Threats to fetus:
● Presence of fetal fibronectin (protein produced ● Uterine and fetal infections
by trophoblast cells) - preterm contractions are ● Increased pressure on the umbilical cord (cord
ready to occur prolapse)
● Absence of fetal fibronectin labor will not occur ● Potter -like syndrome - distorted facial features
-at least 14 days and pulmonary hypoplasia from pressure
THERAPEUTIC MANAGEMENT: ASSESSMENT:
● Woman usually admitted ● Sudden gush of clear fluid from vagina
● Bed rest ● Test with nitrazine paper- turns blue (alkaline)
● lV fluids hydration may stop contractions
● Tocolytic agent - halt labor (terbutaline) THERAPEUTIC MANAGEMENT:
● Advise to limit strenuous activities If labor does not begin, and fetus is at point of viability:
● Fetal assessment - count to 10 test ● Woman is placed on bed rest and receives
used Fund corticosteroid
ADMINISTRATION OF TERBUTALINE: solution water s ● Administration of- broad-spectrum antibiotics
● Mixed with Lactated Ringer's -replace 's ● Membranes resealed by fibrin-based
electroly
● Piggy back commercial sealant
● Microdrip
● Check blood pressure and pulse rate
 LESSON 5:
NURSING CARE OF THE HIGH RISK PREGNANT CLIENT – PART 3

on a random sample and 5g on a

PREGNANCY INDUCED HYPERTENSION 24 hr sample, oliguria, cerebral
or visual disturbances,
● Vasospasm occurs during pregnancy in both pulmonary or cardiac
involvement, extensive
small and large arteries
peripheral edema, hepatic
● Used to be called toxemia dysfunction, thrombocytopenia
(decrease in the no. of platelets)
epigastric pain
Occurs most frequently in women:
Eclampsia Seizure or comma accompanied
● Of color by signs and symptoms of pre
● Multiple pregnancy eclampsia

● Primiparas younger than 20 years or older than

● 40 years MANAGEMENT: MILD PRE ECLAMPSIA
● Low socioeconomic backgrounds poor nutrition ● Promote bed rest
● Who have had five or more pregnancies ● Anti platelet therapy
● Hydramnios -excess amniotic fluid ● Promote good nutrition
● Underlying disease heart dse, diabetes, renal ● Provide emotional support
involvement
CLASSIFICATIONS: MANAGEMENT FOR SEVERE PRE ECLAMPSIA:
● Gestational hypertension ● Support bed rest
● Mild eclampsia ● Monitor maternal well being
● Severe eclampsia ● Monitor fetal well being
● Eclampsia hypertension in pregnancy
-

● Support nutritious diet

● Administer medications to prevent eclampsia
Assessment
● Hypertension MANAGEMENT OF ECLAMPSIA:
urine
● Proteinuria of protein
in
-
4 level ● Tonic-clonic seizures -

● Edema
SYMPTOMS OF PREGNANCY INDUCED
HYPERTENSION
Hypertension Type Symptoms
Gestational HPN BP 140/90 or SBP elevated 30
mm Hg or DBP elevated 15 mm
above pre pregnancy level; no
proteinuria or edema, BP returns
to normal after birth
Mild pre eclampsia BP 140/90 or SBP elevated 30
prioritize safety of px
● Maintain patent airway
● Administer oxygen
● Turn to side
● Administer Magnesium sulfate (Antidote:
Calcium Gluconate) or Diazepam (Valium)
● Assess FHT
● Check for vaginal bleeding
HELLP SYNDROME
● Variation of PIH
● H-emolysis (lysis of RBC)
-

↳+21bs/wk- 2nd
mm or DBP elevated 15 mm
above pre pregnancy level; ● E-levated L-iver enzymes
L 11bs/wk
+
3rd
+

proteinuria of 1- + on a random
L m. edema x ex. fact sample, weight gain over 2
● L-ow P-latelet count
lbs/week in 2nd trimester and 1 ● Increased BP. edema, proteinuria+
lb/wk on the 3rd trimester mild
edema in upper extremities of ● Nausea, epigastric pain, general malaise, RUQ
face tenderness
Severe pre eclampsia BP of 160/110, proteinuria 3-4+
 MANAGEMENT:
● Improve platelet count by transfusion of fresh
frozen plasma or platelets

MULTIPLE PREGNANCY
● A woman's body must adjust to the effects of
more than one fetus
- IDENTCAL

MONOZYGOTIC TWINS:
↓
-Iorum, sperm, zygole/eaetical
● Single ovum and spermatozoon, zygoteNdivides
has the

identical into two-

most
IDENTICAL individuals
DNA ● One placenta, one chorion. 2 amnions, 2
ASSESSMENT:
amnioticsac
umbilical cords
● Uterus increase in size at a rate faster than usual
● Alpha-fetoprotein levels elevated
DIZYGOTIC(FRATERNAL/NON-IDENTICAL):
● Quickening - flurries of action at different
● Double ova-2 placentas, 2 chorions, 2 amnions. 2
portions of abdomen
umbilical cord
● Reveals by ultrasound

THERAPEUTIC MANAGEMENT:
● eCloser prenatal supervisions

excessive amniotic
HYDRAMNIOS -
fluid

● Normal amniotic fluid volume 500-1000mL

● Fluid index above 24 cm or more than 2000 mL
● Suggests difficulty with the fetus' ability to
swallow
● Unusual enlargement of uterus
● Difficult to auscultate FHT
● Shortness of breath
● Increase weight gain
● Hemorrhoid
● Varicosities
● Polyhydramnios - is excessive amniotic fluid
surrounding the fetus (more)
 ● If normal (0) or minimal (below 1:8) test
MANAGEMENT repeated in the 28th week
● Bed rest ● If normal no therapy
● Assess VS and edema ● If elevated (1:16) - fetal condition monitored
● NSAID (Non-Steroidal Anti-inflammatory Drugs) -every 2 weeks
● Amniocentesis- almost daily
THERAPEUTIC MANAGEMENT:
~less than
OLIGOHYDRAMNIOS
● Pregnancy with less than the average amount of ● Passive Rh (D) antibodies against the Rh factor is
amniotic fluid administered to women who are C Rh-negative at
● Caused by bladder or renal disorder -28 weeks
● Fetus is cramped for space ● Given in the-1 st 72 hours-after birth -
days
● Uterus fails to meet expected growth rate ● Cord blood is tested if Rh positive (Coombs'
-
● Mgt: Amniotransfusion negative) large amount of antibodies are not
O
present in the mother, mother will receive RhIG
POST TERM PREGNANCY C
injection
● Pregnancy that exceeds 42 weeks ● If Rh negative injection not necessary
● Common in receiving salicylates (analgesics)
● If there is evidence of placental insufficiency INTRAUTERINE TRANSFUSION
● Mgt: - oxytocin to initiate- labor or CS is ● Injection of RBC directly into the vessel of the
- performed fetal cord or depositing them in the fetal
ISOIMMUNIZATION abdomen
● Occur when an Rh negative mother carries a
fetus with an Rh positive blood (D antigen)

Maternal antibodies may cross the placenta causing: FETAL DEATH

● Hemolytic disease of the newborn or ● If labor does not begin, it will be induced by a
Erythroblastosis fetalis (RBC destruction, combination of prostaglandin gelsuch as
decreased 02 supply) misoprostol (Cytotec) and oxytocin
● Cytotec shouldO not be given to pregnant women
ASSESSMENT because it can trigger abortion; it is meant for
-

● Anti D antibody titer-done at 1 st pregnancy visit ulcer

 NURSING CARE OF A FAMILY EXPERIENCING PREGNANCY COMPLICATIONS FROM PRE-
EXISTING OR NEWLY ACQUIRED ILLNESS - PART 1
Cardio vascular disorders and pregnancy

Cardio vascular disorders and pregnancy • Rheumatic fever 90%

Concerns: • Congenital defects
• Can a woman get pregnant? • Arteriosclerosis
• If the couple decides to get pregnant, how will it • Myocardial infections
affect the health condition of the woman and • Pulmonary diseases
the growing fetus? • Renal diseases
• How does it affect the decision making of the • Heart surgery
couple?
Examples of cardiac diseases
Cardiac disease • Left sided heart failure
Variety of health conditions both congenital and • Right sided heart failure
acquired that complicate pregnancy • Cardiomyopathy
Cardiac output • Hypertensive vascular disease
• Rises significantly • Thromboembolic disease
• Plateau is⑧ 28-32 weeks • Rheumatic heart disease

Factors increasing cardiac output Classification of heart disease

• Blood volume Class 1- No limitation of physical activities, regular
• Hormonal influences activity do not produce symptoms
• Autonomic nervous system -
ANS Class 2- Slightly compromised, slight limitation,
asymptomatic at rest but regular activities produce
Blood volume
palpitations, fatigue, dyspnea and anginal pains
• Increases by plasma volume expansion and RBC
Class 3- Marked limitations, ordinary/ regular activities
multiplication
cause symptoms
• Heart rate increases and dilated systemic
vasculature is maintained Class 4- Marked limitation, symptomatic
mitral value, back pre... pulmonary
Left sided heart failure
-

Hormonal influences • -Mitral valve cannot effectively push blood

• Increased estrogen forward
vein +25mming
• Systemic vasodilation pulmonary • eBack pressure on the pulmonary circulation
X
• Lowered peripheral resistance fluid orcapillaries
-
• If pressure w/in the pulmonary vein reaches 25
interstitial space
• Increased cardiac output in alveoli mm hg, fluids pass from capillary membranes to
interstitial space surrounding the alveoli
Autonomic nervous system
• Pulmonary edema
• Cardiovascular system is hyperfilled from
• Dyspnea, blood specked sputum, change in vital
increased blood volume and hyperdynamic
signs, orthopnea, paroxysmal nocturnal
Pt will likely report signs and symptoms that mimic dyspnea shortnerathe sleep
-> during
cardiac disease -rvc received by AA from VC
Right sided heart failure
• Dyspnea -shortness of breathe
• Orthopnea hypertension
-
in low lying position ↓ • Output of right ventricle<blood volume
congestion -
received T
by right atrium from the vena cava
• Edema
• Back pressure=congestion of the sytemic
of systemic
out
• Syncope -
fainting/passing
heart beat venous venous circulation and less cardiac output to
• Palpitations -

pounding
circ.=[ the lungs
cardiac
Risk factors
output to the
s
 • Jugular venous distention, increased portal • Persistent heart murmur
circulation
Maternal effects
Extreme dyspnea • Patients with valvular problems causing atrial
Pain fibrillation-susceptible to embolic episodes
Ascites • Cyanotic heart disease-increase the maternal
Peripheral edema mortality by 50%
Peripartal Cardiomyopathy -final mos +5mos aft
Fetal and neonatal effects
Weakness and enlargement of the heart muscle that
• Compromised maternal circulation- uterine
usually occurs from around the final month of
blood flow will be reduced
pregnancy through about five months after pregnancy
• Spontaneous abortion- Growth retardation and
• No previous history of heart disease Mental retardation
• Shortness of breath • Fetaldistress- Preterm delivery and fetal
• Chest pain morbidity/fetal death
• Edema

Usual medical management and protocols for nurse

Rheumatic heart disease practitioners
• Compilation of rheumatic fever in which the General management
heart valves are damaged • Team approach
• Affects the valves of the heart secondary to • Adjust cardiac medications
previous exposure to beta hemolytic
- • Bed rest/restricted activity
streptococcus such as streptococcal pharyngitis
-
• Prophylactic antibiotic
Aeria
Assessment • Careful titration of fluid volume
• History of pre pregnancy cardiac status • Advance planning for route of delivery
• Level of exercise performance Drug therapy
• Physical assessment
• Heparin –anticoagulant
• Diagnostic tests
• Warfarin-pulmonary embolism/prosthetic
• Fetal assessment valves
Criteria for establishing a diagnosis of cardiac disease • Furosemide-diuretic
in pregnancy • Digitalis-crosses placental barrier
• Persistent murmur • Tocolytics
• Permanent cardiomegaly- enlargement of the • Beta blockers-treat hypertension
heart
heartbeat
• Severe dysrhythmias
-irregular
• Severe dyspnea prior to stage of pressure on Nursing implementations
the diaphragm
• Encourage early, frequent and regular prenatal
visits
• Encourage compliance with therapeutic
Signs of cardiac decompensation regimen
pas
• Moist cough
lomeferities, Decrease workload of the heart
8-
• Pedal edema • Adequate rest and sleep
• Dyspnea • Treat early anemia
• Tachycardia • Prevent exhaustion, fatigue, stress
• Tachypnea
• Chest pain on exertion Avoid activities that decrease oxygenation
• Cyanosis • Smoking
 • Overcrowded place Intrapartum period goals
• Oxygen per mask
Avoid constipation
• Forceps or vaccuum extraction
• Daily fruits
• Elective CS
• Vegetables
• Regular bowel movement Primary goal:
• Regular exercise • Reduce risks for complications

Proper nutrition Achieved by:

• Well balanced diet • Education
• Adequate protein • Routine assessment
• Low sodium, fats and carbohydrates • Proper referral
• No junk foods and stimulants • Facilitation of patient participation in decision
• Being an advocate and coordinator for the
Intrapartum period goals
multidiciplinary team approach
• Minimize changes in pulse and blood pressure:
• Lateral position
• Adequate pain relief
• Avoidance of hemorrhage
• Avoidance of infection
 iron supplement: stains teeth
A fiber diet
take iron (juice) w/ straw

NURSING CARE OF A FAMILY EXPERIENCING PREGNANCY COMPLICATIONS FROM PRE- righ take

EXISTING OR NEWLY ACQUIRED ILLNESS - PART 2 vit C for absorption,

HEMATOLOGIC DISORDERS AND PREGNANCY ferrous sulfate cation
-

↑ check
*

turn
for gastric irritation,
black
stools

HEMATOLOGIC DISORDERS AND PREGNANCY Prevention/Management

ANEMIA ● Pre natal vitamins containing iron
● Decrease in oxygen carrying capacity of the supplement of - 60 mg elemental iron
blood due to decrease hemoglobin (protein ● Diet high in iron such as green leafy
in the red blood cells that carries oxygen) in vegetables, meat, legumes (beans) and fruits
the blood ● If with deficiency :C 120-200 mg/day
Risk Factors: ● Severe anemia- IV iron dextran (substitute
● Decrease nutritional intake for blood plasma or transfusion)
● Heredity Nursing Implementations
● Increased demands as in pregnancy and ● Promote a balance of activity and rest with
adolescence avoidance of fatigue
● Poor absorption * Low socio-economic level ● Provide dietary instructions
Iron Deficiency Anemia ● Encourage regular intake of ordered
● Most common hematinics (ferrous sulfate)
● Diet low in iron -green leafy vegetable Folic Acid Deficiency
● Heavy menstrual period ● Folic acid-B vitamin necessary for the normal
● Unwise weight reduction program formation of red blood cells
● Woman experiences fatigue and poor ● Leads to megaloblastic anemia (abnormally
exercise tolerance large, immature and dysfunctional red blood
RBC’s Are: cell)
● Microcytic - exceptionally small RBC ● Becomes apparent in the ! 2nd trimester of
● Hypochromic - decreased hemoglobin in the pregnancy
RBC ● More common in multiple pregnancy
Assessment Findings -conjunctiva, pale palm Causes
● Pale skin and mucous linings ● Alcohol abuse (alcohol prevents absorption
● Pearl white sclera of several nutrients especially the B
● Brittle flattened nails vitamins)
● Low Hgb - less than 10 g/dl ● Poor diets (common in alcoholics, the
● Low Hematocrit (measures how much space elderly, those living alone or in poverty, and
in the blood is occupied by red blood cells) - infants especially those with infections or
less than 33% diarrhea)
● Serum Iron (< 65ug/100 ml blood) ● Impaired absorption because of intestinal
May lead to dysfunction
● Low birth weight ● Bacteria competing for available folic acid
● Preterm birth ● Overcooking of food, destroying valuable
● Increased incidence of abortion and water-soluble nutrients, including a high
premature labor percentage of folic acid
which
● Limited storage capacity in infants
* Pica-eating disorder in a
person
eat things notconsidered food
 ● Prolonged drug therapy, especially from prevent:folic ● The chances of passing it to the offspringacid

folic rich food

anticonvulsants and estrogens depends on genetic composition of the
->

● Not addressing increased folic acid needs of ↑ parents advice genetic counselling
-

could lead to infection

certain age groups
May contribute to -tetus keep of normal saline
give propylactic
-> moist

RENAL AND URINARY DISORDERS

-
anti.

~
● Early miscarriage neural tube defect
*
● Urinary tract Infection (UTI)
● Early separation of placenta abdominal wall defects ● Chronic Renal Failure
*

Prevention/Management Incidence
● C 400 ug of folic acid daily before getting ● Infection - 1-5% of pregnancies (un)
pregnant saluyot, spinach (expensive) ● Chronic kidney disease - 6 to 12 cases per
~ Kangkong,
● Folacin rich food: green leafy vegetables, 10,000 pregnancies CCRF)
// n- 12/1000preg
oranges, dried beans Kidneys
● During pregnancy :C 600 ug/day ● Excrete water, electrolytes and nitrogenous
waste product
SICKLE CELL ANEMIA ● Acid-base balance
● Caused by abnormal amino acid in the beta ● Secretes erythropoietin - kidney hormone
chain of hemoglobin that increases the number of RBC in cases of
● Recessively inherited anemia
● Majority of RBCs are irregular or sickle ● Renin - angiotensin - aldosterone system
shaped and cannot carry much hemoglobin Renin - hormone released in the kidney in
-
● If amino acid valine is replaced - sickle response to either decrease BP or plasma
hemoglobin (Hbs) sodium concentration
● If amino acid T
- -
lysine is replaced - non sickling ● Accounts 20-25 % of the cardiac output
usually in joints
Urinary Tract Infection
-
● Ureters dilate from the effect of
progesterone - urine stasis/stagnation
● Minimal glucosuria - growth of
microorganisms

infectioni
Ascending Infection
evital ● Caused by Escherichia coli
Descending Infection
● Streptococcus B
May result to: Assessment
● Blockage to placental circulation ● Frequency and pain on urination
● Low birth weight partially blocked
- ● Pain in the lumbar region
● Fetal death -severely blocked ● Nausea and vomiting
Therapeutic Management ● Malaise
oxygen
● Exchange transfusion sickle-no cannot carry oxygen
cells
● Temperature elevation fever -

● Administering oxygen ↑ Maternal Effects

- -
-

● Controlling pain sickle cell-common

-
joints ● May lead to preterm labor
in

make blood viscous

● Increasing fluid volume -to not
● Bacteremia causing A septic shock
Folic
* acid supplement replace
-
RBC Therapeutic MGT
No
*
routine iron supplement -> bind
cannot w/ sickle cell

period of standing - pulls

gravity blood - lower extremeties
Limitlong
*
G thrombophlebities
venous return ->
walking, rest. Trendelenburg position
*
Encourage
 sufonamides not near form:hyperbilirubenimia in NB
-

Notadvised L Tetracyclines = retardation of bone

growth

● Urine C & S ● Increased glomerular filtration rate /

● Administration of antibiotics creatinine level
● Amoxicillin and ampicillin are safe to Medical Management
administer + cephalosporins ● ACE inhibitor-preserves kidney function but
TRIMETHOPRIM fetotoxic
● Antibiotic used mainly in the prevention and ● Low dose aspirin
treatment of urinary tract infections ● Urine output monitoring
● Folic acid antagonist (neutralizes the effect ● Ultrasound every 2 weeks from 24 wks of
of another drug) gestation
● Must 0 not be given on the first trimester ● Non stress test removal

Care of the woman with chronic renal disease de

of fluid
Prevention of UTI does not e
~dialysis -

● Void frequently -every 2 hours ● If undergoing dialysis, peritoneal (removal of

tapping
or

● Wiping perineal area from front to back fluid from the abdominal cavity) is more
diet
low k

● Wearing cotton underwear preferred - monitor for preterm labor

hemodialysis progesterone
L
● Voiding immediately after sexual intercourse ● Nutrition consultation
=

be removed
might
G a RISK since proges
Nursing Implementations ● Emotional support Heparin may
*
preg. is needed in

● AdviseO 3-4L of water/day Nursing Interventions be given

● Knee chest position - to promote urine ● Monitor I and O

● Evaluate degree of edema ↑take lung
sound
drainage
● Compliance to medications ● Make referral to a dietician regulate diet -

● Teach home blood pressure monitoring

● Teach pt signs and symptoms of preterm -

labor -

Chronic Renal Disease ● Educate on the importance of drinking

dehydration - -
* release
oxytocin
● Results in accumulation of waste products in variety of fluids
-
↳> contracts

● Empty bladder at least everyC

muscle
the blood, electrolyte abnormalities and 2 hours Preterm ↳
labor

anemia ● Perineal hygiene from front to back

● CBC may indicate anemia

I
● May develop severe anemia Cerythropoietin) A mild abdominal cramps
s/s of
↳ cramps - back

preferbor *broke
bag water
of -> effacement a dilatation
NURSING CARE OF A FAMILY EXPERIENCING PREGNANCY COMPLICATIONS FROM PRE-EXISTING OR NEWLY ACQUIRED
ILLNESS - PART 3
Respiratory disorders and pregnancy

Respiratory conditions • Terbutaline & Albuterol – tapered, close to term

• Acute Nasopharyngitis because they may reduce labor contractions
• Influenza • Cromolyn sodium
• Pneumonia • Montelukast sodium
• Asthma Nursing interventions
• Tuberculosis • Review various asthma medications
• Teach importance of avoiding environmental
Acute nasopharyngitis/common cold allergens
• Woman experiences nasal congestion due to • Pollens
estrogen • Molds
• If viral, no medication is needed • Dusts
• Nuts
INFLUENZA • Fish
• Caused by virus
• High fever TUBERCULOSIS
• Body aches • Lung tissue invaded by mycobacterium
• Sore throat tuberculosis
• May receive immunization • Calcification and scarring of the lungs
• Anti pyretic
• Tami Flu (new anti-viral drug) Assessment
• Mantoux test /purified protein derivative (PPD)
Asthma - If positive, should undergo chest radiograph
• Asthma is a disorder marked by reversible airway • Sputum culture confirms the diagnosis
obstruction, airway hyperactivity and airway • Chronic cough
inflammation • Weight loss
• Trigerred by allergens-release of histamine- • Coughs out blood (hemoptysis)
bronchial smooth muscle constriction • Night sweat
• Most serious medical condition to complicate • Low grade fever
pregnancy • Chronic fatigue
• Difficulty releasing air
• High pitched whistling sound(wheezes) Therapeutic management
• Chest tightness Isoniazid (INH) and ethambutol hydrochloride
• Sputum production (Myambutol)
• drugs of choice
Maternal effects
Adequately controlled -risk of complication is no greater Treatment regimen
than non asthmatic With active disease in pregnancy:
Poorly controlled - increased risk of hypertension and • Isoniazid (INH) 300 mg combined with rifampin(
hyperemesis gravidarum (excessive vomiting) RIF) 600 mg and ethambutol 1 gram daily for 2
months
Effect on fetus • RIF and INH for additional 7 months
• Preterm birth • Pyrodoxine (vitamin B6) taken with INH - to
• Growth restriction prevent peripheral neuritis
• Ethambutol – may cause optic atrophy & loss of
Management green color recognition. Monthly, Snellen chart
• Beclomethasone test – if with s/s, discontinue the drug.
• Budesonide
Health education:
 • Maintain an adequate intake of calcium – to
ensure that tuberculosis pockets form or are not
broken down.
• Wait 1 to 2 years to be negative of infection
before deciding to conceive
• Woman with history of tuberculosis should have
three negative sputum culture before she can
hold/cares for her infant
• If with active infection-INH prophylaxis
AUTOIMMUNE RHEUMATIC DISEASES
• Result from the body’s immune system inability
to distinguish “self” from “non self”
• Body manufactures T cells and antobodies
directed against its own cells
Most common examples
• Systemic lupus erythematosus
• Antiphospholipid syndrome
Systemic lupus erythematosus
• Suppression of the body’s normal immunity
• Targets skin, joints, kidneys, lungs, cardiac and
nervous system
• In pregnancy , causes inflammation of the
connective tissue of the decidua resulting to
problem in implantation and functioning
Signs and symptoms
• Depends on the target organ
• Most common are fever, malaise, fatigue, weight
loss, skin rashes and polyarthralgia
11 criteria
1. Butterfly rash
2. Rash on face,scalp,ear ,arms, chest
3. Photosensitivity
4. Oral ulcers
5. Arthritis (inflammation of a joining. Usually
accompanied by pain, swelling, and stiffness)
6. Pericarditis (inflammation of the lining around
the heart
7. Renal disorder
8. Neurologic disorder
9. Hematologic disorder
10. Immunologic disorder
11. ANA positive titer (Anti-Nuclear Antibody) -
presence of the antinuclear antibody which is
associated with several autoimmune diseases
Maternal Effects
• If SLE is active during conception, exacerbation
(worsening/increasing in the severity) is
common
• If pt has renal insufficiency (kidneys are no
longer able to handle their jobs) before
pregnancy, disease deterioration is common
Fetal and neonatal effect
• Increase risk of spontaneous abortion
• Intrauterine growth restriction
• Still birth
General Management
• Counselling
• Planning pregnancy
• At least 6 months on remission (reduction or
disappearance of the signs and symptoms)
Drug therapy
• Corticosteroids - prednisone
• Decrease swelling, tenderness and pain
associated with inflammation
• Low dose aspirin
• For pain and anticoagulant
• Anti malaraialagents (hydroxychloroquine)
• Skin rashes
• Cytotoxic agent
Nursing interventions
• Emphasize frequent pre natal visits
• Assess weight gain
• Measure BP each day
• Balance between activity and rest
• Teach prevention and recognition of preterm
labor
• Instruct on skin care
•
• Fetal surveillance
• Evaluate fetal growth by UTZ every 3-4 weeks
after 24 weeks AOG
• Fetal movement counting
• Assess coping styles and ability to cope with
chronic illness
Anti phospholipid syndrome
• Antibodies formed against plasma protein
leading to a pro coagulant state
• Superficial thrombophlebitis
• Deep vein thrombosis
• Pulmonary embolism

Maternal effects
May lead to life threatening event for the mother • Prednisone
(pulmonary emboli, stroke)
Nursing management
Fetal and neonatal effects • Provide adequate information
• Increases pregnancy loss • Collaborate with medical management plan
• Recurrent spontaneous abortion and • Reinforce preconceptual counselling
unexplained 2nd and 3rd trimester fetal death • Interpret clinical information in lay terms
• Increased risk in cardiac or neurologic anomalies • Be vigilant in physical and psychosocial
assessment
Clinical criteria
• Vascular thrombosis Nursing interventions for APLS
• Venous • Discuss medical and pregnancy risks
• Arterial • Pre natal visits
• Fetal loss • Screen for pre eclampsia and pre-term labor
• One or more unexplained fetal death beyond 10 • Teach self adminsitration of prescribed
weeks AOG medications
• One or more preterm birth before 34 weeks AOG • If heparin is used,take 1000mg of calcium,
• 3 or more unexplained consecutive spontaneous Vitamin D and weight bearing exercises
abortion without hormonal or chromosomal • Serial ultrasound every 3 to 4 weeks starting 17
abnormalities to 18 weeks AOG
• 32 weeks- daily fetal movement and BPS
Laboratory criteria (Bronchopulmonary Sequestration)
• Anticardiolipin antibody • Teach prevention and recognition of preterm
• Lupus anticoagulant labor

General management
• Low dose aspirin ( 81 mg)
• Heparin
NURSING CARE OF A FAMILY EXPERIENCING PREGNANCY COMPLICATIONS FROM PRE-EXISTING OR NEWLY ACQUIRED
ILLNESS - PART 4
DIABETES

Diabetes • Retinopathy - damaged of the retia caused by

Disease characterized by the inability to produce or use complications of diabetes
sufficient endogenous insulin to metabolize glucose • Hypoglycemia
properly Fetal and neonatal effects
• Hypoglycemia
3 types • Hyperglycemia
Type 1- absolute insulin deficiency
Type 2- receptor sites are resistant to insulin HYPERGLYCEMIA
Type 3- Gestational Diabetes mellitus
Congenital defects
Gestational diabetes mellitus • Risk is 3 to 5 times more often
Carbohydrate intolerance that is first recognized during • Directly affects the yolk sac development
pregnancy particularly in the 3rd trimester • Neural tube defects
• Congenital cardiac anomalies
Impaired fasting blood glucose (IFG) • GI and renal anomalies
FBS level that is 100 mg/dL or higher but lower than 126 • Directly related to diabetic control in the 3
mg/dL months before conception and the 1st 2 months
of pregnancy
Impaired glucose tolerance
2 hour post prandial blood sugar level higher than 140 Macrosomia
mg/dL but lower than 200 mg/dL • Elevated fetal glucose
• Fetal hyperinsulinemia
Signs and symptoms of GDM in a previous pregnancy • Increase growth and fat deposition
• Prior delivery of an infant weighing more than 9 • Birth trauma
pounds
• Previous stillbirth of an infant with congenital Intrauterine growth retardation
defects Placental insuffiency or vascular disease
• Polyhydramnios
• Hx or recurrent monilial vaginitis Delayed lung maturity
Interfere with production of phosphatidyl glycerol (fetal
Signs of gdm in the current pregnancy surfactant)
• Recurrent monilial vaginitis
• Macrosomia of the fetus on ultrasound Neonatal hypoglycemia
• Polyhydramnios At birth, the supply of increased glucose is suddenly cut
off, but insulin is still produced
Maternal effects
Risk is directly related to glucose control initiated before Learning disabilities
and throughout pregnanc • Fetal brain cell damage and decresaed brain
growth
Risks: • Low intelligence quotient (IQ)
• Spontaneous abortion
• Pre eclampsia Childhood obesity and TYPe 2 diabetes mellitus later in
• Preterm labor life
• Polyhydramnios 70% chance of developing type 2 DM and obesity
• Infection
• Diabetic ketoacidosis - body produces high levels ESTABLISHING DIAGNOSIS
of blood acids called ketones
• Cesarean or instrumental birth and induction Criteria for the diagnosis of GDM
 lispro(Humalog) and
Criteria Aspart (Novolog)
• Fasting plasma glucose (FPG) 126 mg/dl or B. Short acting: regular (Humulin R)
greater after 8 hour fasting C. Intermediate acting:
• Two hour post prandial glucose >200 mg/dl after neutral protamine hagedorn (NPH, Humulin N)
75 g glucose load
• Polyuria, polydypsia and unexplained weight loss Rapid acting insulin
• Works within 10-15 minutes
Two-step approach: glucose challenge test • Shorter duration (3-5 hours)
• Give 50 g of oral glucose, test blood sugar level • Must eat as soon as injection is administered
after 1 hour • Good for high glycemic index foods: bread, rice
• 139 mg/dL or less rules out GDM and potatoes
• More than 139 to 199 mg/dL –follow up with
OGTT Short acting
• If 200mg/ dL or greater, treat as GDM • Onset is 30 minutes or longer
• Duration of 6-8 hours
Two or three hour glucose tolerance test
• 150 g of complex carbohydrates should be eaten Normal serum blood glucose values
for 3 days
Time of Carpenter and National diabetes
• NPO 8 hours before the test measurement coustan critera data group
• Draw an FBS sample
• Start timer, pt drinks 100 g of glucose solution Fasting <95 <105
within 10 minutes
• Blood samples are drawn 1, 2, and 3 hours 1 hour <180 <190

2 hour <155 <165

Antepartum glycemic management 3 hour <140 <145
• Blood glucose monitoring
• Urine testing • Snacks are essential in the morning, afternoon
• Insulin management and bedtime
• Exercise recommendations
• Antepartum fetal surveillance Comparison chart for human insulins

Blood glucose monitoring Type Appearance Onset Peak Duration

• Daily self-monitoring of blood glucose-3 to 10
times per day Rapid acting Clear solution 10-15 1½ 3-5 hrs
• Capillary blood glucose samples are taken before min hr
meals and snacks, 60-90 minutes after meals, at
Short acting Clear 0.5 hr 3-4 hr 6-8 hrs
bed time, ocassionally between 2 -4 AM
• Hb A1c tests every 4-6 weeks Intermediate Cloudy 2-4 hr 2-14 12-24
acting suspension hrs hrs
Urine testing
• Ketones
• Sugar Calculation guidelines for insulin during pregnancy

Trimester Insulin dosage (unit /kg

body weight)
Insulin management
Usual type is biosynthetic human insulin (Humulin) Pre pregnant 0.6

Classification: First trimester 0.7

A. Rapid acting:
 Exercise recommendations
Second trimester 0.8
Exercise can lead to improved sensitivity to insulin after
Third trimester until 36 0.9 4 weeks
weeks
Antepartal fetal surveillance
36-40 weeks 1.0 • Ultrasound
• Maternal alpha-fetoprotein
Post partum 0.6 • Fetal biophysical tests
• Amniocentesis

Diet management
In consideration to pre pregnancy weight, general health
status, dietary habits, activity level and insulin therapy
NURSING CARE OF A FAMILY EXPERIENCING PREGNANCY COMPLICATIONS FROM PRE-EXISTING OR NEWLY ACQUIRED
ILLNESS - PART 5

GASTROINTESTINAL DISORDERS AND PREGNANCY

GASTRO ESOPHAGEAL REFLUX DISEASE/HIATAL Assessment

HERNIA • Experiences nausea and vomiting
• Liver is tender (painful) on palpation
GERD - Reflux of acid stomach secretions into the • Dark yellow urine
esophagus • Hepatomegaly - enlargement of the liver
• Jaundice
HIATAL HERNIA - portion of the stomach extends and
protrudes up through the diaphragm into the chest THERAPEUTIC MANAGEMENT
cavity • Bed rest
• High calorie diet
Symptoms • CS delivery
• Heartburn • Standard infection precautions
• Gastric regurgitation
• Dysphagia – impaired swallowing Inflammatory bowel disease
• Possible weight loss Crohn’s disease – inflammation of the terminal ileus
• Hematemesis - vomiting of blood Ulcerative colitis – inflammation of the distal colon

Management Inflammatory bowel disease

• Antacids • Bowel develops shallow ulcers
• Histamine receptor antagonist (ranitidine) • Woman develops chronic diarrhea, weight loss,
• Proton pump inhibitor (esomeprazole-Nexium) occult blood in stool, nausea and vomiting
• Loose clothing
• Sleep with head elevated Fetal effects
• Interferring with fetal growth
PANCREATITIS • Total rest for GI tract
• Inflammation of the pancreas • Sulfasalazine (Azulfidine)
• Nasogastric suction
• Bowel rest NEUROLOGIC DISORDERS AND PREGNANCY
• Analgesia – pancreatic pain is sharp SEIZURE DISORDER
• Intravenous hydration May be due to head trauma or meninigitis
Common drugs:
Hepatitis • Trimethadione (Tridione)
Liver disease that may occur from invasion of the A,B,C, • Valproic acid
D or E virus • Carbamazepine
• Phenytoin
Hepatitis A
• Spread by fecal-oral contact MUSCULOSKELETAL DISORDERS AND PREGNANCY
• Ingestion of fecally contaminated water or
shellfish SCOLIOSIS
• May be given prophylactic gamma globulin

Hepatitis b & C
• Spread by exposure to contaminated blood or
blood products
• Can be spread by contaminated semen or vaginal
secretions
 Boston Brace

• Lateral curvature of the spine

• Noticed in girls between 12-14 years old

SCOLIOSIS
Surgical Management
ASSESSMENT
• Visible curve fails to straighten when the child
bends forward and hangs arms down toward
feet
• Hips, ribs and shoulders are asymetrical
• Apparent leg length discrepancy

SCOLIOSIS CAN INTERFERE

• With respiration and heart action because of
chest compression
• Pelvic distortion can interfere with childbirth IMPLEMENTATION POST OPERATIVELY
MANAGEMENT • Maintain proper alignment
BRACES • Logroll when turning
• Usually worn 16-23 hours a day • Neurovascular assessment of lower extremity
• Inspect skin for breakdown function
• Keep skin clean • Monitor for Mesenteric Artery Syndrome
• Advise to wear soft non irritating clothes under Disorder (MASD) – mechanical changes in the
the brace position of abdominal contents during surgery
• Unless modified it cannot be worn during the last (emesis/vomiting, abdominal distention)
half of pregnancy
Brace for scoliosis CANCER AND PREGNANCY
Incidence
1 in 1000 pregnancies

First trimester option

• Delay treatment or
• End pregnancy
NURSING CARE OF A FAMILY EXPERIENCING A
COMPLICATION OF LABOR OR BIRTH
DYSTOCIA

Difficult labor Arise from main components:

 Power
 Passenger
 Passageway
 Psyche

Complications with the Power (Force of Labor)

Uterine Contractions INERTIA

• Basic force moving the fetus through the birth canal
• Denotes sluggishness of contractions or force of labor
• Occur because of the interplay of adenosine
triphosphate and electrolytes such as sodium, calcium, Dysfunctional labor
potassium, contractile proteins, epinephrine, HYPOTONIC CONTRACTIONS
norepinephrine, oxytocin, estrogen, progesterone, and • Number of contractions is unusually low or infrequent
prostaglandin
• Resting tone remains less than 10 mmHg
Normal uterine contractions
• 2 phases: • Strength does not rise above 25 mmHg .

Contraction (systole) Relaxation (diastole)
• Pacemaker - situated at the uterine end of the right
fallopian tube
- Moves downward to the cervix and then to the fundus
30 mm Hg or more - initiates cervical dilatation
• Active labor - 50-80 mmHg
Second stage: 100 mmHg
• Early labor: resting tone 5-10 mmHg
• Active labor :12-18 mm Hg
Cervical dilatation during active phase
Nullipara: 1.2 cm/hr
Multipara: 1.5 cm /hr
*May occur after administration of analgesia or if there
is bladder distention
• Occur in uterus which is overstretched, larger than
usual single fetus, hydramnios, or lax uterus
HYPERTONIC CONTRACTIONS
• Increase in resting tone to more than 15 mm Hg
• Occurs frequently in the latent phase of labor
• More painful, myometrium becomes tender because
of lack of relaxation
 Ineffective
 Uterine pacemakers arise in other areas of the
uterus
Danger
*Could lead to fetal anoxia

*Contractions are strong but ineffective

Management

Apply external uterine and fetal monitor

Prepare for possible cesarean birth

UNCOORDINATED CONTRACTIONS  Usually associated with cephalo pelvic
• More than one pacemaker may be initiating disproportion or fetal malposition
contractions or  Prolonged if cervical dilatation does not occur
at a rate of 1.2 cm/hr in a nullipara or 1.5 cm/hr
• Receptor points in the myometrium may be acting in a multipara or
independently  if active phase lasts longer than 12 hrs (primi)
 Longer than 6 hours in multigravida
*Occur erratically, may be difficult for
Management
woman to rest between contractions
*Augmentation of labor - if cephalo pelvic disproportion
Management
(CPD) is not present
• Apply uterine and fetal monitor
• Cesarean birth - malposition
*Oxytocin administration
DYSFUNCTION AT THE 2ND STAGE OF LABOR
Length of phases and stages of normal labor in hours
 PROLONGED DESCENT
Nullipara Multipara  ARREST OF DESCENT
Phase Average Upper Average Upper
PROLONGED DESCENT
Normal Normal
Latent 8.6 20 5.3 14  Occurs if the rate of descent is less than 1.0
Active 5.8 12 2.5 6 cm/hr in a nullipara or 2.0 cm/hr in a multipara
Second 1 1.5 0.25 *  2nd stage lasts over 3 hours (multi)
 Contractions have been of good quality and
DYSFUNCTION AT THE FIRST STAGE OF LABOR proper duration
 Contractions become infrequent and poor
 PROLONGED LATENT quality
 PHASE PROTRACTED ACTIVE PHASE
 PROLONGED DECELERATION PHASE Management

Prolonged latent phase  Rest

 Fluid intake
 Latent phase that is longer than 20 hours in a  IV oxytocin
nullipara or 14 hours in multipara  Artificial rupture of membranes
 Occur if the cervix is not ripe  Artificial rupture of membranes is Amniotomy
 Excessive analgesic
 Uterus in a hypertonic state Arrest of descent

Etiology  Results when no descent has occurred for 1

hour in multipara or 2 hours in a nullipara
• "longing to complete the pregnancy"  *Expected descent or engagement does not
occur
* "having difficulty managing the uncertainty"
 Most common cause is CPD
MANAGEMENT
Pathologic Retraction Ring (Bandl's Ring)
 Rest the uterus
 Hard band forms across the uterus. At the
 Adequate hydration
junction of the upper and lower uterine
 Pain relief
segment
 Providing comfort measures
 Interferes with fetal descent
 Oxytocin to assist labor
 Fetus is gripped and cannot advance beyond
 Amniotomy
the point
 Cesarean birth
MANAGEMENT
PROTRACTED ACTIVE PHASE
  IV morphine sulfate - to relieve a retraction ring Attempted Vaginal Birth with Subsequent Uterine
 Tocolytic Rupture
 Emergency CS
 Danger: uterine rupture, neurologic damage to
fetus

Precipitate labor

 Uterine contractions are so strong

 Woman gives birth within a few contractions
 Completed in less than 3 hours
 Primipara- dilation is 5 cm or more /hour
 Multipara- 10 cm /hr
 Detected in the active phase

UTERINE RUPTURE

 Occurs when uterus undergoes more strain

than it is capable of sustaining
Uterine Rupture Following Previous Cesarean Section
Contributing Factors Copyrighted

 Prolonged labor Mal Condition During Labor

 Abnormal presentation
 Multiple gestation
 Unwise use of oxytocin
 Obstructed labor
 Traumatic maneuvers of forceps or traction

Complete rupture

 Contractions stop
 Two distinct swellings are visible
 Signs of shock

INCOMPLETE RUPTURE

 Localized tenderness
 Persistent, aching pain at the lower uterine
segment

Management

 Fluid replacement therapy

 IV oxytocin - for contraction and to minimize
bleeding
 Possible laparotomy (hysterectomy and tubal
ligation)
INVERSION OF THE UTERUS

 Uterus turns inside out

 May occur if traction is applied to the umbilical
cord to remove the placenta
 Pressure applied to the fundus if not
contracted
 If placenta is attached at the fundus


Signs and symptoms when amniotic fluid embolism

already reaches in other lungs:

 Hypotension: Blood pressure may drop

significantly with loss of diastolic measurement.
 Dyspnea: Labored breathing and tachypnea
may occur.
Signs of inverted uterus
 Seizure: Tonic clonic seizures are seen in 50% of
 Sudden gush of blood patients.
 Fundus not palpable in the abdomen  Cough: This is usually a manifestation of
 Signs of blood loss dyspnea.
 Cyanosis: As hypoxia/hypoxemia progresses,
MANAGEMENT circumoral and peripheral cyanosis and changes
in mucous membranes may manifest.
 Never replace the inversion  Fetal bradycardia: In response to the hypoxic
 Never attempt to remove placenta if still insult, fetal heart rate may drop to less than 110
attached beats per minute (bpm). If this drop lasts for 10
 Start an IV fluid line minutes or more, it is a bradycardia. A rate of
 Administer oxygen *Assess vital signs 60 bpm or less over 3-5 minutes may indicate a
 Tocolytic agent to relax uterus terminal bradycardia.
 General anesthesia  Pulmonary edema: This is usually identified on
 Manual replacement chest radiograph.
 Oxytocin  Cardiac arrest
 Antibiotic therapy  Uterine atony: Uterine atony usually results in
excessive bleeding after delivery. Failure of the
AMNIOTIC FLUID EMBOLISM
uterus to become firm with bimanual massage
 Amniotic fluid is forced into an open maternal is diagnostic.
uterine blood sinus through defects in the  Coagulopathy or severe hemorrhage in absence
membrane, rupture of the membrane, of other explanation (Disseminated
premature separation of the placenta Intravascular Coagulation - DIC occurs in 83% of
 Woman in strong labor sits up suddenly grasp patients.
her chest because of sharp pain and inability to  Altered mental status/confusion/agitation
breathe
MANAGEMENT
 Pale and bluish gray
 Oxygen administration
  Flat or in a slight Trendelenburg position - to
improve the venous blood return and perfusion
of the central nervous system.
 Fluid therapy
 Administration of pharmacological agents
 Electrocardiographic monitoring to detect and
treat arrhythmias

PROBLEMS WITH PASSENGER

BIRTH COMPLICATIONS

 Premature infant
 Prolapse of the umbilical cord
 Multiple gestation
 Problems with fetal position, presentation or
size ASSESSMENT:
It tends to Occur with the following conditions:  Cord may be felt as the presenting part on an
initial vaginal examination.
 Premature rupture of the membranes
 It also can be identified during sonogram
 Fetal presentation other than cephalic
 CS is necessary before rupture of the
 Placenta previa
membranes occurs.
 Intrauterine tumor preventing the presenting
 Membrane rupture - causes the cord to slide
part to engage
 A small fetus down into the vagina from the pressure exerted
 CPD preventing from engagement by the amniotic fluid.
 Cord prolapse is first discovered only after the
 Hydramnios
membranes have ruptured.
 Multiple gestation
 Variable deceleration FHR pattern suddenly
Prolapse of the umbilical cord becomes apparent

Premature Rupture of Fetal Membranes with Prolapse

of Umbilical Cord
THERAPEUTIC MANAGEMENT:

 Relieve pressure on the cord - to relieve

compression and the resulting fetal anoxia.
 Placing the gloved hand in the vagina and
manually elevating the fetal head off the cord.
 Place the woman in a knee-chest or
Trendelenburg position which cause the fetal
head to fall back from the cord.
 Administer oxygen at 10 L/min by face mask to
the mother help improve oxygen to the fetus
 Tocolytic agent
  If the cord has prolapsed to the extent that it is Common multiples are two and three, known as
already exposed to room air, drying will begin twins and triplets.
leading to atrophy of the umbilical vessels. Do  Multiple birth siblings are either monozygotic or
not attempt to push any exposed cord back into dizygotic.
the vagina. This may add to the compression by
causing knotting or kinking. MULTIPLE PREGNANCY
 Cover the exposed portion with a sterile saline
• Terminology
compress to avoid drying.
 If the cervix is fully dilated at the time of Monozygotic - multiple (typically two) fetuses produced
prolapse, deliver the infant quickly, possibly by the splitting of a single zygote
with forcep - to prevent fetal anoxia.
 If dilatation is incomplete, the birth method of Dizygotic - multiple (typically two) fetuses produced by
choice is upward pressure on the presenting two zygotes
part
Polyzygotic - multiple fetuses produced by two or more
zygotes
Knee chest position
Presentation

 First twin presents vertex, one twin transverse:

75%
 Both twins vertex: 45%
 One twin vertex, one twin Breech: 37%
 Both twins Breech: 10%

AMNIOINFUSION
• Addition of sterile fluid into the uterus

• Prevents additional cord compression

*Sterile catheter is introduced

*Warmed normal saline or Lactated Ringer

Complications:

A. ANTEPARTUM
1. Premature labor

2. Congenital malformations - twice as high singletons

3. Higher spontaneous abortion rate

4. Higher incidence of maternal anemia

5. Pregnancy induced hypertension

MULTIPLE GESTATION
6. Hydramnios
 Occurs when more than one fetus is carried to
term in a single pregnancy. B. INTRAPARTUM
 Different names for multiple births are used, 1. Placenta previa
depending on the number of offspring.
2. Abruptio placenta • Be prepared for postpartum hemorrhage, i.e. oxytocin
use postpartum, large-bore IV is in place, blood
3. Dysfunctional or prolonged labor available for transfusion.
4. Abnormal fetal presentation • Placenta and membranes should be examined and
sent to Pathology.
5. Cord prolapse

6. Higher incidence of cesarean section

Problems with Position, Presentation, or Size
C. POSTPARTUM: Occipitoposterior Position:
1. Greater incidence of maternal blood transfusions • In approximately one tenth of all labors, the fetal
position is posterior rather than anterior.
2. Postpartum hemorrhage/uterine atony
• The occiput is directed diagonally and posteriorly,
MANAGEMENT: either to the right (ROP) or to the left (LOP).

Antepartum Management: • In these position, during internal rotation, the fetal

 All pregnancies complicated by multiple
gestation are high risk and need specialized
antepartum, intrapartum, and postpartum care
and management.
 Encourage bed rest beginning at 20 weeks with
twins, earlier with triplets.
 Patients must be instructed as to signs and
symptoms of premature labor, premature
rupture of membranes and preeclampsia.
 Screen for diabetes at time of diagnosis and
repeat at 26-28 weeks. May screen earlier and
more often with positive family history.
 Serial ultrasounds (q 4 weeks) for fetal growth.
Intrapartum Management:
head must rotate, not through a 90 degree arc, but an
approximately 135 degrees.
MANAGEMENT:
 Pain reliever
 Counter pressure on the sacrum (back rub,
change position)
 Apply hot and cold (which ever feels best) -
Position lying on the side opposite the fetal
back
 Maintain knee position to help the baby rotate
 Empty the bladder
 Determine the last time she ate
 CS if contractions are ineffective

 Delivery should occur at a hospital with the

appropriate level of care (Obstetric and
Pediatric). In preterm gestations (<37 weeks)
maternal transport to Tertiary Center for
delivery should be considered.
 Two obstetricians should be available for
delivery.
 Anesthesia personnel should be available in the
Delivery Room.
 Appropriate personnel skilled in neonatal
resuscitation should be present in the Delivery
Room (one pediatrician and one nurse for each
neonate).

MANAGEMENT: BREECH PRESENTATION:

* Continuous fetal monitoring must be employed
• Cesarean section is advisable for all breech-vertex
and other abnormal presentations (interlocking twins)
and for all pregnancies with three or more fetuses.
Most fetus are in breech presentation early in
pregnancy. By week 38, a fetus normally turns to
cephalic presentation.
  Fetal head presenting at a different angle than
expected
 Eg. Face and brow presentation

ASSESSMENT:

 Head feels more prominent than normal, with

no engagement apparent on leopold's
maneuver.
 Head and back are both felt on the side of the
uterus.
Breech Presentation:
 The back is difficult to outline because it is
 NORMAL concave
 COMPLETE  If the back is extremely concave, fetal heart
 FOOTLING tone may be transmitted to the forward-thrush
chest.
CAUSES OF BREECH PRESENTATION
Face presentation
 Gestational age less than 40 weeks
 Abnormality in fetus (hydrocephalus,
anencephaly)
 *Hydramnios that allow for free movement, the
fetus fits within the uterus in any position.
 Congenital anomaly of the fetus (midseptum, it
traps the fetus in a breech position)
 Any space occupying mass in the pelvis
 Pendulous abdomen, the uterus will fall
forward.
 Multiple gestation -presenting infant cannot
turn to a vertex position
High Risks:
ASSESSMENT:
• Contracted pelvis or placenta previa
 Fetal heart rate usually heard high in the
*Relaxed uterus of a multipara or prematurity
abdomen
 Leopold's maneuver, ultrasound and *Hydramnios
vaginal exam can reveal the presentation . In a
breech birth, the mechanism of labor are the *Fetal malformation
same in vertex birth.
 Monitor FHR and uterine contractions *This is a warning sign -something abnormal is causing
continuously, the face presentation.
 if possible to allow early detection of fetal
MANAGEMENT:
distress.
-Ultrasound to confirm
Face Presentation
• Measurement of the pelvic diameter
 Presenting part is the face
 A face presentation is confirmed by vaginal Note:
examination, when the nose, mouth or chin can
be felt as the presenting part. *if the chin is anterior - NSD

*if the chin is posterior - CS

Asynclitism
Take note:
*otherwise it would be necessary to wait for long
posterior to anterior rotation to occur and can possibly
result to uterine dysfunction.
*Observe the infant for patent airway
*Babies born after face presentation have a great deal
of facial edema.
* Some infant, lip edema is severe that they unable to
suck for a day or two.
*Gavage feeding may be necessary to allow the infant
to obtain enough fluid until he/she can suck effectively.
*The infant may be transferred to the ICU for the first
24 hrs.
*Reassure the parents that edema is transient and will
disappear in a few days.
BROW PRESENTATION
*It occurs in multipara with relaxed abdominal muscles.
*It almost invariably results in obstructed labor,
because the head becomes jammed in the brim of the
pelvis as the occipitomental diameter presents.
•CS will be necessary to deliver the infant safely.
TRANSVERSE LIE
* It may occur in infant with hydrocephalus or
abnormality that prevents the head from engaging.
*A transverse lie usually obvious during inspection.
example of horizontal lie
OVERSIZED FETUS (Macrosomia)
*Size may become a problem in a fetus who weighs
more than 4,000 to 4,500 g (Approximately 9 to 10 lbs)
. Most frequently born to women who enter pregnancy
with diabetes or develop gestational diabetes.
• Oversized infant may cause uterine dysfunction
during labor or birth because of overstretching of the
fiber of the myometrium.
*For oversized fetus, CS is the birth method of choice.
example of normal newborn size while isa is
macrosmia
SHOULDER DYSTOCIA
 A birth problem that is increasing in incidence
along with the increasing average weight of
newborns.
 The problem occurs at the second stage of
labor, when the fetal head is born but the
shoulders are too broad to enter and be born
through the pelvic outlet.
 This is hazardous to the mother because it can
result in vaginal or cervical tears.
 It is also hazardous to the infant if the cord is
compressed between the fetal body and the
bony pelvis.
 PROBLEMS WITH THE PASSAGE

FETAL ANOMALIES
*Hydrocephalus - fluid filled ventricles

*Anencephaly - absence of the cranium Relationship between the passage and the fetus

Hydrocephalus  Engagement
 Station
 Fetal position

The Birth Passage

*Implications of Pelvic types for Labor and Delivery

Anencephaly

CEPHALOPELVIC DISPROPORTION (CPD)

*Disproportion between the size of the normal fetal
head and the pelvic diameters.

*This results in failure to progress in labor.

Inlet Contraction
*Narrowing of Anteroposterior AP diameter to less than
11 cm or
• Transverse diameter to 12 cm or less
*Engagement will not occur
• Measure pelvis before 24 weeks of pregnancy
*CPD-floating-malposition-ROM-cord prolapse
Outlet Contraction
• Narrowing of the transverse diameter at the outlet to
less than 11cm. This is the distance between the ischial
tuberosities, a measurement that is easy to make during
prenatal visit, so the narrow diameter can be
anticipated before labor begins
CEPHALOPELVIC DISPROPORTION (CPD)
• Is the turning of a fetus from a breech to a cephalic
position before birth.
• It may be done as early as 34 to 35 weeks, although
the usual time is 37 to 38 wks of pregnancy.
MANAGEMENT:
- During the procedure, FHR and possibly ultrasound are
recorded continuously,
*Tocolytic agent may be given.
*The breech and vertex position of the fetus are located
and grasped transabdominally by the examiner's hands
on the woman's abdomen.

*Gentle pressure is then exerted to rotate the fetus in a

forward direction to a cephalic lie.

External Cephalic Version

1. The baby is in breech position.

2. The doctor feels for the baby's head and bottom.

3. The doctor turns the baby around.

4. The baby is now for normal delivery.

TRIAL LABOR
*If a woman has a borderline inlet measurement and
the fetal lie and position are good, her physician or
nurse midwife may allow her a " trial labor" to
determine whether a labor can progress normally.

*A trial labor continues as long as descent of the

presenting part and dilatation of the cervix are occuring.

MANAGEMENT

* Monitor uterine contraction and monitor fetal heart Contraindication:

sound continuously.
*Multiple Gestation
• Urge the woman to void every 2 hrs- to empty the
bladder to allow the fetal head to use all space • Severe Oligohydramnios
available.
*Cord coil
• After rupture of the membranes, assess FHR carefully
(if the fetal head is still high, there is an increased *Unexplained third trimester bleeding
danger of prolapsed of the cord or fetal anoxia.

External Cephalic Version

 *Deep attachment of the placenta in the uterine
myometrium, placenta will not loosen and deliver

Anomalies of placenta and cord • Manual removal may lead to hemorrhage

*Hysterectomy or treatment with methotrexate to

destroy the still-attached tissue.

Type Description Percent

Placenta An invasion of the myometrium 75-78%
accreta which does not penetrate the
entire thickness of the muscle.
This form of the condition
accounts for around 75% of all
cases.
Placenta Occurs when the placenta further 17%
Increta extends into the myometrium.
NORMAL PLACENTA Placenta The worst form of the condition is 5-7%
Percreta when the placenta penetrates the
Placenta & Cord - examined for anomalies after birth entire myometrium to the uterine
NORMAL PLACENTA: serosa (invades through entire
• Weighs 500g (approximately 1/6 of the fetus) uterine wall). This variant can
lead to the placenta attaching to
* Diameter 15-20 cm other organs such as the rectum
or bladder.
*Thickness 1.5 to 3.0 cm Type:
*Enlarged in women with diabetes placenta accreta
*So large in women with syphilis or erythroblastosis - Description:
1/2 the fetus' wt.
An invasion of the myometrium which does not
* If uterus has scars or septum - placenta may be wide penetrate the entire thickness of the muscle. This form
in diameter to find implantation space of the condition accounts for around 75% of all cases.
Placenta succenturiata Percent:
*Placenta that has one or more accessory lobes
connected to the main placenta by blood vessels 75-78%

• Placenta appears torn at the edge - Remaining lobes Vasa Previa

removed manually - Umbilical vessels of a velamentous cord insertion cross
the cervical os, & therefore deliver first before
Battledore placenta
- Cord is inserted marginally rather than centrally the fetus

*No known clinical significance.
Velamentous insertion of the cord
• Cord separates into small vessels that spreads the
placenta by spreading across a fold of amnion
*Common in multiple gestation
*May result to fetal anomalies
Placenta accreta
*Vessels may tear with cervical dilatation & may result
to sudden fetal blood loss
- Infant needs to be born by cesarean birth
Two-Vessel Cord
• Absence of one of the umbilical arteries is associated
with congenital heart and kidney anomalies
• Loss of the vessel affected other mesoderm germ
layer structures
Unusual Cord length. Induction of labor by oxytocin
*Unusually short umbilical cord- result in premature Oxytocin
separation of the placenta or an abnormal fetal lie
• Pitocin
*Unusually long umbilical cord- results in twist or knot
*10 IU in 1000ml of Lactated Ringer's (LR)
THERAPEUTIC MANAGEMENT OF PROBLEMS OR
POTENTIAL PROBLEMS IN LABOR AND BIRTH *Use infusion pump

Induction of labor Safe induction by oxytocin

*Labor is started artificially
• Proper regulation
Augmentation of labor
*Assess pulse and BP every 15 minutes
• Assisting labor that has started spontaneously but is
not effective * Monitor FHR and uterine contractions
Reasons for inducing labor: * 02 administration- if necessary
• Presence of pre eclampsia • Observe for signs and symptoms of H2O intoxication -
due to antidiuretic side effect of oxytocin
*Eclampsia
*Monitor I & O
• Severe hypertension
*Keep IVF at 150 ml/hr
* Diabetes
• Keep terbutaline sulfate or magnesium sulfate ready -
• Rh sensitization
to decrease myometrial activity.
*Prolonged rupture of the membrane Intrauterine
Forceps delivery/vacuum extraction
growth restriction

• Post maturity

AUGMENTATION
*For hypotonic, too weak or infrequent contractions

Conditions for induction of labor

•Fetus is in longitudinal lie

* Cervix is ripe, ready for birth

*Presenting part is engaged

*There is no CPD
Indications:
* Fetus is mature
• Woman unable to push
CERVICAL RIPENING
• Cessation of descent in 2nd stage
 Stripping the cervix -separating the membranes
from the lower uterine segment manually, using a • Fetus is in abnormal position
gloved finger in the cervix
*Fetus is distressed
• Hygroscopic suppositories - gradually and gently urge
Before forceps are applied:
dilatation (laminaria technique)

• Prostaglandin gel (misoprostol/Cytotec) -produces • Membranes must be ruptured

cervical dilatation CPD must not be present
• The cervix must be fully dilated
• Woman's bladder, must be empty
Vacuum Extraction
• Disk shaped cup is pressed against the fetal scalp over
the posterior fontanelle
• Little anesthesia is necessary
. Fewer lacerations
Disadvantages:
*Marked caput on the fetus
*Should not be used for premature and if fetal scalp
sampling was obtained
Postpartum Complications
*The changes brought about by involution are
considered to be normal physiologic processes;
however, they border closely between health and
illness because the changes are marked and rapid that a
departure from a condition of wellness is highly
probable.
LESSON: APRIL 25
Postpartum Complications
The changes brought about by involution are
considered to be normal physiologic processes;
however, they border closely between health and
illness because the changes are marked and rapid that a
departure from a condition of wellness is highly
probable.
Hemorrhage
Hemorrhage, defined as uterine blood loss over 500ml.
can occur at anytime during pregnancy but is a major
danger during the immediate post partum period
because of the grossly unprotected area left after
placental delivery.
Hemorrhage classified into two:
1. Early Post partum hemorrhage
 it occurs during the first 24hrs postpartum.
Causes:
A. Uterine Atony - inability of the uterus to maintain a
contracted state.
Factors:
a. Multiple pregnancy
b. Polyhydramnios
C. Excessively large babies
d. Placental accidents (Abruptio and Previa)
Management
Massage
Ice Compress
Oxytocin Administration
Emptying of the bladder
Bimanual extraction
Hysterectomy
B. Lacerations -are accidental tears of the perineum
which occur when episiotomy had not been done or as
extension of an episiotomy.
CLASSIFICATIONS:
1. First degree -involved vaginal mucous membrane and
the skin of the perineum
2, Second degree -involved vaginal mucous membrane,
perineal skin, fascia, and muscles and perineal body
3. Third Degree -involved the vaginal mucous
membrane, perineal skin and muscle, external sphincter
to the rectum either partially or completely.
4. Fourth degree - involved entire perineum, rectal
sphincter and some of the mucous membrane of the
rectum
Management
 Encourage increase fluid intake
 Food high in fiber
 Stool softener for the first week postpartum.
2. Late Post partum hemorrhage
 it occurs after the first 24 hours post partum
Causes:
a. Retained Placental Fragment
Management:
1. Proper inspection of the placenta for completeness
2.D and C (Dilatation and Curettage)
Infection of the Perineum
This condition usually refers to infection of the suture
line and is often localized, so the woman may or may
not have elevated body temperature.
Signs and Symptoms
 Pain, heat and a feeling of pressure in the
perineum
 Inflammation of the suture lines with pus
 One or two stitches may be sloughed away, or
area may be open
Management
• Antibiotic or Analgesic administration
• Sitz bath or warm compress to hasten drainage and
cleanse the area
• Removal of the perineal sutures to open the area for
drainage
• Frequent change of perineal pads to avoid further
infection
Endometritis
Infection on the lining of the uterus and is usually
manifested on the 3rd or 4th day postpartum.
Assessment
 Fever, chills, loss of appetite and general
malaise
 Some with abdominal tenderness
 Uterus painful to touch and not well contracted
 Lochia usually dark brown in color and have a
foul odor
Management
 Antibiotic and analgesic administration
 Oxytocin to promote uterine contraction
 Putting the woman in fowler's position to drain
out the dark brown, fouls smelling lochia
Mastitis
Infection of the breast may occur as early as the 7th day
postpartum or even at the end of lactation.
Assessment
 Cracked nipples
 Localized pain
 Swelling and redness
 Fever and breastmilk becomes scanty
Management
 Cold compress - pain relief
 Warm Compress-reduce inflammation and
edema Good bra support
 Antibiotic
 Discontinue breastfeeding if both breasts are
affected
Thrombophlebitis
Infection of the lining of the blood vessels with
formation of blood clots and is usually an extension of
endometritis.
Assessment
 Elevated body temp, chills and gen. malaise
 Stiffness, pain and redness on the affected part
 Swelling of the leg below the affected part
 Pain in the calf when the foot of the affected leg
is dorsiflexed (Positive Homan's sign)
Management:
 Bed rest with the affected leg elevated to
improve circulation.
 Antibiotics and analgesic to arrest infection
 Avoid rubbing or massaging the affected leg
 Administration of anti-coagulant (heparin)
Sub-involution
 Incomplete return of the uterus to its
prepregnant size and shape
 Results from retained placental fragments,
endometritis, etc
 Uterus is still enlarged and soft
 Lochia still present
Management:
Methergine – to improve uterine tone and complete
involution
If with endometritis – antibiotic is prescribed
Puerperal Infection
After rupture of membranes, pathogens can invade
uterus
Risk of infection is greater if tissue edema & trauma are
present
Management:
Antibiotic – after culture and sensitivity test of the Management
isolated organism
Bladder Training - indwelling catheter will be clamped
and released for a short time, then removed

Peritonitis Urinary Tract Infection

Infection of the peritoneal cavity, usually an extension Prone to develop UTI because bacteria may be
of endometritis introduced into the bladder at the time of
catheterization
Abscess may form in the cul-de-sac of Douglas (lowest
point of the peritoneal cavity) - gravity causes infected Assessment
material to localize there
 Burning sensation during urination
Assessment  Hematuria
 Feeling of frequency to urinate
 Rigid abdomen (guarding)  Low-grade fever
 Abdominal pain  Lower abdominal pain
 High fever
 Rapid pulse Management:
 Vomiting
 Amoxicillin or ampicillin
Management:  Sulfa drugs - contraindicated if breastfeeding
because they cause neonatal jaundice
 NGT insertion - prevents vomiting & rest the  A glass of fluid every hour - to help flush the
bowel infection from her bladder
 IVE or TPN  Analgesic - for pain
 Analgesics - for pain
 Antibiotics - for infection POSTPARTAL PREGNANCY-INDUCED HYPERTENSION
Mild pre-existing hypertension may increase in severity
Pulmonary Embolus during the first few hours or days after birth
Obstruction of the pulmonary artery by a blood clot,
usually a complication of thrombophlebitis Assessment

Assessment  Cardinal symptoms are the same with prenatal

PIH
 Sudden, sharp chest pain  Proteinuria Edema
 Tachypnea  Hypertension
 Tachycardia
 Orthopnea Management:
 Cyanosis
 Treatment are the same with antepartal PIH:
Management:  Bedrest
 Quiet atmosphere
 Oxygen administration  Monitoring of VS & urine output,
 ICU - for continuing care, at risk for cardio  Administration of MgSO4/antihypertensive
pulmonary arrest drugs
 If postpartal PIH is due to retained placental
Urinary Retention fragments - D & C shall be performed and BP
 Bladder sensation for voiding is decreased due will be normal after the procedure
to bladder edema caused by the pressure of
birth EMOTIONAL AND PSYCHOLOGICAL COMPLICATIONS
 Bladder fills to overdistention OF PUERPERIUM
 Permanent damage may occur from loss of Post Partum Blues
bladder tone, leading to permanent
incontinence
  During the postpartal period, as many as 50% of religious training, traumatic events in childhood
women experience some feeling of and delusions.
overwhelming sadness
 They may burst into tears easily or feel let down Situational Factors
or irritable.
 include difficulties related to place, time, or
 This is a temporary feeling after birth
partner.
Assessment  also includes marital discord, boredom, or
negative emotions (anger, fear, shame )
 Tearfulness
 Feeling of inadequacy Physical Factors
 Mood lability
 include physical disorder and use of
 Anorexia
medications that affect the normal sexual
 Sleep disturbance
response
Management
TYPES OF SEXUAL DYSFUNCTIONS
 Reassure the mother
Sexual Desire Disorder/ Hypoactive Sexual Desire
 Anticipatory guidance and individualized
Disorder
support (allow her to verbalized her feelings)
✓characterized by a deficient, absent or extreme
 Keeping the lines of communication always
aversion to and avoidance of sexual activity that caused
open
a marked strain in interpersonal relationships. This
Post Partum Depression disorder affects more women than men.
30% of women experience a more serious level of
Causes:
sadness after birth.
 Hormonal imbalance: testosterone level less
Management
than 300mg/dl in male
 Formal counseling  Boredom or unhappiness in the relationship
 Psychiatric Care  Depression
 Substance abuse
 Prescription drugs: antihypertensives
SEXUAL DYSFUNCTIONS  Traumatic events in childhood
 characterized by inhibition or interference in  Suppression of sexual fantasies
the normal human sexual response cycle.  Dysfunctional family
 may involve both subjective and objective
components of sexual response. Signs and Symptoms:

LIFELONG - no satisfying sexual experience has ever  Lack of interest in sex

occurred.  Infrequent sexual activity
 Engages in sex often only to satisfy partner
ACQUIRED - developed after a period of normal
function; may be limited to certain situations or
partners Treatment:

Removing the cause, treats the disorder

Causes of Sexual Dysfunction:
Sexual Aversion Disorder
Psychologic Factors
 It is characterized by persistent or recurrent
 often associated with negative feelings towards dislike and avoidance of sexual activity or
partner or the sexual activity such as anger, fear genital contact with a sexual partner.
and guilt.  More common in females than males
 may also be due to depression, anxiety, aging,
Causes:
ignorance, stressful situation, inappropriate
Traumatic sexual experience (incest, rape, initial *Enhances the effect of nitric oxide released during
intercourse that caused dyspareunia) sexual stimulation

Causes:

 Traumatic sexual experience (incest, rape, initial

intercourse that caused dyspareunia)
 Rigid religious training childhood
 Repressive Childhood

Treatment:

 Marital therapy
 Psychotherapy if due to painful past sexual
experience
 Behavioral therapy
 Sexual counseling for client and partner
Sexual Arousal Disorder
Partial or complete failure to achieve a physiologic or
psychologic response to sexual activity.
Orgasm Disorder
Delay in or absence of orgasm or premature ejaculation.
ERECTILE DYSFUNCTION
Formerly referred to as impotence, is the inability of a
man to produce or maintain an erection long enough
for vaginal penetration or partner satisfaction.
CAUSES:
 Physical (aging, atherosclerosis, diabetes)
 Side effects of a certain drugs
A. Antihypertensives
Natural Remedy
L-Arginine
L-arginine is an amino acid that the body uses to make
nitric oxide, a substance signals smooth muscle
surrounding blood vessels to relax, which dilates the
blood vessels and increases blood flow. Relaxation of
smooth muscle in the penis allows for enhanced blood
flow, leading to an erection.
Mechanical Devices
 Vacuum constriction device
 Vacuum constriction device (VCD) is an external
pump with a band on it that a man with erectile
dysfunction can use to get and maintain an
erection.

B. Psychotropic drugs Vacuum constriction device:

C. Endocrinologic agents

MANAGEMENT:

 Medications like Viagra, Levitra, Cialis taken

once daily to stimulate penile erection
 Surgical Implant to aid erection and the use of
vacuum pressure are possible alternatives
 Testosterone injections for male may help

Viagra
Interferes with breakdown of biochemical, involved in
smooth muscle relaxation of the corpus cavernosum
necessary to produce erection

Levitra
 Characterized by dyspareunia or persistent genital pain
before, during, or after sexual activity.

VAGINISMUS

 Involuntary contraction of the muscles at the

outlet of the vagina when coitus is attempted.
This muscle contraction prohibits penile
penetration.
 Sexual or psychological counseling is necessary
to reduce this response.

Types:

 Primary
 Secondary

Associated with:

 Vaginal vestibulair syndrome more or less

synonymous to focal vaginitis a so-called
subclinical inflammation. No pain is perceived,
until some form of penetration is tried.
 Urinary tract infections or vaginal yeast
infections.
 sexual abuse, rape, or attempted sexual abyse
 Knowledge of (or witnessing) sexual or physical
Premature Ejaculation
abuse of others, without being personally
 orgasm and ejaculation occurring before, during abused domestic violence or conflict in the early
or shortly after penetration and before the man home environment having been taught that sex
desires is immoral, vulgar, or demoralizing fear of pain
 often cause is a combination of psychologic and associated with penetration, particularly the
physiologic factors popular misconception of
 rapid ejaculation, rapid climax,  'breaking' the hymen upon the first attempt at
premature climax, or early ejaculation penetration, or the idea that vaginal
penetration will inevitably hurt the first time it
CAUSES: occurs
 Being sexualized or told about sex in violent or
 Psychological inappropriately graphic terms before an age at
 Doubt about masculinity which one is comfortable with such information
 Fear of impregnating a woman which prevent  Any physically invasive trauma
the man from sustaining erection  Generalized anxiety
 Stress
Management:
Management
 Wearing of condom
 Relaxation and guided imagery  Psychological
 Mechanical devices (constrictive rings)  Physical –desensitization with vaginal dilators
 Teach partner to avoid excessive stimulation  Botox treatment-anesthetic agent
Intracavernous Pharmacotherapy DYSPAREUNIA / VESTIBULITIS
Injection of vasodilator directly into the penis to help
control premature ejaculation and sustain erection  Pain during coitus
 Vestibulitis – inflammation of the vestibule.
Sexual Pain Disorder
CAUSES:
  Endometriosis (abnormal placement of Normal is 20 million/ml of seminal fluid
endometrial tissues)
 Vaginal infection Congenital anomalies:
 Hormonal changes (cases like menopause)
a. Varicocele - abnormal dilatation of the veins of
 Psychological factor
the spermatic cord
MANAGEMENT: b. Cryptorchidism - failure of one or both testes to
descend from the abdominal cavity to the srotum
 Encouraging open communication between
sexual partners Obstructed or impaired sperm motility
 Serotonergic antidepressant may help Obstruction may occur at any point along the pathway
 Sexual counseling may help to reduce stress to
 Mumps orchitis - testicular inflammation and
alleviate the problem.
scarring due to mumps virus
 Lubricants
 Epididymitis
NURSING CARE OF THE SUBFERTILE COUPLE:  Tubal infections
Infertility
Ejaculation problems
Inability to conceive a child or sustain a pregnancy to
birth  Psychological problems
 CVA
Subfertility
 DM
Couples have the potential to conceive but they are just
 Drugs
less able to do this without additional help.
 Primary - If man has never been able to achieve
Pregnancy has not occurred for at least a year of erection and ejaculation
unprotected coitus  Secondary –man has been able to achieve
ejaculation in the past but now has difficulty
Primary subfertility
There have been no previous conceptions.
Female Subfertility Factors
Secondary subfertility
There have been a previous viable pregnancy but the  Anovulation
couple is unable to  Tubal transport problems
 Uterine problems
conceive at present  Cervical problems
 Vaginal problems
Sterility
Inability to conceive because of a known condition, such Anovulation
as the absence of a uterus
 May be secondary to Turner’s Syndrome
Male subfertility factors (hypogonadism)- non-functional ovaries
 Hormonal imbalance
 Disturbance in spermatogenesis  Ovarian tumors
 Obstruction in the seminiferous tubules, ducts  Exposure to x-ray
or vessels preventing movement of  Poor diet
spermatozoa  Stress
 Qualitative or quantitative changes in the
seminal fluid preventing sperm motility Tubal transport problems
 Development of autoimmunity that immobilizes
sperm  Scarring in the fallopian tube
 Problem in ejaculation  Previous tubal ligation
 Pelvic inflammatory disease
Inadequate sperm count
Number of sperm in a single ejaculation or in a milliliter Uterine problems
of semen
 Tumors
 Congenitally deformed uterine cavity
  Hormonal imbalance  Record BBT
 Endometriosis  Dip in BT, then rises to a level not higher than
the normal BT
Cervical problems
In vitro fertilization
 Stenotic cervical os or obstruction The woman is stimulated with injected medications to
 Cervical infection develop multiple follicles in the ovaries. Each follicle
 Scar tissue contains a microscopic egg. These injections continue to
 Tightening of cervical os stimulate follicle and egg growth and development for
about 8 - 10 days.
Vaginal problems
Blood and ultrasound testing is done every 1-3 days to
 Acidic vaginal pH
monitor the development of the follicles (egg-
 Sperm immobilizing
containing structures) in the ovaries.
 Sperm agglutinating antibodies
We need to get a minimum number of 3 follicles to
FERTILITY ASSESSMENT
develop to maturity in order to be able to proceed with
 HEALTH HISTORY the egg retrieval.
 MENSTRUAL HISTORY
When a sufficient number of the woman's follicles are
 PHYSICAL ASSESSMENT
mature, a transvaginal ultrasound-guided egg retrieval
 FERTILITY TESTING
(egg aspiration) procedure is performed to remove the
FERTILITY TESTING eggs from the follicles
SEMEN ANALYSIS
The average duration of the egg retrieval procedure is
OVULATION MONITORING under 10 minutes, with a range of about 2-15 minutes

TUBAL PATENCY ASSESSMENT Powerful anesthesia medications are used so that the
woman is "out" during this procedure and does not feel
SEMEN ANALYSIS or remember anything.

 Man ejaculates by masturbation into a clean dry

specimen jar after 2-4 days of sexual abstinence
 Repeat after 2-3 mos
 Spermatogenesis (30-90 days) - production of
sperm cells

The eggs are then fertilized in the laboratory with

partner's sperm

The embryos are cultured in the IVF laboratory for 2-6

days.

The embryo transfer procedure is done which places

the embryos in the woman's uterus where they will
hopefully implant and develop to result in a live birth
Ovulation monitoring
 DIAGNOSTIC TESTS
 Chest radiography
 Bronchography
 Pulmonary function studies

Disorders of the upper respiratory tract

TONSILLITIS
 Infection and inflammation of the palatine
tonsils
 Adenitis (infection and inflammation of the
adenoid or pharyngeal tonsils)

ASSESSMENT
 Painful swallowing
 Drooling of saliva
 Fever
Lesson 3: April 27, 2022  Lethargy
Nursing care of a family when a child has Respiratory  Pus
Disorder  Change in speech quality
 Difficulty of hearing
ASSESSING RESPIRATORY ILLNESS IN CHILDREN CROUP
 Inflammation of the larynx, trachea and major
PHYSICAL ASSESSMENT bronchi
 COUGH  H. Influenzae
 RATE AND DEPTH OF RESPIRATION  Barking cough
 RESTLESSNESS  Inspiratory stridor
 CYANOSIS  Marked retractions
 CLUBBING OF FINGERS
 ADVENTITIOUS BREATH SOUNDS CROUP Management
 CHEST DIAMETER  Run the shower or hot water tap in a bathroom
until the room fills with steam
LABORATORY TESTS  Cool moist air with corticosteroid
 ARTERIAL BLOOD GAS ANALYSIS  Epinephrine for bronchodilation
 NASOPHARYNGEAL CULTURE ASPIRATION
 SPUTUM ANALYSIS  Inhalation of a foreign object into the airway
 Choking, hard forceful coughing
  Or the child may not be able to cough at all  Tuberculosis
ASPIRATION MANAGEMENT
 Subdiaphragmatic abdominal thrusts “Heimlich
Maneuver” Bronchitis
 Inflammation of the major bronchi and trachea
 Influenza viruses
 Adenovirus
 Mycoplasma pneumoniae
 Fever
 Dry hacking cough
 Rhonchi and rales on auscultation

Asthma (Grk-panting)
 Due to hypersensitiveness to allergens
 Mast cells release histamine and leukotrienes
 Inflammation
 Bronchoconstriction
 Mucus production
Place the infant stomach-down across your forearm and Asthma -Allergens
give a five quick, forceful blows on the infant’s back  Pollens
with heel of you hand  Molds
Newborn  House dust
 Food
 Other air pollutants
Therapeutic Management
 Avoidance of allergen
 Skin testing and hyposensitization
 Pharmacologic agents

Pneumonia
 Infection and inflammation of the alveoli
 Pneumococcal, streptococcal, staphylococcal or
viral in origin
 Maybe hospital acquired
(pneumo/streptococcal)
 Community acquires (chlamydial/viral)
Toddler
 Assessment findings: depend on causative
agent

Tuberculosis
 CA: Mycobacterium tuberculosis
 Primary infection: cough,anorexia, weight
loss,night sweat and low grade fever
 Primary complex in children

Tuberculosis Assessment
 Mantoux test /purified protein derivative test-
positive reaction 5-15 mm of reddened
Disorders of the lower respiratory tract induration
 Bronchitis  Chest radiograph
 Asthma  Sputum exam
 Influenza Therapeutic Management
 Pneumonia
  INH –drug of choice, add Pyridoxine (Vitamin
B6)
 Rifampin -2nd drug of choice, used in
combination with INH
 Ethambutol

Cystic Fibrosis
 Generalized dysfunction of the exocrine glands
 Tenacious secretions in the pancreas and lungs
 Abnormality in chromosome 7, sweat contains
much chloride
 Sweat testing-presence of sodium chloride (
Incentive Spirometry
n=20 mEq/L)
 Expand your lungs to fully help you breathe
 Lack of weight gain
fully
 Feeding problem
 Balls are your guide
 Large and greasy stool
 Respiratory infection

THERAPEUTIC TECHNIQUES
EXPECTORANT THERAPY
 Liquefying agents
 Humidification
 Vaporizers
 Nebulizers
 Coughing
 Mucus clearing device (flutter device)
 Chest physiotherapy
Therapy to Improve Oxygenation
 Oxygen administration
 Incentive spirometry
 Breathing techniques
 Tracheostomy
 Intubation
 Assisted ventilation

Chest Physiotherapy
 Performed by physical respiratory therapist
 To helps loosen the phlegm in the secretions in
the lungs.
 Prior to suctioning of the lungs
 Nursing care of a family when a Child Has a
Tracheostomy Cardiovascular Disorder
 Placed in the hole to keep the patient
breathing
 Tracheotomy
Pulmonary valve >
Blood Flow
From SC, svc & IVC Heart diseases in children
to RA to RV Via Iv  Embryonic structures necessary for fetal life did
to PA to the LUNGS via Pv not close at birth
to PV to LA to LV via Mv  Heart originally formed inappropriately
to Aorta via Av
Assessment of heart disorders in children
 History
 Physical assessment
 Vital signs assessment
History
 Thorough pregnancy history
 How much activity before a child becomes tired
 Position
 Frequency of infection
 Urination
PA and VS
Three Shunts  Height
Ductus arteriosus.  weight
Ductus venosus  IPPA
Foramen ovale
Diagnostic testing
Electrocardiogram
 Written record of the Electrical voltages
generated by the contracting heart
 Heart rate, rhythm, state of the myocardium
and presence of hypertrophy, ischemia,
necrosis
Hypertrophy - an increase and growth of muscle cells
Ischemia - a condition in which the blood flow (and
thus oxygen) is restricted or reduced in a part of the
body. Cardiac ischemia is the name for decreased blood
flow and oxygen to the heart muscle.
Necrosis - the death of body tissue
 P wave - atrial contraction
 QRS spike - ventricular depolarization
 T wave - ventricular recover/repolarization
Radiography
 Furnish accurate picture of the heart
Echocardiography
 Primary diagnostic test for heart disease
 Locate and study the movements and
dimensions of cardiac structures
Phonocardiography
Phonocardiogram
 Diagram of heart sounds translated into
electrical energy by a microphone placed on a
child’s chest and then recorded as
diagrammatic representation of heart sounds
Congenital heart disorders
MAJOR CLASSIFICATIONS:
1. Acyanotic Heart Disease oxygenated to unoxygenated
blood or left-to-right shunts
2. Cyanotic Heart Disease deoxygenated blood to
oxygenated blood or right-to-left shunts
Four classifications:
 Increased pulmonary blood flow
 Obstruction to blood flow leaving the heart
 Mixed blood flow
 Decreased pulmonary blood flow
Increased pulmonary blood flow
 Blood flow from the left to the right side of the
heart
Disorders with increased pulmonary blood flow
 Ventricular septal defect
 Atrial septal defect
 Patent ductus arteriosus
 Atrioventricular canal defect
Ventricular septal defect
 — right ventricular hypertrophy — ineffective
heart action
 Wide pulse pressure
 Machinery murmur (upper left sternal
border/under left clavicle)
Patent ductus arteriosus

 Easy fatigue
 Loud harsh, pansystolic murmur
 Palpable thrill

VSD
 Opening is present in the septum between
ventricles Therapeutic management
 IV indomethacin
 Left to right shunting
 Ibuprofen
 If small closes on its own
 Cardiac catheterization (6 mos to 1 year) to
 May require surgery (over 3 mm) and
prophylactic antibiotic evaluate heart function and diagnose
cardiovascular conditions
Atrial septal defect
 Abnormal communication between the two
Cardiac catheterization
atria
 Shunting of blood from left to right atria
 Harsh systolic murmur
 Surgery done between 1-3 years old

Disorders with obstruction to blood flow

 Pulmonary stenosis
Assessment  Aortic stenosis
 Harsh systolic murmur  Coarctation of the aorta
 Fixed splitting of the 2nd heart sound Obstruction to blood flow
 Vessel or valve is narrower than usual
Patent ductus arteriosus  Prohibit blood from reaching its intended site
 Ductus arteriosus-connects pulmonary artery to Pulmonary stenosis
the aorta  Narrowing of the pulmonary valve or
 Closes at first breath, at 7-14 days of age pulmonary artery
 Full closure at 3 mos  Asymptomatic or
 Blood shunts from the aorta to the pulmonary  With cyanosis
artery-leads to increased pulmonary pressure  Right sided heart failure
Therapeutic management
Balloon angioplasty
Assessment
 Asymptomatic
 Typical murmur
 Thrill
 Faint pulses
 Hypotension
 Tachycardia
 Inability to suck
 Chest pain similar to angina
Therapeutic management
 Beta blocker
 Calcium channel blocker
 Balloon valvuloplasty
 Prosthetic valve

Aortic stenosis
 Stricture of the aortic valve prevents blood from
passing freely from the left ventricle of the
heart into the aorta
 Increased pressure and hypertrophy of the left
ventricle occur
 Back pressure in the pulmonary veins
 Pulmonary edema Coarctation of the aorta
Aortic stenosis  Narrowing of the lumen of the aorta due to a
constricting band
 Blood pressure increases proximal to the
coarctation and decreases distal to it
 Elevated upper body blood pressure
 Headache vertigo
 Exceptional irritability
 Epistaxis
 CVA
 Absence of palpable femoral pulses
 Leg pain on exertion
 Collateral arteries enlarge
Coarctation of the aorta Mixed disorders
Mixing of blood from the pulmonary and systemic
circulation in the heart chambers
Transposition of the great arteries
Transposition
 Aorta rises from the right ventricle instead of
the left
 Pulmonary artery arises from the left ventricle
instead of the right
Assessment
 Cyanotic
 Low oxygen saturation
 Enlarged heart
Therapeutic management Therapeutic management
 Digoxin  Surgical correction
 Diuretics  1-3 months of age
 Interventional angiography  PGE (prostaglandin) to keep ductus arteriosus
 Scheduled by two years of age, children achieve patent
the greater part of their adult height Disorders with decreased pulmonary blood flow
Involve some type of obstruction to blood flow in the
pulmonary artery

Tricuspid atresia
Tricuspid atresia

Disorders of mixed blood flow

 Allows no blood to flow from the right atrium to

the right ventricle
 Blood crosses through patent foramen ovale
into the left atrium bypassing the lungs
 Shunted back to PDA for oxygenation
Assessment
 Extreme cyanosis
 Tachycardia
 Dyspnea
 IV infusion of PGE1
 Glen Shunt baffle/Fontan procedure
 Fontan procedure
 Tetralogy of fallot
TOF/TET

 Pulmonary stenosis
 VSD
 Overriding aorta
 Hypertrophy of the R ventricle
Assessment
 Polycythemia
 Dyspnea
 Growth restriction
 Clubbing of the fingers
 Syncope (fainting)
 Hypoxic episode (tet spells)
Therapeutic management
 Surgery 1-2 years old
 Knee-chest position
 Inderal –beta blocker
 Blalock-Taussig procedure
 BLALOCK-TAUSSIG procedure
MAY 25, 2022
FINALS
NCM 109 LEC: CARE OF MOTHER, CHILD AT RISK OR WITH PROBLEMS (ACUTE AND CHRONIC)
LESSON 1:
NURSING CARE OF CHILDREN WITH ALTERED HEMATOLOGICAL FUNCTION

REVIEW OF STRUCTURE AND FUNCTION OF

BLOOD

HEMATOLOGIC SYSTEM

Overview of Anatomy and Physiology ERYTHROCYTES OR RBC

The structures of the hematologic or hematopoietic
system include the blood, blood vessels, and
blood-forming organs (bone marrow, spleen, liver,
lymph nodes, and thymus gland). The hematologic
system also plays an important role in hormone
transport, the inflammatory and immune
responses, temperature regulation, fluid
electrolyte balance, and acid-base balance.
❖ RBC's travel through the body delivering
oxygen and removing waste.
❖ RBC's are red because they contain a protein
chemical called hemoglobin which is bright
red in color.
❖ Hemoglobin contains iron, making it an
excellent vehicle for transporting oxygen and
carbon dioxide.

BONE MARROW

A.Contained inside all bones, occupies interior of

spongy bones and center of long bones;
collectively one of the largest organs of the body
(4%-5% of total body weight)

B. Primary function is hematopoiesis (All blood

cells start as stem cells in the bone marrow; these LEUKOCYTES OR WBC
mature into the different, specific types of cells
❖ These are battling blood cells.
collectively referred to as formed elements of blood
or blood components: erythrocytes, leukocytes ❖ The white blood cells are continually on the
and thrombocytes look out for signs of disease.
❖ When a germ appears the WBC will:
BLOOD - produce protective antibodies.
- surround it and devour the bacteria.
Composed of plasma (55%) and cellular
components (45%)

Plasma

A. Liquid part of blood; yellow in color because of

pigments
B. Consists of serum (liquid portion of plasma) and
fibrinogen
C. Contains plasma proteins such as albumin, WHITE BLOOD CELLS AND THEIR
serum globulins, fibrinogen, prothrombin. FUNCTIONS

TYPE FUNCTION
CELLULAR COMPONENTS
1. Neutrophils Phagocytosis -process
of destroying bacteria,
viruses, or foreign
bodies
 2. Eosinophils Allergic reactions

3. Basophils Inflammatory reactions

4. Monocytes Phagocytosis, antigen

(macrophages) processing

5. Lymphocytes Humoral immunity (B

cells), cellular
immunity (T cell)

THROMBOCYTES OR PLATELETS
RESPIRATORY MANIFESTATIONS
❖ Smallest cells in the blood.
❖ They are irregularly shaped, colorless ❖ Dyspnea on exertion
bodies that are present in blood.
❖ Decreased oxygen saturation levels
❖ Their sticky surface lets them form clots to
stop bleeding. NEUROLOGIC MANIFESTATIONS
ERYTHROCYTES/RBC DISORDERS ❖ Increased somnolence and fatigue
❖ Headache
ANEMIA
Reduction in the total number of erythrocytes in the
MACROCYTIC-NORMOCHROMIC ANEMIAS
circulating blood or in the quality or quantity of
hemoglobin ❖ Also termed megaloblastic anemias
❖ Impaired erythrocyte production ❖ Characterized by very large nuclueated,
immature erythrocyte but normal
❖ Acute or chronic blood loss
hemoglobin concentrations.
❖ Increased erythrocyte destruction - Caused by deficiencies in vitamin B₁2
❖ Combination of the above or folate
- Coenzymes for nuclear
GENERAL SIGNS OF ANEMIA maturation and the DNA
synthesis pathway
1. Fatigue, pallor, dyspnea, and tachycardia - Results in the unequal growth of the
2. Severe anemia may lead to angina if oxygen nucleus and cytoplasm
supply to the heart is insufficient.
3. Chronic severe anemia may cause CHF
(Congestive Heart Failure)
4. Other affects may include hair and skin
changes.

KEY FEATURES OF ANEMIA

INTEGUMENTARY MANIFESTATIONS

❖ Pallor of ears, nail beds, palmar creases,

conjunctiva, and around mouth
❖ Cool to touch 1. PERNICIOUS ANEMIA
❖ Intolerance of cold temperatures
Results in vitamin B₁₂ deficiency related to
❖ Nails become brittle, overtime become
vegetarian diets, or diets lacking in dairy products,
concave and fingers are club-like in
or poor absorption of B₁2 in conditions such as
appearance.
small bowel resection, tapeworm, or overgrowth of
intestinal bacteria
CARDIOVASCULAR MANIFESTATIONS
❖ Loss of appetite, abdominal pain, beefy red
tongue (atrophic glossitis), icterus
❖ Tachycardia, murmurs, gallops when
(jaundice), and splenic enlargement
anemic, severe orthostatic hypotension
Treatment
Parenteral or high oral doses of vitamin B₁2
2. FOLATE DEFICIENCY ANEMIA
❖ Absorption of folate occurs in the upper small
intestine
❖ Similar symptoms to pernicious anemia
except neurologic manifestations generally
not seen -Not dependent on any other factor
Treatment
requires daily oral administration of folate
MICROCYTIC-HYPOCHROMIC ANEMIAS
Characterized by red cells that are abnormally
small and contain reduced amounts of hemoglobin
Related to:
❖ Disorders of iron metabolism
❖ Disorders of porphyrin and heme synthesis
❖ Disorders of globin synthesis
1. IRON DEFICIENCY ANEMIA
❖ Most common type of anemia worldwide
❖ Nutritional iron deficiency Metabolic or
functional deficiency
❖ Progression of iron deficiency causes:
- Brittle, thin, coarsely ridged, and
spoon-shaped nails
- A red sore, and painful tongue
❖ Insufficient iron impedes synthesis of
hemoglobin, reducing the amounts of
oxygen transported in blood
❖ Results in microcytic (small cell)
hypochromic (less color) erythrocytes due
to a low concentration of hemoglobin in
each cell.
NORMOCYTIC-NORMOCHROMIC ANEMIA
Produces a destruction or depletion of normal or
mature erythrocytes. Although the erythrocytes are
relatively normal in size and in hemoglobin
content, they are insufficient in number.
The anemia is usually mild to moderate and non-
progressive
Most of the patients have few symptoms and do
not require treatment
1. APLASTIC ANEMIA
is a rare disease caused by a decrease in or
damage to marrow stem cells, damage to the
microenvironment within the marrow, and
replacement of the marrow with fat
it results in bone marrow aplasia (markedly
reduced hematopoeisis) or reduced RBC
production
caused by infections in pregnancy, certain
medications, chemicals or radiations (eg Benzene)
2. POSTHEMORRHAGIC ANEMIA
blood loss from the vascular space
3. HEMOLYTIC ANEMIA
The RBC's have shortened lifespan; thus the
number of RBC in the circulation is reduced.
Destruction or hemolysis of RBC at a rate that
exceeds production
It has various forms:
1. Sickle cell -An autosomal recessive genetic
disorder of inadequate production of normal
hemoglobin develops a sickle or crescent shape.
2. Thalassemia -causes synthesis of a defective
hemoglobin; RBC's are fragile and have a
shortened lifespan; this leads to anemia and
hypoxia.
3. G6PD deficiency -Most common type of
congenital hemolytic anemia where this enzyme is
lacking in the RBC energy production when
exposed to certain drugs or toxins the aging RBC
easily break
4. Hereditary spherocytosis -characterized by the
production of red blood cells that are sphere-
shaped rather than bi-concave disk shaped
(Donut-Shaped), and therefore more prone to
hemolysis.
GENERAL PLANNING AND IMPLEMENTATION
1. Assist hydration through IV fluids and oral ❖ Peripheral Blood Stem Cell Transplant
intake. (PBSCT)
2. Increase tissue perfusions by administering
oxygen and blood products as ordered; this helps 4. LYMPHOMAS
prevent from sickling. Cancer of the lymphatic system
3. Promote and encourage rest; schedule activities ❖ Hodgkin’s
of daily living and play to maximize rest and ❖ Non-Hodgkins
comfort. Presentation
4. Assist the child and family to avoid emotional
❖ Swelling of the lymph nodes
stress as much as possible
5. Assess for signs/symptoms of worsening ❖ Fever, night sweats, anorexia, weight loss,
anemia, shock and altered neurological function fatigue, and pruritis
6. Provide emotional support during crisis, as well Management
as on an ongoing basis when the child is well and ❖ Follow general treatment guidelines
in the home setting ❖ Utilize isolation techniques to limit risk of
infection
MYELOPROLIFERATIVE RBC DISORDERS
HODGKIN’S LYMPHOMA
1. POLYCYTHEMIA Incidence:
Overproduction of red blood cells ❖ Peaks in mid to late 20's
Relative polycythemia ❖ And> 50 (males affected more in > 50)
❖ Result of dehydration
❖ Fluid loss results in relative increase of red Causes
cell counts and Hgb and Hct values ❖ Probably viral or chemical
❖ Usually originates in a single or chain of
LEUKOCYTES DISORDERS nodes
❖ Reed-Sternberg cells (characteristic
1. LEUKOPENIA/NEUTROPENIA marker)
Too few white blood cells or neutrophils.
❖ Follow general treatment guidelines and Assessment:
provide supportive care. enlarged painless node or nodes, fever, malaise,
night sweats
2. LEUKOCYTOSIS
An increase in the number of circulating white Diagnosis:
blood cells, often due to infection. Biopsy reveals R-S cells
❖ Leukemoid reaction
Staging:
3. LEUKEMIA crucial-treatment is based on extent of disease
Cancer of hematopoietic cells Prognosis: one of most curable forms of cancer

Initial presentation Treatment

❖ Acutely ill, fatigued, febrile and weak,
anemic.
❖ Thrombocytopenia (decreased platelets in
the blood)
❖ Often have a secondary infection.
❖ Stage 1-2: extensive radiation
❖ More extensive: radiation with aggressive
multiagent chemotherapy
❖ Nursing management focuses on side
effects

Management NON-HODGKIN'S LYMPHOMA

❖ Follow general treatment guidelines. ❖ Cancers of the lymph tissue that are not
❖ Utilize isolation techniques to limit risk of Hodgkin's
infection. ❖ Most occur in older adults

Drug therapy Causes unknown

❖ Intensive combination chemotherapy Suspect viral, radiation, chemical
❖ Major side effects: bone marrow
depression Prognosis:
- Increases vulnerability to infection ❖ Dependent on cell type
- Antibiotics, antifungals, antivirals
❖ Bone marrow transplantation (BMT)
 ❖ Ranges from excellent to poor Treatment
and nursing care similar to Hodgkin's
lymphoma

CLOTTING DISORDERS
1. THROMBOCYTOSIS
An abnormal increase in the number of platelets

2. THROMBOCYTOPENIA ❖ Coffee ground emesis

An abnormal decrease in the number of platelets ❖ Cola-colored urine
❖ Tarry stools
❖ Sequestration 4. DISSEMINATED INTRAVASCULAR
❖ Destruction (ITP-Idiopathic COAGULATION
Thrombocytopenic Purpura)
❖ Decreased production System activation of coagulation cascade.

Management Results from sepsis, hypotension, OB

Provide supportive care and follow general complications, severe tissue or brain injury,
treatment guidelines. cancer, and major hemolytic reactions.

❖ Immunosuppressants (chemicals to Characterized by:

suppress immunological responses) ❖ Low platelet and fibrinogen levels
❖ Plasma exchange ❖ Prolonged PT, aPTT, thrombin time
❖ Platelet aggregation inhibitors ❖ Elevated D-dimer

3. HEMOPHILIA Clinical manifestations:

(Inherited blood disorder)
Deficiency or absence of a blood clotting factor Bleeding from mucous membranes, venipuncture
❖ Deficiency of factor VIII causes hemophilia sites, Gl and urinary tracts
A.
❖ Deficiency of factor IX causes hemophilia Treatment:
B ❖ Most important: identify and treat cause
❖ Deficiency is a sex-linked, inherited ❖ Correct secondary effects of tissue
disorder. hypoxia
- Defective gene is carried on the X ❖ Replace depleted coagulation factors
chromosome. ❖ Heparin infusions (controversial)
● No cure
● Avoid injury and meds that promote 5. MULTIPLE MYELOMA
bleeding (blood thinners, aspirin)
● Good nutrition ❖ Cancerous disorder of plasma cells.
● Good dental hygiene
❖ Pathologic fractures are common.
● IV administration of deficient clotting factor
● Visual disturbances
GENERAL MANAGEMENT
● Prolonged nosebleeds
● Bruises easily
1. Assess frequently for bleeding and neurological
● Warm, painful, swollen joints with
status
movement
2. Closely monitor platelet count 3. Use soft
bristled toothbrush
Signs & Symptoms
4. Avoid using rectal thermometer and aspirin like
Numerous bruises, deep muscle bleeding, and
products
joint bleeding.
5.Steroids are ordered to avoid inflammatory
processes
6. IV immunoglobulins may also be used to avoid
auto immune problem
 LESSON 2
Nursing Care of a Child with Urinary Disorders

● Epispadias - opening of the urinary

RENAL DISORDERS IN CHILDREN meatus on the dorsal or superior surface if
the penis
Structural abnormalities of the urinary tract
● Skin around the bladder is excoriated
● Patent urachus ● Kidney function
● Exstrophy of the bladder ● Waddling gait
● Hypospadias
Therapeutic Management
Patent Urachus
● Surgical closure of the bladder
● When the bladder first forms in utero, it
PREOPERATIVE
is joined to the umbilicus by a narrow tube,
the urachus ○ Cover the bladder by a sterile plastic
● If this fails to close a fistula is left bowel bag
between the bladder and umbilicus (Patent ○ A & D ointment
Urachus) ○ Ace bandages
● Common in males than females ○ Change diaper immediately after each
defecation
Assessment ○ Supine position
● Fluid draining from the base of the ○ Sponge bath rather than tub bath
umbilical cord while changing the diaper
POST OPERATIVE
● Acidic
● Ultrasound can confirm the diagnosis ○ Supine position
○ Suprapubic or indwelling catheter
Management ○ Analgesic
● Few heals spontaneously ○ Antispasmodic
● Others surgical correction ○ Kegel exercise

EXSTROPHY OF THE BLADDER HYPOSPADIAS

● A midline closure defect that occurs
during the embryonic period of gestation (8th
weeks)
● Bladder lies open and exposed on the
abdomen
● More frequent in male than female ratio
of 2:1
Assessment
● Fetal Ultrasound there is no anterior wall
of the bladder and no anterior skin covering
on the lower anterior abdomen
● Bladder appears bright red and
continually drains urine from open surface
● Male: penis is often unformed or
malformed
● Females: urethra abnormally formed
● Non Closure of the pelvic arch
● A urethral defect in which the urethral
opening is no at the end of the penis but on
the ventral (lower) aspect of the penis
● With familial tendency
● 1:300 male
Assessment
● Short chordee-fibrous band that
causes the penis to curve downward
(cobra head appearance)
● Cryptorchidism - undescended testes
Management
● Meototomy surgical procedure in which
the urethra is extended in the normal
position
● 12-18 mos. Chordee maybe released
● Surgery maybe delayed at 3-04 years
 ● Testosterone cream
● Daily injection of Testosterone
● Analgesic and Antispasmodic after
surgery
HYDRONEPHROSIS
● Enlargement of the pelvis of the
kidney with urine as a result of back
pressure in the ureter.
● Back pressure is cause by :
○ Obstruction either of the
ureter or of the point where the
ureter joins with the bladder
○ Common in 1st 6 months of
life
Assessment
● Some are asymptomatic
● Repeated UTI’s from urinary stasis
● HPN
● Flank or abdominal pain
● Abdominal palpation reveals
abdominal mass
● IVP or UTZ will show the enlarged
pelvis and point of obstruction
Treatment
Assessment
● URINE is collected after the child has
been recumbent during the night (a 1st
voided urine) and then again after the
child has been up and active for several
hours
● Record also the child activity during
urine collection
● No therapy is needed but needs to be
documented because some of these
children develop some form of kidney
disorder later in life
ACUTE POSTSTREPTOCOCCAL
GLOMERULONEPHRITIS
● Glomerulonephritis inflammation of the
kidney
● Immune complex disease after
infection with nephrotogenic
streptococci (group A beta hemolytic
streptococci)
● Tissue damage occurs from a
complement fixation reaction in the
glomeruli
● Complement- a cascade of proteins
activated by antigen-antibody reactions
and actually plugs or obstructs
glumeruli

● Surgical correction of the obstruction ● IgG antibodies is detected

before glomerular or tubular destruction
● Intravascular coagulation in the minute
occurs
renal vessels
POSTURAL (ORTHOSTATIC) PROTEINURIA
● Ischemic damage
● Also called postural albuminuria
● Decreased GFR
● Few children will spill albumin into the
● CHON molecules escape into the
urine when they stand upright for an
filtrate
extended period of time
Assessment
● Amount of spilling decreases when
they rest in supine position
● Common in 5-10 years old and male, during
● Have no apparent damage on to winter and spring
glomeruli ● Gross hematuria
● Proteinuria
● Attributable to the effect of gravity on ● Urine specific gravity is elevated
glomerular function ● HPN
● Hypervolemia
● Abdominal pain
● Low grade fever ● SAME WITH Acute Poststreptococcal
● Edema
● Anorexia Management
● Vomiting
● SAME WITH Acute Poststreptococcal
● Headache
● Orthopnea Additional Management
● Cardiac enlargement
● Enlarged liver ● Corticosteroid
● Pulmonary edema
● Reverse isolation
● Galloping heart rhythm
● ECG-T wave inversion and prolonged PR ● Hemodialysis or peritoneal dialysis
interval
● Heart failure ● Worst - needs kidney transplant
● Low blood protein level (hypoalbuminemia)
NEPHROTIC SYNDROME (NEPHROSIS)
● Mild anemia
● ESR increase ● Nephrosis - altered glomerular
● BUN and Creatinine increase permeability due to fusion of the
If BP is 160/100 mmHg leads to encephalopathy glomeruli membrane surfaces causes
abnormal loss of protein in urine
Management
● Cause is hypersensitivity to an antigen
● 1-2 weeks antibody reaction

● Antibiotics ineffective because the ds. ● T lymphocyte dysfunction

Is caused by antigen antibody
inflammatory response ● Highest at 3 years old male

● Lasix 3 forms of Nephrotic Syndrome

● Semi fowler ● Congenital - occurs as an autosomal

recessive disorder
● Oxygen inhalation
● Secondary progression of
● Anti HPN drugs glomerulonephritis or Sickle cell
anemia SLE
● Aluminum Hydroxide
● Idiopathic unknown and rare
● Bed rest
According to amount of membrane destruction
● Salt restriction
● Minimal Change Nephrotic Syndrome
● Weigh daily (MCNS) little scarring of the glomerulus

CHRONIC GLUMERULONEPHRITIS ● Focal Glomeruloscrelosis (FGS)

● Occurs as a primary ds. After acute ● Membranoproliferative (MPGN) bothe

glumerolunephritis was so mild and it involve scarring of glomeruli
was undiagnosed
4 characteristics of Nephrosis
● Renal biopsy shows permanent
destruction of glomeruli membranes ● Proteinuria
● Edema
● Alport’s syndrome - includes hearing ● Hypoalbuminemia
loss and ocular changes is a ● Hyperlipidemia
progressive chronic GN inherited as a
X linked disorder

Assessment
Assessment
 ● Periorbital edema ● Exposure to mercury

● Ascites Assessment

● Boys (scrotal edema) ● Oliguria

● Anorexia ● Azotemia (accumulation of nitrogenous

waste in the bloodstream)
● Vomiting
● Uremia extra accumulation of nitrogen
● Diarrhea wastes in the bld with additional toxic
symptoms of cerebral irritation
Management
● Hyperkalemia
● Corticosteroid
● Hyperphosphatemia
● Lf pt. Respond poorly to Corticosteroid
● Hypocalemia
● Lasix maybe given
Therapeutic Management
● Supplemental Potassium
● IVF
● IV albumin
● Sodium Bicarbonate
RENAL FAILURE
● IV glucose and insulin
● Acute or Chronic
● Lasix
Acute occurs because of sudden body insult such
as severe DHN ● Diet low in CHON, K, and Na but High
in CHO
Chronic results from extensive kidney ds.
● Limit fluid intake as per doctor’s order
● Other causes of Acute Renal Failure
● Weigh daily
● Prolonged anesthesia
● TPN
● Hemorrhage

● Severe diarrhea

● Sudden traumatic injury

● Swallow arsenic (found in rat poison)

 LESSON 3:
NURSING CARE OF A CHILD WITH ALTERATIONS IN IMMUNE SYSTEM

ASSESSMENT OF ALLERGY IN CHILDREN Antihistamine - block histamine release as a result

it control itching, sneezing and rhinorrhea
1. Family History
2. Determine the exact symptoms of allergy to e.g. Diphenhydramine hydrochloride (Benadryl),
identify allergens Cetirizine (Zyrtec), Loratidine (Claritine)

e.g. Decongestant -decrease nasal edema and help

rhinitis - airborne antigen
urticaria (swelling, itching) caused by ingested
antigen
Contact dermatitis (often a rash) from something
that contacts the skin in that area
enlarge breathing space
e.g Pseudoephedrine (Sudafed)
Intranasal Corticosteroid - reduce inflammation

3. The time of the year that the allergy occurs may COMMON IMMUNE REACTION
also due to its cause
1. Anaphylactic Shock
LABORATORY TESTING immediate life threatening, type 1
1. Determination of IgE serum antibodies - sensitivity reaction that occur after
associated with allergy (Inc. Eosinophil count to exposure to an allergen
5% or more is significant)
e.g sting by an insects or drugs to which a child
2. Skin Testing - is done to determine the presence has been sensitized
of IgE in the skin. The test should be read in 20
mins ASSESSMENT
1. Initially a child become nauseated, w/ vomiting
2 TYPES OF SKIN TESTING and diarrhea
2. Urticaria
1. Applying a patch or using a scratch 3. Bronchospasm becomes so severe, the child
2. Intracutaneous injection becomes dyspneic
Note: 1 ml of epinephrine (adrenaline) should be 4. Seizure and death
ready on hand to counteract anaphylactic reaction
from skin testing MANAGEMENT:
Epinephrine - drug of choice to treat anaphylaxis
Therapeutic Management
3 Goals for therapy
1. Reduce the child's exposure to allergens 2. Urticaria or hives
2. Hyposensitize the child to produce a state of ❖ Refer to wheals surrounded by erythema
increased clinical tolerance to allergens arising from the chorion layer of skin, they
3. Modify the child's response to the allergens with are intensely pruritic
pharmacologic agent ❖ No causative allergens

ENVIRONMENTAL CONTROL
Removal of as many common allergens as
possible from the child's environment

HYPOSENSITIZATION
Or immunotherapy is done when the child's allergy
symptoms cannot be controlled by avoidance of
the allergens or conventional drug therapy

PHARMACOLOGIC THERAPY:
Hyposensitization procedures - these drugs do not
change the sensitivity to allergens but they only
relieve the symptoms 3. Angioedema
 ❖ Edema of the skin and subcutaneous
tissue. Frequently occur in the eyelid, feet, Therapeutic Management
genitals and lips ❖ Avoidance of allergens
❖ Apparent where skin is loosely bound by ❖ Use of pharmacologic agents
Sub Q tissues (antihistamine, corticosteroid)
❖ Immunotherapy

Common cause of Urticaria and Angioedema

1. Drugs
2. Foods
3. Insect stings

ATOPIC DISORDER
Individual with atopy are prone to all allergic
response
ATOPIC DERMATITIS
ALLERGIC RHINITIS
Caused by immediate hyposensitivity immune Primarily a disease of an infant, beginning as early
response as the 2nd month of life and possibly lasting until
age 2 to 3 years
Assessment
❖ Sneezing Causes
❖ Horizontal crease across the nose ❖ Food allergy
(Dennie's line) due to constant wiping away ❖ Sweat
of nasal secretions
❖ Heat
❖ Dark patches under their eye due to back
❖ Tight clothing
pressure from nasal congestion (allergic
shiners) ❖ Contact irritants such as soap.
Assessment:
❖ Nasal engorgement
❖ With papular and vesicular skin eruptions
❖ Profuse watery nasal discharge
with surrounding edema
❖ Mucous membrane of the nose is pale
❖ With sticky secretions that form crust on the
❖ Conjunctiva of the eyes maybe pruritic skin as they dry
❖ Rubbing the nose in an upward motion ❖ Linear excoriation (lesions are extremely
(allergic salute) pruritic, the child scratches and further
❖ Children older than 6 years old may report irritates)
full frontal headache ❖ Common sites for lesions include the scalp
❖ Some children feel exhausted, lethargic and forehead, cheeks, neck, behind the
and cannot function well in school ears and the extensor surface of the
❖ Recurrent otitis media may occur extremities
❖ Increase eosinophils will be revealed after ❖ Irritable
smear of nasal discharge ❖ They cannot eat well
❖ No fever unlike in URTI

Causes
Pollens or molds rather than food and drugs

PERENNIAL ALLERGIC RHINITIS

Allergens that are capable of affecting the child for Therapeutic Management
a year round such as dust, mites or pet hair
 ❖ Hydrating the skin by bathing or applying
wet dressing (wet with tap water for 15-
20min. Then apply hydrating emollient like
petroleum jelly
❖ Antihistamine
❖ Topical steroids
ATOPIC DERMATITIS IN CHILDREN
May occur at any age but frequently at puberty or
late adolescence
Signs and Symptoms
❖ Lesions prominent on the flexor surface of
the extremities and on the dorsal surface of
the wrist and ankles
❖ Depigmentation or hyperpigmentation is
usually present
❖ The fingernails have a glossy sheen
❖ Itch-scratch cycle in response to stress
Therapeutic Management
❖ Do not use ordinary soap only prescription
soap to prevent skin drying
❖ Avoid swimming in a chlorinated pool
❖ After period of activity in which sweating
occur, suggest that the child may take
shower to remove perspiration, which is
irritating to skin
❖ Avoid tight clothing at the flexor portions
❖ Caution children not to use medication for
acne cover-up on atopic lesions to prevent
dryness of the skin and will increase
itchyness
❖ Medical management same with infant with
atopic dermatitis
NURSING DIAGNOSIS
❖ Situational low self-esteem related to
feelings of inadequacy and embarrassment
❖ Risk for impaired parenting related to
feeling of inadequacy secondary to infant's
chronic atopic dermatitis
❖ Impaired skin integrity related to infantile
atopic dermatitis
EVALUATION
❖ Evaluation for the older child with atopic
dermatitis should include how well the
lesions are healing and how the child is
adjusting and coping to school and family
❖ A child who enters adulthood with poor self
esteem because of chronic allergic
disorder could have difficulty achieving a
high level of adult wellness
 LESSON 4:
Infectious Disease
THE INFECTIOUS PROCESS
STAGES OF INFECTIOUS DISEASE
1. Incubation Period
❖ The time between the invasion of an
organism and the onset of symptom of
infection
❖ Microorganism grow and multiply
❖ Incubation period varies depending on
the pathogens Common interval is 7-10
days
2. Prodromal Period
❖ Time between the beginning of non
specific symptoms: lethargy, low grade
fever, fatigue and malaise
❖ Children are infectious this time
❖ Prodromal stage from hours to a few
days
3. Convalescent period
❖ The interval between when symptoms
first begin to fade and the child return to
full wellness
❖ Time until full energy is restored, is often
longer than anticipated
Assessing a Child with Common Signs &
Symptoms of Infectious Disorder
A. History (Chief Concern)
❖ Does the child have fever, general
malaise, vomiting, or diarrhea?
❖ Was the child recently exposed to
someone with an infection?
B. Past Medical History: Are child's
immunization current?
As healthcare professionals, it is important to
understand two things about infection:
1.the various ways infection can be transmitted
2. the ways the infection chain can be broken
There are six links in the chain of infection:
1st- The Infectious Agent -any disease-causing
microorganism (pathogen) Bacteria, virus, protist,
parasite, fungi
2nd - The Reservoir Host -the organism in which
the infectious microbes reside (reservoir can be
environmental, the hospital setting or the water
supply, or in a living organism, a rodent, bird or
even snail.)
What are "Carrier Hosts" Hosts that do not show
any outward signs or symptoms of a disease but
are still capable of transmitting the disease are
known as carriers.
3rd- The Portal of Exit -route of escape of the
pathogen from the reservoir. Examples:
respiratory secretions, blood exposure, breaks in
skin.
4th- The Route of Transmission -method by which
the pathogen gets from the reservoir to the new
host
Transmission may occur through:
direct contact
INDIRECT CONTACT
❖ air
❖ insects
5th-The Portal of Entry -route through which the
pathogen enters its new host
Respiratory System - Inhalation
Gastrointestinal System- Ingestion
Urinary and Reproductive System
Break in protective skin barrier
6th-The Susceptible Host -the organism that
accepts the pathogen The support of pathogen life
& its reproduction depend on the degree of the
host's resistance.
Organisms with strong immune systems are better
able to fend off pathogens.
Organisms with weakened immune systems are
more vulnerable to the support & reproduction of
pathogens.
How to interrupt the chain of infection:
The essential part of patient care and self-
protection
1. Pathogen Identification -identification of
infectious agent & appropriate treatment
2. Asepsis & Hygiene -potential hosts & carriers
must practice asepsis & maintain proper personal
hygiene
3. Control Portals of Exit -healthcare personnel
must practice standard precautions: (Control body
secretions & wash hands according to protocol.)
4. Prevent a Route of Transmission
1. Disinfection & sterilization techniques
2.Isolation of infected patients
3. Proper handwashing
4. Not working when contagious
5. Protect Portal of Entry -Health professionals
must make sure that ports of entry are not
subjected to pathogens. (nose, mouth, eyes,
urinary tract, open wounds, etc.)
6. Recognition of Susceptible Host -health
professionals must recognize & protect high-risk
patients
1. CANCER PATIENTS
2. AIDS and HIV PATIENTS
3. TRANSPLANT PATIENTS
4. INFANT AND ELDERLY
Remember--breaking the chain of infection is the
responsibility of each health professional.
Standard and Transmission-Based Precaution
for Infection Control
1. Hand washing...
2. Wear gloves appropriately...
3. Wear mask, protective eye wear and gown
during any patient care activity when splashes or
sprays of body fluids are likely to happen.
4. Handle needles and other sharp instruments
safely. Do not recap needles but dispose in
puncture resistant containers
5. Routinely clean and disinfect frequently touched
surface including bed rails, examination tables and
bed side table
6. Do not touch linens soiled with blood or bloody
fluids with bare hands. Used plastic bag to
transport soiled linen.
7. Place patient whose blood or body fluids are
likely to contaminate surface or other patient in
isolation room.
8. Minimize the use of invasive procedure to avoid
potential injury and accident exposure.
9. When a specific diagnosis is made, find out how
the disease is transmitted. Used precautions
according to transmission risk.
AIRBORN PRECAUTION
1. Place the patient in isolation room that is not air-
conditioned or where air is not circulated to the rest
of the health care facility.
2. Wear a HEPA or other biosafely mask when
working with the patient and in the patient room
3.AIRBORN PRECAUTION
3. Limit movement of the patient from the room to
the other areas. Place a surgical mask on the
patient who must be moved
DROPLET PRECAUTION
1. Place the patient in an isolation room.
2. Wear a biosafely mask when working with
patient
3. Limit the movement of the patient from the room
to the other areas. If the patient must be moved,
placed a surgical mask on the patient.
CONTACT PRECAUTION
1. Place the patient in an isolation room and limit
access.
2. Wear gloves during contact with patients ar with
infectious body fluids or contaminated items.
Reinforce hand washing
3. Wear two layers or protective clothing
4. Limit movement of the patient from isolation
room to the other areas.
5. Avoid sharing equipment between patients.
Designate equipment for each patients, if supplies
allow. If sharing equipment is unavoidable, clean
and disinfect it before use with the next patient.
Identify the infection link that the , nurse is
breaking...
1. A nurse washing her hands after leaving the
patients → room
2. A nurse autoclave infected instruments
3. Nurse avoid contacting Hepatitis C by avoiding
being punctured by a needle X
4. A nurse administers chicken pox vaccine to a ASSESSMENT
pediatric patient
5. A nurse bandages a wound infected with MRSA
(Methicillin-Resistant Staphylococcus Aureus -
bacteria, Staphylococcus aureus, that are resistant
to a number of antibiotics, including methicillin).
Assessing a child with common/s of infectious
disorder
MEASLES
❖ Causative Agent: Measles Virus
❖ Incubation Period- 10 to 12 days
❖ Period of communicability - 5th day of
incubation period through the 1st day of t
rash appears
❖ Mode of transmission - direct and indirect
contact with droplet
❖ Contacting the dse. offers lasting natural Management
immunity
ASSESSMENT
❖ Also called brown or black or 7 days (to
differentiate it with rubella/German
measles or 3-day)
❖ Lymph node enlargement High fever
❖ Malaise Coryza (rhinitis and sore throat)
Conjunctivitis with photophobia Cough
Pathognomonic sign (Koplik's spot) small
irregular bright red spots with blue white.
❖ If the rash is red it fades on pressure if it is
brown it does not fade
❖ Fine desquamation but the hands and feet
do not desquamate
❖ Complication – Pneumonia
approximately 5 days after the rash
appears
❖ Mode of transmission - direct and indirect
contact with droplet Contacting the dse.
offers lasting natural immunity
- low grade fever
- headache
- malaise
- anorexia
- mild conjunctivitis
- sore throat
- mild cough
- swollen lymph nodes
❖ After 1-5 days of Prodromal signs a
discrete pink red maculopapular rash
begins on the face then spreads downward
to the trunk and extremities on the 3rd day
the rash disappears
❖ No desquamation but flaking of the skin
❖ Arthritis (joint pain) with effusion on the 3rd
day 'til 5-10 days
- Antipyretic
- Droplet precaution
OTHER BACTERIAL INFECTIONS
❖ Diphtheria
❖ Causative Agent: Corynebacterium
❖ diphtheriae (Klebs-Loffler bacillus)
❖ Incubation Period- 2 to 6 days
❖ Period of communicability - rarely more
than 2 weeks to 4 weeks in untreated
persons; 1 to 2 days in children treated with
antibiotics
❖ Mode of transmission - direct and indirect
contact with droplet
❖ Contacting the dse. offers lasting natural
immunity

MANAGEMENT
❖ Antipyretic
❖ Lubricating jelly to area prevent excoriation
❖ Cough suppressant Wearing dark glasses
❖ Airborne precaution
GERMAN MEASLES (Rubella)
❖ Causative Agent: Rubella Virus
❖ Incubation Period- 14-21 days Period of
communicability - 7 days before to
ASSESSMENT
❖ Inflammation and necrotizing cells form a
characteristic gray membrane on the
nasopharynx
❖ Purulent nasal discharge Brassy cough
❖ If untreated myocarditis with heart failure
Severe neuritis
❖ Paralysis of the diaphragm, pharyngeal
and laryngeal muscles
❖ Diagnostic
❖ Throat culture
❖ Prevention - Immunization (DPT)
MANAGEMENT
❖ Intravenous administration of antitoxin
Penicillin or erythromycin Complete bed
rest Droplet precaution
❖ Careful observation to prevent airway
obstruction
FUNGAL INFECTION
CANDIDA ALBICANS
Candida Albicans -Fungus responsible for
monilial infection
❖ Oral trush or oral candidial infection
❖ Characterized by white plaques on an
erythematosus base on the buccal
membrane and surface of the tongue
❖ Mouth painful
❖ Child does not eat well MONILIAL DIAPER
RASH
❖ Severe bright red sharply circumscribed
diaper area rash
❖ Management: Nystatin ointment for diaper
rash
Common Parasitic Infection
• SCABIES Organism: female mite (Acarus
scabiei)
ASSESSMENT
- Extreme pruritus
- Black burrow filled with mite feces 1-2
inches long, usually between fingers and
toes, on palms or in axilla or groin
- Management
❖ Wash bed sheets and recently worn
clothes
❖ Vacuum pillows, mattresses, or other items
unable to be washed
❖ Caution children that groin infestation
might be spread by physical intimacy
❖ Wash area with lindane (Kwell) lotion or
permethrin (Elimite) All contagious disease
are infectious, but not all infectious disease
are contagious..!
 LESSON 5:
NURSING CARE OF A FAMILY WHEN A CHILD HAS A MALIGNANCY
MALIGNANT/CANCEROUS
❖ Cells that are growing and proliferating
in a disorderly, chaotic fashion
❖ Immature white blood cells (WBC)
overgrowth, or LEUKEMIA – most
frequent type of cancer in children
Symptoms of malignancy in children
are often difficult to identify
❖ NEOPLASM abnormal growth, either
BENIGN (growth is limited) or
❖ MALIGNANT (cancerous or with
unlimited growth)
❖ BIOPSY-surgical removal of cells for
laboratory analysis
❖ TUMOR STAGING - malignant tumor's
extent and progress are documented
TUMOR STAGING
malignant tumor's extent and progress are
documented:
• Stage 1 -tumor that has not extended
into the surrounding tissue and may be
completely removed surgically
• Stage II -some local spread but the
chance for complete surgical removal is
good
• Stage III -cancer cell have spread to
local lymph nodes • Stage IV-tumors
spread systemically (metastasis)
• TNM System describes: (T) tumor's
size, (N) any presence in the lymph
nodes, (M) cancer cells metastasized
or spread to other organs
• TNM system is applicable to solid
tumors only & does not apply to
malignancy of the bone marrow
(leukemias)
TYPES OF CANCERS IN CHILDREN
LEUKEMIAS
distorted & uncontrolled proliferation of WBC's
(leukocytes) & most common type of cancer in
children
a. Acute Lymphocytic Leukemia (ALL)-
immature lymphocytes, limits production of
RBC's and platelets
b. Acute Myeloid Leukemia (AML)- over
proliferation of granulocytes, risk for infection
2. LYMPHOMAS
malignancies of the lymph or
reticuloendothelial system
a. Hodgkin Disease - Reed-Sternberg
Cells develop (non-functioning cells)
b. Non-Hodgkin Disease -malignant
disorders of the lymphocytes (either B
or T cells). Burkitt Lymphoma, involves
B-lymphocytes cells
3. Brain Tumors
2nd most common form of cancer & most
common solid tumor in children. Common
brain tumors are cerebellar, astrocytomas,
medulloblastomas, & brainstem gliomas
4. Bone Tumors
tumors derived from connective tissue, such
as bone & cartilage, muscle, blood vessels, or
lymphoid tissue are termed SARCOMAS
a. Osteogenic Sarcoma- malignant
tumor of long bone
b. Ewing Sarcoma- bone marrow
5. Neuroblastoma
tumors of the sympathetic nervous system,
common in the abdomen or spinal ganglia
6. Rhabdomyosarcoma
tumor of striated muscle
7. Nephroblastoma (Wilm's Tumor)
malignant tumor of the kidney
8. Retinoblastoma
malignant tumor of the retina of the eye
9. Skin Cancer
a. Basal Cell Carcinoma- a surface
epithelial growth that appears as a
small ulcer that does not heal
 b. Squamous Cell Carcinoma- a
tumor of the epidermis that appears as
a white scaly lesion
c. Malignant Melanoma- a tumor
originating in melanocytes or nevi that
appears as a mole changing in
appearance. Melanomas can be
differentiated from benign moles by an
A-B-C-D assessment: Asymmetry,
Border irregularity, Color (variable or
dark pigmentation), and Diameter (over
6mm)

ASSESSING A CHILD FOR SIGNS OF

CANCER
History
Chief concern: Weight loss, loss of appetite,
easy bruising, swelling in a body part,
headache, eye deviations.
Past medical history: Family member with a
history of cancer.

Physical examination
▪ Swollen lymph glands (Hodgkin
2020 NATIONAL HEALTH GOALS disease)
RELATED TO CANCER AND CHILDREN ▪ Nausea and vomiting (brain tumor)
❖ REDUCE THE OVERALL CANCER ▪ Weight loss
DEATH RATE FROM A BASELINE OF ▪ Ecchymotic marks (leukemia)
178.4 PER 100,000 TO 160.6 PER ▪ Pain and swelling in a large joint
100,000 OF THE POPULATION. (osteosarcoma or Ewing sarcoma)
❖ INCREASE THE PROPORTION OF ▪ Headache (brain tumor)
ADOLESCENTS IN GRADES 9 ▪ Eye deviations (brain tumor,
THROUGH 12 WHO FOLLOW retinoblastoma)
PROTECTIVE MEASURES THAT MAY ▪ Palpable mass in abdomen
REDUCE THE RISK OF SKIN CANCER (neuroblastoma or Wilms tumor)
FROM 9.3% TO 11.2%. GENERAL SIGNS AND SYMPTOMS OF
❖ REDUCE THE RATE OF MELANOMA CANCER
CANCER DEATHS FROM A BASELINE ❖ Unexplained fever
OF 2.7 PER 100,000 TO A TARGET ❖ Bleeding/bruising
LEVEL OF 2.4 PER 100,000 OF THE ❖ Morning headaches and neurologic
POPULATION. changes
❖ Palpable abdominal mass
ASSESSING CHILDREN WITH CANCER ❖ Swollen lymph nodes
❖ History ❖ One and joint pain
❖ Physical and laboratory examination ❖ Fatigue
- Biopsy
- Staging
 ASSESSING THE LEUKEMIAS
ACUTE LYMPHOCYTIC
(LYMPHOBLASTIC) LEUKEMIA
ACUTE MYELOID LEUKEMIA
▪ Pallor, low-grade fever, lethargy, low
thrombocyte count, petechiae, bleeding
from oral mucous membranes, easy
bruising on arms and legs, abdominal
pain, vomiting, anorexia, bone and joint
pain, headache or unsteady gait,
painless, generalized swelling of lymph
nodes, elevated leukocyte count,
lesions on long bones, blast cells in csf
▪ Bone marrow aspiration identifies type
of wbc involved
ASSESSING THE LYMPHOMAS
HODGKIN DISEASE
❖ One painless, enlarged, rubbery-
feeling cervical lymph node followed by
enlargement of other nodes and liver,
spleen, bone marrow, cns, anorexia,
malaise, night sweats, elevated
sedimentation rate, anemia
❖ Biopsy of lymph nodes, chest,
abdominal ct, lymphangiogram
ASSESSING THE LYMPHOMAS
NON-HODGKIN LYMPHOMA
ENLARGED LYMPH GLANDS OF NECK
AND CHEST, POSSIBLY OF AXILLARY,
ABDOMINAL, INGUINAL NODES, IF
MEDIASTINAL LYMPH GLANDS INVOLVED,
COUGH OR CHEST "TIGHTNESS, EDEMA
OF FACE BIOPSY OF AFFECTED LYMPH
NODES, BONE MARROW
BURKITT LYMPHOMA
ENLARGED, PAINLESS LYMPH NODE OF
NECK OR ABDOMEN BLOCKING A BODY
SYSTEM, GROWTH SO RAPID CELL MASS
MAY DOUBLE IN SIZE IN AS FEW AS 24
HOURS
ASSESSING NEOPLASMS OF THE BRAIN
TYPES OF BRAIN TUMORS
• CEREBELLAR ASTROCYTOMAS:
slow-growing, cystic tumors that arise
from glial or support tissue surrounding
neural cells
• MEDULLOBLASTOMAS: fast-growing
tumors found most commonly in
cerebellum
• BRAINSTEM GLIOMAS: often cause
paralysis of the fifth, sixth, seventh,
ninth, and tenth cranial nerves
• SYMPTOMS OF INCREASED
INTRACRANIAL PRESSURE
o Headache occurs on arising, may
be intermittent throughout day,
intense on straining
o Vomiting occurs on arising, not
nauseated, will eat immediately
after, morning after morning,
eventually projectile
o Diplopia, ptosis, or strabismus,
papilledema
o Skull films, bone scan, ultrasound or
mri, cerebral angiography, or a ct
scan, possibly myelography, lumbar
puncture
ASSESSING BONE TUMORS
OSTEOGENIC SARCOMA
▪ Taller than average, painful, swollen
site, possibly inflamed, feels warm,
report of recent trauma to site
▪ Elevated serum alkaline phosphatase,
biopsy of site
EWING SARCOMA
▪ Intermittent pain at site, becomes
constant and severe, "onion. Skin
reaction on x-ray
▪ Bone scan, bone marrow aspiration,
biopsy, CT scan of lungs, and iv
pyelogram or kidney MRI
ASSESSING OTHER CHILDHOOD
NEOPLASMS
NEUROBLASTOMA
▪ Palpable abdominal mass after
weight loss, anorexia, possibly
excessive sweating, flushed face,
hypertension, possibly abdominal
pain, constipation, possibly loss of
motor function in lower extremities
▪ Arteriogram, ultrasound, CT, or MRI
scan of chest, abdomen, pelvis,
gallium bone scan, bone marrow
aspiration and biopsy
NEPHROBLASTOMA (WILMS TUMOR) bone marrow of a well person to a child
with cancer
▪ Palpable firm, nontender abdominal
mass, possibly hematuria, CANCER TREATMENT
▪ Low-grade fever, anemia • ct scan
or ultrasound, glomerular filtration RADIATION THERAPY
rate or blood urea nitrogen assays • Immediate side effects
• Long-term side effects
RETINOBLASTOMA
• Effects on bone
▪ Pupil appears white, strabismus • Effects on hormones
▪ CT scan, MRI, and ultrasound • Effects on nervous system
NURSING DIAGNOSES • Effects on organs of chest, abdomen
▪ Pain • Before treatment
▪ Imbalanced nutrition • During treatment
▪ Risk for infection • After treatment
▪ Disturbed body image CHEMOTHERAPY
▪ Compromised family coping TYPES
▪ Alkylating agents
CANCER TREATMENT MEASURES IN ▪ Antimetabolites
CHILDREN ▪ Plant alkaloids
• Radiation Therapy - changes the DNA ▪ Antitumor antibiotics
component of a cell's nucleus & ▪ Nitrosoureas
prevents replication (external beam ▪ Corticosteroids
radiation, brachytherapy, stereotactic ▪ Immunotherapy
radiosurgery) PROTOCOLS
• Chemotherapy - A chemotherapeutic SIDE EFFECTS AND TOXIC REACTIONS
agent is a drug that is capable of
destroying malignant cells, ensures ▪ ALOPECIA-hair loss
maximal tumor cell death. With side ▪ CUSHINGOID APPEARANCE -facial
effects like alopecia, fever, vomiting, puffiness and weight gain
diarrhea that can lead to dehydration STEM CELL TRANSPLANTATION
• Surgery - an operation/procedure done ▪ Pain relief
for the removal of tumors
• Stem Cell Transplantation-
transplantation of stem cells from the
 LESSON 6:
Nursing care of a family when a child has gastrointestinal disorder
Assessment
• Vomiting appears effortless
• Irritable
• May experience period of apnea
• Presence of gastric secretions in the
esophagus

Therapeutic management
• Feed infant in an upright position
• Keep the infant upright in an infant chair
Assessing gastrointestinal illness in
for 1 hr. After feeding to prevent reflux
children
Medication (proton pump inhibitor)
Physical assessment
omeprazole (prilosec), ranitidine (zantac) to
• Vomiting
prevent irritation in the esophagus.
• Diarrhea
• Poor skin turgor
Laparoscopic or surgical procedure
• Dry mucous membrane
tighten/suture esophageal sphincter.
• Weight
Pyloric stenosis
Diagnostic tests
• Constriction of the outlet of the stomach
• X-ray with contrast medium
• Hypertrophy (increase in the size) or
• Endoscopic exam
hyperplasia (overgrowth of a tissue) of
• Abdominal ultrasound
the muscle surrounding the pyloric
• MRI-magnetic resonance imaging
sphincter.
• Serum analysis
• Fluid concentration thru urine test

DISORDERS OF THE STOMACH AND

DUODENUM

Gastroesophageal reflux (Achalasia)

Assessment
is a neuromuscular disturbance in which the
• Vomiting - spitting and progress to
gastroesophageal (cardiac) sphincter and the
projectile vomiting soon after the end of
lower portion of the esophagus are lax and
feeding.
thus allow easy regurgitation of the gastric
• Changes in stool
content into the esophagus.
• Failure to gain weight
• Lethargy

Diagnostic evaluation
• Palpation of pyloric mass in conjunction
with persistent, projectile vomiting is
"pathognomonic sign"
• Ultrasound evaluation
• Barium swallow upper G.I. series
 • Test for metabolic alkalosis

Treatment
Initial treatment
• A. Rehydrate to correct electrolytes
• B. Correct alkalosis
• Surgery- Ramstedt pyloromyotomy

HIATAL HERNIA assessment

Is the intermittent protrusion of the stomach up
through the esophageal opening.
• Jelly like stool with blood and mucous
• Acute episodic abdominal pain
• A sausage shaped - mass palpated in
the right upper quadrant
• Vomiting up bile
• Lethargy

Management
• Abdominal x-ray - show obstruction
• Barium or air enema (pneumatic
Assessment insufflation)
• Periodic vomiting similar to esophageal • Surgery - straighten the invaginated
reflux portion
• Pain accompanies vomiting
• Shortness of breath VOLVULUS
• Twisting of the intestine
Diagnostic tests • The twist leads to obstruction of the
• Ultrasound passage of feces and compromise of
• Barium swallow the blood supply of intestine involved.

Management
• Baby kept in upright position to prevent
condition from recurring
• Laparoscopic surgery - to reduce
stomach ability to protrude through the
diaphragm Assessment
• Intense crying
INTESTINAL DISORDERS • Pain
• Pulling up the legs
Intussusception • Abdominal distention
• Is the invagination of one portion of the • Vomiting
intestine into another.
• The distal ileal segment of bowel has Diagnostic tests
invaginated into the cecum. • Abdominal x-ray
• Barium enema

Medical management
• Correction of fluids and electrolytes
• Treatment of shock if present
 • Intestinal intubation- rectal tube to
decompress an area
Surgery
A. Laparotomy -incision made in the
abdominal wall
B. Segmental resectioning
C. Anastomosis - joining together of
two or more hollow organs
D. Temporary or permanent
colostomy Assessment:
• Infant do not pass meconium
DISORDERS OF THE LOWER BOWEL • Abdominal distention
• Sometimes babies develop infection in
HIRSCHSPRUNG'S DISEASE the intestines
• Other term is Aganglionic megacolon
Treatment:
• Is a disease of the large intestine
• Surgery - pull through operation
• Absence of ganglionic innervation to
the muscles of a section of the bowel -
in most instances, the lower portion of
the sigmoid colon just above the anus.
• Birth defect in which some nerve cells
are missing in the large intestine, so a
child's intestine can't move stool and
becomes blocked
 LESSON 7:
Nursing Care of a Child with Endocrine Disorders
● Delayed growth of pubic, facial, axillary
ENDOCRINE DISORDERS and genital hair

ENDOCRINE SYSTEM Therapeutic management:

Ductless glands that work together with the
neurologic system to regulate and coordinate
a body systems
GROWTH HORMONES (SOMATOTROPIN)
increases bone and cartilage growth and
increase gastrointestinal absorption of
calcium.
DWARFISM
if growth hormone production is inhibited
GIGANTISM
if growth hormone production is excessive
1. Administration of intramuscular
recombinant human growth 2 or 3 times
a week
2. Growth hormone should be given at
bedtime, the time of the day at which
the GH normally peaks
GROWTH HORMONE EXCESS
● Over production of GH is caused by a
tumor of the anterior pituitary
(adenoma)
● If an over production occurs before the
epiphyseal lines of the long bones have
closed, excessive growth results

DIABETES INSIPIDUS
● A disease in which there is decreased
release of antidiuretic hormones (ADH)
by the pituitary gland
● This cause less absorption of fluid in
the kidney tubules

PARTS OF THE ENDOCRINE SYSTEM:

Assessment:
Pituitary gland ● Excessive thirst (polydipsia)
directed by the hypothalamus, organ located ● Polyuria, first as bedwetting in a toilet
in the center of the brain trained child
● Weight loss because of the large
PITUITARY GLAND DISORDERS:
volume loss
GROWTH HORMONE DEFICIENCY
● If untreated may lead to severe
Production of the human growth hormone dehydration and death
(somatotropin) is deficient, children cannot
grow to full size Diagnostic procedures:
● Radiography
Assessment: ● Ct scanning
● Normal in size and weight at birth
● Ultrasound
● First few years of life, the child begins Note: to determine lesion or tumor
to fall below the 3rd percentile of height
and weight on growth chart Management:
● The face that appears infantile because Administration of vasopressin (pitressin) - to
the mandible is recessed and immature rule out kidney disease
● The nose is usually small
1. Surgery if tumor is present
● Voice is high pitched
 2. If the condition is idiopathic, it can be
controlled by administration of
desmopressin an arginin vasopressin
Note: for emergency cases it can be given iv,
but for long term intranasally
THYROID GLAND
● controlling the rate of metabolism in
the body through production of
hormones thyroxine (t4) and
triiodothyroxine (t3) by its follicular cells
Assessment of thyroid function:
1. Radioimmunoassay of t3 and t4
THYROID GLAND DISORDERS:
Congenital hypothyroidism
Causes reduced production of t3 and t4
CONGENITAL HYPOFUNCTION
Reduced or absent function. Usually occur as
a result of an absent or non functioning thyroid
gland.
Assessment:
● Child sleep excessively
● Tongue becomes enlarged (causing
resp. Difficulty, noisy respiration, or
obstruction)
● Child may suck poorly because Of
sluggishness or choking
● Skin of the extremities usually feels
cold and over all body temperature
maybe subnormal due to slowed
metabolism
● Slow pulse and respiratory rate due to
slowed metabolism
● Prolonged jaundice (due to immature
liver and inability to conjugate bilirubin)
● Anemia may increase child lethargy
and fatigue
● Child’s neck appear short and thick
● Facial expression is dull
● Open mouthed because of the child’s
attempt to breathe around the enlarged
tongue
● Extremities are short and fat with
hypotonic muscle giving the infant a
floppy, rag doll appearance
● Slow deep tendon reflex
● Generalized obesity
● Hair is brittle and dry
● Dentition is delayed and teeth may be
defective when they do erupt
● Sonogram reveals small or absent
thyroid gland
● Hypotonia (lessened muscle tone)
affect intestinal tract as well, so the
infant develop chronic constipation
● The abdomen enlarges because if
intestinal distention and poor muscle
tone
● Skin is dry and scaly
● Decreased t3 and t4
● Increases TSH (thyrotropin)
CRETINISM
● Old term for the state of mental and
physical retardation
● Resulting from untreated congenital
hypothyroidism, due to iodine
deficiency from birth
Management:
1. Administration of thyroid hormones
(sodium levothyroxine)
● Treatment may start within the
1st 1-2 weeks of life
2. Recognized the disease as early as
possible so that there is time to
stimulate growth before epiphyseal
lines close at puberty
2. ACQUIRED HYPOTHYROIDISM
● Hashimoto’s disease
● Most common form of acquired
hypothyroidism in childhood
● Onset is often 10-11 years of age
● Hx. Of family with thyroid disease
● Caused by autoimmune phenomenon
that interferes with thyroid production
● Increased tsh when thyroid hormones
decreases in an attempt to cause the
thyroid to be more effective
Assessment:
● Hypertrophy of the thyroid gland
(goiter)
● Impaired body growth due to lack of
thyroxine
● Infant - congenital goiter can lead to
airway obstruction
● Children - obesity, lethargy, delayed
sexual development
● Anti-thyroid antibodies is present if the
illness is caused by an autoimmune
process
● Thyroid becomes enlarge and nodular
due to over secretion of TSH
Diagnostic procedure
● Administration of radioactive iodine
RESULTS: if the nodes are benign there is
generally rapid uptake of radioactive iodine
(hot nodes)
Carcinoma - if there is no uptake (cold nodes)
Therapeutic management:
● Administration of thyroid hormone
(sodium levothyroxine)
Note: obesity will diminish and growth begins
again
HYPERTHYROIDISM
● Grave’s disease
● Over secretion of thyroid hormones by
the thyroid gland
● Usually occur the time of puberty or
during adolescence
● In children it is due to autoimmune
reaction that results in overproduction
of IgG (stimulates thyroid gland to
overproduce thyroxine)
• Intolerance to heat
• Fine, straight hair
• Bulging eyes
• Facial flushing
• Enlarged thyroid
• Tachycardia
• Increased systolic BP
• Breast enlargement
• Weight loss
• Muscle wasting
• Localized edema
• Finger clubbing
• Tremors
• Increased diarrhea
 • Menstrual changes (amenorrhea)
Assessment:
● With nervousness due to production of
t3 and t4 - loss of muscle strength and
easy fatigue
● Increased BMR, BP, PR
● They perspire freely
● Always hungry although they eat
constantly
● They do not gain weight and may even
loss weight because of an increase bmr
● Swelling of the anterior neck-goiter
● Fines tremors are present
● Eye globe are prominent
(exophthalmos)
Laboratory test:
● T3, T4 AND TSH
Therapeutic management:
● Beta adrenergic blocking agent such as
propranolol to decrease antibody
response
● Anti thyroid drug is given (tapazole -
can cause decrease WBC and platelet)
to suppress the formation of
thyroxinered
● The effect of drugs will be after 2-3
weeks
● The child needs to take the drugs for 2-
3 years
● Exophthalmos may not recede but will
not become worse
● For non compliance with the medication
radioiodine ablative therapy is done to
reduce the size of thyroid gland
● Thyroidectomy (surgical removal of the
thyroid gland, or portions of it)
● After radioiodine ablative therapy and
thyroidectomy is done, supplemental
thyroid hormone is needed since the
glands no longer produce adequate
amount
TYPE 1 DIABETES MELLITUS
● Is a disorder that involves an absolute
or relative deficiency of insulin
● Formerly referred to as juvenile
diabetes or insulin dependent diabetes
Assessment:
● Onset is abrupt
● Increased thirst (polydipsia)
● Polyuria
● Increased urination may begin as
bedwetting (enuresis) in a previously
toilet trained child
● May have constipation due to
dehydration
Laboratory studies:
● Random plasma glucose level greater
than 200 mg/dl
Normal range:
● Fasting - 70 -100 mg/dl
● Non fasting - 90- 180 mg/dl
● Fasting blood glucose level greater
than 126 mg/dl
● 2 hour plasma glucose level greater
than 200 mg/dl during an oral glucose
tolerance test (gtt)
● Glycosylated hemoglobin (hba1c)
Therapeutic management :
1. Initial regulation of insulin
- When children first diagnosed with
diabetes, they are usually
hyperglycemic
2. Insulin administration
- Injection technique
3. Proper nutrition
4. Urine testing to determine presence of
ketones
5. Self blood glucose monitoring
6. Stress adjustment
7. Management of complications
 LESSON 8:
NEUROLOGICAL DISORDERS OF INFANCY AND CHILDHOOD
• Widening systolic and diastolic blood
Topics: pressure
● Neurological assessment • Decreased pulse rate
● Spina bifida • Headache increased temperature
● Hydrocephalus • Pain on neck
● Cerebral palsy • Flexion ineffective sucking
● Seizure disorders • Decreased respiratory rate
● Altered states of consciousness • Spasticity of muscles
● Meningitis
NEURO ASSESSMENT

Glasgow Coma Scale

Assessment Reaction
● Head Eye Opening • Spontaneously 4
● Eyes response • To speech 3
● Mouth • To pain 2
● V/s • No response 1
● Muscles Motor • Obeys verbal
● Neck response command 6
History: • Localizes pain 5
• Flexion withdrawal 4
Chief concern: seizure, loss of
• Flexion 3
consciousness, delay in developmental task,
• Extension 2
headache, clumsiness at motor tasks • No response 1
Past medical history: infection during Verbal • Oriented x3 - 5
pregnancy: difficult birth: difficulty with Response • Conversation
initiating respirations at birth; head injury from confused 4
fall or accident • Inappropriate speech
Family medical history: history of seizures or 3
headache in other family members • Incomprehensible
sounds 2
• No response 1
Physical examination
● A score of 3 to 8 denotes severe trauma
• Increased head circumference
● 9 to 12, moderate trauma
• Bulging fontanelles ● 13 to 15 slight trauma
• Bulging forehead ● Closure of the neural tube occurs
• Unequal size and response of pupils; during the 3rd and 4th week AOG
unequal eye globe movements
• Projectile vomiting
 SPINA BIFIDA
● Abnormality of embryonic neural tube
● Most common developmental disorder
of CNS - multifactorial inheritance
● 1-5 per 1000 live births
● Prenatal testing
● Folic acid use
● Spina bifida with meningocele
Care of myelomeningocele sac
● Wet dressings, normal saline
● Sterile field
● Closely inspect for leaks and notify
physician immediately
● Latex allergies (18% - 60%)
Prevention / prognosis
● Depends on neurological deficit
● Depends on early intervention
● Folic acid use will prevent 50-70%
● Education

Pathophysiology
● Failure of the neural tube to close
● Degree of neurological dysfunction is
directly related to the anatomic level of
the defect and the nerves involved HYDROCEPHALUS
● Imbalance in the production and
absorption of CSF in the ventricular
system
● Causes passive dilation of ventricles
with S & SX of increased ICP
● Incidence: 1.2 in 1000 births
● Hydrocephalus with spina bifida - 3 to 4
in 1000 births

Diagnostic evaluation
Based on clinical manifestations and exam of
sac
● Prenatal detection
● Labs - alpha - fetoprotein at 16-18
weeks
● Amniocentesis
● Fetal ultrasound
● CT and myelography after birth

Therapeutic management
Multidisciplinary approach:
● Antenatal microsurgical closure
● Initial care of newborn
● Early closure during 1st 24 hours
● Bladder / bowel dysfunction
● Family support
Diagnostic evaluation
● Primary diagnostic tools: CT & MRI
● Infancy - serial head measurements
● Early to late childhood - S & SX of
increased ICP and space - occupying
lesions Nursing care management
● Manifestations: depends on ● Watch for increased ICP - S & SX
developmental stage (headache, nausea, vomiting, seizure)
Therapeutic management ● Prevent infection
● Bypass blockage: surgery with VP ● Avoid scalp vein IV’s
shunt ● Observe for abdominal distention
● Treatment of complications ● Family support
● Management of problems ● Education
● Prevention of infection CEREBRAL PALSY
● Chronic, nonprogressive disorder of
posture and movement

Etiology & manifestations

Most common permanent physical disability of
childhood
● Prenatal, perinatal, or postnatal
damage to motor system
● Incidence: 2 in 1000 live births
Prognosis ● Abnormal posturing, perceptual
● If surgically treated with follow - up, 80 problems, language deficits, intellectual
% survival rate impairment
● Highest incidence of mortality within 1st
year of treatment Pathophysiology
● Surviving children - 1/2 have neurologic ● Cerebral assault: loss of voluntary
disabilities and 1/3 are normal muscular control
 ● Neuromuscular disability: ● Provide educational opportunities
determined by area of brain damage ● Promote socialization

Diagnostic evaluation
● Moro reflex
● Neuro exam & history
● Test: r/o other pathology
● Primitive reflexes continue
● Physical signs include poor head SEIZURE DISORDERS
control after 3 months of age, feeding ● Brief paroxysmal behavior due to
difficulties and floppy or limp body malfunctions of the brain’s electric
posture system (excessive discharge of
neurons)
● Most common observed neurologic
dysfunction in children
● 3% - 5% children under 18 mos
● 3% - 4% children 6 mos - 3 yrs (febrile)
● Neonatal seizures: 20 % of preterm
infants
● Epilepsy: seizure onset before 18 yrs:
60%
EPILEPSY:
a chronic seizure disorder with recurrent and
unprovoked seizures. Seizures are
characteristic of epilepsy: not every seizure is
epileptic.

Therapeutic management
● Early recognition and intervention to
attain optimum development, maximum
abilities
● Multidisciplinary approach
● Establish locomotion, communication
and self help
Etiology
● Symptomatic of altered neuronal
activity in cns
● Primary: no underlying brain structure
abnormality
● Secondary: structural or metabolic
abnormality
● 50 % idiopathic (cause unknown)
● Most common in the first 2 years of life
Classification:
● Generalized - consciousness impaired
, onset any age
● Tonic - clonic - abrupt arrest of activity
/ impaired consciousness
● Atonic - abrupt loss of postural tone,
consciousness impairment, confusion,
lethargy, & sleep
● Myoclonic - brief random contractions
of muscle group ; usually school-age or
adolescent
● Absence - brief altered consciousness,
twitching, eyelid fluttering, blank face,
onset after 5 yrs, outgrow
● Partial - onset any age, simple or
complex - odd sensations, disrupted
memory, etc.
Diagnostic evaluation
● Health history & family history
● Behavior prior, during, & after seizure
● Video recording and EEG
(electroencephalogram)
● Complete physical and neurological
exam
● Lab tests (metabolic causes)
● CT and MRI (trauma, tumor,
congenital)
● Neonates: torch titers (torch infections:
toxoplasmosis, other agents, rubella,
cytomegalovirus, & herpes simplex to
exclude viral infections)
Therapeutic management
● Discover cause and effect
● Live normal life
● Medication
● Oral care
● Don’t stop medication abruptly! Reduce
medication dose gradually.
Nursing care management
● Assessment
● Protect from harm during seizure
● Reorient to environment
● Determine trigger factors
● Medication
● Family support
STATUS EPILEPTICUS
continual or recurrent seizures lasting 30
minutes or more with no return to normal
consciousness
● Support and maintenance of vital
● functions
● iv administration of diazepam (valium)
● or lorazepam (ativan)
● iv phenobarbital (2nd round)
● monitor closely
● safety
Febrile seizures
● During temperature rise › 102°f,
(38.8°c)
● Increased susceptibility in families
● Accompany uri infection (90%)
● Boys affected twice as often as girls
● 3% develop epilepsy
Meningitis
Most common CNS infectious process:
Bacterial or viral
● Primary: bacteria or viruses
● Secondary: neurosurgery, trauma,
Sinus, ear, or systemic infections
● Most common between 1 month and 5
years; any age
● > in boys; › in african-americans
Etiology:
2mos-12 years: h. Influenzae type b
N. Menigitidis, & streptococcus
Pneumonia (95% of bacterial
Meningitis)
● Neonatal: e. Coli & group b strep
● Older children/adolescents:
Meningococcal (droplet transmission)

Pathophysiology
● Vascular dissemination from infection
elsewhere: most common
● Entry by direct implantation
● Spread to CSF
● Ill child with petechial rash medical care
immediately

Diagnosis: Therapeutic management

● LP ● Medical emergency
● Blood cultures ● Isolation (droplet) precautions for 24
● CBC hours after antibiotic treatment begins
● Signs of meningeal irritation: ● Antimicrobial therapy
1. Nuchal rigidity (+ Brudzinski’s sign and ● Hydration reduce increased ICP
Kernig’s sign) ● Management of bacterial shock
2. Opisthotonos (back is arched & neck is ● Control seizures
hyperextended) ● Control temp extremes
● Treatment of complications
Nursing care
● Assessment: history and pe
● Neuro: headache, photophobia,
hearing loss, seizures, change in loc,
pupil changes, nuchal rigidity, muscle
flaccidity, irritability
● Nausea & vomiting, loss of appetite
● HX recent immunizations or illness
● Prophylaxis for others exposed
● Family support

Prognosis
● Age of child
● Type of organism
● Severity of infection
● Duration before therapy
● Sensitivity of organism to antimicrobial
drugs
● Infants - communicating hydrocephalus
● Older children - inflammatory process
or vasculitis
 ● Mortality rate & poor neurological ● Symptoms present 6 months or more,
outcome: highest with pneumococcal before age 7, present in 2 settings (e.g.,
meningitis home, school, recreation, church)

ADHD (ATTENTION - DEFICIT Therapeutic management

HYPERACTIVITY DISORDER) ● Medication : methylphenidate Ritalin ,
Most common chronic behavioral disorder of Dexedrine, Adderall
children ● Environmental manipulation
● Developmentally inappropriate degrees ● Classroom education
of inattention and concentration, ● Support to family
impulsiveness, and hyperactivity ● Parenting classes
● Incidence: 1 % - 20 %, 4 % - 12 %
● 3:1 males to females Nursing care management
● Onset: 3-4 years ● Education
● Focus on type of learning disabilities to
Diagnostic evaluation provide direction for family
● Battery of tests ● Support to family
● Hand eye coordination ● Parenting classes
● Auditory and visual perception
● Comprehension, memory, IQ
 LESSON 10:
CHILD WITH MUSCULO-SKELETAL PROBLEM
FLAT FOOT (PES PLANUS) medial surfaces of the knees will be more
● Condition where the longitudinal arch or than 2 inches apart.
instep of the foot collapses and comes in ● Common at 2 yrs. old
contact with the ground.
● Relaxation of the longitudinal arch of the
foot.
Some common symptoms of a flat foot are:
● A flat look to one or both of you feet
● Uneven shoe wear and collapse of you
shoe toward the inside of you flat foot
● Lower leg pain
● Pain on the inside of your ankle
Management
● Swelling along the inside of your ankle
● No treatment is necessary
● Foot pain
● Problem tends to correct itself as the child
Management
grows (3 yrs. old)
● Flat feet that are painless do not require
● For those who have the abnormality
treatment.
needs to be referred to an orthopedist
● If flat feet cause pain, an evaluation with
a health care provider is needed to
determine the cause.
● Walkin in tip toe for 5-10 mins. Or daily
picking up of marbles with toe
● Some common treatments are : shoe
inserts, ankle braces, rest, surgery, pain
medication, and anti-inflammatory
medication.
Knock Knees (Genu Valgum)
Opposite of genu varum
● Medial surfaces of knee touch and medial
surfaces of the ankle malleoli are
separated by more than 3 inches
● Common at 3-4 yrs. old
Management
● No treatment is necessary
● Problem tends to correct itself as the child
Bowlegs (Genu Varum)
grows
● Lateral bowing of tibia
● For those who have the abnormality
● Malleoli (rounded prominence on either
needs to be referred to an orthopedist
side of the ankle) will be touching and the
Osteogenesis Imperfecta
 ● A connective tissue disorder in which
fragile bone formation leads to recurring
(pathologic fractures)
● 2 forms :
A) Osteogenesis Imperfecta Type 1
- A severe autosomal dominant form that is
recognized at birth
B) Osteogenesis Imperfecta Type 3
- Autosomal recessive form where
symptoms develop later in life
Assessment
Osteogenesis Imperfecta Type 1
➢ Born with countless fracture already
present from the force of birth
➢ Radiograph shows particular ribbon-like
or mosaic pattern in bones
➢ Sclera is blue in color
Osteogenesis Imperfecta Type 3
➢ Associated deafness and dental
deformities with tendency of the bone to
fracture easily
➢ Limb and spinal deformities
Management
● Growth hormone
● Calcitonin
● Biphosphonates pamidronate (increase
bone mass)
● Protection from trauma
● Fractures need to be aligned with a cast
● Lifestyle education
● Lightweight leg braces or intermedullary
rod insertion
● Keep side rails up
● Keep floors dry and remove objects that
can fall easily
● Lift child gently and avoid lifting them by
1 hand or arm only
Slipped Capita Femoral Epiphysis
● Coxa Vera
● Slipping of the femur head in relation to
the neck of the femur at the epiphyseal
line
● Proximal femoral head displaces
posteriorly and inferiorly
● Common in pre-adolescence
● 2x as frequent in young African-American
and boys
Assessment
● Limping and holding their legs externally
rotated
● Knee pain
● Internal rotation of the hip is difficult
● Radiographs reveals slipped epiphysis at
the femoral head
Management
● Surgery with pinning
● External fixation
● Health education
● Frequent visit of friends and telephone
calls
Legg-Calve-Perthes Disease
● Is a vascular necrosis of the proximal
femoral epiphysis
● Associated with incomplete clotting
factors
● More often in boys than girls
● Peak between 4-8 years old
● Usually unilateral
Assessment
● Pain in the hip joint accompanied by
spasm and limited motion
4 stages
A) Synovitis stage or period of painful
inflammation
B) Necrotic stage = bone in the femur head
shrinks in size and shows increased
density on X ray, 6-12 months
C) Fragmentation stage = resorption of dead
bone occurs over a period of 1-2 years
 D) Reconstruction stage = marks final
healing with deposition of new bone
Management
● Rest
● Containment devices (brace, cast and
etc.)
● Parent and children education about the
treatment
● NSAID (Non-steroidal anti-inflammatory
drug)
● Corrective surgery (osteotomy) - a bone
is cut to shorten, lengthen, or change its
alignment
Dysplasia of the Hip
● Head of the femur is improperly seated in
the acetabulum, or hip socket of the
pelvis
● Can be congenital or developed after
birth
Assessment
Neonates
● Laxity of ligaments around the hip
● Allows femoral head to be displaced in
the acetabulum upon manipulation
Infants beyond newborn
● Asymmetry of the gluteal and thigh
skinfolds when the child is placed prone
● Limited ROM
● Asymmetric abduction of the affected hip
when the child is placed supine with
knees and hips flexed
Toddler
● Trendelenburg’s Sign

Implementation
● Splinting of the hips with Pavlik Harness
● Following neonatal period-traction and /
or surgery to release muscle and tendons
Causes ● Following surgery - spica cast
● Congenital ● Profoundly affected - osteotomy
● Hereditary
● Breech presentation
● Swaddling infant
● Use of cradle board

*Short leg Hip Spica Cast*

 Congenital Clubfoot or Congenital Talipes
Equinovarus
● Congenital malformation of the lower
extremities
● Maybe unilateral or bilateral
● Foot is plantar flexed with an inverted
heel and adducted forefoot

Osteomyelitis
● Infection of the bone
● Caused by staphylococcus aureas
● Children with sickle cell anemia have a
special susceptibility to Salmonella
invasion in long bones
● Organism is carried out to the bone by
septicemia
● Occurs after impetigo (pustular
inflammatory dse. Of the skin), burn,
furuncle (boil or abscess) , penetrating
wound, open fracture or contamination
during surgery

Causes
● Genetic defect
● Breech presentation
● Oligohydramnios Signs and Symptoms
Management ● Systemic malaise
● Serial manipulation and castings weekly ● Fever
● If not successful within 3-6 months ● Irritability
surgery is indicated ● Sharp pain at the bone metaphysis
● Monitor for pain ● Warm to touch
● Assess NVS of the toes ● Edema
● Sequestrum-dead bone tissue
Management
● Limitation of weight bearing on the
affected part
● Bedrest
● Immobilization
● Administration of antibiotic
ex . Oxacillin
● Bisphosphonates- prevent loss of bone
density
 LESSON 11: NEONATAL BASIC LIFE SUPPORT (BLS)
Neonates are newborns who are less than a month
old. It's important to note that there are some
significant differences between resuscitating
neonates compared to infants.
As with infants, it's most common for the
respiratory drive or lack of oxygen to contribute to
the neonate's unresponsiveness versus a cardiac-
driven event. This is important as it reflects how we
perform rescue breaths and CPR. The following
CPR instructions are for respiratory distress.
Pro Tip #1: The rescue mask for neonates is
extremely small. It's important to have rescue
masks to fit every size patient, as an adult mask
could prove useless when trying to resuscitate a
newborn.
How to Provide Care
After making sure the scene is safe, that your
gloves are on, and that you have your rescue mask
with a one-way valve, begin to assess whether or
not the newborn is responsive.
If you don't get an initial response and you can see
that the infant still isn't breathing normally, place
your hand on his or her forehead and tap on the
bottom of the newborn's feet. If you still do not get
a response, proceed with the following steps.
• Call 911 and activate EMS or call in a code
if you're in a healthcare setting. If there is a
bystander nearby, you can ask for their
help – calling 911, locating an AED, etc. In
the event that you do not know how to
proceed, call 911 on your cell phone, put it
on speaker, and follow their instructions.
• Continue to assess the victim's
responsiveness and vital signs – signs of
breathing normally, signs of a pulse, etc.
• Check for a pulse using the brachial artery,
located on the inside of the arm between
the bicep and tricep against the humerus
bone. Use the flat parts of your index and
middle fingers and press on that artery.
Spend no more than 10 seconds looking for
a pulse.
Pro Tip #2: If the newborn's pulse is 100 beats per
minute or less but not less than 60, perform rescue
breathing – one rescue breath every two to three
seconds.
Rescue breathing (for pulse rates between 60 and
100) – one breath every two to three seconds,
enough air for the newborn's chest to rise and fall.
Do this for two minutes. Then check again for a
brachial pulse.
If the newborn's pulse is less than 60, begin to
perform full neonatal CPR – three chest
compressions followed by one rescue breath.
CPR Technique for Neonates
• Just as you would for infants (the
landmarks are the same), draw an
imaginary line across the newborn's
nipples and place two fingers on the lower
part of the sternum in the center of the
infant's chest. Your fingers should be
perpendicular to the baby's chest, meaning
your knuckles are directly above your
fingers during compressions.
• Stand or kneel directly over the patient's
chest. As less pressure is needed when
performing CPR on neonates, use only
your fingers to supply the force for the
chest compressions, and count as you
perform them.
• Conduct compressions that go to a depth
of 1/3 of the newborn's chest cavity, and at
a rate of between 100 and 120
compressions per minute, which amounts
to two compressions per second.
• Perform three chest compressions.
• Grab the rescue mask and seal it over the
victim's face and nose.
• Breathe once into the rescue mask and
wait for the chest to rise and fall.
• Continue to perform three chest
compressions to one rescue breath for two
minutes then reassess for vital signs. If the
neonate's pulse is still slow or there is no
pulse, continue CPR until help arrives, an
AED arrives, or the victim is responding
positively and breathing normally.
Pro Tip #3: Although most situations involving an
unresponsive neonate will be due to a respiratory
problem, remember that there is a difference in
how we resuscitate an unresponsive newborn who
has had a cardiac-related event that led to their
current condition. If their condition was due to a
congenital heart defect or cardiac arrest, perform
15 compressions to two rescue breaths and
repeat.
Performing Neonate CPR in a Two-Responder
Setting
This two-responder scenario is more likely to be
found in a clinical or professional health setting. It
allows the responders to incorporate things like
high-flow oxygen with a bag valve mask and the
use of circumferential thumb compressions. This is
much more efficient when performing just three
compressions to every breath, as one responder
can handle the bag while the other performs the
compressions.
A Word About Vital Signs (By Age)
Assessing a patient's vital signs is a crucial first
step in providing care. Therefore, it's important to
know what range is normal when it comes to pulse
rates and respirations.
For Adults (12 years and older)
Pulse rate – 60 to 100 beats per minute
Respirations – 12 to 20 breaths per minute
For Children (1 year to 12 years old)
Pulse rate – 80 to 100 beats per minute
Respirations – 15 to 30 breaths per minute
For Infants (1 month to 12 months old)
Pulse rate – 100 to 140 beats per minute
Respirations – 25 to 50 breaths per minute
For Neonates (full term to 30 days)
Pulse rate – 120 to 160 beats per minute
Respirations – 40 to 60 breaths per minute
Transcript:
So though neonatal resuscitation is not necessarily
part of the normal BLS program, we think it's
important that, for those of you who have an infant
that's less than a month old, or for those of you who
actually work with neonates, that you have an
understanding of the differentiation between baby
or infant CPR and neonatal resuscitation. So we're
going to highlight some of the aspects of both the
single and the two-rescuer CPR for the neonate.
So we understand that a neonate is a baby that not
necessarily falls into the category of premature, but
is newborn up to 30 days. We're also going to
understand that this baby, if they are in trouble, is
in most cases going to be in trouble because of
respiratory drive or a lack of oxygen, versus
cardiac-driven cardiac arrest. So a lot of what
you're going to see here is respiratory-driven
respiratory response. And you'll see that reflected
in how we give rescue breaths, but also in how we
do CPR for a neonate that we do not suspect had
cardiac arrest, and then that's why they're
unresponsive. Now keep in mind that the rescue
mask is very small. It's going to be important that
you have it be the size appropriate for the neonate.
They actually do have smaller face shields for
preemies, and so it's important that if you're in a
clinical setting, that you have the appropriate size
equipment for the appropriate size patient. Now as
we try to elicit a response from this baby, we find
that they're not breathing normally, they're
cyanotic, and they're not responsive. If we've not
already called a code or called for 911 or EMS,
we're now going to call for EMS. "You in the plaid
shirt, go call 911, come back. I might need your
help. And if you can find an AED bring it with you."
If you're in a clinical setting, call a code and bring
the cardiac resuscitation team in. Now I'm going to
be checking for a brachial pulse for no more than
10 seconds. Now this baby in this situation has a
pulse rate that is less than 100 beats per minute,
but not less than 60. In this case I'm going to begin
rescue breathing at a rate of 1 breath every 3
seconds. How much air do we put in, you say?
Enough to get chest rise and fall. So 1 breath every
3 seconds. We're going to do this for 2 minutes.
After 2 minutes I reassess for a brachial pulse, and
now the brachial pulse is less than 60 beats per
minute. I'm now going to go into neonatal
resuscitation, which is going to be 3 chest
compressions followed by 1 rescue breath, then
followed by 3 more compressions and 1 rescue
breath. And we keep that 3:1 ratio going for
another 2 minutes. Landmarks are still the same,
imaginary line across the nipples, 2 fingers down
on the sternum. We're going to be compressing at
the depth of 1/3 the chest of the baby, and we're
going to be compressing no less than 100 times
per minute, up to 120 times per minute. We're
going to do this 3:1 for 2 minutes, reassess for a
brachial pulse. If there is still a slow pulse, or no
pulse, we're going to continue CPR, 3
compressions, 1 rescue breath, until EMS arrives,
until the baby revives, or until an AED arrives. Now
let's discuss the difference between single rescuer
and two rescuer neonatal resuscitation. Now
again, remember, there's a bit of a difference in
how we resuscitate if we believe that the
unresponsive neonate is due to a cardiac-related
situation that led them to this versus a respiratory-
driven problem. If it's respiratory-driven arrest, or
bradycardia, meaning slow pulse, we're going to
be doing 3 compressions to 1 rescue breath. If we
believe though that there's a congenital heart
defect or there was a cardiac arrest that led to their
unresponsiveness and no breathing, we're going
to do 15 compressions to 2 rescue breaths. So just
a special note to keep in mind there. But when I
have a second rescuer, this works extremely well,
and it's usually going to be found more in a clinical
or a professional healthcare provider related
scenario. So with the second rescuer, we can
incorporate things like high flow oxygen with bag
valve mask, and we can also incorporate the
circumferential thumb compression, which allows
for a lot of efficiency when it comes to 3
compressions and 1 rescue breath. We're still
going to do the setup the same way. We're still
going to activate a code or EMS, but when we
deliver the CPR, you'll see how we orchestrate
two-rescuer into this. So we check for the baby's
responsiveness and normal breathing. They are
not breathing normally and they're not responding
to my taps and shouts. I'm now going to activate
EMS or call a code, and now we're going to assess
the baby for a brachial pulse for no more than 10
seconds. If at that time I feel a pulse of 100 or less,
but not less than 60, the rescue breather is going
to give 1 rescue breath every 3 seconds. >>
speaker 2: Breathe. >> speaker 1: 1 1000, 2 1000,
3 1000. >> speaker 2: Breathe. >> speaker 1: After
2 minutes of rescue breathing we're going to
reassess a brachial pulse. If at that time the pulse
rate is less than 60, we are now going to
incorporate full neonatal CPR with 3 compressions
followed by a rescue breath. 3 compressions,
rescue breath. We're going to continue to do that
until the patient begins to respond or an AED
arrives. If the AED arrives, we're going to stop only
to put the pads on, and then we'll move into the
actual defibrillation mode. But we're going to
LESSON 12: PEDIATRIC ADVANCED LIFE SUPPORT (PALS)
1. High-quality cardiopulmonary resuscitation
(CPR) is the foundation of resuscitation. New
data reaffirm the key components of high-quality
CPR: providing adequate chest compression
rate and depth, minimizing interruptions in CPR,
allowing full chest recoil between compressions,
and avoiding excessive ventilation.
2. A respiratory rate of 20 to 30 breaths per minute
is new for infants and children who are (a)
receiving CPR with an advanced airway in place
or (b) receiving rescue breathing and have a
pulse.
continue to do this resuscitative effort until either
the baby starts breathing normally or the next level
of care comes to take over.
Source:
https://www.protrainings.com/training_video/neon
atal-bls
9. Naloxone can reverse respiratory arrest due to
opioid overdose, but there is no evidence that it
benefits patients in cardiac arrest.
10. Fluid resuscitation in sepsis is based on patient
response and requires frequent reassessment.
Balanced crystalloid, unbalanced crystalloid,
and colloid fluids are all acceptable for sepsis
resuscitation. Epinephrine or norepinephrine
infusions are used for fluid-refractory septic
shock.

3. For patients with non-shockable rhythms, the

earlier epinephrine is administered after CPR
initiation, the more likely the patient is to survive.

4. Using a cuffed endotracheal tube decreases the

need for endotracheal tube changes.

5. The routine use of cricoid pressure does not

reduce the risk of regurgitation during bag-mask
ventilation and may impede intubation success.

6. For out-of-hospital cardiac arrest, bag-mask

ventilation results in the same resuscitation
outcomes as advanced airway interventions
such as endotracheal intubation.

7. Resuscitation does not end with return of

spontaneous circulation (ROSC). Excellent
post–cardiac arrest care is critically important to
achieving the best patient outcomes. For
children who do not regain consciousness after
ROSC, this care includes targeted temperature
management and continuous
electroencephalography monitoring. The
prevention and/or treatment of hypotension,
hyperoxia or hypoxia, and hypercapnia or
hypocapnia is important.
8. After discharge from the hospital, cardiac arrest
survivors can have physical, cognitive, and
emotional challenges and may need ongoing
therapies and interventions.
Note: According to research council guidelines, at any
point during the resuscitation, CPR should be interrupted
for no longer than 5 seconds.
Nursing Responsibilities
• Check a response from the patient. (Use a
verbal and physical pain response stimulus)
• Look in the airway. There are 2 possible options:
• If the airway if apparently clear and
there doesn’t appear to be any foreign
body in the airway, then move on to
 opening it and securing it with some sort
of airway adjunct.
• The other is, there could be some sort
of any foreign object obstructing the
airway and that could take a number of
different forms: it could be liquid
(mucus, blood, vomit) or it could be a
physical foreign object that the patient
has swallowed but then subsequently
choke it on.
• Next is to remove it. With a large physical object,
provider will use McGill’s forceps to remove
them. But if it is a liquid, use postural drainage
coupled with a finger sweep potentially and
suction to clear the prior to opening it.
• Expose the chest. Look, listen, and feel for
breathing for up to 10 seconds.
• In the event of having no breathing, give five
rescue breaths. Then reassess for 10 seconds.
• Start CPR.
• Attach the
pads.

• OPA is removed.
• Laryngoscope is inserted and the
ET Tube is inserted.

• Once the patch is attached, switch on the

defibrillator and a rhythm check as soon as
possible.
• Correctly identify the rhythm that you’re in.
• Charge the defibrillator with on going CPR.
• Prepare the equipment for intubation.
• Secure the ET tube manually.
• Position the patient in a “Sniffing the Morning
Air”
• Depending on the cuff of the tube, you may
have to be inflated or you may not in the
smaller tube.
• Check the tube placement by looking for equal
rise and fall of the chest.
• Auscultating both sides of the chest and over the
epigastric region.
• Connect wave from capnography.
• Remember that in doing all of these, aim for no
longer than 5 seconds off the chest at any one
point.
 • Once we verify placement, secure the
tube.
• Do another rhythm check.
• Move on now to IV/IO cannulation.
• Next is the drug administration. It is
important to check the dosages

Source:
https://www.protrainings.com/training_video/neon
atal-bls

And Patricia Olpindo’s work on Grp 4 compilation

NOTE:
MISSING TOPIC LESSON 9
SENSORY