Module No.

01
Date: 02-13-22
Topic: Complications in Pregnancy

CUES/QUESTIONS/KEYWORDS NOTES
“Disease process should be understood in order for a nursing
intention to be made.”

ASSESSMENT FOR RISK FACTORS

1) Biophysical factors
 originate from the mother or fetus
 impact the development or function of mother/fetus
 include genetic, nutritional imbalance, medical, and
obstetric issues.

2) Psychosocial factors
 maternal behaviors/lifestyles that negatively affects the
mother or fetus.
Ex. smoking, caffeine use, alcohol/drug use, and psychological
status.

3) Sociodemographic factors
 variables that pertain to the woman and her family and place
the mother and the fetus at increased risk.
Ex. access to prenatal care, age, parity, marital status, income,
and ethnicity.

MULTIPLE PREGNANCY

How do monozygotic twins Monozygotic Twins Dizygotic Twins

and dizygotic twins differ in
development?
 To form monozygotic twins,
1 fertilized egg (ovum)
splits and develops into 2
babies with exactly the
same genetic information.
 To form dizygotic twins, 2
eggs (ova) are fertilized by
Risk Factors
2 sperms and produce 2
genetically unique
children.
 Identical  Nonidentical, Fraternal
 Single Ovum +  2 ova, 2 spermatozoa
Spermatozoon  2 placenta, 2 chorion,
 1 placenta, 1 chorion, 2 amnions, 2 umbilical
2 amnions, 2 umbilical cords
cords  Has either same or diff.
 Always have same sex sex
 In-vitro fertilizations
 “IVF babies” or “test tube babies”
 More frequent in non-whites than in whites
  Multiparity
 Refers to more than 1 pregnancy
 Advanced maternal age
 > 35y.o.
 Heredity
 Genetic

Assessment
 Uterus begins to increase in size at a rate faster than usual.
 Elevated AFP
 It denotes multiple pregnancy
 Flurries of action at different portions of the abdomen during
quickening.
 Multiple sets of fetal heart sounds are heard upon
Note: Fetal heart is heard auscultation.
better on fetal back.  If one or more fetus has his or her back positioned toward
a woman’s back, only one fetal heart sound may be
heard.
 An ultrasound can reveal multiple gestation sacs early in
pregnancy.
 In some instances, early ultrasound examinations reveal
multiple amniotic sacs but then later in pregnancy, in as many
as 30% of women, only one fetus remains - vanishing twin
syndrome.
 More susceptible to complications of pregnancy:
- PIH / Pre-eclampsia
- Hydramnios
- Placenta previa
- Preterm labor
- Anemia
- Postpartum bleeding
 Higher risk for:
- Congenital anomalies – spinal cord defects
- Velamentous cord insertion
 Twin-to-twin transfusion – monozygotic
 Knotting and twisting of umbilical cords – single amnion

HYDRAMNIOS
Normal Amniotic Fluid
 Excess fluid more than 2000mL
 500 – 1000ml
 AFI above 24cm
 “normohydramnios”
Implications
- Anencephaly
- Tracheoesophageal fistula with stenosis
- Intestinal obstruction
- DM
 Complications
- Fetal malpresentation
- PROM

Assessment
 Assess fundic height
 Possible signs:
 Rapid enlargement / Excessive growth of uterus
 Unpalpable due to excess water
 Cannot be auscultated due to constant repositioning of
fetus
 Weight gain
 May have varicosity due to infused weight
 Shortness of breath due to compressed diaphragm caused
by distended uterus
 Hemorrhoids – possible due to pressure
 Confirmatory test: Ultrasound
 Insert grading of edema (associated symptom)

Therapeutic Management
SEVERE HYDRAMNIOS
 Bed rest
 Assess VS, lower extremity edema
 Therapeutic amniocentesis
 Avoid constipation, encourage a high-fiber diet, stool
What is Amniocentesis?
softener
It’s a procedure used to take
 Increase bulk in diet to reduce
out a small sample of the
pressure/constipation
amniotic fluid for testing.
 Health Teaching:
 Report any sign of ruptured membranes or uterine
What is Therapeutic
contractions
Amniocentesis?
 Assess infant for factors that may have interfered with
It is an attempt to remove
the ability to swallow in utero.
enough amniotic fluid in
 Therapeutic amniocentesis
pregnancies complicated by
 To prevent premature separation of placenta
symptomatic hydramnios to
leave a normal volume of AF.  w/ ultrasound

OLIGOHYDRAMNIOS
 A pregnancy with less than the average amount of amniotic
fluid.
 Smaller than expected growth rate
- Fetal bladder or renal disorder that interferes with
voiding.
- Severe growth restriction
- Hypoplastic lungs
 Potter’s syndrome
  Distorted features of fetus
 Amniotransfusion
 Process of transform

PREMATURE RUPTURE OF MEMBRANES (PROM)

 Rupture of fetal membranes with loss of amniotic fluid during
pregnancy before 37 weeks
 Occurs in 5% to 10% of pregnancies
 May be mistaken as urine

Complications
- Infection
- Pressure on umbilical cords
- Cord prolapse

Assessment
Results of Nitrazine test
 Blue → alkaline → amniotic
fluid
 Yellow → acidic → urine
Indication of Ferning test
Positive: presence of fern-like
patterns of amniotic fluid
crystals
 A woman usually describes a sudden gush of clear fluid from
her vagina, with continued minimal leakage.
 Occasionally, a woman mistakes urinary incontinence caused
by exertion for rupture of membranes.
 Nitrazine paper
 Used to measure vaginal pH
 Microscopic ferning
 Swabbing and drying of amniotic fluid on a slide
 High AFP in the vagina
 Ultrasound → amniotic fluid index
 Cultures for Neisseria gonorrhoeae, Streptococcus B, and
Chlamydia
 WBC, C-reactive protein
 Avoid doing routine vaginal examinations

Therapeutic Management

If fetus is mature enough… If fetus is not mature enough…

 Induction of labor
 Strict bed rest when fluid is
leaking
 Monitor for fever → sign of
infection
 Corticosteroid
 Prophylactic broadspectrum
antibiotics
 To prevent infection
 Tocolytic agents
 To mature lungs
 To inhibit contractions
 PREMATURE CERVICAL DILATATION
 Indicates possible labor
 Previously termed incompetent cervix
 A cervix that dilates prematurely and therefore cannot hold a
fetus until term.
 Dilatation is usually painless.

Symptoms
 Show – pink-stained vaginal discharge
 Increased pelvic pressure → ROM

Risk Factors
Normal Cervix  Increased maternal age
2 – 3cm  History of difficult birth, forceful D&C
 Congenitally short cervix

Therapeutic Management
 If with history in previous pregnancy, cervical cerclage can be
performed.
 Purse-string sutures are placed in the cervix by the vaginal
route under regional anesthesia. (Shirodkar or McDonald
cerclage)
 To tighten
 Sutures are removed during labor/ new labor to dilate
 Sutures are then removed at weeks 37 to 38 of pregnancy so
the fetus can be born vaginally.

PRETERM LABOR & BIRTH

 Premature labor
 the onset of labor before 37 weeks’ gestation.
 Preterm birth
 refers to gestational age at birth of less than 37
weeks.

Diagnosis of Preterm Labor

Effacement
 Persistent uterine contractions, four every 20 minutes
 Refers to thinning and
 Cervical effacement over 80% or dilation over 1 cm
shortening of cervix as it
stretches
Risk Factors
 Measured by percent
 Dehydration
 Urinary tract infection
 Periodontal disease
 Chorioamnionitis
 African American women
 Adolescents
  Inadequate prenatal care
 Strenuous work
 Women born small, partner is overweight
 Intimate partner abuse

Common Symptoms of Early Preterm Labor

 persistent, dull, low backache
 vaginal spotting
 pelvic pressure or abdominal tightening
 menstrual-like cramping
 increased vaginal discharge
 uterine contractions
 intestinal cramping

Focus: Prevention of early delivery

Therapeutic Management
Medical attempts can be made to stop labor IF
Signs of fetal distress  the fetal membranes are intact
 Tachycardia  fetal distress is absent
 Bradycardia
 there is no evidence that bleeding is occurring
 Amniotic bleeding
 the cervix is not dilated more than 4 to 5 cm
 Dilated cervix (> 4 – 5cm)
 effacement is not more than 50%
Contraindications to treating preterm labor include:
 Active hemorrhage
 Severe maternal disease
 Fetal compromise
 Chorioamnionitis
 Fetal death

Therapeutic Management
 Nursing assistance to help patient relax
 Bed rest
 IV therapy
 Vaginal, cervical cultures
 Clean-catch urine sample
 Antibiotics as needed
 Tocolytic agents
- B-sympathomimetics
- Causes blood vessels and bronchi to relax along with
uterine muscle
- Have mild hypotensive and tachycardic effect
- Potassium shift into cells → blood glucose and plasma
insulin levels increase
- Should be used cautiously in patients with DM and
thyroid dysfunction
 - Common side effects: headache, nausea and vomiting
- Obtain baseline blood data
 Hct, serum glucose, K, Na, pCO2
- Mix with PLR, piggyback; may titrate until uterine
contractions are halted
- VS q15mins, measure I&O; assess for chest pain,
dyspnea; wof pulmonary edema (rales)
- After contractions halt, a tocolytic infusion usually is
continued for 12 to 24 hours, and then oral
administration of terbutaline is begun
 Corticosteroid Therapy
- Pregnancy under 34 weeks
- Betamethasone 12mg/IM q24h x 2 doses
 Lower rates of respiratory distress
- Dexamethasone 6mg/IM q12h x 4 doses
- It takes about 24 hours for betamethasone to have an
effect, so it is important labor be halted for at least this
long.
- The effect lasts approximately 7 days

Labor that cannot be halted:

 Membranes have ruptured
 Cervix is more than 50% effaced
 Cervix is more than 3 to 4 cm dilated

If fetus is very immature → CS birth to reduce pressure on fetal head

→ reduce possibility of subdural or intraventricular hemorrhage
from a vaginal birth.

POST-TERM PREGNANCY
 Post mature / Post dated
 More than 42wks AOG
 Baby may be poisoned by own feces
 Remaining in utero for longer than 2 weeks beyond term
creates a danger to a fetus for several reasons:
 Meconium aspiration
 Macrosomia
 Calcification of placenta

Risk Factors  women receiving salicylates, myometrial quiescence

Method to check gestation
 LMP If labor has not begun by 41 weeks
 Indicates that date was probably miscalculated:
- Maternal vaginal fibronectin level
- Nonstress test
- Biophysical profile
  Labor induction
- Prostaglandin gel
 To cause cervical dilation
- Misoprostol (Cytotec)
 “pampalaglag”
- Oxytocin
 Uterine contraction

ABORTION
 Any interruption of a pregnancy before a fetus is viable.
Age of viability  Spontaneous abortion: 15-30% of all pregnancies
 24 weeks
Causes
below age of viability  Systemic infection
 Abortion  Rubella
 Syphilis
What is removed in  Poliomyelitis
spontaneous abortion?  Cytomegalovirus
“product of conception”  Toxoplasmosis infections
 UTI
 Ingestion of a teratogenic drug
 Isotretinoin
 Ingestion of alcohol

Types
1) Threatened Abortion
 Cervix closed, but bleeding, cramping and backache
occur
 Pregnancy may be continued
 Medication may be given
2) Imminent or Inevitable Abortion
 Bleeding and cramping become more severe, cervix
dilates and membranes may rupture
3) Incomplete Abortion
 All the products of conception are not expelled after
dilation of cervical os
 D+C (dilatation and curettage)
4) Complete Abortion
 All products of conception expelled within 24-48
hours
 Confirm thru ultrasound
5) Missed Abortion
 Fetus dies in utero but not expelled; client must be
monitored for DIC
6) Habitual Abortion
 Three consecutive pregnancies that end in abortion

 Incompetent cervix
 “hindi makabuo”
Assessment  to AVOID ABORTION
 Confirmation of pregnancy
 Signs of shock
 Rigid abdomen
 Cullen’s sign – bluish tinge in the umbilicus

Diagnostics
 Leukocytosis
 Transvaginal ultrasound
 Falling hCG or serum progesterone level
 Laparoscopy, culdoscopy
 Aspirate cul de sac using culdoscope

Therapeutic Management
Pharmacological
 Methotrexate – folic-acid antagonist chemotherapeutic
agent
 To prevent redevelopment
 Leucovorin
 Negative hCG titer, hysterosalpingogram
 Mifepristone – abortifacient
A ruptured ectopic pregnancy is an emergency situation!
 CBC, typing and cross-matching
 For possible blood transfusion
 hCG if pregnancy is not yet confirmed
 Large-bore IV fluid
 Laparoscopy to ligate bleeders and repair or remove
damaged
 fallopian tube

 provide emotional support

 monitor for shock management in surgery

GESTATIONAL TROPHOBLASTIC DISEASE

 Abnormal proliferation and then degeneration of the
trophoblastic villi.
 As the cells degenerate, they become filled with fluid and
appear as clear fluid-filled, grape-sized vesicles.
 Associated with choriocarcinoma

Risk Factors
 Low protein intake
 > 35 years old
 Women of Asian heritage
 Blood group A women who marry blood group O men
 Molar Pregnancy
 no fetus or amnion
Partial molar pregnancy
 a fetus or amniotic sac present
Invasive mole
 locally invasive to surrounding tissues
Choriocarcinoma
 may occur years after a hyatidiform mole

Assessment
 Larger uterus  indication for present mole
 Fetal parts are unpalpable; has dough-like consistency
 Si/sx of hypertension, hyperemesis common
 Potential for uterine perforation, hemorrhage, and infection;
passing of “grapelike” substance
 Vaginal bleeding appears brownish, prune juice
Hysterectomy is a surgical  Absence of FHT or activity
procedure to remove the  Confirmation by ultrasonography
womb (uterus)
Therapeutic Management
What is hCG?  Spontaneous evacuation
 Human chorionic  Evacuation by D&C or hysterectomy
gonadotropin (hCG)
 Continued follow-up of serum gonadotropin
 Hormone produced by
 Prevent pregnancy is essential for 1 year
placenta
 Chemotherapy if malignant
 Can be detected in urine
 hCG is monitored for:
 Measured to check
 1 year, 2x weekly
wellness of pregnancy
 If hCG is high, mattress is removed
progression

PLACENTA PREVIA
 Implantation of the placenta in the lower uterine segment
 May be partially or completely/total covered

Note: Normal segment of the placenta is ABOVE

Types
1) Type I: Low-lying
 Placenta is in lower uterine segment next to os. As
uterus stretches, placenta moves away from os.
2) Type II: Marginal
 Placental edge is at the os, but does not cover it.
3) Type III: Partial
 Placental edge partially covers the os
4) Type IV: Complete
 Placenta is centered over the os
Risk Factors
 Increased parity
 Advanced maternal age
 Past CS births
 Past uterine curettage
 Multiple gestation
 Male fetus

Assessment
 Painless, bright-red bleeding; hemorrhage in the third
trimester
 Pain indicates bleeding (dark red)
 Soft uterus in the latter part of pregnancy
 Signs of infection may be present
 Assess for:
 Signs of shock
 Changes or absence of FHR

Therapeutic Management
 Ultrasonography
 To detect location and degree of obstruction
 Depend on location of placenta, amount of bleeding and
status of fetus
 Home monitoring with repeated ultrasounds may be possible
with type I
 Control bleeding
 Replace blood loss if excessive
 CS birth
 Since obstructed
 Betamethasone

Nursing Interventions
 No admission vaginal examination
 Double set-up
 Maintain bed rest
 FHR, VS monitoring
 Assess for pallor, cyanosis; O2 as needed
 Assess perineal pads; monitor Hgb, Hct; prepare for CS
 IV therapy/blood transfusion

 Maintain bed rest w/ oxygen

 Position: left lateral position to maximize cardiac activity

ABRUPTIO PLACENTAE
 Premature separation of placenta
  May be partial, marginal, complete
 Degree of separation may be mild, moderate or severe
(Grade 1, 2 or 3)
 Painful vaginal bleeding
 Separation of placenta would mean that baby has no oxygen
supply

Note: Normal separation of placenta occurs after delivery

Complications
 Hemorrhage
 Disseminated intravascular coagulopathy
 Hyperfibrinogenemia
 increased level of fibrinogen in the blood

Possible causes
 High parity
 Advanced maternal age
 Short umbilical cord
 Gestational or chronic hypertension
 Maternal cocaine use
 Previous history of abruptio placentae
 Trauma
 Aggressive Pitocin induction
 Chorioamnionitis

Assessment
 Concealed bleeding if center of the placenta separates and
margins are intact
 Dark-red blood may not be evident with partially detached
placenta at margins
 Moderate to agonizing abdominal pain
 Persistent uterine contraction
 Firm to board-like abdomen
 Hyperactivity THEN cessation of fetal movements
 Changes in or absence of FHR
 Level of anxiety usually increases
 WOF si/sx of shock

Therapeutic Management
 Replacement of blood loss
 Emergency CS birth
 Oxygenation if necessary
 Maintain F&E

Nursing Interventions
  Maintain bed rest in lateral recumbent
 FHR, VS close monitoring
 Assess for pallor, cyanosis – O2 prn
 Blood typing, cross-matching, coag studies, Hgb, Hct
 Kleihauer-Betke test
 To determine oxygen of blood
 May be fetal of maternal
 Assess abdominal pain, tonicity of abdomen, perineal pads
 Prepare for CS birth
 IV therapy/blood transfusion

BLEEDING THROUGH PREGNANCY

FIRST TRIMESTER Threatened miscarriage

Imminent (inevitable) miscarriage
Missed miscarriage
Incomplete miscarriage
Complete miscarriage
Ectopic pregnancy
SECOND TRIMESTER Hyatidiform mole
Premature cervical dilatation
THIRD TRIMESTER Placenta previa
Abruptio placentae
Preterm labor

 Any degree of bleeding during pregnancy is potentially serious.

 The placenta has loosened, cutting off nourishment to
the fetus.
 The amount visualized may only be a fraction of the
blood lost.

Disease Process
1) Blood loss

2) Decreased intravascular volume

3) Decreased venous return, decreased CO, lowered BP

4) Body compensating by increasing HR, vasoconstriction of

peripheral vessels. Increased RR, feeling of apprehension

5) Cold, clammy skin, decreased uterine perfusion

6) Reduced renal, uterine and brain perfusion

7) Lethargy, coma, decreased renal output


Sign & Symptoms of Hypovolemic Shock
Hypovolemic Shock is an
emergency condition in which
severe blood or other fluid loss
makes the heart unable to
pump enough blood to the
body.
Emergency Interventions
DISSEMINATED INTRAVASCULAR COAGULATION
8) Renal failure
9) Maternal and fetal death
Increased pulse rate  Heart attempts to circulate the
decreased blood volume
Decreased blood  Less peripheral resistance because of
pressure decreased blood volume
Increased  Increases gas exchange to better
respiratory rate oxygenate decreased red blood cell
volume
Cold, clammy skin  Vasoconstriction occurs to maintain
blood volume in central body core
Decreased urine  Inadequate blood is entering kidneys
output because of decreased blood volume
Dizziness or  Inadequate blood is reaching
decreased level of cerebrum because of decreased
consciousness blood volume
Decreased central  Decreased blood is returning to heart
venous pressure because of reduced blood volume
 Left side-lying position
 IV fluids – D5LRS with 16- or 18- gauge angiocath; possible CVP
 O2 prn – 6-10L/min via face mask
 Monitor uterine contractions, VS q15 mins
 Omit vaginal examination
 Put on NPO
 Secure blood for possible blood transfusion
 Monitor I&O, weigh perineal pads, save any tissue passed
 Ultrasound examination
 Acquired disorder of blood clotting in which the fibrinogen
level falls to below effective limits.
 An emergency  it can result in extreme blood loss.
 Occurs when there is such extreme bleeding and so many
platelets and fibrin from the general circulation rush to the
site that not enough are left in the rest of the body.
 Paradox: at one point in the circulatory system, the person
has increased coagulation, but throughout the rest of the
system, a bleeding defect exists
Risk Factors
 premature separation of the placenta
 pregnancy-induced hypertension
 amniotic fluid embolism
 placental retention
 septic abortion
 retention of a dead fetus

Platelets quickly form a seal

over a point of bleeding

thrombin activates Intrinsic and extrinsic

fibrinolysin, a clotting pathways then
proteolytic enzyme, to activate and strengthen
begin to digest excess this plug by fibrin
fibrin threads threads to produce a
(anticoagulation) firm, fixed structure

Release of fibrin
degradation products

Diagnostics
 Testing clotting time can be done by placing a small amount
of blood in a test tube.
 After 30 minutes, a clot should not only form but retract and
the volume of serum in the tube should exceed the size of the
clot.
 If this does not occur, a low fibrinogen level is suggested

PLATELETS Decreased to =/<100,000/uL

PROTHROMBIN Low Depends on the conversion of
fibrinogen to fibrin
THROMBIN TIME Elevated Measures the time necessary for
conversion of
fibrinogen to fibrin
FIBRINOGEN Decreased to <150mg/dL Fibrinogen has been used up
FIBRIN SPLIT >40 ug/mL Reflecting the destruction of
PRODUCTS fibrinogen or fibrin

Therapeutic Management
 The underlying insult that began the phenomenon must be
halted.

DIABETES MELLITUS
Diabetes  to siphon, pass
through
Mellitus  honeyed, or sweet
Types of Diabetes
Risk Factors
Macrosomia is used to
describe a baby that’s larger
than average
 The marked coagulation must be stopped so that coagulation
factors can be freed and normal clotting function can be
restored.
 Heparin
 Blood or platelet transfusion
 Common condition in pregnancy
 A chronic metabolic disease characterized by hyperglycemia
as a result of limited or no insulin production.
 Polyuria
 Frequent urination
 Polydipsia
 Extreme thirstiness
 Polyphagia
 Eats excessive amounts of food
1) Type 1 or Insulin dependent DM (IDDM)
 autoimmunity of beta cells of the pancreas resulting in
absolute insulin deficiency
 can be managed with insulin
 has no known cause
2) Type 2 or Non-Insulin dependent DM (NIDDM)
 Characterized by insulin resistance and inadequate
insulin production.
3) Gestational DM
 Occurs during pregnancy
 Has possible risk for type 2
 Obesity
 Age over 25 years
 History of large babies (10 lb or more)
 History of unexplained fetal or perinatal loss
 History of congenital anomalies in previous pregnancies
 History of polycystic ovary syndrome
 Family history of diabetes (one close relative or two distant
ones)
 Member of a population with a high risk for diabetes (Native
American, Hispanic, Asian)
Assessment
 Hyperglycemia/hypoglycemia
 Glycosuria → polyuria
 Oral glucose tolerance test (OGTT)
 Fasting plasma glucose: =/> 126 mg/dL
 Non-fasting: =/> 200 mg/dL
 Glycosylated hemoglobin (HbA1C)

Complications
 Infection
 Preterm labor
 Pregnancy-induced hypertension
 Macrosomia → CPD → shoulder dystocia, CS birth

Therapeutic Management
 Insulin
 Early in pregnancy, a woman with diabetes may need less
insulin
 Later in pregnancy, she will need an increased amount
 OHA’s are not used for regulation during pregnancy.
 Blood glucose monitoring

Note: Always prepare client for induction of labor

Nursing Interventions
For the mother
 Encourage preconception counseling and early
medical and prenatal supervision.
 Teach and encourage adherence to dietary and
insulin regimens
 Teach signs and symptoms of hyperglycemia
(acidosis) and hypoglycemia (insulin reaction)
 Teach serum glucose testing, insulin administration
and record keeping
 Reinforce need for various tests for fetal well-being,
such as ultrasound, stress and nonstress tests,
biophysical profile, and amniocentesis for
phosphatidylglycerol levels and L/S ratio
 Prepare client for induction of labor or cesarean birth
if indicated.
  Continue monitoring for fluid and electrolyte balance
and ketoacidosis during intrapartum and postpartum
periods
 Monitor glucose levels for the first 48 postpartum
hours; women who were not insulin-dependent
before pregnancy probably will not require it after
delivery

For the neonate

 Admit infant to neonatal intensive care unit if
necessary
 Keep the infant warm because of poor temperature
control mechanisms
 Observe respirations (stomach aspiration performed
at time of birth, because hydramnios inflates
stomach, which rises and interferes with diaphragm)
 Observe for signs of hypoglycemia and hypocalcemia
such as lethargy, poor sucking reflex, cyanosis, or
muscular twitching; decreased blood glucose (30-
45mg/dL)
 Provide glucose water feeding
 to prevent acidosis (with poor sucking reflex,
glucose should be given parenterally)
 provide thru IV
 Observe for congenital anomalies; there is an
increased incidence in infants of diabetic mothers
 Promote early mother-infant interaction

PREGNANCY-INDUCED HYPERTENSION
 A condition in which vasospasm occurs during pregnancy in
both small and large arteries.
 Characterized by:
Proteinuria is increased levels  hypertension
of protein in the urine  proteinuria
 Edema

Risk Factors
 Women of color
 Multiple pregnancy
 Primiparas younger than 20 years old, older than 40 years old
 Low SES
 Five or more pregnancies
 Hydramnios
  Underlying disease such as heart disease, diabetes with vessel
or renal involvement and essential hypertension

Assessment
 Classic signs of PIH:
 Hypertension
 Proteinuria
 Edema

Classification
1) GESTATIONAL HYPERTENSION
 Elevated blood pressure (140/90 mmHg)
 But NO proteinuria or edema
 No drug therapy needed

2) MILD PRE-ECLAMPSIA
 Elevated blood pressure (140/90 mmHg) on two
occasions at least 6 hours apart.
 1+ or 2+ proteinuria
 Orthostatic proteinuria
 First morning urine sample
 Weight gain more than 2lb/week in 2nd trimester,
1lb/week in 3rd trimester

Nursing Interventions
 Clients with mild pre-eclampsia can be managed
at home with frequent follow-up care.
 Monitor antiplatelet therapy
 Promote bed rest
 Promote good nutrition
 Provide emotional support

3) SEVERE PRE-ECLAMPSIA
 BP rises to systolic 160mmHg, diastolic 110mmHg on
at least 2 occasions 6 hours apart at bed rest
 3+ or 4+ proteinuria
 Extensive edema is present
 Abdominal edema/ischemia to the pancreas and
liver → severe epigastric pain, N&V
 Pulmonary edema → SOB
 Cerebral edema → blurred visions, seeing spots,
severe headache, hyperreflexia, ankle clonus
 Decreased UO to 400-600mL/24hrs

Nursing Interventions
 >/= 36 weeks AOG
 Induced labor
 CS birth
 Less than 36 weeks AOG
 Interventions to alleviate symptoms and
allow fetus to come to term.
 Support bed rest
 Private room, darken room, peace and
quiet
 Monitor maternal well-being
 VSq4h, CBC, blood chem
 Inc. Hct levels d/t edema
 Daily weights
 IFC, UO >600mL/24hr, >30mL/hr
 Doppler q4h
 O2 as needed
 Support a nutritious diet
 Moderate-high CHON, moderate Na
 Large-bore IV

Pharmacological Interventions
Anti-hypertensive Medications
 Hydralazine - peripheral vasodilator
 Labetalol – betablockers
 Nifedipine – Ca-channel blockers
 These drugs lower blood pressure by
peripheral dilatation and do not interfere
with placental circulation
 Can cause maternal tachycardia, obtain
baseline VS
 WOF diastolic BP <80-90mmHg → inadequate
placental perfusion

 MgSO4 – cathartic
 aka magnesium sulfate
 Reduces edema by causing a fluid shift from
extracellular spaces into the intestine
 Has CNS depressant action → lessens
possibility of seizures
 Loading dose (LD) given via IV bolus
 acts almost immediately, but effect lasts only
30-60 minutes; administration must be
continuous
  To act as anticonvulsant, blood serum level: 5-
8mg/100mL
 >8mg/100mL → respiratory depression,
cardiac arrhythmia, cardiac arrest

 MgSO4 overdose: decreased UO, depressed

respirations, reduced
 consciousness, decreased DTR
 Monitor UO closely; ensure UO is above 25-
30mL/hr
 10%calcium gluconate  antidote for
magnesium toxicity
 Notify paediatrician that woman has been
receiving MgSO4 → can cause respiratory
depression
 May be given up to 12-24 hours postpartum
to prevent eclampsia
 Must be discontinued before breastfeeding

4) ECLAMPSIA
 Most severe classification of PIH
 Can happen up to 48hrs postpartum
 Cerebral edema is so acute → grand mal seizures or coma
occurs
 Maternal mortality rate: 20%
 Poor fetal prognosis: hypoxia → fetal acidosis
 Immediately before a seizure, BP and temp spike d/t
increased cerebral pressure

Tonic-clonic seizures
 Aura
 Tonic phase
 approx. 20 secs, may bite tongue, respirations
halt
 Clonic phase
 may last up to 1min, bladder and bowel
muscles contract and relax → incontinence
 Post-ictal state
 A woman is semi-comatose and cannot be
roused except by painful stimuli for 1-4 hours
 Assess for placental separation, labor
initiation
 Painful stimulus may initiate another seizure

Nursing Interventions for Eclampsia

 Maintain a patent airway
  Turn woman to her side
 Administer O2 via face mask
 Assess O2 sat
 Keep NPO
 Pharmacological: MgSO4, Diazepam
 Assess fetal well-being
 FHT via fetal heart monitor
 Check for vaginal bleeding to detect placental
separation
 Birth
 If the pregnancy is more than 24 weeks along, a
decision about birth will be made as soon as a
woman’s condition stabilizes, usually 12 to 24
hours after the seizure.
 There is some evidence that a fetus does not
continue to grow after eclampsia occurs
 Fetal lung maturity appears to advance rapidly
with PIH
 Cesarean birth is always more hazardous for the
fetus because of the association of retained lung
fluid
 A woman with eclampsia is not a good candidate
for surgery
 Vaginal birth is preferable, but CS is indicated if
fetus is compromised

HELLP Syndrome
 H-emolysis – anemia
 E-levated L-iver enzymes – epigastric pain
 L-ow P-latelets – abnormal bleeding/clotting,
petechiae

Si/sx:
 Proteinuria
 Edema
 Elevated BP
 Nausea
 Epigastric pain
 General malaise
 RUQ tenderness

Diagnostics
 RBC hemolysis – PBS appear fragmented
 Thrombocytopenia – PC <100,000/mm3
 Elevated liver enzymes – ALT, AST elevated due to
haemorrhage and necrosis of the liver
 Complications
 Subcapsular liver hematoma
 Hyponatremia
 Renal failure
 Hypoglycemia
 Maternal Risks
 Cerebral haemorrhage
 Aspiration pneumonia
 Hypoxic encephalopathy
 Fetal Complications
 Growth restriction
 Preterm birth

Therapeutic Management
 FFP, platelet transfusion
 Correct hypoglycemia via IV glucose
 Infant is born as soon as feasible by either vaginal
or CS birth
 WOF maternal haemorrhage
 Epidural anesthesia is contraindicated

CARDIOVASCULAR DISORDERS
 Cardiovascular disease now complicates only approximately
1%of all pregnancies.
 However, because it can lead to serious complications: it is
responsible for 5% of maternal deaths during pregnancy.
 Left-sided heart failure = pulmonary symptoms, orthopnea,
paroxysmal nocturnal dyspnea
 Right-sided heart failure = systemic symptoms, jugular vein
distention, increased portal circulation → liver enlargement
→ SOB, distention of abdominal muscles → ascites, peripheral
edema

Assessment
 Fatigue
 Cough
 Increased RR; tachycardia
 Poor FHT variability from poor tissue perfusion
 Decreased amniotic fluid from IUGR
 ECG, echocardiogram, chest radiography

During Labor & Birth

 Monitor fetal heart rate and uterine contractions during labor
in all
  women with heart disease.
 Assess a woman’s blood pressure, pulse, and respirations
frequently.
 A rapidly increasing pulse rate (100 beats per minute)
is an indication that a heart is pumping ineffectively
and has increased its rate in an effort to compensate.
 Side-lying position; semi-Fowler’s position
 Oxygen administration
 Continuous hemodynamic monitoring
 Anesthetic of choice: epidural
 Low forceps or vacuum extractor

Postpartum Nursing Interventions

 With delivery of the placenta, the blood that supplied the
placenta is now released into her general circulation,
subsequently increasing her blood volume 20% to 40%.
 The increase in pressure takes place within 5 minutes, so the
heart must make a rapid and major adjustment.
 For severe CHF: decreased activity, anticoagulant and digoxin
therapy
 until circulation stabilizes.
 Anti-embolic stockings and ambulation
 Prophylactic antibiotics
 Oxytocin must be used with caution

Venous thromboembolic disease

 Deep vein thrombosis
 Si/sx: pain and redness usually in the calf of a leg
 Dx: Doppler ultrasonography
 Management:
 Bed rest
 IV heparin for 24-48 hours
 Subcutaneous heparin administration
 Injection sites: arms and thighs
 Frequent PTT determinations

 The chief danger of thrombophlebitis is pulmonary embolism

or a clot lodging in the pulmonary artery and blocking
circulation to the lungs and heart.
 Symptoms of pulmonary embolism include:
 Chest pain
 Sudden onset of dyspnea
 Cough with hemoptysis
 Tachycardia or missed beats
 Severe dizziness or fainting from lowered blood pressure
ANEMIA IN PREGNANCY
True anemia is present when a woman’s hemoglobin concentration
is less than 11g/dL (hematocrit 33%) in the first or third trimester of
pregnancy or hemoglobin concentration is less than 10.5 g/dL
(hematocrit 32%) in the second trimester

Iron-deficiency anemia (IDA)

 Most common anemia of pregnancy, complicating as
many as 15%to 25% of all pregnancies.
 Microcytic, hypochromic anemia

Causes
 Diet low in iron
 Heavy menstrual periods
 Unwise weight-reduction programs
 Previous pregnancy less than 2 years before current
pregnancy

Si/sx
 Pica
 Extreme fatigue
 Poor exercise tolerance

Therapeutic Management
 Iron-rich diet
 Iron supplement – 60 mg as prophylactic therapy
 Therapeutic iron supplement – 120-200mg ferrous
sulfate, ferrous fumarate

Nursing Interventions
 Iron is best absorbed in an acid medium
 Orange juice or Vit. C supplement.
 Constipation or gastric irritation
 Ferrous sulfate turns stool black
 IM or IV Dextran

Folic Acid-Deficiency Anemia

 Megaloblastic Anemia
 Formation of red blood cells, neural tube defects
 1-5% of pregnancies

Risk Factors
 Multiple pregnancy
 Secondary hemolytic illness
 Women taking hydantoin
 Oral contraceptives
  Gastric bypass

Nursing Interventions
 Women expecting to become pregnant are advised
to begin a supplement of 400 ug folic acid daily
 Eating folacin-rich foods: green leafy vegetables,
oranges, dried beans
 During pregnancy, the folic acid requirement
increases to 600 ug/day.

Sickle Cell Anemia

 recessively inherited hemolytic anemia caused by an
abnormal amino acid in the beta chain of hemoglobin
 clumping due to reduced oxygen tension as in high
altitudes, dehydration

Risk Factors
 1/10 African Americans has the sickle cell trait
 1/400 African Americans has the disease

Nursing Interventions
 All African American women who have not been
previously tested should be screened for sickle cell
anemia at a first prenatal visit.
 A woman with sickle cell disease may normally have
a hemoglobin level of 6 to 8 mg/100 mL.
 Unless she receives active interventions to raise this
level, she will maintain it during pregnancy,
reducing oxygen to the fetus.
 Diet: sufficient amount of folic acid, fluid intake
monitoring.
 Assess for varicosities or pooling of blood in leg veins
→ red cell destruction
 Prolonged standing increases pressure, encourage
sitting, lying on Sim’s position
 Help a woman plan her day so she has limited long
periods of standing and adequate rest periods.

Therapeutic Management
 Periodic exchange transfusions to prevent sickle cell
crisis.
 Also removes increased bilirubin
 !!! Women with sickle cell are not given iron
supplement during pregnancy!

WOF
 infection → fever → sweating → dehydration
  Resp infxn → decreased PO2

URINARY TRACT INFECTION

 4-10% of nonpregnant women have asymptomatic bacteriuria.
 Progesterone → ureters dilate → urine stasis
 10-15%of pregnant women = asymptomatic UTI
 Can progress to pyelonephritis, preterm labor, PROM

 E.Coli
 Streptococcus B

Assessment
 Frequency in urination
 Painful urination
 Flank pain, tender to touch
 Fever
 Urine culture: 100,000 organisms /mL

Therapeutic Management
 Clean catch urine specimen for c/s
 Amoxicillin, ampicillin, cecphalosporins
 Sulfonamides – may not be used near term

CONTRAINDICATED
 Tetracyclines

INFLUENZA
 Caused by a virus

Si/sx
 high fever
 extreme prostration
 aching pains in the back and extremities
 sore throat

Treatment
 Antipyretic
 flu vaccine

PNEUMONIA
 Bacterial or viral, acute inflammatory response
 Can induce preterm labor d/t oxygen deficit

Treatment
  Antibiotics
 oxygen administration

ASTHMA
Airflow obstruction, airway hyperactivity, and airway inflammation

Treatment
 Inhaled corticosteroids (beclomethasone, budesonide)
 B-adrenergic agonists (terbutaline, albuterol)

PULMONARY TUBERCULOSIS
Caused by Mycobacterium tuberculosis

SI/SX
 chronic cough
 weight loss
 hemoptysis
 night sweats
 low-grade fever
 chronic fatigue

Treatment
 Isoniazid
 Ethambutol
 A woman must have 3 negative sputum cultures before she
holds or cares for her infant.

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Acid reflux into esophagus

Si/sx
 Heartburn
 gastric regurgitation
 dysphagia
 possible weight loss
 hematemesis

Management
Advise to wear loose clothing and sleep with head elevated

Diagnostics
 direct endoscopy
 ultrasound
Pharmacological
 Antacids
 H2 receptor antagonist
 PPI

CHOLECYSTITIS & CHOLELITHIASIS

Risk Factors
 Women older than 40 years
 Obesity
 Multiparity
 ingestion of a high-fat diet

Si/sx
 constant aching and pressure in R epigastrium
 may be accompanied by jaundice

Management
 lower fat intake
 NPO
 IV fluids
 laparoscopic surgery

HEPATITIS
Hepatitis A
 Fecal-oral contact
 Ingestion of fecally-contaminated water or shellfish
 Incubation period: 2-6 weeks
 Prophylactic gamma globulin for pregnant women
 Not known to be transmitted to the fetus

Hepatitis B
 Exposure to contaminated blood or blood products,
sexually transmitted, maternal/fetal transmission
 1/2000 pregnancies
 Incubation period: 6 weeks to 6 mos.
 Prophylactic immune globulin (HepaBIg), vaccine
(Hepavax)

Hepatitis C
 Exposure to contaminated blood or blood products,
sexually transmitted, maternal/fetal transmission
 Demonstrate fewer symptoms
 May not be present for 12months after exposure
 Most common cause of chronic liver disease and liver
transplantation
Management
 High-calorie diet
 CS birth may be planned to reduce maternal-fetal blood
exchange
 The mother may breastfeed
 Hepatitis during pregnancy may lead to spontaneous
miscarriage or
 preterm labor

SEIZURE DISORDERS
 Recurrent seizures have several causes:
 Head trauma
 Meningitis
 Idiopathic
 No contraindication to pregnancy exists for women with
seizures as long as the medication they take is at the lowest
dose possible and serum levels are carefully monitored.
 Seizure medications are mildly teratogenic.
 Need to be certain the medications they are taking are the
least teratogenic ones possible and the dosage they are
taking is the lowest possible to control seizures

Therapeutic Management
Early Trimester
 Remind women to continue to take their antiseizure
medications despite the nausea or vomiting of early
pregnancy.
 Be certain they understand that the rule “Do not take
medication
 during pregnancy” does not apply to their antiseizure
medications.
 The risk of adverse maternal or fetal outcome from
seizures during pregnancy, however, is greater than
the risk of teratogenicity from taking anticonvulsant
drugs.
 !!! PHENYTOIN
 Dilantin can cause a syndrome involving fetal
cognitive impairment and a peculiar facial
proportion not unlike that of fetal alcohol
syndrome.
 Competition for folic acid binding sites → neural tube
disorders
 Also prone to hemorrhagic disease of the newborn
because of decreased levels of vitamin K coagulation
factors at birth from phenytoin.
  Women may be prescribed vitamin K during labor or
the last 4 weeks of gestation.
 Women who have been taking phenytoin (Dilantin)
may have developed chronic hypertension.

HYPERTHYROIDISM
 Graves’ disease
 If undiagnosed, may develop heart failure d/t increased heart
rate.
 More prone to symptoms of hypertension of pregnancy, fetal
growth
 restriction, and preterm labor than the average woman.

Si/sx:
 increased HR
 palpitations
 exophthalmos
 heat intolerance
 nervousness
 weight loss

Management
 Thioamides – reduces thyroid activity
 Methimazole (Tapazole) – lesser evil
 Propylthiouracil (PTU)
 !!! TERATOGENS!
 Can lead to congenital hypothyroidism fetus airway
obstruction

 If hyperthyroidism is not regulated during pregnancy, an

infant may be born with symptoms of hyperthyroidism
because of the excess stimulation he or she receives in utero.
 A woman should be regulated on the lowest possible dose of
drug and cautioned to keep a careful record of doses taken so
she does not forget or accidentally duplicate a dose.
 Surgical treatment – not TOC during pregnancy

SUMMARY

ASSESSMENT FOR RISK FACTORS

1. Biophysical factors
 originate from the mother or fetus
2. Psychosocial factors
 maternal behaviors/lifestyles
3. Sociodemographic factors
 variables that pertain to the woman and her family and place
MUTIPLE PREGNANCY
 Monozygotic Twins
 Dizygotic Twins

HYDRAMNIOS
 Excess fluid more than 2000mL
OLIGOHYDRAMNIOS
 A pregnancy with less than the average amount of amniotic fluid.

PREMATURE RUPTURE OF MEMBRANES (PROM)

 Rupture of fetal membranes with loss of amniotic fluid during pregnancy before 37 weeks

PREMATURE CERVICAL DILATATION

 A cervix that dilates prematurely and therefore cannot hold a fetus until term.
 Indicates possible labor

PRETERM LABOR & BIRTH

 Premature Labor
 the onset of labor before 37 weeks’ gestation
 Preterm Birth
 refers to gestational age at birth of less than 37 weeks
 POST-TERM PREGNANCY
 More than 42wks AOG

ABORTION
 interruption of a pregnancy before a fetus is viable
 Threatened Abortion
 Imminent or Inevitable Abortion
 Incomplete Abortion
 Complete Abortion
 Missed Abortion
 Habitual Abortion

ECTOPIC PREGNANCY
 Implantation occurs outside the uterine cavity

GESTATIONAL TROPHOBLASTIC DISEASE

 Abnormal proliferation and then degeneration of the trophoblastic villi.
 Molar Pregnancy
 no fetus or amnion
 Partial molar pregnancy
 a fetus or amniotic sac present
 Invasive mole
 locally invasive to surrounding tissues
 Choriocarcinoma
  may occur years after a hyatidiform mole

PLACENTA PREVIA
 Implantation of the placenta in the lower uterine segment
 May be partially or completely/total covered
 Type I: Low-lying
 Placenta is in lower uterine segment next to os. As uterus stretches, placenta
moves away from os.
 Type II: Marginal
 Placental edge is at the os, but does not cover it.
 Type III: Partial
 Placental edge partially covers the os
 Type IV: Complete
 Placenta is centered over the os

ABRUPTIO PLACENTAE
 Premature separation of placenta
 May be partial, marginal, complete

BLEEDING THROUGH PREGNANCY

 Any degree of bleeding during pregnancy is potentially serious
 The placenta has loosened, cutting off nourishment to the fetus
 The amount visualized may only be a fraction of the blood lost

DISSEMINATED INTRAVASCULAR COAGULATION

 Acquired disorder of blood clotting in which the fibrinogen level falls to below effective limits.

DIABETES MELLITUS
 Common condition in pregnancy
 A chronic metabolic disease characterized by hyperglycemia as a result of limited or no insulin
production.
1) Type 1 or Insulin dependent DM (IDDM)
2) Type 2 or Non-Insulin dependent DM (NIDDM)
3) Gestational DM

PREGNANCY-INDUCED HYPERTENSION
 A condition in which vasospasm occurs during pregnancy in both small and large arteries
1) GESTATIONAL HYPERTENSION
2) MILD PRE-ECLAMPSIA
3) SEVERE PRE-ECLAMPSIA
4) ECLAMPSIA

Other complications:
 Cardiovascular Disorders
 Anemia In Pregnancy
 Urinary Tract Infection
 Influenza
 Pneumonia
 Asthma
 Pulmonary Tuberculosis
 Gastroesophageal Reflux Disease (Gerd)
 Cholecystitis & Cholelithiasis
 Hepatitis
 Seizure Disorders
 Hyperthyroidism
Name: Posa, Aliyah Nicole J.
Yr. / Block: 2A

Module No. 02
Date: 02 – 18 – 2022
Topic: Complications of Labor & Delivery

CUES/QUESTIONS/KEYWORDS NOTES

What to check when woman is COMPLICATIONS WITH THE POWER

in labor: Abnormal/ineffective contractions usually leads to ineffective labors
 Vital signs
 Contraction Dysfunctional labor - prolongation in the duration of labor in the
 Interval first stage of labor
 Frequency
 Pattern  Primary – occurs at the onset of labor
 Fetal heart rate  Secondary – occurs later in labor

Complications
Health Teaching during labor:  Maternal post-partal infection
 Correct positioning &  Hemorrhage
breathing  Infant mortality
 Where to hold
 Newborn care
 Breastfeeding INEFFECTIVE UTERIN FORCE
 Cord care
Hypotonic Contractions
 The number of contractions is usually low or infrequent
 Not more than 2 or 3 in a 10-minute period
 Resting tone: <10mmHg
 Strength contraction: <25mmHg
 Most apt to occur during the active phase of labor
 Contractions are not exceeding painful, because of lack of
intensity
 May occur after the administration of analgesia
 If cervix is not dilated to 3 to 4cm
 If bowel or bladder distention prevents descent or
firm engagement

Risk Factor
 Multiple Gestation
Note: Insert catheter if bladder is  Larger-than-usual single fetus
distended  to lower fetal head  Hydramnios
 Grand multiparity

When to monitor Management

 15mins in 1st 2hrs  WOF postpartal hemorrhage
 30mins in 3rd hour  Up to 1hr postpartum, palpate the uterus and assess the
 1hr in 4th hour lochia q15min

Hypertonic Contractions
Check fundus  Increased in resting tone >15mmHg
 Occur frequently and are most commonly seen in the latent
Normal location of fundus after phase of labor.
labor  More painful than usual, because the myometrium becomes
 1cm below umbilicus tender from constant lack of relaxation and the anoxia of
uterine cell that results
Uterus must be FIRM  Fetal anoxia

Management
For continuous contraction,  Uterine and fetal heart monitor
check fetal heart rate  Deceleration in FHR, or abnormally long first stage of labor –
CS birth

Normal dilation  1cm per hour Criteria Hypertonic Hypotonic

Phase of labor Latent Active
Symptoms Painful Limited pain
Must know hours of labor to Medications Used:
Oxytocin Unfavorable reaction Favorable reaction
determine dilation
Sedation Helpful Little value

Uncoordinated Contractions
“Ripe cervix”  doesn’t become
More than one pacemaker may be initiating contractions, or
thin and dilate
receptor points in the myometrium may be acting independently of
the pacemaker.
Station  the location of
Management
engagement
 Uterine and fetal heart monitor
 Higher location means (–)
 Assess the rate, pattern, resting tone and fetal response to
 Lower location means (+)
contractions for at least 15 minutes to reveal abnormal
pattern
 Oxytocin administration
3 Kinds of placental invasion
 For continuous contraction
 Based on degree of
invasion
Lengths of Phases and Stages of Normal Labor in Hours
1) Accrete Nullipara Multipara
2) Increta Phase Average Upper Average Upper
3) Percreta Normal Normal
Latent phase 8.6 20.0 5.3 14.0
Active phase 5.8 12.0 2.5 6.0
 Second stage 1 1.5 0.25 -*
Hysterectomy is the surgical
* There is no limit to the length of the second stage as long as progress is being made
removal of the uterus. It may and fetal distress is not present.
also involve removal of the
cervix, ovaries, fallopian tubes,
and other surrounding DYSFUNCTION AT FIRST STAGE OF LABOR
structures. Usually performed by
a gynecologist, a hysterectomy Prolonged Latent Phase
may be total or partial  Latent phase that is longer than 20 hours in nullipara or 14
hours in multipara
 The uterus tends to be in hypertonic state
 Relaxation between contraction is inadequate
 Contractions are only mild (less than 15mmHg) and therefor
ineffective
 May occur if the cervix is not “ripe” at the beginning of labor
and time must be spent getting truly ready for labor
 May occur if there is excessive use of an analgesic early in
labor.

Management
 Help uterus rest
 Provide adequate fluids
 Pain relief such as MG04
 Changing the linens and women’s gown, darken lights,
decrease noise and stimulation
 CS birth
 Anatomy
 Oxytocin infusion
 To induce labor

Protracted Active Phase

 Usually associated with CPD or fetal malposition
 Ineffective myometrial activity
 Cervical dilatation occurs at <1.2cm/hr in a nullipara and
<1.5cm/hr in a multipara
 Tens to be hypotonic

Management
 If with CPD – CS birth
 Baby cannot enter pelvis due to tight passage
 If no CPD – Oxytocin management

Prolonged Deceleration Phase

 A deceleration phase has become prolonged when it extends
beyond 3 hours in a nullipara or 1 hour in a multipara
 Most often result from abnormal fetal head position
 CS birth
Secondary Arrest in Dilatation
 No progress in cervical dilatation for longer than 2 hours
 CS Birth

DYSFUNCTION AT SECOND STAGE OF LABOR

Prolonged Descent
 Rate of Descent: <1cm/hr in nullipara, <2cm/hr in multipara
 2nd stage of labor last over 3hrs in a multipara
 Contractions have been good quality and proper duration, and
enforcement and beginning dilatation have occurred, but then
the contractions become infrequent and poor quality and
dilatation stops.

Management
 Rest and fluids for hypertonic contractions
 Intact BOW – amniotomy
 IV oxytocin
 Semi-Fowler’s position, squatting, kneeling, or more effective
pushing

Arrest Descent
 No descent has occurred for I hour in multipara or 2 hours in
nullipara
 Expected descent of the fetus does not begin or engagement
or movement beyond 0 station has not occurred.
 Most likely cause is CPD
 CS birth
 Oxytocin administration

Contraction Rings
 A hard band that forms accros the uterus at the junction of
the upper and lower uterine segents and interferes with the
fetal descent
 The most frequent type seen is termed a pathologic retraction
ring (Bandi’s Ring)
 Warning signs that severe dysfunction labor is occurring as it is
formed by the excessive retraction of the upper uterine
segment
 Early labor
 uncontrolled contraction
 Pelvic division of labor
 Obstetric manipulation or oxytocin administration

Management
  Ultrasound
 IV MS04, inhalation of amyl nitrate
 Tocolytics
 CS Birth

Precipitate Labor
 Labor that completed in fewer than 3 hours
 Precipitate dilatation: cervical dilation that occurs at a rate of
% cm or more per hour in primipara or 10 cm or more per
hour in multipara

Risk factor
 Grand multiparity
 Induction of Labor by oxytocin
 Amniotomy

Complications
 Abruptio placentae
 Hemorrhage
 Fetal subdural hemorrhage
 Perineal Laceration

Management
 Tocolytics

Uterine Rupture
 Vertical scar from a previous CS birth or hysterotomy tears
 <1% in low transverse CS
 4-8% in classic CS
 Prolonged labor
 Abnormal presentation
 Multiple gestation
 Unwise use of oxytocin
 Obstructed labor
 Traumatic maneuvers of forceps or traction

Assessment
 Impending rupture > pathological ring
 Strong uterine contractions without cervical dilatation.
 A sudden, severe pain during a strong labor contraction.
 She may report a "tearing" sensation.
 Incomplete rupture
 Intact peritoneur
 Localized tenderness and persistent aching pain over area
of the lower uterine segment,
 Fetal and maternal distress;
 ‘fHR Vs changes
  ‘Lack of contractions
 Confirmed by ultrasound

Complete rupture
 Endometrium, myometrium, peritoneum layers
 Uterine contractions will immediately stop
 Two distinct welling:
 Retracted uterus
 Extrauterine fetus
 Hemorrhage
 Signs of shock

Management
 Highly vascular > Ill uterine rupture is an immediate
emergency situation
 Emergency fluid replacement therapy
 IV oxytocin
 Prepare for possible laparotomy
 Viability of the fetus: extent of rupture and time elapsed
between rupture and abdominal extraction
 Woman's prognosis: Depends on extent of the rupture and
the blood loss.
 Most women are advised not to conceive again after a rupture
of the uterus, unless the rupture occurred in the inactive
lower segment.
 Consent for cesarean hysterectomy or tubal ligation

Uterine inversion
 The uterus turning inside out with either birth of the uterus or
delivery of the placenta
 1/20,000 births
 Inversion occurs in varying degrees
 May lie within the uterine cavity or vagina
 Total inversion protrudes from vagina

Risk factors
 traction is applied to the umbilical cord to remove the
placenta
 pressure is applied to the uterine fundus when the uterus is
not contracted
 the placenta is attached at the fundus so that, during birth,
the passage of the uterus pulls the fundus down

Assessment
 Large amount of blood suddenly gushes from the vagina
 Fundus isa not palpable in the abdomen
 Prolonged bleeding
  Hypovolemic shock

Management
 NEVER attempt to replace inversion
 NEVER attempt to remove the placenta if it is still attached
 Oxytocic drugs will make the uterus more tense and harder to
replace
 IV fluid replacement
 O2 via face mask
 Assess VS, anticipate need for CPR
 General anesthesia, nitroglycerin, tocolytic drug before
replacing manually
 Prophylactic antibiotic therapy
 CS for any subsequent pregnancies

Amniotic fluid embolism

 Amniotic fluid is forced into an open maternal uterine blood
sinus through:
 Some defect in the membranes
 After the membrane rupture
 Partial premature separation of the placenta
 Occurs in 1/20,000 births; accounts for 10% of maternal
deaths in the US
 It is not preventable because it is not predictable

Risk factors
 Oxytocin administration
 abruptio placentae
 hydramnios

Assessment
 A woman, in strong labor, sits up suddenly and grasps her
chest because of sharp pain and inability to breathe as she
experiences pulmonary artery constriction
 She becomes pale and then turns the typical bluish gray
associated with pulmonary embolism and lack of blood flow to
the lungs

Management
 O2 administration
 endotracheal intubation
 CPR-death
 Even if the woman survives initial insult, high risk for DIC

PROBLEMS WITH THE PASSENGER

Umbilical Cord Prolapse
 A loop of the umbilical cord slips down in front of the
presenting part

Risk factors
 Premature rupture of membranes
 Fetal presentation other that cephalic
 Placenta previa
 Intrauterine tumors preventing the presenting part from
engaging
 A small fetus
 Cephalopelvic disproportion preventing firm engagement
 Hydramnios
 Multiple gestation

Prolapse of umbilical
Umbilical cord.
 (A) The cord is prolapsed but still within the uterus.
 (B) The cord is visible at the vulva. In both instances the fetal
nutrient supply is being compromised, although only a cord
such as that shown in B would be visible.
 Both prolapses could be detected by fetal monitoring.

Umbilical cord Assessment

 In rare instances, the cord may be felt as the presenting part
on an initial vaginal examination during labor.
 Ultrasound
 More often, however, cord prolapse is first discovered only
after the
 membranes have ruptured, when a variable deceleration FHR
pattern suddenly becomes apparent.
 The cord may be visible at the vulva.
 Always assess fetal heart sounds immediately after ROM

Management
 Management is aimed at relieving pressure on the cord,
thereby relieving the compression and the resulting fetal
anoxia
 Manual elevation of fetal head off the cord
 Knee-chest or Trendelenburg
 0210 L/min by face mask
 Tocolytic agents
 Amnioinfusion
 If cord prolapse is exposed to air drying dystrophy of umbilical
vessels
 DO NOT attempt to push any exposed cord back into
the vagina. This may add to the compression by
 causing knotting or kinking.
 Instead, cover any exposed portion with a sterile saline
compress to prevent drying.
 If the cervix is fully dilated at the time of the prolapse, the
physician may choose to birth the infant quickly, possibly with
forceps, to prevent fetal anoxia.
 If dilatation is incomplete, apply upward pressure on the
presenting part until CS birth.

Shoulder Dystocia
 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.

Risk Factors
 Women with DM
 Multiparas
 post-date pregnancies
 Maternal Complications
 vaginal or cervical tears
 Fetal complication
 cord compression
 fractured clavicle or brachial plexus injury
 McRobert's maneuver
 Applying suprapubic pressure

SUMMARY
COMPLICATIONS WITH THE POWER
 Dysfunctional labor
 prolongation in the duration of labor

INEFFECTIVE UTERIN FORCE

 occurs when uterine contractions become abnormal or ineffective, as uterine contractions are
the basic force behind moving the fetus through the birth canal
 Hypotonic Contractions
 poor and inadequate uterine contractions that are ineffective to cause cervical dilation,
effacement, and fetal descent, leading to a prolonged or protracted delivery
 Hypertonic Contractions
 a contraction of increased duration or increased amplitude
 Uncoordinated Contractions

DYSFUNCTION AT FIRST STAGE OF LABOR

 Prolonged Latent Phase
 Protracted Active Phase
  Excessively prolonged active or pushing phase of labor
 Prolonged Deceleration Phase
 progress in dilation slows after 8 cm and uterine contractions become dysfunctional, even
after oxytocin administration
 the cervix starts to swell and take on fluid. In this situation, a C-section may be needed
 Secondary Arrest in Dilatation
 diagnosed when there has been no change in cervical dilation for at least 2 hours

DYSFUNCTION AT SECOND STAGE OF LABOR

 Prolonged Descent
 abnormally slow cervical dilation or fetal descent during active labor
 Arrest Descent
 the head of the fetus is in the same place in the birth canal during the first and second
examinations, which your doctor performs one hour apart
 signifies that the baby hasn't moved farther down the birth canal within the last hour
 Contraction Rings
 a spasmodic contraction of the lower portion of the uterus which usually occurs during the
first phase of labor, but persists into the second stage
 the ring contracts round the child's neck and prevents the child descending, thus delaying
and preventing delivery
 Precipitate Labor
 extremely rapid labor and delivery
 expulsion of the fetus within less than 3 h of commencement of regular contractions
 Uterine Rupture
 spontaneous tearing of the uterus that may result in the fetus being expelled into the
peritoneal cavity
 Complete rupture
 often seen as a very traumatic injury and almost always requires surgery in order to regain
proper function, regardless of where it is and of what type of tissue
 Uterine inversion
 occurs when the uterine fundus collapses into the endometrial cavity, turning the uterus
partially or completely inside out
 Amniotic fluid embolism
 occurs when amniotic fluid — the fluid that surrounds a baby in the uterus during
pregnancy — or fetal material, such as fetal cells, enters the mother's bloodstream

PROBLEMS WITH THE PASSENGER

 Umbilical Cord Prolapse
 occurs when the cord drops through the open cervix into the vagina before your baby
moves into the birth canal.
 Shoulder Dystocia
 occurs when one or both of your baby's shoulders get stuck during vaginal delivery
Name: Posa, Aliyah Nicole J.
Yr. / Block: 2A
Module No. 3
Date: March 6, 2022
Topic: POSTPARTUM COMPLICATIONS

CUES/QUESTIONS/ NOTES
KEYWORDS

POSTPARTAL HEMORRHAGE
Note: First 4 hours (most  Any blood loss from the uterus greater than 500 mL within a
difficult, should be monitored) 24-hour period.
 Early within the first 24 hours
 Late after 24 hours-6 weeks

Causes
 Uterine Atony
 Lacerations
 Retained placental fragments
 Uterine inversion
 DIC (Disseminated intravascular coagulation)

Uterine Atony
 relaxation of the uterus

Conditions That Leave the Uterus Unable to Contract Readily

 Deep anesthesia or analgesia
 Labor initiated or assisted with an oxytocin agent
 Maternal age greater than 35 years
 High parity
 Previous uterine surgery
 Prolonged and difficult labor
 Possible chorioamnionitis
 Secondary maternal illness (e.g., anemia)
 Prior history of postpartum hemorrhage
 Endometritis
 Prolonged use of magnesium sulfate or other tocolytic
therapy

Therapeutic Management
 Attempt uterine massage
 “conduct a nursing management first”
 Remain with the woman after massaging her fundus
 to be certain the uterus is not relaxing again
 Observe carefully, including fundal height and
consistency and lochia, for the next 4 hours.
 Check padding
 IV Oxytocin

Lacerations
 Small lacerations or tears of the birth canal are common and
 Large lacerations, however, can cause complications.
Episiotomy is performed to
control risk of laceration
 10-40 U/1000 mL PLR
 Duration of action: 1 hour
 If -----
 Methylergonovine maleate (Methergine)
 Ergot compound
 Given IM q2-4hrs x 5 doses
 Contraindicated to high blood pressure
 Carboprost tromethamine (Hemabate)
 Prostaglandin derivative
 May be given q15-90 mins x 8 doses
 Rectal misoprostol
 To relieve hemorrhage
 Prostaglandins tend to cause diarrhea
 Offer a bedpan or assist the woman with ambulating
to the bathroom at least every 4 hours
 Respiratory distress: O2 4L/min via face mask, supine
position
 Monitor VS, WOF si/sx of hypovolemic shock
 Blood transfusion
 To replace losses hypovolemia
 Process immediately
 Hysterectomy or suturing
 If indicated
may be considered a normal consequence of childbearing.
They occur most often:
 With difficult or precipitate births
 In primigravidas
 With the birth of a large infant (9 lb)
 With the use of a lithotomy position and instruments
Cervical Laceration
 Usually found on the sides of the cervix, near the
branches of the uterine artery.
 Arterial blood = bright red
 Repair is difficult due to poor visualization
 Be certain that a physician or nurse-midwife has
adequate space to work, adequate sponges and
suture supplies, and a good light source.
Vaginal Laceration
 Easier to assess than cervical lacerations, because
 they
 are easier to view.
 Vaginal tissue is friable.
 Some oozing often occurs after a repair, so the vagina
 may be packed to maintain pressure on the suture
line.
 IFC
 Document when and where the packing is placed.
 Packing left in more than 24-48hrs can lead to TSS.

Perineal Lacerations
Classification Involvement

First Degree Vaginal mucous membrane and skin of the perineum

to the fourchette
Second Degree Vagina, perineal skin, fascia, levator ani muscle, and
perineal body
Third Degree Entire perineum, extending to reach the external
sphincter of the rectum
Fourth Degree Entire perineum, rectal sphincter, and some mucus
membrane of the rectum

Therapeutic Management
 Perineal lacerations are sutured and treated as an
episiotomy repair.
 Document the degree of laceration.
 High fluid diet and stool softeners
 3rd- and 4th-degree lacerations should not have an
enema, rectal suppository or have rectal
temperature taken.
 4th-degree lacerations can lead to long-term
dyspareunia, rectal incontinence, or sexual
dissatisfaction.

Retained Placental Fragments

 Portion retained keeps the uterus from contracting fully →
uterine bleeding occurs
 Every placenta should be inspected carefully after birth to see
that
 it is complete.
 May also be detected by ultrasound.
 Blood serum sample: hCG → placenta is still present
 Large fragments → bleeding will be apparent in the
immediate post-partal period
 Small fragments → bleeding may not be detected until
postpartum day 6-10
 Abrupt discharge, large amount of blood
 Usually, the uterus is not fully contracted upon
 palpation.

Therapeutic Management
 Removal of the retained placental fragment is necessary
to stop the bleeding.
 D&C
 Balloon occlusion and embolization of the internal iliac
arteries
 Methotrexate

Subinvolution
 Incomplete return of the uterus to its prepregnant size and
shape.
 At a 4- or 6-week postpartal visit, the uterus is still enlarged
and soft.
 Lochial discharge usually is still present.

Causes
 Small retained placental fragment
 Mild endometritis
 Accompanying problem such as uterine myoma

Therapeutic Management
 Oral methylergonovine 0.2mg QID
 Oral antibiotic for endrometritis
 Health teaching:
 How to recognize normal process of involution,
lochial discharge before hospital discharge

Perineal Hematoma
 A collection of blood in the subcutaneous layer of tissue of the
perineum. The overlying skin, as a rule, is intact with no
noticeable
 trauma.
 Can be caused by injury to blood vessels in the perineum
during birth.
 Most likely to occur after rapid, spontaneous births and in
women
 who have perineal varicosities
 May occur at the site of an episiotomy or laceration repair if a
vein was punctured during repair.

Assessment
 Severe pain in perineal area or a feeling of pressure
between her legs.
 Inspect the perineal area for a hematoma.
  Area of purplish discoloration with obvious swelling,
tender to palpation
 May feel fluctuant, but as seepage into the area
continues and tissue is drawn taut, it palpates as a firm
globe.

Management
 Report the presence of a hematoma, its size, and the
degree
 Administer a mild analgesic as ordered for pain relief.
 Ice pack → to prevent further bleeding
 Incision and ligation under local anesthesia.

PUERPERAL INFECTION
 Theoretically, the uterus is sterile during pregnancy and until
the membranes rupture.
 After rupture, pathogens can invade.
 The risk of infection is even greater if tissue edema and
trauma are present.
 A puerperal infection is always potentially serious, because,
although it usually begins as only a local infection, it can
spread to involve the peritoneum (peritonitis) or the
circulatory system (septicemia).

Conditions That Increase a Woman’s

 Risk for Postpartal Infection
 Rupture of the membranes more than 24 hours before
birth
 Retained placental fragments
 Postpartal hemorrhage
 Pre-existing anemia
 Prolonged and difficult labor, particularly instrument
births
 Internal fetal heart monitoring
 Local vaginal infection was present at the time of birth
 The uterus was explored after birth for a retained
placenta or abnormal bleeding site

Endometritis
 Infection of the endometrium, the lining of the uterus

Assessment
 Fever manifests on 3rd-4th day pp, T >38C
 WBC is normally elevated during postpartum
 Chills, loss of appetite, general malaise
 Uterus is not well contracted and painful to touch
  May feel strong afterpains, lochia usually dark brown
and has a foul odor
 Poor uterine involution → increased amount
 High fever → may be scant or absent

Therapeutic management
 Antibiotics determined by culture of lochia
 Oxytocic agent such as Methergin
 Additional fluid
 Analgesics
 Infection control measures
 Health teaching
 Si/sx of endometritis

Infection of the Perineum

 Episiorrhapy → portal of entry

Assessment
 Localized infection, pain, heat, feeling of pressure,
discharge, appearance of wound
 Slough, purulent drainage

Management
 May remove perineal sutures to allow for draining,
packing
 Systemic or topical antibiotic
 Analgesics
 For pain
 Sitz bath
 Should be warm
 Infection control measures

Peritonitis
 Infection of the peritoneal cavity, usually occurs as an
extension of endometritis.
 One of the gravest complications of childbearing and is a
major cause of death from puerperal infection.
 The infection spreads through the lymphatic system or
directly through the fallopian tubes or uterine wall to the
peritoneal cavity.
 Abscess may form in the cul-de-sac of Douglas.

Assessment
 Si/Sx:
 rigid abdomen
  abdominal pain
 high fever
 rapid pulse,
 vomiting
 appearance of being acutely ill
 Note that uterus is well-contracted, and abdomen is
soft.
 Paralytic ileus

Management
 NGT, IV fluids or TPN
 Analgesics
 Antibiotics

Mastitis
 Infection of the breast
 May occur as early as the seventh postpartal day or not until
the baby is weeks or months old
 The organism causing the infection usually enters through
cracked and fissured nipples.
 Measures that prevent cracked and fissured nipples also help
prevent mastitis.

Preventive Measures
 Making certain the baby is positioned correctly and
grasps the nipple properly, including both nipple and
areola baby from the breast
 Washing hands between handling perineal pads and
touching the breasts
 Exposing nipples to air for at least part of every day
 Using a vitamin E ointment to soften nipples daily
 If a woman has one cracked and one well nipple,
encourage her to begin breastfeeding (when the infant
sucks most forcefully) on the unaffected nipple.

Assessment
 Mastitis is usually unilateral
 Epidemic mastitis may be bilateral
 Affected breast is painful, swollen, and reddened
 Fever accompanies these first symptoms within hours,
and breast milk becomes scant.

Management
 Antibiotics
 Breastfeeding is continued, keeping the breast emptied
 to prevent growth of bacteria
  Manual expression
 Cold/ice compress pain relief
 Warm/hot compress reduce inflammation and edema
 Good supportive bra

EMOTIONAL AND PSYCHOLOGICAL COMPLICATIONS OF THE

PUERPERIUM
 Any woman who is extremely stressed or who gives birth to
an infant who in any way does not meet her expectations may
have difficulty
 bonding with her infant.
 Inability to bond is a postpartal complication with far-reaching
implications, possibly affecting the future health of the entire
family.

A Woman Whose Newborn Has Died

 Most women are interested in seeing the baby. This is
generally therapeutic because it helps them begin grieving.
 Clean the baby, wrap the baby in an infant blanket, and bring
him or her to the parents. Remain with them, but give them
time to handle and inspect the child as they wish.

Postpartal Blues
Onset 1 – 10 days after birth
Symptoms Sadness, tears
Incidence 70% of all births
Etiology  Probable hormonal changes
 stress of life changes
Therapy Support, empathy
 let them know you understand them
Nursing Role Offer compassion and understanding

Postpartal Depression
Onset 1 – 12 months after birth
Symptoms Anxiety, feeling of loss, sadness
Incidence 10% of all births
Etiology  History of previous depression
 Hormonal response
 lack of support
Therapy Counseling, drug therapy
 refer
Nursing Role Refer to counseling
 Postpartal Psychosis
Onset Within first year after birth
Symptoms Delusions or hallucinations of harming infant or
self
Incidence 1-2% of all births
Etiology  Possible activation of previous mental illness
 hormonal changes
 family hx of bipolar d/o
Therapy Psychotherapy, drug therapy
Nursing Role Refer to psychiatric care, safeguarding mother
from injury to self or the newborn

SUMMARY

POSTPARTAL HEMORRHAGE
blood loss from the uterus that’s greater than 500 mL within a 24-hour period.

Causes
 Uterine Atony
 Failure of the uterus to contract
 Relaxation of the uterus
 Normal: FIRM, 1cm below umbilicus, no bleeding + products of conception
 Palpate to assess
 Lacerations
 May be cervical, vaginal, uterine, perineal
 Uterine laceration
 Caused by; macrosomia, instruments used, primigravida
 Retained placental fragments
 Most common
 Uterine inversion
 Inside out uterus
 Usually cause by pulling the placenta that’s still attached to the uterus
 Normal time to deliver placenta: 5-30 mins
 DIC

PUERPERAL INFECTION
 Endometritis
 inflammation of the endometrial lining of the uterus
 Peritonitis
 redness and swelling (inflammation) of the tissue that lines your belly or abdomen
 Mastitis
 inflammation of breast tissue that sometimes involves an infection

EMOTIONAL AND PSYCHOLOGICAL COMPLICATIONS OF THE PUERPERIUM

  Postpartum blues
 Postpartum depression
 Postpartum psychosis

Name: Posa, Aliyah Nicole J.

Yr. / Block: 2A

Module No. 04
Date: March 31, 2022
Topic: The High-Risk Newborn
 CUES/QUESTIONS/
KEYWORDS
Newborn at Risk because of ALTERED GESTATIONAL AGE
Gestational age refers to no.
of weeks that the infant
remained in the utero. Can be
determined by:
1) MacDonald’s rule
 measure of the size
of the uterus in cm
 distance from top
of the uterus to
symphysis pubis
2) LMP (-3mos, - 7days,
+1yr)
Dysmature infant may be born
before term or post-term, or
who is underweight or
overweight for gestational age
Full term AOG: 37 – 42wks
Pre-term AOG: < 37wks
Post-term AOG: > 43wks
Vernix caseosa acts as a
waterproof barrier to protect
the baby's skin against the
amniotic fluid and facilitates
extra-uterine adaptation of
skin in the first postnatal week
if not washed away after birth.
Meconium is a newborn's first
NOTES
Preterm Infant
 A live born infant born before the end of 37 weeks
gestation
Assessment
 Ballard Score or Maturity Scale
Complications
 Anemia of Prematurity
 a baby born early does not have enough red
blood cells
 Kernicterus
 type of brain damage that can result from
high levels of bilirubin in a baby's blood
• Persistent Patent Ductus Arteriosus (PDA)
 a persistent opening between the two major
blood vessels leading from the heart
 results from lack of surfactant, therefore,
lungs are noncompliant
 surfactant is injected to inflate lungs and
support breathing
• Periventricular/Intraventricular Hemorrhage,
intracranial hemorrhage
• Respiratory distress syndrome (RDS)
• Retinopathy of prematurity (ROP)
• Necrotizing enterocolitis (NEC)
 a serious disease that affects the intestines of
premature infants
 happens within the first 2 weeks of life in
babies who are fed formula instead of breast
milk
 bacteria invade the wall of the intestine
Post-term Infant
 A live born infant born after the 42 weeks AOG
Post-term syndrome
 Dry, cracked, almost leatherlike skin from lack of
fluid
 Absence of vernix
 AF less than usual, may be meconium-stained
 Long fingernails
poop
Complications
 Meconium aspiration
 Hypoglycemia
 Impaired thermoregulation
 Polycythemia, dehydration

Newborn at Risk because of ALTERED BIRTH WEIGHT

Altered Gestational Age
 Colorado (Lubchenco) Intrauterine Growth Chart
 used to determine if the weight of infant is small,
average or large for gestational age
 reference to monitor the premature newborn's
growth
 Low birth weight (LBW) infants – under 2500g
 Very low birth weight (VLB) – 1000-1500g
 Extremely very low birth weight (EVLB) – 500-1000g

AGA  Appropriate for Gestational Age

 10th - 90th Percentile of weight for their age

SGA  Small for Gestational Age

 Below 10th Percentile of weight for their age
 They experience intrauterine growth restriction
(IUGR)
 failed to grow at the expected rate in utero
Uterine perfusion involves the
transport of nutrients and
oxygen to the placenta and the Risk factors
fetus  Malnutrition
 Adolescent pregnancy
 Placental anomaly – most common
 Systemic diseases that decrease uterine perfusion
 Smoking, narcotic use
 Intrauterine infection- rubella, toxoplasmosis

Assessment
Acrocyanosis is blueness of
the extremities and the center
of your face like the nose and
ears.
 May be detected in utero – fundic height, sonogram
 At birth:
 Overall wasted appearance
 Small liver → difficulty regulating glucose,
protein, bilirubin
 Poor skin turgor, appear to have a large head
relative to body size
 High Hct count/polycythemia → acrocyanosis
 Hypoglycemia is common
 LGA  Large for Gestational Age
 Above 90th Percentile of weight for their age
 Also termed macrosomia
 Appears deceptively healthy, but immature
development

Risk factors
 Mothers with GDM (gestational diabetes mellitus)
or are obese
 Multiparity

Other conditions associated with LGA:

 Transposition of the great vessels
 Beckwith syndrome
 classified as an overgrowth syndrome
 affected infants are larger than normal
(macrosomia)
 Omphalocele
 birth defect of the abdominal (belly) wall
 organs stick outside of the belly through the
belly button

Assessment
 Unusually large uterus for gestational age
 Difficulty or prolonged labor → shoulder dystocia
 At birth:
 Immature reflexes, signs of prematurity
 Extensive bruising or birth injury
 Caput succedaneum, cephalhematoma,
molding

Complications
 Bruising
 Polycythemia → cardiovascular dysfunction
 Hypoglycemia

Illness in the Newborn

Transient Tachypnea of the Newborn (TTN)
 Respiratory rate that remains at 80-120 bpm beyond 1
hour after birth

Cause
 retained lung fluids

Assessment
 Mild retractions
  (-) cyanosis
 Difficulty feeding
 CXR, UTZ will reveal lung fluids

Risk Factors
 CS birth
 Extensive fluid administration of mother during
labor
 Preterm infants

Management
 Observe closely, WOF progression to more serious
illness
 O2 prn
 Peaks at 36HOL then fades, usually ends at 72HOL

Apnea
 A pause in respirations longer than 20 seconds with
accompanying bradycardia

Risk factors
 Presence of infection
 Hyperbilirubinemia
 Hypoglycemia
 Hypothermia

Management
 Gently stimulate the infant to breathe again
 Close monitoring, document duration x episode/min

Respiratory Distress Syndrome (RDS)

 Hyaline membrane disease
 Pathologic feature: hyaline-like (fibrous) membrane
lines the bronchioles, alveolar ducts, alveoli,
preventing gas exchange
 Caused by low level or absence of surfactant
 Surfactant does not form until the 34th week
AOG

Assessment
 Most infants who develop RDS have difficulty
initiating respirations at birth.
 After resuscitation:
 Low body temperature
 Nasal flaring
  Sternal and subcostal retractions
 Tachypnea (more than 60 bpm)
 Cyanotic mucus membranes
 Grunting - caused by closure of the glottis →
increases pressure in alveoli on expiration
 As distress increases:
 Seesaw respirations
 Heart failure, evidenced by decreased UO and
edema of extremities
 Pale gray skin
 Periods of apnea
 Bradycardia
 Pneumothorax

Diagnostics
 CXR – ground glass (haziness)
 ABG – respiratory acidosis
 R/O group B beta-hemolytic infections
 Blood, CSF, skin gs/cs
 Antibiotic and aminoglycoside started while
culture reports pending: Ampicillin and
Amikacin respectively

Therapeutic Management
 Surfactant replacement
 Endotracheal administration
 Mechanical ventilator
 Oxygen administration
 Mechanical ventilator
 CPAP – continuous positive airway pressure
 Pharmacological
 Indomethacin or Ibuprofen – closure of PDA
 Pancuronium IV – decrease risk of
pneumothorax
 ECMO – extracorporeal membrane oxygenation
 Liquid ventilation – perfluorocarbon
 Supportive care: keep thermoregulated, provide
hydration and nutrition

Meconium Aspiration Syndrome (MAS)

 An infant may aspirate meconium either in utero or
with the first breath at birth.
 Fetal hypoxia → stimulation of vagus nerve →
relaxation of rectal sphincter
 Can cause severe respiratory distress:
 Causes inflammation of the bronchioles
 
Block bronchioles by mechanical plugging

Decreased surfactant production through lung
trauma
 May lead to pneumonia

Assessment
 Meconium-stained AF
 Difficulty establishing respirations at birth
 Low APGAR score
 Tachypnea
 Retractions
 Cyanosis
 Barrel chest
 ABG:  PO2, increased PCO2
 CXR: bilateral coarse infiltrates in the lungs, with
spaces of hyperaeration (honeycomb effect);
diaphragm pushed downward by overexpanded
lungs

Therapeutic Management
 Amnioinfusion – to dilute the meconium in AF and
reduce risk of aspiration
 May have CS birth once meconium-stained AF is
detected
 Suction with a bulb syringe or catheter while at the
perineum, before the birth of shoulders, to prevent
meconium aspiration.
 Don’t administer oxygen under pressure (bag and
mask) until intubated and suctioned.
 Post-birth and tracheal suction, oxygen
administration and assisted ventilation.
 Antibiotic therapy as prophylaxis for secondary
pneumonia !!! meconium is sterile
 Surfactant administration
 WOF pneumothorax, pneumomediastinum, si/sx of
heart failure, hypoxia.
 Maintain neutral temp environment to prevent →
metabolic oxygen demands.
 Chest physiotherapy: clapping, vibration
 ECMO

Sudden Infant Death Syndrome (SIDS

 Sudden unexplained death in infancy
 Peak age of incidence: 2-4 months old

Risk Factors
  Adolescent pregnancy
 Closely spaced pregnancy
 Underweight, preterm infants
 Infants with bronchopulmonary dysplasia
 Twins
 Native American, Alaskan Native
 Economically disadvantaged black infants
 Infants of narcotic dependent mothers

Clinical Findings
 After being put to bed at night or for a nap, infant is
found dead a few hours later.
 They do not appear to make a sound as they die
 Many infants are found with blood-flecked sputum
or vomitus in their mouth – most likely occur as
result of death, not as a cause
 Did not suffocate from bedclothes, choke from
overfeeding, underfeeding, or crying.

Client Teaching
 American Academy of Pediatrics recommendation:
put newborns to sleep on their backs with pacifier
reduced SIDS incidence by 50%

Hemolytic Disease of The Newborn

 Hemolysis → hyperbilirubinemia
 Most common cause: ABO incompatibility
 ABO incompatibility
 Maternal blood type is O+, fetal blood type is
A, B, AB
 Progressive jaundice usually occurs within the first 24
hours of life

Diagnostics: TB, B1, B2

Therapeutic Management
 Initiation of early feeding
 Phototherapy
 Exchange transfusion

Nursing Considerations
 Place lights 12-30 inches above the infant.
 Eye and genital shield
 Stool often becomes bright green, loose and
irritating to the skin. Urine may be dark-colored.
 Keep thermoregulated; WOF skin breakdown
 Retinopathy of Prematurity
 acquired ocular disease that leads to partial or total
blindness in children
 caused by vasoconstriction of immature retinal blood
vessels d/t delivery of high concentration of oxygen.
 ROP screening routine for premature babies

Ophthalmia Neonatorum
 Eye infection that occurs during birth or during the
first month

Most common causative agents

 N. gonorrhea
 Chlamydia trachomatis

Assessment
 generally bilateral fiery red conjunctiva with thick
pus
 edematous eyelids

Prevention
 Erythromycin eye prophylaxis

Therapeutic Management
 Individualized depending on organism cultured
 gonococci – Ceftriaxone, Penicillin
 chlamydia – Erythromycin eye ointment
 Standard and contact precaution
 Eye irrigation with NSS using sterile medicine
dropper or bulb syringe, administered laterally to
prevent cross-contamination

SUMMARY
Newborn at Risk because of ALTERED GESTATIONAL AGE
Preterm Infant
 A live born infant born before the end of 37 weeks gestation
 Assessed with Ballard Score or Maturity Scale

Post-term Infant
 A live born infant born after the 42 weeks AOG

Newborn at Risk because of ALTERED BIRTH WEIGHT

Altered Gestational Age
 Colorado (Lubchenco) Intrauterine Growth Chart is used to assess and classify infant’s
 weight/growth
 Low birth weight (LBW) infants – under 2500g
 Very low birth weight (VLB) – 1000-1500g
 Extremely very low birth weight (EVLB) – 500-1000g

AGA  Appropriate for Gestational Age

 10th - 90th Percentile of weight for their age

SGA  Small for Gestational Age

 Below 10th Percentile of weight for their age

LGA  Large for Gestational Age

 Above 90th Percentile of weight for their age
 Also termed macrosomia
 Appears deceptively healthy, but immature development

Illness in the Newborn

Transient Tachypnea of the Newborn (TTN)
 Respiratory rate that remains at 80-120 bpm beyond 1 hour after birth
 Caused by retained lung fluids

Apnea
 A pause in respirations longer than 20 seconds with accompanying bradycardia
 Absence of respiration

Respiratory Distress Syndrome (RDS)

 Hyaline membrane disease
 Pathologic feature: hyaline-like (fibrous) membrane lines the bronchioles, alveolar
ducts, alveoli, preventing gas exchange
 Caused by low level or absence of surfactant

Meconium Aspiration Syndrome (MAS)

 An infant may aspirate meconium either in utero or with the first breath at birth.
 Fetal hypoxia → stimulation of vagal nerve → relaxation of rectal sphincter
 Can cause severe respiratory distress:
 Causes inflammation of the bronchioles
 Block bronchioles by mechanical plugging
 Decreased surfactant production through lung trauma
 May lead to pneumonia

Sudden Infant Death Syndrome (SIDS

 Sudden unexplained death in infancy
 Peak age of incidence: 2-4 months old

Hemolytic Disease of The Newborn

 Hemolysis → hyperbilirubinemia
 Often caused by ABO incompatibility (Maternal blood type is O+, fetal blood type is A,
 B, AB)
 Progressive jaundice usually occurs within the first 24 hours of life

Retinopathy of Prematurity
 acquired ocular disease that leads to partial or total blindness in children
 caused by vasoconstriction of immature retinal blood vessels d/t delivery of high
concentration of oxygen.
 ROP screening routine for premature babies

Ophthalmia Neonatorum
 Eye infection that occurs during birth or during the first month
 Commonly caused by N. gonorrhea and Chlamydia trachomatis
 Administer erythromycin for prevention

Name: Posa, Aliyah Nicole J.

Yr. / Block: 2A

Module No. 05
Date: 04.07.2022
Topic: Pediatric Illnesses
CUES/QUESTIONS/ NOTES
KEYWORDS

CONGENITAL HEART DISORDERS

CLASSIFICATION
Based on physical sign of cyanosis
Acyanotic Heart Disease  involves heart or circulatory anomalies
that moves blood from the arterial to the venous system
 Oxygenated to unoxygenated blood
 Left-to-right shunts

Cyanotic Heart Disease  blood is shunted from venous to arterial

system as a result of abnormal communication between the two
systems
 Unoxygenated blood to oxygenated blood
 Right-to-left shunts

Four Classifications
1) Increased pulmonary blood flow – VSD, ASD, PDA
2) Obstruction to blood flow leaving the heart – pulmonary
stenosis, aortic stenosis, COA
3) Mixed blood flow (oxygenated and deoxygenated blood mixing
in the heart or great vessels) – TGA, truncus arteriosus
4) Decreased pulmonary blood flow – tricuspid atresia, TOF

Ventricular Septal Defect

 most common type of congenital cardiac disorder
 an opening is present in the sputum between the two
ventricles
 greater pressure on the left ventricle
 left to right shunt (acyanotic disorder)

Symptoms
 begin around 4-8wks of age
 easy fatigue
 loud, harsh pansystolic murmur at 3rd – 4th interspace
 palpable thrill

Dx
 Doppler of MRI  R ventricular hypertrophy, pulmonary
artery dilatation
 ECG  R Ventricular Hypotrophy

Management
 Up to 85% close spontaneously
  Open-heart surgery before 2yo

Atrial Septal Defect

 Abnormal communication between the two atria
 Left to right shift (acyanotic effect)

Assessment
 Harsh systolic murmur over the 2nd-3rd interspace
 Fixed splitting – second heart sound auscultated as split
 Dx: Doppler – enlarged right side of the heart, increased
pulmonary circulation

Therapeutic Management
 Surgery to close the defect is done electively between 1-
3 y/o.
 Without closure  infectious endocarditis  heart
failure

Patent Ductus Arteriosus

 Ductus arteriosus - fetal structure that connects the
pulmonary artery to the aorta.
 Closure begins with first breath, usually complete between 7-
14 days of age; full closure may be up to 3 mos.
 Blood shunts from aorta to the pulmonary artery (acyanotic)
 blood returns to L atrium  L ventricle  aorta 
pulmonary artery.
 Increased pressure in the pulmonary circulation  R
ventricle hypertrophy and ineffective heart action

Assessment
 Twice as common in girls as boys.
 Wide pulse pressure
 Continuous “machinery murmur at the upper left
sternal border or under the left clavicle
 Echocardiography – visualization of the patent ductus.

Management
 IV indomethacin, ibuprofen, prostaglandin inhibitors.
 Cardiac catheterization
 Surgical intervention: ductal ligation via thoracotomy

Pulmonary Stenosis
 Narrowing of the pulmonary valve or the pulmonary artery
just distal to the valve.
 Accounts for 10% of congenital heart anomalies
 Narrowing creates obstruction  unable to empty the right
ventricle  R ventricular hypertrophy
Assessment
 Asymptomatic, or signs of mild R-sided heart failure
 If severe, cyanosis
 Systolic ejection murmur, grade IV or V crescendo-
 decrescendo loudest at left sternal border
 Echocardiography – R ventricle hypertrophy

Therapeutic Management
 Depends on the age and severity
 Balloon angioplasty via cardiac catheterization
 After the procedure, the child may always have a
residual heart murmur

Aortic Stenosis
 Stenosis or stricture of the aortic valve.
 Prevents blood from passing freely from L ventricle to the
aorta  increased pressure and L ventricle hypertrophy 
increased pressure in L atrium  back-pressure in pulmonary
veins  pulmonary edema

Assessment
 Generally asymptomatic, typical murmur heard loudest
in the second right interspace
 Thrill may be present – suprasternal notch
 If severe, decreased cardiac output evidenced by:
 Faint pulses
 Hypotension
 Tachycardia
 Inability to suck for long periods
 When child is active 🡪 chest pain, similar to angina
 ECG or echocardiography 🡪 L ventricular hypertrophy

Therapeutic Management
 Beta blocker or calcium channel blocker – reduce
hypertrophy before the defect is corrected
 Balloon valvuloplasty – surgical treatment of choice
 For severe defects 🡪 dividing the stenotic valve, or
dilating a constrictive aortic ring
 Artificial valve replacement

Coarctation of the Aorta (COA)

 Narrowing of the lumen of the aorta due to a constricting
band
 Occurs more frequently in boys than in girls.
 Results in increased BP in the heart and upper body,
decreased BP in lower body 🡪 BP in arms at least 20 mmHg
 higher than in legs

Assessment
 Mild: absent palpable femoral pulses
 As child grows older 🡪 leg pain on exertion d/t
diminished blood supply
 Echocardiography, MRI, X-ray – L sided heart
enlargement
 Soft or moderately loud systolic murmur may or may
not be present

Therapeutic Management
 interventional angiography (balloon catheter)
 surgery: narrowed portion of the aorta is removed, new
ends are anastomosed
 subclavian artery graft
 infants: digoxin therapy, diuretics pre-op

Transposition of the Great Arteries

 aorta arises from right ventricle instead of the left
 blood enters from vena cava to r atrium  r ventricle 
aorta completely deoxygenated then returns by vena
cava
 pulmonary artery arises from left ventricle instead of the right
 blood enters from pulmonary vein  l atrium  l
ventricle  pulmonary artery
 creates two closed circulatory system
 this defect is incompatible with life
 may also occur along with ASD/VSD
 tends to occur in large newborns and more often in boys than
girls

Assessment
 Usually cyanotic at birth
 No murmur, or various murmurs in presence of other
defects
 Echocardiography  enlarge heart
 Cardiac catheterization  low O2 sat

Therapeutic Management
 If no septal defect: PGE1 to keep ductus arteriosus
patent
 Balloon atrial septal pull-through: open the foramen
ovale
 Surgical correction at 1 week to 3 months of age –
arterial switch procedure
Truncus Arteriosus
 Rare defect, approximately 1%
 One major artery or “trunk” arises from left and right
ventricles
 Usually with accompanying VSD
 Cyanotic and may have typical VSD murmur
 Repair – restructuring the common trunk to create separate
vessels
 May need a second surgical procedure as the graft inserted is
outgrown

Tricuspid Atresia
 Extremely serious disorder because the tricuspid valve is
completely closed
 No blood flow from right atrium to the right ventricle
 Instead, blood crosses patent foramen ovale into L atrium 
bypasses lungs and therefore oxygenation
 Oxygenation by shunt via PDA
 As long as foramen ovale and ductus arteriosus remain open,
the child can obtain adequate oxygenation, but eventually
they will close
 Surgery: construction of vena cava to pulmonary artery shunt
(Fontan procedure or Glenn Shunt baffle)

Tetralogy of Fallot
 Four anomalies:
 Pulmonary stenosis
 VSD (usually large)
 Dextroposition (overriding) of the aorta
 Hypertrophy of the right ventricle
 A number of children with this disorder show a deletion
abnormality of chromosome 22

Assessment
 Absent or minimal cyanosis immediately after birth, but
becomes cyanotic thereafter.
 Polycythemia
 If not corrected:
 Severe dyspnea
 Growth restriction
 Clubbing of the fingers
 Child assumes squatting or knee-chest position
 Loud harsh widely transmitted murmur or a soft,
scratchy,
 localized systolic murmur in the L 2nd, 3rd or 4th
parasternal interspace.
 Echocardiography, ECG – enlarged R side of the heart,
 decrease in size of pulmonary artery, reduced blood
flow to the lungs
 Cardiac catheterization and angiography – definitive
evaluation
 CBC inc. Hgb, Hct, dec. O2 sat

Therapeutic Management
 Surgical correction at 1-2 years of age
 O2 administration
 To prevent hypercyanotic episodes
 Place the baby in knee-chest position
 MSO4
 To generally reduce symptom
 Propanolol
 To aid pulmonary artery dilation
 Blalock-Taussig procedure
 temporary or palliative, creates a shunt between
the aorta and the pulmonary artery (creating a
PDA)
 Brock procedure
 full repair

DISORDERS OF THE RESPIRATORY SYSTEM

Acute Nasopharyngitis (Common Cold)
 Incubation period: typically 2-3days
 Common infectious agents: rhinovirus, coxsackievirus, RSV,
adenovirus, and parainfluenza and influenza viruses

Assessment
 nasal congestion
 watery rhinitis
 low-grade fever (except for infants)
 cervical lymph nodes may be swollen and palpable
 may progress into a cough and/or sore throat
 infants may develop secondary symptoms such as
vomiting and diarrhea

Therapeutic Management
 There is no specific treatment for a common cold.
 Symptomatic management:
 Acetaminophen or ibuprofen for fever
 !!! Children below 18 years old must not be given
ASA
 Saline nose drops or nasal spray for infants
 Guaifenesin – expectorant

Pharyngitis
  Infection and inflammation of the throat

Viral pharyngitis
 Causative agent: adenovirus
 Si/Sx: sore throat, fever, general malaise, erythema on in
back of pharynx and palatine arch, increased WBC
 Warm compress, gargle with warm water, WOF dehydration

Streptococcal pharyngitis
 Group A beta-hemolytic streptococcus
 All streptococcal infections must be taken seriously 🡪 can
lead to cardiac and kidney damage from the accompanying
autoimmune process
 Si/Sx: erythematous back of throat and palatine tonsils
(bright red), enlarged tonsils, white exudate in the tonsillar
crypts, high fever, extremely sore throat, difficulty
swallowing, lethargy, headache
 Throat culture: (+) Streptococcus bacteria

Management
 10-day course oral antibiotics:
 Pen G
 Clindamycin
 Cephalosporins or broad-spectrum macrolides – (+)
resistance
 Si/sx of acute glomerulonephritis (AGN) appear in 1-2
weeks
 Child may be asked to come back after 2 weeks for a
urine test

Tonsillitis
 Infection and inflammation of the palatine tonsils.
 “Adenitis” – infection and inflammation of the adenoid
(pharyngeal) tonsils

Assessment
 same symptoms as pharyngitis
 drooling – the throat is too sore for them to swallow
saliva
 swallowing described as swallowing bits of metal or
glass
 high fever, lethargy
 tonsillar tissue appears bright red and enlarged
 pus can be detected or expelled from the tonsillar crypts
 Adenoid: nasal quality of speech, mouth breathing,
difficulty hearing, halitosis and sleep apnea
 throat culture
Therapeutic Management
 Tonsillectomy – removal of the palatine tonsils
 Adenoidectomy – removal of the pharyngeal tonsils
 done once the child is well; if done while the infection is
active, might spread the pathogen and cause septicemia
 WOF si/sx of hemorrhage: a child may be swallowing
blood

Epistaxis
 Nosebleed

Causes
 trauma
 homes that lack humidification
 strenuous exercise
 tends to occur during respiratory illnesses
 associated with several systemic illnesses: rheumatic
fever, scarlet fever, measles, chickenpox

Management
 Keep in upright position with head tilted slightly forward
to minimize blood pressure in nasal vessels
 Apply pressure to the sides of the nose with your fingers
 Keep the child quiet or help stop crying
 Nasal pack – cold compress
 Epinephrine (1:1000)

Sinusitis
 Infection and inflammation of the sinuses
 Rare in children younger than 6 years of age 🡪 frontal sinuses
do not
 develop fully until age 6
 Si/sx: fever, purulent discharge, headache, tenderness over
the affected sinuses
 (+) nose and throat culture
 Management
 antipyretic
 analgesic
 antibiotic for specific organism
 Oxymetazoline hydrochloride – nasal drops or nasal
spray

Laryngitis
 Inflammation of the larynx
 May occur as complication of phrayngitis or from excessive
use of voice, shouting or loud cheering
  Si/sx: brassy, hoarse voice sounds or inability to make audible
voice sounds
 Management
 Sips of fluid – warm or cold, whichever feels best.
 Have the child rest the voice for at least 24 hours
 For infants, attend to their needs before they start
crying
 Older child – caution them not to speak; provide a
whiteboard or paper and pencil for communication

Croup (Laryngotracheobronchitis)
 inflammation of the larynx, trachea, and major bronchi
 Common causative agent: viral infection such as parainfluenza
virus; H. influenzae

Assessment
 Mild upper respiratory tract infection symptoms at
bedtime
 Temperature is normal or slightly elevated
 During the night, they develop a barking cough (croupy
cough), inspiratory stridor, and marked retractions
 They wake in extreme respiratory distress
 These severe symptoms typically last several hours and
then, except for a rattling cough, subside by morning.
Symptoms may recur the following night

Therapeutic Management
 Run the shower or hot tap to fill the room with steam
and keep the child inside until symptoms are relieved
 If not relieved, bring child to emergency department
 Corticosteroid or racemic epinephrine via nebulizer
 IV therapy; monitor I&O and urine specific gravity

Aspiration
 Inhalation of a foreign object into the airway
 Occurs most frequently in infants or toddlers
 Initial reaction is choking, and hard, forceful coughing 🡪 can
dislodge the object
 Cough with no sound 🡪 airway is obstructed; intervention is
necessary
 subdiaphragmatic abdominal thrusts
 for infants, use back thrusts

Influenza
 Inflammation and infection of the major airways
 Caused by the orthomyxovirus influenza type A, B, or C
 Si/sx: cough, fever, fatigue, aching pains, a sore throat, and
 often accompanying GI symptoms such as vomiting or
diarrhea.
 Management
 antipyretics – acetaminophen (Tylenol)
 Oseltamivir (TamiFlu) – children over 1 year old
 Flu vaccine

Bronchitis
 Inflammation of the major bronchi and trachea

Assessment
 mild URTI for 1-2 days  fever and dry, hacking cough
(hoarse and mildly productive in older children)
 cough is serious enough to wake a child from sleep
 si/sx may last a week, full recovery up to 2 weeks
 On auscultation, rhonchi and coarse crackles
 CXR: diffuse alveolar hyperinflation and some markings
in the hilus of the lungs

Therapeutic Management
 Therapy is aimed at relieving respiratory symptoms,
reducing fever, and maintaining adequate hydration
 Antibiotics – bacterial infections
 Expectorants

Respiratory Syncytial Virus Bronchiolitis

 RSV – pathogenic RNA virus that is most common cause of
bronchiolitis in young children

Si/sx
 mild URTI that quickly extends to bronchioles
 Infant quickly becomes lethargic and possibly cyanotic
 Dehydration
 Resp. distress – nasal flaring, retractions, grunting, rales,
 wheezing noted on auscultation
 !!! Monitor for apnea

Management
 Supportive therapy
 Supplemental oxygen
 Hydration
 Life-threatening apnea may need mechanical ventilation
 Ribavirin
 Isolate infants with RSV

Asthma
 Immediate hypersensitivity (type 1) response
  Most common chronic illness in children
 Tends to occur in children with atopy or hypersensitive to
allergens.
 pollens, molds, house dust, food, cold air, irritating
odors, air pollutants (e.g. cigarette smoke)
 Mast cells release histamine and leukotrines  triad of
inflammation, bronchoconstriction, and increased mucus
production  diffuse obstructive and restrictive airway
disease

Assessment
 History
 what the child was doing at the time of the attack
 what actions were taken by the parents or child to
decrease or arrest the symptoms
 describe the home environment, including any
pets, the child’s bedroom, outdoor play space,
classroom environment, and type of heating in
the house, etc.
 Physical Assessment
 wheezing so loud it can be heard without
auscultation
 Cyanosis
 Elevated eosinophil count
 Bronchospasm  CO2 trapping and retention 🡪
air-filled lungs  hyperresonant to percussion
 Longer expiration phase than inspiration
 Retractions
 Decreased wheezing means less air can go in 
hypoxemia  cyanosis
 Chronic sufferers:
 barrel-shaped chest
 clubbing of fingernails

Therapeutic Management
 Goals of therapy:
 avoidance of allergen by environmental control
 skin testing and hyposensitization to identified
allergens
 relief of symptoms by pharmacologic agents
 Cough suppressants are CONTRAINDICATED
 Pharmacological Tx:
 inhaled anti-inflammatory corticosteroid such as
fluticasone
 long-acting bronchodilator at bedtime
 short-acting beta-2–agonist bronchodilator, such
as albuterol or terbutaline
  leukotriene receptor antagonists such as
montelukast
 WOF dehydration
 Encourage to drink fluids, but avoid milk or milk
products

Status Asthmaticus
 Child fails to respond to first-line therapy (aerosol
administration of a bronchodilator)
 an extreme emergency

Assessment
 Acute respiratory distress
 Increased HR, RR
 O2 sat, PO2 low
 PCO2 elevated 🡪 acidosis
 Breath sounds limited (wheezing no longer heard)
 Often triggered by respiratory infection
 obtain cultures from coughed sputum
 broad-spectrum antibiotics until culture results
are available

Therapeutic Management
 Continuous nebulization with an inhaled beta-2-agonist
 IV corticosteroids
 Oxygen via face mask or nasal cannula to
 maintain the PO2 at more than 90 mm Hg.
 Drinking tends to aggravate coughing  IVF of D5
0.45NaCl
 Do not offer cold drinks  can trigger bronchospasm
 Monitor I&O, urine specific gravity

Pneumonia
 Infection and inflammation of the alveoli
 Types: hospital-acquired and community acquired
 May be bacterial, viral or aspiration
 Pneumocystis carinii pneumonia – associated with HIV/AIDS

Pneumococcal pneumonia
 Therapeutic Management
 Antibiotics: ampicillin or a third-generation
cephalosporin
 Amoxicillin-clavulanate (Augmentin) -
penicillin-resistant organisms
 Children need rest to prevent exhaustion
 Turn and reposition a child frequently to avoid pooling
of secretions
  IV therapy to supply necessary fluids; infants may tire
of sucking
 Humidified oxygen
 Assess oxygen saturation via pulse oximeter
 Chest physiotherapy
 Pneumococcal vaccine

Viral pneumonia
 generally caused by the viruses of upper respiratory tract
infection: the RSVs, myxoviruses, or adenoviruses.
 Assessment
 Si/sx of URTI for first 1-2 days 🡪 low-grade fever,
nonproductive cough, tachypnea
 Diminished breath sounds and fine rales upon
auscultation
 RSV may cause apnea
 CXR: diffuse infiltrated areas
 Therapeutic Management
 Symptomatic management
 Anti-pyretics
 IV fluid if w/ dehydration

Rheumatic Fever
 Autoimmune disease  reaction to group A beta-hemolytic
streptococcal infection
 Inflammation  fibrin deposits on the endocardium and
valves, esp. mitral valve, as well as major body joints.
 Often follows an attack of pharyngitis, tonsillitis, scarlet fever,
“strep throat”, or impetigo.
 Occurs most often in children 6-15 y/o, peak incidence at 8
y/o.
 Children do not develop immunity to streptococcal infections
 infections can recur
 Si/Sx of original infection subside in a few days, child appears
well  after 1-3 weeks, onset of rheumatic fever symptoms

Assessment
 Jones criteria
 Major
 Carditis
 Erythema marginatum – macular rash found
predominantly
 on the trunk
 Subcutaneous nodules
 Sydenham’s chorea – sudden involuntary
movement of the
  limbs
 Polyarthritis
 Minor
 Arthralgia
 Fever
 Hx of previous rheumatic fever; prolonged
PR interval
 Elevated ESR, C-reactive protein,
leukocytosis

Therapeutic Management
 Full course is 6-8 weeks
 Maintain on bedrest during acute phase of illness
 Monitor VS, apical pulse
 Penicillin therapy; single IM benzathine penicillin
 Oral ibuprofen – arthralgia, inflammation
 Corticosteroids – if not responding to ibuprofen
 Phenobarbital, diazepam – chorea
 Digoxin, diuretics – if heart failure is present

Kawasaki Disease
 Mucocutaneous lymph node syndrome
 A febrile, multisystem disorder that occurs almost exclusively
in
 children before the age of puberty
 The peak incidence is in boys under 4 years of age
 Vasculitis (inflammation of blood vessels) is the principal (and
life- threatening) finding because it can lead to formation of
aneurysm and myocardial infarction
 Infection  altered immune function  increased antibody
production  circulating immune complexes (antigen-
antibody) bind to the vascular epithelium  inflammation of
blood vessels  aneurysm, platelet accumulation, thrombi
formation

Assessment
 Acute phase (Stage 1)
 High fever (39-40C) that doesn’t respond to
antipyretics
 Lethargic, or irritable
 Reddened swollen hands and feet
 Conjunctivitis
 Strawberry tongue and red, cracked lips
 Rashes
 Enlarged cervical lymph nodes
 Abdominal pain, anorexia, diarrhea
 Arthritic joints
  WBC, ESR elevated
 Subacute phase (10 days after onset)
 Desquamation, esp. on palms and soles
 PC rises
 Convalescent phase (stage II)
 25th-40th day
 Stage III
 From 40 days until ESR returns to normal

Treatment
 ASA, ibuprofen
 Abciximab is a platelet receptor inhibitor specific for
Kawasaki disease
 IV immune globulin (IVIG)
 Children should not receive routine
immunizations while taking IVIG or the
immunization will be ineffective.
 Steroids are contraindicated

DISORDERS OF THE GASTROINTESTINAL SYSTEM

Pyloric Stenosis
 Pyloric sphincter - opening between the lower portion of the
stomach and the beginning portion of the intestine, the
duodenum
 Narrowing in the pyloric sphincter, possibly due to
hypertrophy or hyperplasia of the muscles surrounding the
sphincter

Assessment
 At 4 to 6 weeks of age, infants begin to vomit almost
immediately after each feeding  projectile vomiting
 Formula-fed – at 4 weeks; breastfed – at 6 weeks onset
 Sour-smelling vomitus
 Disinterest in eating, excessive drooling, or chewing on
tongue suggests nausea
 History taking:
 What is the duration? Begins at 6 weeks of age
 What is the intensity? Projectile vomiting
 What is the frequency? Immediately after eating
 What is the description of the vomitus? Sour but
contains no bile
 Is the infant ill in any other way? No
 Signs of dehydration: lack of tears, dry mucous
membranes, sunken fontanelles, fever, decreased UO,
poor skin turgor, weight loss
 Alkalosis  hypopnea
 A definitive diagnosis is made by watching the infant

NOTE: Fluid is unable to pass
easily through the stenosed
and hypertrophied pyloric
valve
drink.
 Before the child drinks - attempt to palpate the
right upper quadrant of the abdomen for a pyloric
mass – round and firm approximately the size of
an olive
 As the infant drinks, observe for gastric peristaltic
waves passing from left to right across the
abdomen. The olive-size lump becomes more
prominent. The infant vomits with projectile
emesis
 UTZ  hypertrophied sphincter
 Endoscopy  direct visualization
Therapeutic Management
 Surgical or laparoscopic correction (pyloromyotomy)
 Correct electrolyte imbalance/dhn/starvation pre-op
 IVF PNSS or D5NSS
 NPO
 Pacifier for non-nutritive sucking
Intussusception
 Invagination of one portion of the intestine into another
 Usually occurs in the second half of the first year of life
 Infants <1 year old: idiopathic
 Infants >1 year old: “lead point”
 Meckel’s diverticulum, polyp, hypertrophy of Peyer’s
patches,
 bowel tumors
 The point of the invagination is generally at the juncture of
the distal ileum and proximal colon
Assessment
 During peristaltic wave: child will draw up legs and cry
(severe pain); may vomit
 Vomitus will begin to contain bile
 After approx. 12 hours, blood appears in stool and
possibly in vomitus
 “currant jelly” appearance
 If with necrosis: elevated temp, peritoneal irritation
(tender abdomen, guarding), increased WBC, rapid
pulse
 History taking
 What is the duration of the pain? It lasts a short
time, with
 intervals of no crying in between.
 What is the intensity? Severe
 What is the frequency? Approximately every 15 to
 20 minutes
 What is the description? The child pulls up legs
with crying.
 Is the child ill in any other way? Yes. Vomits;
refuses food; states stomach feels “full.”
 Confirmed by ultrasound or CT scan

Therapeutic Management
 Surgical emergency
 Reduction of the intussusception must be done
promptly by either instillation of a water-soluble
solution, barium enema, or air (pneumatic insufflation)
into the bowel or surgery to reduce the invagination
before necrosis of the effected portion of the bowel
occurs
 Observe the child for 24 hours for recurrence of
intussusception

Necrotizing Enterocolitis (NEC)

 The bowel develops necrotic patches, interfering with
digestion and possibly leading to a paralytic ileus. Perforation
and peritonitis
 may follow
 Shock or hypoxia  vasoconstriction of blood vessels 
ischemia or poor perfusion  necrosis
 Lower incidence in breastfed compared to formula-fed

Assessment
 Distended abdomen; delayed gastric emptying 🡪 return
of undigested milk of more than 2mL
 (+) occult blood in stool
 Apneic episodes, si/sx of blood loss d/t intestinal
bleeding: dec. BP, ineffective thermoregulation
 X-ray: air invading intestinal wall

Therapeutic Management
 Put on NPO  IV, TPN
 Antibiotics
 Handle the abdomen gently to lessen the possibility of
bowel perforation
 Surgical removal of necrosis
 If perforation occurs  peritoneal drainage, laparotomy
 Temporary colostomy

Appendicitis
 Inflammation of the appendix
 The most common cause of abdominal surgery in children
  Fecal material enters the appendix 🡪 hardens and obstructs
the appendiceal lumen 🡪 inflammation, edema 🡪 compression
of blood vessels, cellular malnutrition 🡪 necrosis and pain
 If the condition is not discovered early enough, the necrotic
area will rupture and fecal material will spill into the
abdomen, causing peritonitis—a potentially fatal condition

Assessment
 Simple gastroenteritis
 Pain is a late symptom
 Diagnosis via symptom cluster: anorexia, pain,
tenderness in the
 RLQ, N/V, elevated temp, leukocytosis
 Abdominal pain is diffuse at first, then localized to RLQ
 (McBurney’s point)
 Rebound tenderness
 Reduced or absent bowel sounds
 Ultrasound, CT scan to confirm the appendicitis
 History Taking
 How was the child on Monday? Not herself. She
was not eating
 How was she Monday night? She had generalized
abdominal pain
 Tuesday morning? She had sharp localized pain
 Now? She has localized pain, vomiting, and fever

Therapeutic Management
 Surgical removal of the appendix prior to rupture
 Ruptured appendix:
 Position child in semi-Fowler’s
 IV for hydration
 Antibiotics
 Assess for signs of peritonitis: board-like abdomen,
shallow respirations, increased temp

Celiac Disease
 Malabsorption syndrome; gluten-induced enteropathy
 Sensitivity or abnormal immunologic response to protein,
particularly the gluten factor of protein found in grains—
wheat, rye, oats, and barley
 Ingestion of gluten 🡪 changes in intestinal mucosa or villi 🡪
prevents food absorption, esp. fat 🡪 steatorrhea, ADEK
deficiency, distended abdomen
 Rickets, loss of calcium from bones, hypoprothrombinemia,
hypochromic anemia, hypoalbuminemia
 Occurs most frequently in children of a northern European
background
  increased incidence in children of type 1 diabetes mellitus, IgA
deficiency, and Down syndrome

Assessment
 Child tends to be anorectic and irritable; fall behind
other children their age in height and weight
 Appear skinny, with spindly extremities and wasted
buttocks
 Face may be plump and rounded
 History
 bulky stools, malnutrition, distended abdomen,
and anemia
OGTT  oral glucose  become noticeable between 6 and 18 months
tolerances test  Serum analysis of antibodies against gluten (IgA
antigliadin antibodies)
 biopsy of the intestinal mucosa (done by endoscopy)
 OGTT
 Stool test for fat content

Therapeutic Management
 Gluten-free diet for life
 Water-soluble forms of vit. A & D; iron and folate
Biopsy  medical test that supplements
involves extraction of sample  Celiac Crisis
cells/tissue for examination to  Occur when child develops any type of infection
determine presence of a
 Extreme symptoms
disease
Hirschsprung’s Disease
 Aganglionic megacolon
 Absence of ganglionic innervation to the muscle of a section
of the bowel, usually the lower portion of the sigmoid colon
just above the anus
 Absence of nerve cells 🡪 no peristaltic waves in the section 
chronic constipation, ribbonlike stool 🡪 bowel proximal to the
obstruction dilates 🡪 abdominal distention
Ganglion  collection of
 Gene abnormality on chromosome 10
neuronal bodies found in the
 Higher incidence among siblings
voluntary and autonomic
 More often in males than in females
branches of the peripheral
nervous system (PNS)
Assessment
 Infants who fail to pass meconium by 24 hours;
Chromosome 10  genes that abdominal distention
provide instructions for  Symptoms may not become apparent until 6-12mos of
making protein age
 History of constipation:
 What is the duration of the constipation? It may
have been a problem from birth
  What do parents mean by constipation? Children
do not have a bowel movement more than once a
week
 What is the consistency of the stool? Ribbonlike
or watery
 Is the child ill in any other way? Children with
aganglionic disease of the intestine tend to be
thin and undernourished, sometimes deceptively
so because their abdomen is large and distended
 True constipation – examining finger will touch hard,
caked stool
 With Hirschsprung’s – rectum is empty
 Barium enema – use with caution
 Biopsy of affected segment – definite; will show the lack
of innervation
 Anorectal manometry - technique to test the strength or
innervation of the internal rectal sphincter by inserting a
balloon catheter into the rectum and measuring the
pressure exerted against it

Therapeutic Management
 Dissection and removal of the affected section, with
anastomosis of the intestine (termed a pull-through
operation)
 In infants, two-stage surgery:
 Temporary colostomy
 Bowel repair at 12-18 months

DISORDERS OF THE GENITOURINARY SYSTEM

Urinary Tract Infection (UTI)
 Occurs more often in females than in males
 Ascending infection from perineum most common, usually
gram- negative rods, such as E. Coli

Assessment
 Pain on urination, frequency, burning, and/or hematuria
 With cystitis: low grade fever, mild abdominal pain,
enuresis
 Pyelonephritis: high fever, abdominal or flank pain,
vomiting, malaise
 Any child with a fever and no demonstrable cause on
physical examination should be evaluated for UTI
 Urine c/s – clean catch, suprapubic aspiration,
catheterization
 Bacteriuria: bacterial colony count >100,000/mL
 Negative: <10,000
 Proteinuria – d/t presence of bacteria
  Hematuria – mucosal irritation
 Elevated pH >7

Therapeutic Management
 Oral antibiotics specific to causative organism
 IOFI – increase oral fluid intake
 Cranberry juice – acidifies urine 🡪 more resistant to
bacterial growth
 Mild analgesic e.g. Acetaminophen

Glomerulonephritis
 Inflammation of the glomeruli of the kidney.
 Usually occurs as an immune complex disease after infection
with nephritogenic streptococci (most commonly subtypes of
gABHS)
 Complement – a cascade of proteins activated by antigen-
antibody reactions and actually plufs or obstructs glomeruli
 Complement fixation reaction  tissue damage 
intravascular coagulation occurs in the minute renal vessels 
ischemic damage  scarring and decreased glomerular
function  decreased GFR (glomerular filtration rate) 
accumulation of Na and H2O in the bloodstream;
inflammation increases permeability  protein molecules
escape into the filtrate

Assessment
 History of recent respiratory infection (within 7-14 days)
or impetigo
 (within 3 weeks)
 Sudden onset hematuria and proteinuria – 24-hr urine
collection
 Urine appears tea-colored, reddish-brown, or smoky
 Oliguria
 Elevated urine specific gravity
 Abdominal pain, anorexia, vomiting
 Low-grade fever, headache
 Edema
 Hypertension d/t hypervolemia
 Cardiac involvement r/t difficulty managing excessive
plasma fluid
 Orthopnea
 Cardiac enlargement
 Enlarged liver
 Pulmonary edema
 Galloping heart rhythm
 ECG: T-wave inversion, prolonged PR interval
 Heart failure
  Hemodynamics:
 Hypoalbuminemia d/t massive proteinuria
 Low serum complement
 Mild anemia
 Increased ESR rate
 Increased urea, BUN, creatinine
 BP 160/100 and higher  encephalopathy  headache,
irritability, seizures, vomiting, coma or lethargy

Therapeutic Management
 Course of AGN: 1-2 weeks
 Little specific therapy
 Heart failure
 Place child in semi-Fowlers, digitalization, O2
therapy
 Diastolic pressure >90 mmHg: antihypertensive therapy
(Ca channel blocker)
 Phosphate binders, kayexalate

INFECTIOUS DISEASES
Rubella (German Measles)
 Causative Agent: Rubella virus
 Incubation period: 14-21 days
 Period of communicability: 7 days before to approx. 5 days
after rash appears
 Mode of transmission: Direct and indirect contact with
droplets
 Immunity: Contracting the disease offers lasting natural
immunity; a high rubella titer reveals infection has occurred
 Active artificial immunity: Attenuated live virus vaccine
 Passive artificial immunity: Immune serum globulin is
considered for pregnant women

Assessment
 1-5 days prodromal period
 Low-grade fever
 Headache
 Malaise
 Anorexia
 Mild conjunctivitis
 Sore throat, mild cough
 Swollen lymph nodes
 After prodromal period
 A discrete pink-red maculopapular rash begins on
the face, then spreads downward to the trunk and
extremities.
 On 3rd day, rash disappears
  (-) desquamation; if so, fine flaking of the skin

Management
 Comfort measures for rash
 Antipyretic, analgesic
 Droplet precaution for 7 days after onset

Measles (Rubeola)
 Causative agent: Measles virus
 Incubation period: 10 to 12 days
 Period of communicability: Fifth day of incubation period
through the first few days of rash
 Mode of transmission: Direct or indirect contact with droplets
 Immunity: Contracting the disease offers lasting natural
immunity
 Active artificial immunity: Attenuated live measles vaccine
Passive artificial immunity: Immune serum globulin

Assessment
 10- to 11-day prodromal period
 Lymphoid tissue becomes enlarged
 High fever (39.5-40C), malaise
 2nd day of prodromal period
 coryza – rhinitis and a sore throat
 Conjunctivitis with photophobia
 Cough
 Koplik’s spots – small, irregular, bright-red spots
with a blue-white center point on buccal
membrane
 4th day of fever
 Deep-red maculopapular eruption begins at the
hairline of the forehead, behind the ears, and at
the back of the neck and then spreads to the face,
the neck, upper extremities, trunk, and finally the
lower extremities
 After 5-6 days, rash completely fades  fine
desquamation

Management
 Comfort measures for rash
 Antipyretic, decongestants
 WOF complications: pneumonia, otitis media, airway
obstruction, acute encephalitis

Chickenpox (Varicella)
 Causative agent: Varicella-zoster virus
 Incubation period: 10 to 21 days
  Period of communicability: 1 day before the rash to 5 to 6
days after its appearance, when all the vesicles have crusted
 Mode of transmission: Highly contagious; spread by direct or
indirect contact of saliva or vesicles
 Immunity: Contracting the disease offers lasting natural
immunity to chickenpox; may be reactivated at a later time as
herpes zoster (shingles)
 Active artificial immunity: Attenuated live virus vaccine
 Passive artificial immunity: There is little passive placental
immunity to chickenpox

Assessment
 Low-grade fever, malaise
 In 24hrs, rash that begins as macule 🡪 papule (6-8hrs)
 vesicle  crust
 Lesions are usually 2-3mm in diameter, accompanied by
elevated temp, mostly found in the trunk

Therapeutic Management
 Allow scabs to crust and fall of naturally; picking on
scabs will leave a white, round, slightly indented scar at
the site
 Advise children not to scratch and remove scabs
 Antihistamine, antipyretic
 Acyclovir
 Airborne and contact precaution until all lesions are
crusted
 Complications: secondary infection of lesions,
pneumonia, and encephalitis

Poliovirus Infections: Poliomyelitis

 Causative agent: Poliovirus
 Incubation period: 7 to 14 days
 Period of communicability: Greatest shortly before and after
onset of symptoms, when virus is present in the throat and
feces (1 to 6 weeks)
 Mode of transmission: Direct and indirect contact
Polio  Greek word for
 Immunity: Contracting the disease causes active immunity
“grey”, the color of the spinal
against the one strain of virus causing the illness.
cord after it atrophies from the
 Active artificial immunity: Inactivated polio virus vaccine (IPV)
effect of the poliomyelitis virus
 Passive artificial immunity: None
 Polio is Greek for “gray” – the color of the spinal cord after it
atrophies from the effect of the poliomyelitis virus

Assessment
 Enters via GI, where it multiplies
 Fever, headache, nausea, vomiting, abdominal
 pain
 Moderate pain of the neck, back, and legs soon
develops
 CSF – increased protein and lymphocytes
 Followed by intense pain and tremors of extremities 
paralysis occurring immediately or over a period of 1-7
days
 Kernig’s sign – test for meningeal irritation
 Tripod sign – cannot sit without placing both arms and
hands behind them to brace themselves
 DTR are hyperactive at first, then diminish as CNS is
fully invaded
 Laryngeal paralysis makes swallowing or talking difficult
 Respiratory paralysis can halt respiration

Therapeutic Management
 Bedrest
 Analgesia, moist hot packs
 Long-term ventilation
 Progressive muscle atrophy (survivors) or severe
arthritis in late
 adulthood

Mumps (Epidemic Parotitis)

 Causative agent: Mumps virus
 Incubation period: 14 to 21 days
 Period of communicability: Shortly before and after onset of
parotitis
 Mode of transmission: Direct or indirect contact
 Immunity: Contracting the disease gives lasting natural
immunity
 Active artificial immunity: Attenuated live mumps vaccine
Passive artificial immunity: Mumps immune globulin

Assessment
 Fever, headache, anorexia, malaise
 Within 24 hours, “earache” occurs, but child will point
to the jawline just in front of the ear lobe.
 Chewing movements aggravate the pain
 By next day, parotid gland is swollen and tender
 Boys also may develop testicular pain and swelling

Therapeutic Management
 Soft or liquid die until swelling recedes (about 6 days)
 Analgesics, antipyretic
 Droplet and standard precautions
 Children are infectious for at least 5 days after
 symptoms appear
 Complications: mumps orchitis, meningoencephalitis,
severe permanent hearing impairment

Diphtheria
 Causative agent: Corynebacterium diphtheriae (Klebs- Löffler
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 or indirect contact
Diphtherial Bacilli invade and  Immunity: Contracting the disease gives lasting natural
grow in nasopharynx  immunity
exotonin production   Active artificial immunity: Diphtheria toxin given as part of
massive cell necrosis and DTaP vaccine
inflammation  necrosing  Passive artificial immunity: Diphtheria antitoxin
material feeds the bacilli more  Diphtheria bacilli invade and grow in nasopharynx  exotoxin
production  massive cell necrosis and inflammation 
necrosing material feeds the bacilli more

Assessment
 Characteristic gray membrane on the nasopharynx
 Purulent nasal discharge
 Brassy cough
 If untreated, myocarditis, CNS involvement may occur
 Diagnosis via throat culture

Therapeutic Management
 IV antitoxin
 Penicillin or erythromycin
 Complete bedrest
 Droplet precaution
 WOF airway obstruction  ET intubation

Whooping Cough (Pertussis)

 Causative agent: Bordetella pertussis
 Incubation period: 5 to 21 days
 Mode of transmission: Direct or indirect contact
 Period of communicability: Greatest in catarrhal (respiratory
illness) stage
 Immunity: Contracting the disease offers lasting natural
immunity
 Active artificial immunity: Pertussis vaccine given as part of
DTaP vaccine
 Passive artificial immunity: Pertussis immune serum globulin
3 Stages
1. Catarrhal stage
 URTI symptoms, coryza, sneezing, lacrimation,
cough, low grade fever
 Children are irritable and listless
 Lasts from 1-2 weeks
2. Paroxysmal stage
 Lasts 4-6 weeks
 Cough changes from mild to paroxysmal, 5-10
short, rapid coughs followed by a “whoop” or
high-pitched crowing sounds
3. Convalescent stage
 Gradual cessation of coughing and vomiting
 Children younger than 6 months of age: “whoop”
of the cough may be absent
 B. pertussis may be cultured from nasopharyngeal
secretions
 Increased WBC

Therapeutic Management
 Maintain on bedrest, seclude from environmental
factors
 Frequent small meals
 May be admitted to health care facility d/t tenacious
secretions needing airway suction
 Full 10-day course erythromycin/azithromycin
 Droplet precaution until 5 days after child starts
antibiotics
 Complications: pneumonia, atelectasis, emphysema,
seizures from asphyxia, epistaxis, alkalosis and
dehydration if with insufficient fluid intake

Helminthic Infections
 Helminths are pathogenic or parasitic worms
 Because children tend to be careless about washing their
hands before eating or tend to suck their thumbs, they are
prone to these infections

Roundworms (ascariasis)
 Eggs are excreted in feces  larvae hatch and
penetrate intestinal wall and enter circulation
 Loss of appetite, nausea, vomiting
 Intestinal obstruction may occur
 Anthelmintic – pyrantel pamoate

Pinworms
 Small, white, threadlike worms live in the cecum
  At night, female pinworm travels to anus to deposit
eggs on the anal and perianal region  child awakens
at night crying and scratching
 Some eggs are carried from child’s fingernails to the
mouth, cycle is repeated
 Worms are large enough to be seen if child’s buttocks
are separated while sleeping.
 Press a piece of cellophane tape against anus 
microscopic examination to reveal pinworm eggs
 Treatment: single dose mebendazole or pyrantel
pamoate
 All family members are treated for pinworm infestation
 Teach child to avoid nail biting and to wash their hands
before food preparation or eating

Name: Posa, Aliyah Nicole J.

Yr. / Block: 2A

Module No. 06
Date: 05.03.2022
Topic: Physical and Developmental Disorders

CUES/QUESTIONS/ NOTES
KEYWORDS

GASTROINTESTINAL SYSTEM
Ankyloglossia
  tongue-tied
 abnormal restriction of the tongue caused by an abnormally
Lingual frenulum  mucous tight frenulum
membrane fold found  surgical intervention to release
underneath the tongue
Cleft Lip and Cleft Palate
Cleft Lip
NOTE: Maxillary and Medial  failure to maxillary and median nasal processes to fuse
nasal processes develop during  may range from a small notch in the upper lip to a total
9-12wks or intrauterine life separation of the lip and facial structure up to the floor of
the hose with even upper teeth and gingiva absent
 may be unilateral/bilateral
“teratogenic” – something  more prevalent w/ boys
that can disturb the  hereditary, transmission of multiple genes, or teratogenic
development of embryo/fetus factors such as viral infection of folic acid deficiency
(ex. Radiation, maternal Cleft Palate
infection, chemicals, and  opening of the palate, usually on the midline and may
drugs) involve anterior hard palate, the posterior soft palate or
both
NOTE: Palate process closes at  usually occurs in conjunction w/ cleft lip
weeks 9-12 intrauterine life
Tracheoesophageal Atresia and Fistula
 Atresia
Sonogram  An orifice or passage in the body is closed or absent
 Similar to ultrasound  Fistula
 Produces pictures of  Abnormal or surgically made passage between a hollow
certain area or tubular organ and the body surface or between two
 Much affordable hollow or tubular organs
 Esophageal Atresia
Utero fetal surgery  Obstruction of the esophagus
 Aka in utero surgery
 Done to treat congenital 5 Types
malformities during fetal a) The esophagus end in blind pouch; there’s a
period tracheoesophageal fistula between the distal part of the
esophagus and the trachea
b) The esophagus ends in a blind pouch; there’s no
TPN  total parenteral connection to the trachea
nutrition c) A fistula is present between an otherwise normal
 To support nutrition esophagus and trachea
 Hydration d) The esophagus ends in a blind pouch. A fistula connects
 Electrolyte imbalance the blind pouch of the proximal esophagus to the
trachea
e) There is a blind pouch end portion of the esophagus.
Fistula are present between both widely spaced
segments of the esophagus and the trachea

Omphalocele & Gastroschisis


Hernia  a tear in muscle or
tissue that allows a part of the
insides to bulge out
NOTE: OGT  much prone to
aspiration, NGT  mostly used
in infants and may depend on
use
NOTE: Assess for size
appearance, color, cm after
delivery for evaluation
 Omphalocele
 Protrusion abdominal contents through the abdominal
wall of the point of the junction of the umbilical cord
and the abdomen
 Herniated contents are usually intestines, but may
include stomach and liver
 Usually covered with UC protruding from the
 Gastroschisis
 Similar to omphalocele but abdominal organs are not
contained by a membrane but spill freely from abdomen
Intestinal Obstruction
 Stenosis = narrowing
 Mechanical impairment or complete arrest or passage of
contents through the intestines are to pathology that causes
blockage of the bowel
 NPO
 Feeding can cause distension which can result to
pain/discomfort

Diaphragmatic Hernia
 Protrusion of an abdominal organ (usually stomach or
intestine) through a defect in a diaphragm into the chest
cavity
 sonogram
Fetoscopy  insertion of  bowel removal via fetoscopy
camera in uterus to vies fetus  upon birth:
 respiratory difficulty due to compression of lungs by
NOTE: Disorders usually start abdominal organ
in respiratory
 abdomen appears generally sunken
 absent breath sounds on affected side
 cyanosis
 NPO
 NGT
 Surgical repair

Imperforate Anus
 Stricture of the anus
 Detected by sonogram
 NPO
Gastrotomy  feeding  IVT
Colostomy  opening for  Colostomy until repair
poop
NERVOUS SYSTEM
Hydrocephalus
 Abnormal accumulation of CSF in the ventricles or
 subarachnoid spaces
 Communicating/extraventricular hydrocephalus if fluid
reaches spinal cord
 Obstructive/intraventricular hydrocephalus if there’s blockage
to passage
 Also classifies as congenital or acquired
 Formation of CSF  increases head size + hold pressure in
brain  damage brain tissue/function

Neural Tube Disorders

a) Spina bifida occulta
 Occurs when the posterior laminae of the vertebrae fail
Spina bifida  Latin for to fuse
“divided spine”  Noticeable as dimpling, abdominal tufts of hair or
discolored skin at the point of poor fusion
 A benign disorder
Benign disorder  no
immediate surgical b) Meningocele
intervention but needs to be  Meninges covering the spinal cord herniate through
observed unformed vertebrae
 The anomaly appears as a protruding mass, usually
approximately the size of an orange at the center of the
back
 The protrusion may be covered by a layer of skin or only
the dura matter

c) Myelomeningocele
 The spinal cord and the meninges protrude through the
vertebrae the same as with a meningocele
 The spinal cords at the end of the point motor and
sensory function is absent beyond is point  lower
motor neuron damage
 The child will have flaccidity, lack of sensation of LE, loss
of bladder/bowel control
 Often accompanied by talipes disorder + developmental
hip dysplasia
 High placement of myelomeningocele, more likely
accompanied by hydrocephalus
 CT scan / ultrasound / MRI  to differentiate from
meningocele

Anencephaly
 absence of the cerebral hemispheres
 may have difficulty of labor; the underdeveloped head
does not engage in cervix
 many presents as breech
 children can’t survive with this disorder; however, if
Medulla with intact, medulla, the infant may survive several days
 aka medulla oblongata after birth
 lowest portion of
brainstem Microcephaly
 transmits signals  slowed brain growth that falls more than 3 times below
between brain normal on growth charts
 causes
 intrauterine infection (rubella, CMV,
toxoplasmosis)
 severe malnutrition/ anoxia in early infancy
 infant is cognitively challenged d/t lack of functioning
brain tissue

SKELETAL SYSTEM
Developmental Hip Dysplasia
 imperfect development of the hip – can affect femoral head,
acetabulum or both
 head of the femur does not lie deep enough within the
acetabulum and slips out in movement
 occurs in females 7x more than males
 classification
 acetabular dysplasia – mildest form of; femoral head
remain in acetabulum
 subluxation – most common form; femoral head
partially displaced
 dislocation – femoral head not in contact with
acetabulum, displaced posteriorly and superiorly

Absent or Malformed Extremities

 may result from maternal drugs ingestion, virus invasion,
amniotic band formation in utero
 lower extremity prostheses are fitted as early as age 6 months
(so an infant will learn to stand at the normal time)
 upper extremity prostheses early are fitted this early, so an
infant can handle and explore objects readily
 introducing prostheses early also prevents a child from
adjusting to a missing extremity, such as writing with the feet
or sliding across a floor rather than walking

Finger and Toe Conditions

 Polydactyly
 presence of one or more additional fingers or toes
 usually amputated off early

 Syndactyly
 two fingers of toes fused
 webbing  separation of digits can be done
  bones are fused  cannot be fully reconstructed

Chest Deviations
 Pectus Excavatum
 Indentation of the lower position of the sternum
 Decreased lung volume, heart is displaced to the left

 Pectus Carinatum
 Sternum is displaced anteriorly, increasing AP diameter
of the chest

Craniosynostosis
 premature closure of the sutures of the skull
 may occur in utero or in early infancy
 needs to be detected early because a sealed skull will
compromise brain growth
 causes
 dominantly inherited trait
 rickets
 irregularities of calcium or phosphate metabolism

Achondroplasia
 failure of bone growth inherited as a dominant trait
 causes a disorder in cartilage production in utero
 Assessment:
 head appears larger compared to extremities
 can be diagnosed in utero or at birth by comparing the
length of extremities to the normal length
 radiography  characteristic abnormally flaring
epiphyseal lines

Talipes Disorders
 Latin “talus” (ankle) and “pes” (foot)
 Ankle – foot disorders, popularly called “club foot”
 Pseudo-talipes d/o – d/t intrauterine position
 May be corrected via manipulation

Four Types
 Plantarflexion – equinus or “horse foot position”
 Dorsiflexion – anterior foot is flexed towards anterior
leg
 Varus deviation – foot turns in (pikit)
 Valgus deviation – foot turns out (sakang)

SUMMARY
Physical and Developmental Disorders of the Gastrointestinal System
 Ankyloglossia – tongue-tied
  Cleft lip and palate – opening or split in the upper lip, the roof of the mouth or both
 Tracheoesophageal atresia and fistula – abnormal connection of esophagus and trachea
 Omphalocele – congenital defect of abdominal wall  intestinal hernia, has sac covering
 Gastroschisis – congenital defect of abdominal wall, has no sac covering / peritoneal layer
 Intestinal obstruction – mechanical impairment of complete arrest of intestines or food passage
 Diaphragm hernia – a birth defect where there’s a hole in the diaphragm and the abdominal
organs protrude through the hole into infant’s chest
 Imperforate anus – blocked / missing anus

Physical and Developmental Disorders of the Nervous System

 Hydrocephalus – buildup of fluid in the brain’s cavities
 Neural tube disorders
 Spine bifida occulta – baby’s spine isn’t fully developed
 Meningocele – a sac protrudes thru spinal column
 Myelomeningocele – “ has exposed nervous system
 Microcephaly – infant’s head is smaller than average
 Anencephaly – infant is born without parts of the brain and skull

Physical and Developmental Disorders of the Skeletal System

 Developmental hip dysplasia – “ball and socket” joint of infant does not properly form
 Absent or malformed extremities – congenital absence of limb
 Finger and toe conditions
 Polydactyly – presence of extra finger or toe
 Syndactyly – fusion of two fingers/toes
 Chest deviation
 Pectus Excavatum – indented sternum
 Pectus Carinatum – advanced sternum
 Craniosynostosis – failure of bone growth
 Talipes Disorders – “clubfoot”, defect that affects foot + ankle
 Plantarflexion
 Dorsiflexion
 Varus deviation
 Valgus deviation
Name: Posa, Aliyah Nicole J.
Yr. / Block: 2A

Module No. 07
Date: 05.17.2022
Topic: COPD, Acute Glomerulonephritis, Otitis Media, Acute lymphocytic Leukemia,
Pneumonia

CUES/QUESTIONS/ NOTES
KEYWORDS

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

 a progressive disease that makes it hard to breathe
  characterized by a combination of chronic obstructive
bronchitis and emphysema

Two Main Forms of COPD

1. Emphysema
 the walls between the air sacs in the lungs are
damaged where the air sacs lose their shape
and become floppy.
 airflow limitation
 pink puffers

2. Chronic Bronchitis
 inflammation and irritation of the bronchial
tubes.
 Absence of airflow
 Blue bloaters (cyanosis)

Cause
• Smoking
• Air pollutants
• Genes (Alpha-1 antitrypsin deficiency  AATD)

Predisposing Factors
• Exposure to tobacco smoke
• Occupational exposure
• Genetic abnormalities

Precipitating Factors
• Smoking

Medical Management
• Bronchodilators enhance alveolar ventilation
 To increase O2 distribution all thru the lungs
• Supplemental oxygen therapy
Spirometry is the most • Use the results of spirometry to increase motivation to
common type of pulmonary quit smoking.
function or breathing test • smoking cessation program aims to provide support for
smokers in order to improve their ability to become and
stay nicotine-free.

Pharmacological Management
Chronic Pulmonary Medications Save Lungs!!
• Corticosteroids
• Phosphodiesterase-4 inhibitors
• Methylxanthines
• Short-acting Bronchodilators
• Long-acting Bronchodilators

Hematuria  blood in urine
Proteinuria  increased levels
of protein in the urine
Nursing Management
• Monitor VS
• Assess skin color
• Assess medical history
• Assess breath pattern and sound
ACUTE GLOMERULONEPHRITIS
 a syndrome characterized by the abrupt onset of hematuria
 often accompanied by proteinuria, hypertension, edema, and
renal dysfunction
 subdivided into:
• primary glomerular disease
• postinfectious glomerulonephritis
• glomerulonephritis associated w/ systemic disease
 comprises a specific set of renal diseases in which an
immunologic mechanism triggers inflammation and
proliferation of glomerular tissue that can result in damage to
the basement membrane, and capillary endothelium
 a frequent disease in children between 5-10yrs of age w/ boys
being more susceptible than girls to develop the condition
 commonly caused by a previous streptococcal such as a
history of recent respiratory infection (within 7 to 14 days) or
impetigo (within 3 weeks)
OTITIS MEDIA (OM)
 Infection or inflammation of the middle ear
Types
1. Acute otitis media – Middle ear infection occurs
abruptly causing swelling and redness
2. Otitis media w/ effusion – continuous accumulation of
fluid (effusion) and mucus in the middle ear after an
initial infection subsides
3. Chronic otitis media w/ effusion - Fluid remains in the
middle ear for a prolonged period or recurrent, even
though there is no infection
Effects
 severe earache
 Untreated infection can travel from the middle ear to
the nearby parts of the head
 mild to moderate hearing loss
 Speech and language disabilities
 Assessment
1. Medical History
2. Si/Sx
3. PE
 Otoscopy
 Otoscope
 Pneumatic otoscope
 Hearing Test
 Tympanometry

Possible Causes
• malfunction of the eustachian tube
• cold or allergy
• sore throat
• respiratory infection

Treatment
• Antibiotic medication by mouth or ear drops
 High-dose Amoxicillin
• Medication (for pain and fever)
 Acetaminophen
 Ibuprofen
• For complications
 Antihistamine and decongestant
Myringotomy  a procedure  Analgesic
done to create a hole in the • If infection last greater than 3 months or continues to
ear drum for drainage of fluid reoccur
that is trapped in the middle  Myringotomy
ear

ACUTE LYMPHOCYTIC LEUKEMIA (ALL)

 B or T lymphoblast malignancy
 characterized by uncontrolled abnormal growth and creates
immature blood cell
 common in children between 2-5 years of age, especially in
children with Genetic disorder
 typically present with symptoms related to anemia

Risk Factor
 Exposure to high levels of radiation
 Exposure to benzene
 Genetic disease
 Down syndrome
 Bloom syndrome
 Neurofibromatosis type 1
 Ataxia telangiectasia
 Diagnosing
• Blood test
• Imaging Test (X-ray, CT scan, MRI or ultrasound)
• Bone marrow aspiration and Biopsy
• Spinal tap (lumbar puncture)

Treatment
• Chemotherapy
• Targeted Therapy
• Bone Marrow Transplant
• Stem Cell Transplant
• Radiation Therapy
• Immunotherapy
• Physical Therapy and Exercise
• Heat Or Cold Therapy

PNEUMONIA
 a lung and lower respiratory tract infection that occurs below
the level of the larynx
 distinguished by the accumulation of pus and other fluids in
the lung air sacs (alveoli).
 Limits O2 intake and causes difficulty of breathing due to
alveoli being clogged with pus and fluid
 Contagious (blood, airborne droplets, aspiration)
 Categorized as: community-acquired, hospital-acquired and
pneumonia occurring in Immunocompromised individuals
 MILD: can be treated at home and are given antibiotics in
tablet form
 MODERATE: signs include drowsiness and confusion, low
blood pressure, worsening shortness of breath, and risk
factors such as old age and underlying diseases. Needs to
have treatment at a hospital. Some will be given a
combination of two different antibiotics, at least at the
beginning of the treatment.
 SEVERE: heart, the kidneys or the circulatory system are at risk
of failing, or if the lungs can no longer take in enough oxygen.
 Pneumonia in children is only classified as either “not severe”
or “severe.”

Cause
 Streptococcus pneumoniae
 Haemophilus influenzae type b (Hib)
 Respiratory syncytial virus
 Pneumocystis jiroveci
 Atypical bacteria (Chlamydia pneumoniae, Mycoplasma
pneumoniae, Legionella species)
  viruses

Confirmatory Tests
 Blood tests
 C-reactive protein (CRP)
 Chest X-ray
 Pulse oximetry
 Sputum test
 Arterial blood gases test (ABG)
 Complete Blood Count (CBC)
 Blood culture

SUMMARY
• Chronic obstructive pulmonary disease, or COPD, refers to a group of diseases that cause airflow
blockage and breathing-related problems.
• Acute Glomerulonephritis is defined as inflammation and subsequent damage of the glomeruli
leading to hematuria, proteinuria, and azotemia; it may be caused by primary renal disease or
systemic conditions.
• Otitis Media is inflammation or infection located in the middle ear. Otitis media can occur as a
result of a cold, sore throat, or respiratory infection.
• Acute lymphocytic Leukemia is a type of cancer in the blood and bone marrow that appears
mostly in children who are at high risk.
• Pneumonia is an infection-induced inflammation of the lungs.