Pediatric Nursing 4.

Suction the Airway (If Necessary)

Nursing Care of a Family with a High-Risk Newborn ❖ Predisposing factors of infants to respiratory difficulty that needs
resuscitation
Newborn Needs on the First Days of Life
 Low birth weight (LBW) newborns
1. Initiation & maintenance of respirations  Intrauterine Growth Restriction (IUGR)
 A maternal history of diabetes
No effective breathing = residual neurologic morbidities resulting
 PROM
Cerebral hypoxia or Hypoxic-Ischemic Encephalopathy (HIE)  Maternal use of barbiturates
 If the baby inhales this meconium-stained
O Potentially leads to long-term conditions depending on its severity  Irregularities in the fetal heart rate during labor
 Cord prolapse is a medical emergency
Cerebral palsy (brain/weakness)  Low Apgar score (below 7)
 Post-term newborns, born at 42 weeks or later, Small for
Developmental delays
gestational age birthmall for gestational age (SGA) newborns
Intellectual disability  Breech Birth
 Multiple birth Newborns
Death.  Chest, heart, or respiratory tract anomalies

 Symptoms ❖ First signs of respiratory Compromise in newborns

 abnormal breathing
 feeding problems  Increasing respiratory rate (30-60RR;30-40RR sleeping)
 seizures,  Grunting
 Changes in muscle tone or reflexes.  Nasal flaring
 Undress the baby’s chest and look for intercostal retractions
❖ Development of severe acidosis (inward sucking of the anterior chest wall on inspiration)

Born with some degree of respiratory acidosis. Corrected by the spontaneous ❖ Nursing Actions:
onset of respirations w/in 2 minutes to prevent cerebral hypoxia
1. Place the infant under a radiant warmer to help prevent cooling and
Respiratory acidosis in newborn = infant's lungs can't effectively remove acidosis
carbon dioxide (CO₂) from the blood, leading to its accumulation and a 2. Clothing (except diaper, while inside the warmer) should be
decrease in blood pH (making it more acidic). removed

Common causes of RA: √ To promote better respiration and observation.

 Respiratory distress syndrome (RDS) 3. Head of mattress elevated approximately 15 degrees

 Pneumonia
 Meconium aspiration syndrome √ To allow abdominal contents fall away from diaphragm & increased
breathing space
Diagnostics: ABG = pH below 7.35 and an increase PaCO2.
4. Bagging” the infant with a mask and positive-pressure ventilation
Treatment: Give supplemental 02, positive airway pressure (CPAP), or bag for a minute before suctioning
mechanical ventilation to improve the baby's breathing
√ Improve the infant’s oxygen level and prevent it from desaturating to
❖ Patent ductus arteriosus dangerous levels during Suctioning

 Failure of fetal circulatory to shunts 5. Treat the cause of the respiratory distress to correct the difficulty
 Ineffective pump action in the heart

❖ Asphyxia in utero = DOB B4 1ST 2 minutes of life

Infant has no audible heartbeat HR ⬇️60 beats/min

1. ESTABLISHING EXTRAUTERINE CIRCULATION
 Cord compression 
 Maternal anesthesia –  Chest compressions should be started
 Placenta previa
 Intrauterine growth restriction Hold the Infant with fingers encircling the chest and wrapped around the back
 (IUGR) and depress the sternum with both thumbs on the lower third of the sternum,
 Premature separation of the placenta approximately one third of its depth (1 or 2 cm) at a rate of at least 100 times
➤ Reason of deaths occurring during the first 48 hours after birth: per minute

 NB’s inability to establish or maintain adequate respirations  Lung ventilation rate of 30 times per minute = Chest compressions
rate of 90 compressions per minute ratio of three compressions to
one ventilation.
 NB HR > 60 but < 100 beats/min, chest compressions = stopped
❖ Newborn resuscitation but continued ventilations

❖ Initial Steps (First Minute of Life) Adequate ventilation - major priority and should continue until the heart rate -
> 100 beats/min
1. Provide Warmth
2. Dry the Infant Oxygen Saturation
3. Position the Airway
  Pulse oximeter to evaluate respi & cardiac efficiency.  Cover NB with an infant cap
 Palpate femoral pulse.  Wiping the body and head dry with a towel or blanket,
 IV Epinephrine is prescribed if HR < 60 beats/min after at least 30  Kept NB in a radiant warmer or prewarmed incubator
seconds of NNR  Skin-to-skin contact with one of the parents.
 Epinephrine 1:10,000 given (IV) to stimulate heart action  Kangaroo – mother care
 Preterm infants receive surfactant to replace the natural surfactant  Plastic wrap, increasing the room temperature, and warmed
that is not formed in their lungs. mattresses
 Transferred to NICU for continuous cardiorespiratory observation  To prevent heat loss, infant is not placed on a cool X-ray table or
scale
Potential Complications 5. ESTABLISHING ADEQUATE NUTRITIONAL INTAKE
 Gavage feedings is given if rapid Infant’s respiratory rate that NB
❖ Patent Ductus Arteriosus
can’t suck effectively
In preterm infants – normal fetal connection between the aorta and pulmonary  Gastrostomy tubes long-term nutrition concern
artery fails to close after birth, to blood flow to the lungs  Preterm infants should be fed breast milk because of the immune
protection they can get
 Pulmonary edema 6. ESTABLISHING WASTE ELIMINATION
 Respiratory distress  Immature infants void & pass stool within 24 hours / void later
 Strain on the heart and lungs than term newborns.
 Document the time & date any voidings & the passing out of stool
3. MAINTAINING FLUID AND ELECTROLYTE BALANC  Proof hypotension is improving and the kidneys are being
perfused.
❖ Hypoglycemia = results from NRP & effort to begin breathing
 Because meconium has not yet reached the end of the intestine at
 70 and 150 mg/dL (3.9 to 8.3 mmol/L) 1st few week of life. birth.
 1st hour after birth, glucose levels drop as low as 30-40 mg/dL (1.7-  Observing for an expected anal opening and monitoring for the
2.2 mmol/L) before stabilizing passage of meconium within the first 48 hours.
 Treated initially with intravenous 10% dextrose in water to restore
-If an imperforate anus is suspected:
blood glucose level
 Sodium, glucose, and potassium are also given PRN  imaging tests such as an abdominal X-ray
 spinal ultrasound
❖ Dehydration = result from increase water loss by rapid respirations.
 echocardiogram are used to assess the extent of the defect and
 Monitor the rate of fluid administration because a high fluid intake check for associated abnormalities in the urinary tract, spine, and
= fluid overload = patent ductus arteriosus /heart failure.. heart.
 Monitor fluid status both by urine output and urine specific gravity 7. Prevention of infection
values
❖ Conditions that makes an infant high risk for infection:
❖ Inadequate fluid intake if:
 Preterm premature rupture of the membranes
 Output less than 2 ml/kg/hr 24 to 48 hours of life  Risk of adverse neurodevelopmental outcomes from the infection
 Urine specific gravity greater than 1.015 to 1.020 (1.001-1.02 or
❖ Viruses that affect infants in utero & may cause congenital
even lower, such as 1.003)
Anomalies
❖ Hypovolemia fetal blood such as placenta previa or twin-to-twin
transfusion.  Cytomegalovirus
 Toxoplasmosis virus.
S/S:
8. Establishment of a newborn-parent/caregiver relationship
 Tachypnea  Urge parents to spend time with their infant in NICU as possible
 Pallor 9. Institution of developmental care or care that balances physiologic
 Tachycardia needs and stimulation for optimal development
 Decreased Arterial blood pressure  Follow-Up of the High-Risk Infant at Home
 Decreased central venous pressure  Each time parents visit a special/intensive care assess their level of
 Decreased tissue effusion of peripheral tissue, knowledge
 Developing metabolic acidosis.  Additional health teachings and referral to a home care agency

Treatment/ Actions: ❖ Small for gestational age (SGA)

 Isotonic solution (normal saline) to increase blood volume. - Infants who fall below the 10% of weight for their age
 Vasopressor dopamine given to increase blood pressure and
❖ Appropriate for gestational age (AGA).
improve cell perfusion.
- Infants weighing 10th and 90th % of weight for their gestational age,
4. REGULATING TEMPERATURE
regardless if preterm, term, or post term
 Increased metabolism = destructive = 1 oxygen, & w/out O2  Low-birth-weight (LBW) = Weight is < 2,500g@ birth
available because of DOB, body cells become hypoxic.  Very-low-birth-weight (VLBW) = Weight <1500g @birth
 Chilled = heart action, breathing, electrolytic balance, and possibly  Extremely (ELBW) = Weight < 1,000g @ birth
brain function all become compromised.
❖ THE PRETERM INFANT
Ways to provide warmth to the NB (36.5°C & 37.5°C)
 Live-born infant born b4 end of week 37 of gestation.
 Divided in terms of the degree of care needed
  Late preterm (born bet 34 & 37 wks) S/S= appear pale, lethargic, and anorectic.
 Early preterm (born bet 24 & 34 wks)
 Combination of immaturity of the hematopoietic system
❖ Assessments  Delaying cord clamping at birth to allow a more blood from the
placenta to enter the infant = help reduce the development of
 Sole creases anemia
 Skull firmness = softer and more malleable than a full-term baby
 Ear cartilage = lack of fully formed cartilage = pinna very soft and
flexible. NEONATAL HYPOGLYCEMIA
 Ears appear large in relation to the head.
 Eyes appear small & nearsighted ❖ GLUCOSE DEMAND
 No sucking, swallowing and breathing coordination if an infant’s
Usual rate of glucose utilization is 4-8mg/kg/min
age is below 33 weeks;
 Neurologic development = higher risk for both acute brain injuries O Exogenous or endogenous glucose supply is limited
and long-term neurodevelopmental impairments
 Last menstrual period ❖ Severe or prolonged hypoglycemia may result in long term neurologic
 Sonographic estimation of age all can be helpful to determine damage.
gestational age
❖ HYPOGLYCEMIA
❖ NEONATES INTENSIVE CARE UNIT / NICU
A plasma glucose of < 40 mg/dl Glucose levels generally increase to more
 A special area of the hospital that has advanced technology and than 45 mg/dL by 12 hours after birth.
trained healthcare professionals to give special care for the tiniest
patients. In preterm infants, repeated blood glucose levels below 50 mg/dL may be
 Care areas for babies who are not as sick but do need specialized associated with neurodevelopmental delay.
nursing care.
❖ HBA1C AND FBS
❖ Phototherapy
 HbAlc measures the percentage of hemoglobin in your red blood
 Eyes are covered cells that is coated in glucose.
 To prevent retinal damage:  FBS/Fasting Blood Sugar = test that measures your blood glucose
 Phototherapy lights prolonged exposure to the intense blue-green levels.
light spectrum can damage the delicate retinal cells.
❖ RBS & POST PRANDIAL TEST
 To provide comfort: eye covers protect newborn from the
discomfort of the bright light, which can help them remain calm  Postprandial Blood Sugar (PPBS)
during treatment.  Shows how your body responds to food
 Genitals are covered:  Random Blood Sugar (RBS)
 To prevent potential significant risk of developing genital skin  Both tests are used to screen for and monitor diabetes and other
cancer & to avoid sunburn on sensitive skin glucose-related conditions.
❖ Preterm Infant Etiology ❖ UNITS OF MEASUREMENT OF BLOOD SUGAR
 Common Factors Associated With Preterm Birth - milligrams per deciliter (mg/dL)
 Low socioeconomic level - millimoles per liter (mmol/L)
 Poor nutritional status
 Lack of prenatal care ❖ NORMAL BLOOD GLUCOSE FOR A NEONATE
 Multiple pregnancy
 Previous early birth  70 and 150 mg/dL = initial glucose in the 1st week of life fluctuate
 Race (non-Whites have a higher incidence of prematurity than  decrease around 25-30 mg/dl = immediate hours after birth
Whites)  stabilize 4 to 6 hrs to adult levels of about 60-100 mg/dL within the
 Cigarette smoking first few days of life.
 Age of the mother (highest incidence is in mothers younger than
❖ TRANSISTIONAL GLUCOSE METABOLISM
age 20 years)
 Order of birth (early birth is highest in first pregnancies and in  Fetal Glucose Metabolism
those beyond the fourth pregnancy)  Maternal glucose is the only source of fetal glucose
 Closely spaced pregnancies  Baseline fetal blood glucose is 60-70% of maternal serum glucose
 Abnormalities of the mother’s reproductive system, such as  Glycogen stores increase in last month of third trimester.
intrauterine septum
 Infections (especially urinary tract infections) ❖ GLUCOSE METABOLISM AFTER BIRTH
 Pregnancy complications, such as premature rupture of membranes
or premature separation of the placenta.  Cessation of maternal glucose supply
 Early induction of labor  Surge in glucagon, catecholamine Decrease insulin
 Elective cesarean birth  Blood glucose stabilises (~1-2 hrs after birth)

❖ Potential Complications ❖ INCREASED UTILIZATION OF GLUCOSE

- Anemia of Prematurity 1. Diabetic mother

 Normochromic, normocytic anemia (normal cells, just few in 2. Islet cell hyperplasia
number) 3. Insulin producing tumors
4. Maternal tocolytic theraphy with B-sympathomimetric agents
 5. Malposition of umbilical artery catheter * Symptoms of hypoglycemia can be subtle
1. Infant of Diabetic Mother (IDM)
 IDM- fetus to high blood glucose- fetus to produce Treatment focuses : Providing adequate calories
excess insulin.
3. Delayed onset of feeding
 Maternal glucose supply=the newborn’s high insulin
4. Treatment: Oral glucose or IV glucose
levels=hypoglycemia.
 Perinatal stress; condition like birth asphyxia and INCREASED UTILIZATION AND DECREASED PRODUCTION
hypothermia can also cause a temporary, stress-
induced hyperinsulinism. Perinatal stress eg. shock, sepsis, asphyxia
 Congenital hyperinsulinism
 Common cause of neonatal hypoglycemia Enchange transfusion
 Increased metabolic
Defect in carbohydrate metabolism eg. glycogen storage disease Endocrne
demand=hypoglycemia=increased glucose usage
deficiency eg. adrenal insufficiency, hypopituitarism Defect in amino acid
due to conditions like sepsis, congenital heart
metabolism
disease, or polycythermia (excessive red blood cell)
2. Islet cells hyperplasia Polycythemia
 Islet of Langerhans in the pancreas enlarge=
potential cause of hypoglycemia Maternal therapy with B-blocker
 Symptoms of islet cell hyperplasia
- Hypoglycemia (low blood sugar) 1. Perinatal stress eg. shock, sepsis, asphyxia Stressful perinatal disrupt a
 Treatment newborn's glucose metabolism. Perinatal asphyxia = Depletion of glycogen
- Subtotal pancreatectomy stores Sepsis and shock increase a newborn' metabolic demands
- Medication diazoxide 2. Enchange transfusion which triggers a reactive insulin response. = rapid
2. Insulin producing tumor drop in blood sugar causing apnea or convulsions, especially in infants prone
 Insulinomas= persistent hypoglycemia-secrete too to low blood sugar.
much insulin
 Hyperinsulinemia can lead to if not promptly 3. Endocrne deficiency eg. adrenal insufficiency Adrenal insufficiency Lack
diagnosed and treated. of cortisol can lead to glucose production by the liver and decreased glucose
 Seizure uptake by peripheral tissues = hypoglycemia.
 Developmental delays
 Brain damage 4. Defect in amino acid metabolism can cause hypoglycemia due to inborn
errors of metabolism (IEMS) IEMS can cause hypoglycemia
❖ Diagnostics
5. Polycythemia → due to increased blood viscosity.
Whipple’s triad and imaging, followed by surgical removal of the tumor,
which can cure the condition. Common signs of polycythemia

3. Maternal tocolytic theraphy with B-sympathomimetric agents Treatment for symptomatic newborns partial exchange transfusion to lower
the hematocrit and improve blood viscosity
❖ Tocolytic like:
6. Maternal therapy with B-blocker block the effects of catecholamines such
 Ritodrine as epinephrine and norepinephrine = which are crucial for maintaining blood
 Nifedipine sugar and heart rate
4. Malposition of umbilical artery catheter (UAC)
PREDISPOSED INFANTS
Place too high
o Infants of diabetic mothers
Refractory hypoglycemia o can develop asymptomatic hypoglycemia as early as 1 hour after
birth and generally by 12 hours.
Glucose levels returning to normal upon catheter repositioning to a lower, o Maternal use of B-adrenergic agonist/ antagonist
more appropriate position.
o LGA - Large- or small-for-gestational-age infants can develop
asymptomatic hypoglycemia as early as age 3 hours and are at risk
for up to 10 days
❖DECREASED SUBSTRATE AVAILABILITY (PRODUCTION/STORES) o Preterm
o Polycythemia
 Prematurity o Asphyxia
 IUGR
o Sick infant
 Inadequate caloric intake
 Delayed onset of feeding SIGNS AND SYMPTOMS OF HYPOGLYCEMIA
1. Prematurity
Symptoms are Non specific hence need for high index of suspicion
❖ High risk to hypoglycemia due to:
 Jitteriness
 Limited glycogen and fat stores  Apnea
 Immature gluconeogenesis (glucose production)  Irritability
 Higher metabolic demands  Grunting
 Difficulty feeding immediately after birth  Lethargy
2. Inadequate caloric intake  Seizures

Neonates lack sufficient fuel to maintain normal glucose levels. SCREENING

 o Blood glucose or point of care testing (POC) should be done in  If the baby cant take oral, (IV) infusion of dextrose solution (e.g.,
high risk infants within the first 1 to 2 hours after birth 12.5% D/W) is necessary.
o Bedside reagent test-strip glucose results are available rapidly but
might vary from the actual glucose level by up to 10 to 20 mg/dL Severe cases

WHIPPLE'S TRIAD: MEDICAL DIAGNOSTIC CRITERION FOR administering IV dextrose in

HYPOGLYCEMIA
 Ensuring adequate and effective feeding,
The Whipple triad describes indications that signs and symptoms are the result  Educate the mother on signs and symptoms and feeding practices
of hypoglycemia: to prevent recurrence
 Give glucose administration with enteral feeds (breastfeeding or
It constitutes: formula).

 low blood glucose concentration, IV THERAPY

 signs consistent with hypoglycemia,
 resolution of signs and symptoms when blood glucose Indications
concentrations return to normal.
 Inability to tolerate oral feeding
MANAGEMENT  Symptomatic infant
 Lack of response with oral feeds
Constitutes 3 regimens depending on and escalated on the basis of the severity  Glucose < 25 mg/dL, regardless of patient's symptoms
of the NH.
MEDICATION
 Oral feeds
 Intravenous Dextrose infusion therapy Indication
 Medication
 Persistent hypoglycemia despite a GIR > 12 mg/kg/min.
MANAGEMENT Oral Feeds
Critical investigations
o Indicated for asymptomatic at risk infants
 Serum cortisol, insulin, growth hormone when glucose is low and
o Neonate fed on Breastmilk or Formula (never glucose water!!). prior to treatment
o Glucose screening should be done 30 minutes after the first feed.  DO NOT wait >5 minutes for results prior to treating
o Target glucose levels are 45mg/dL or higher before routine meals hypoglycemia
o If the glucose level doesn't rise, a more aggressive therapy may be
needed. HYDROCORTISONE
o At-risk infants should maintain normal plasma glucose on a routine
Indication:
diet for at least 3 feed-fast periods before discharge.
O Hypoglycemia despite GIR > 12 mg/kg/min, hypoglycemia of
PROTOCOL FOR MANAGEMENT OF AT RISK INFANTS
known origin.
From Birth to age 4 hours: O Dose: 10 mg/kg/day IV q 12 hrs
O Precaution: Investigate hormone levels before starting
O Initial feeding should begin within age 1 hour and glucose testing hydrocortisone!!!
30 minutes after the first feeding.
O If the initial glucose level is less than 25 mg/dL, then refeed and
recheck glucose level in 1 hour.
O If the glucose level remains at lower than 25 mg/dL, treat with
intravenous glucose. GLUCAGON
O If the glucose level is 25 to 40 mg/dL, then refeed or treat with
intravenous glucose as needed. Mechanism of Action: Insulin antagonist
O In at-risk asymptomatic infants,
 Management differs for the period from birth to 4 hours vs 4 to 12 Glucagon also relaxes smooth muscles of Gl tract Indications: Treat
hours and during the first 12 hours after birth. hypoglycemia
 Target glucose level is at least 45 mg/dL before feedings.
2ndary to hyperinsulinemia given w/ or w/out t initial IV access
O For symptomatic hypoglycemia,
 Target plasma glucose is 40 to 50 mg/dL. Dose: 0.025-0.3 mg/kg IM/IV (maximum 1 mg)

NURSING INTERVENTIONS ON NEONATAL HYPOGLYCEMIA Should cause recovery of hypoglycemia

 Blood glucose monitoring May not work if

 a heel-prick test
 Monitoring starts within a few hours of birth and continues until Reduced glycogen stores
levels are stable
Glycogen storage disease
Administering carbohydrates via enteral feeding or oral glucose gel

➤ Mild cases
DIAZOXIDE
 Give rapid-acting carbohydrates, such as fruit juice, as soon as
possible. Mechanism of Action: Increases blood glucose by inhibiting pancreatic insulin
release and possibly through an extrapancreatic effect.
A hyperglycemic effect starts within an hour and usually lasts a maximum of ▸ Antibiotics aminoglycosides, amoxicillin ampicillin cotrimoxazole and
8 hours with normal renal function procaine penicillin usually given for 7-10 days.

Dose: 2-5 mg/kg/dose PO q 8 hrs. Muscle relaxants: pancuronium

Indication: Infants who have persistent hyperinsulinemia Diuretics: furosemide

RESPIRATORY DISTRESS SYNDROME ▸ Antacids: sodium bicarbonate, sodium citrate

A severe lung disorder in neonate which is primarily related to lung Indomathacin if patent ductus arteriosus
immaturity.
Supportive management:
▸ breathing > 60 breaths per min
 Maintain adequate hydration and electrolyte status.
▸ use of accesory muscle of respiration WITH grunting.  Administer anti pyretics to reduce fever.
 Maintain acid base balance.
▸ neonate less than 35 wks is prone to develop RDS, w/o surfactant infants are  No nipple or gavage feeding: increase respiratory rate and chance
unable to keep their lungs inflated. Predisposing factors Prematurity Asphyxia of aspiration.
Hypothermia  IV line for fluid/hydration, nutrition and medication

▸ Maternal Anemia Pre eclampsia NURSING MANAGEMENT

▸ Maternal diabetes Caesarian section Pulmonary risk factors: ASSESSMENT:

Pneumonia History taking typically w/in hours, worse over 48-72 hours Nature of the
respiratory distress (rapid, shallow breathing, grunting, retractions, cyanosis),
➤ Pneumothorax Congenital Malformation Upper airway obstruction eg: complications like edema or decreased urine output.
meconium aspiration syndrome
◆Physical examination
Non- pulmonary risk factors : Sepsis
signs of increased breathing effort; including tachypnea (fast breathing)
➤ Cardiac defect
grunting sounds with each breath nasal flaring retractions of the chest muscles
cyanosis Lethargy poor feeding.
Exposure to cold
chest X-ray
Hypoglycemia
 Downe's score
➤ Metabolic acidosis
 Shake test
 Clinical Features Tachypnea (< or = 80-120 breaths per min)
Nursing diagnosis:
 Dyspnea
 Pronounced intercostals or substernal  Ineffective breathing pattern related to surfactant deficiency and
 Fine inspiratory crackles alveolar instability.
 Audible expiratory grunt  Impaired gas exchange related to immature pulmonary function.
 Flaring of external nares  Altered nutriton less than body requirement related to feeding
 Cyanosis or pallor difficulties.
 Place the infant in radiant warmer, incubator.
Manifestation as the disease progress
 Use environmental control
 Apnea  Position the infant properly
 Flaccidity  Maintain optimal nutrition pattern of infant
 Absent spontaneous movement  Once baby is breathing without distress NG feeding is started.
 Unresponsiveness  Involves parent in the care of children and allow frequent visit to
 Diminished breath sound encourage and promote infant - parent bonding.
 Mottling  Skin care with frequent position change.
 Mouth care.
SHAKE TEST  Psychological support and provide adequate information about
child's condition.
 withdraw gastric aspirate to determine lung maturity.
 Mix 0.5 ml of gastric aspirate with 0.5 ml of absolute alcohol in a Complications
test tube and shake for 15 sec. Formation of bubbles indicate
adequate surfactant and less chance of RDS.  Patent ductus arteriosus
 Congestive cardiac failure
MANAGEMENT  Intraventricular hemorrhage
 Retinopathy of prematurity
▸ treated in NICU.  Pneumonia
 Sepsis
Administer IV fluids and oxygen
 Necrotizing enterocolitis
➤ start oxygen therapy @4-6 lit/min. Maintain oxygen saturation between 90-  Neurologic sequele
95%.
Neonatal Sepsis
➤ Administration of exogenous surfactant through ET tube directly into
trachea. Medicines:
 is an invasive infection, usually bacterial, occurring during the neonatal Less vigorous sucking
period
Bradycardia
Neonatal sepsis occurs in 0.5 to 8.0/1000 births.
Anorexia
❖Categories of neonatal sepsis
Temperature instability (hypothermia or hyperthermia)
Neonatal sepsis may be categorized as:
Fever is present in only 10 to 15%
 Early onset (day of life 0-3)
 Late onset (day of life 4 or later Neonates with clinical signs of sepsis

Early-onset neonatal sepsis  respiratory symptoms require chest x-ray.

 Diagnosis is confirmed by isolation of a pathogen in culture.
 is associated acquired from the mother.
 Infection occur via hematogenous, transplacental spread from Prognosis
infected mother / more commonly, via ascending infection from
The fatality rate is 2 to 4 times higher in LBW infants than in full-term infants
the cervix.
The overall mortality rate of: - Early-onset sepsis is 3 to 40% (that of early-
With early-onset sepsis
onset GBS infection is 2 to 10%)
 85% present within 24 hours (median age of onset 6 hours)
- Late-onset sepsis is 2 to 20% (that of late-onset GBS is about 2%)
 5% present at 24-48 hours
Treatment
 Smaller percentage present within 48-72 hours. Onset is most rapid
in premature neonates. If no source of infection is identified clinically, the infant appears well, and
cultures are negative, antibiotics can be stopped after 48 h (up to 72 h in small
The microorganisms most commonly associated with early-onset infection
preterm infants).
include the following:
If maternal group B streptococcus prophylaxis was indicated and given
 Group B Streptococcus (GBS)
appropriately (i.e., penicillin, ampicillin, or cefazolin given IV for ≥ 4 h):
 Escherichia coli
 Coagulase- negative - Infants should be:
 Staphylococcus
 Haemophilus influenzae  Observed in the hospital for 48 h
 Listeria monocytogenes  Testing and treatment are done only if symptoms develop.

Pathophysiology Prevention

Currently, GBS and E coli continue to be the most commonly identified If adequate group B streptococcus prophylaxis was not given:
microorganisms associated with neonatal infection
- Infants are observed in the hospital for 48 hour without antimicrobial
Early onset: Risk factors therapy

 Maternal perinatal and obstetric factors that increase risk: If membranes ruptured ≥ 18 h before birth or gestational age is < 37 wk.:
 Premature rupture of membranes occurring (PROM) ≥ 18 h before *blood culture, CBC with differential, and perhaps a C-reactive protein level
birth Maternal chorioamnionitis is recommended at birth and/or at 6 to 12 h of life.
 Colonization with GBS
 Preterm delivery -The clinical course and results of the laboratory evaluation guide
management.
Hematogenous and transplacental infection occurs in the transmission of
certain: Nursing Assessment

 viral (e.g., rubella, cytomegalovirus)  Body temperature instability (high or low)

 protozoal (e.g., Toxoplasma gondii)  Poor feeding or refusal to feed
 treponemal (e.g., Treponema pallidum) pathogens  Lethargy or irritability
 Respiratory distress or rapid breathing
Late onset: risk factors  Abnormal heart rate or low blood pressure
 Jaundice (yellowing of the skin and eyes)
Important risk factor in late-onset sepsis is preterm delivery. Others include:  Poor weight gain or failure to thrive
 Abdominal distension or vomiting
 Prolonged use of intravascular catheters
 Skin rash or redness
 Exposure to antibiotics (which selects resistant bacterial strains)
 Signs of infection at the site of the umbilical cord or other wounds.
 Associated illnesses
 Prolonged hospitalization
 Contaminated equipment or IV or enteral solutions
LOWER RESPIRATORY TRACT INFECTION
Early signs of neonatal sepsis:
Incidence and etiology
Common early signs include:
Commom in children less than 4 years of age usually associated with previous
Diminished spontaneous activity URI.

Apnea Acute bronchitis

Viral infection Management

Bacterial infection Nebulization with normal saline or bronchodilators.

*Chemical agents/ allergens Broncodilators

(VOCs) from solvents and cleaning agents → Mucolytics

*Allergens Anti-inflammatory medicines

Dust from substances such as cotton or silica Bronchitis nursing interventions

Smoke (including tobacco smoke and air pollution) *Support Airway & Respiratory Function

Specific allergens like pollen and perfumes. Humidified Air

◆ Symptoms: Oxygen Therapy

Coughing mucus production Nasal Suctioning

Allergic bronchitis. Monitoring

Signs & Symptoms Bronchitis nursing interventions

Runny nose *Monitoring & Assessment

Sore throat Cardiorespiratory Monitoring

Malaise Apnea Monitoring

Wheezing Respiratory Status

Chills Signs of Dehydration

Shortness of breath INTRODUCTION

Fever Bronchiolitis is lower respiratory tract infection

Fatigue Viral infection

Back and muscle pain Seasonal, peak in winters.

Coughing Major cause is RSV

Diagnostic evaluation Bronchiolitis is lower respiratory tract infection

History and physical Viral infection

Examination Seasonal, peak in winters.

Cold-like symptoms Major cause is

Persistent cough (initially dry, then productive) RSV

Rapid breathing (respiratory synticial virus)

Nasal flaring, or retractions Definition

X ray ◆Bronchiolitis

Shows increased density of the bronchial walls or thickening of the interstitial A serious illness characterized by inflammation of bronchioles, causing sever
markings dyspnea.

Sputum culture Incidence and etiology

Cough deeply and spit any phlegm that comes up from your lungs into a Common under infant under age of 6 months.
special container.
Viral: RSV, adenovirus, influenza
Management
Bacteria: influenzae, pneumococcus and streptococcus hemolyticus
Antibiotics
Pathophysiology
Cough expectorant
Upper respiratory infection usually by RSV
Antipyretics medicines
Edema, mucus and cellular debris obstruct bronchioles
Steam inhalation
Bronchioles constrict during expiration, causing hyperinflation of lungs Supportive Management

Atelectasis can occur when obstruction is complete Oxygenation:

Normal exchange of gases is impaired Apnea Monitoring

Hypoxemia Feeding

Clinical manifestations Nebulised Hypertonic Saline

Dyspnea Bronchodilators

Diminished Inhaled / Oral Corticosteroids

Nasal flaring Physiotherapy

Cyanosis Nursing diagnosis

Intercoastal, subcoastal. Supracoastal retractions *Ineffective airway clearance related to Increased mucus and nasal discharge

Breath Interventions:

Sounds Assess airway for patency

Crackles Monitor the vital signs

Sound Position patient properly

Wheezing Interventions

History and physical examination. Encourage fluid intake at frequent intervals over 24-h time periods.

Initial cough Assist to perform deep breathing and coughing exercises in child.

Congestion Nebulization should be done as prescribed by the dr.

Fever Administer oxygen as prescribed.

Clinical manifestations Administer medication as prescribed by the dr.: antipyretic, bronchodilaters,

antibiotics
Chest x ray
PNEUMOΝΙΑ
Pulse oximetry-
An inflammation of the lung parenchyma (the respiratory bronchioles and the
SPO2 alveoli)

Cultures Pneumonia is mainly caused by microorganisms which enter the lower

respiratory system and cause infection.
Capillary Blood
CLASSIFICATION
Gas
According to the causative organisms
“Children with less severe symptoms:
Viral pneumonia
Antipyretics, adequate hydration.
Bacterial pneumonia
Hospitalization is warranted for children on severe distress
Fungal pneumonia
Oxygen therapy, critical monitoring of vital signs and blood gas level and
ventilatory support be necessary. Parasitic pneumonia

Bronchiolitis *According to the areas of the lung involved/affected

◆Indications for admission : Lobar pneumonia

Persistent resting oxygen Multilobar pneumonia

Saturation Lobar pneumonia

Elevated respiratory rate ⚫respiratory infection of one or more lung lobes caused by Streptococcus
pneumoniae
Dyspnea
Multilobar pneumonia
Chronic lung disease
Infection in two or more lung lobes, either in the same lung (unilateral) or in
Management
both lungs (bilateral).
*Bronchial pneumonia 1. Exercise

Lung’s bronchi 2. Aspirin

Patchy areas of consolidation in one or more lobes of the lung. 3. Change in temperature

◆Interstitial pneumonia 4. Viral respiratory infection

⚫childhood interstitial lung disease (chILD) 5. Emotional stress

Miscellaneous types: 6. Excitement

Aspiration pneumonia Clinical manifestation

Loffler’s pneumonia (eosinophils) Tachypnea

Hypersensitivity pneumonitis Wheezing

Hypostatic pneumonia Restlessnesss

Pathophysiology Dyspnea

Bacteria enters the respiratory tract and travels down. Abdominal pain

Agent destroy mucous membrane and causes interstial lesions. Cough

Inflammation of air sac or mucous membrane of small bronchioles or Fatigue due to shortness of breath
interstial tissue
Retractions
Destruction of parenchymal tissue
Nasal flaring
Pus or fluid is filled in air sac
Cyanosis
Consolidation occur
Stridor
Causing difficulty in breathing, tachypnea, retractions
Diagnostic evaluations
CLINICAL MANIFESTATION
History taking
Fever with chills
Physical examination
Cough with thick sputum
Sputum culture
Tachypnea
Chest x-ray: shows air trapping
ASTHMA IN CHILDREN
Blood examination shows eosinophilia
Definition of Asthma
Pulmonary function test:.
increased responsiveness of the A reversible, characterized by an airways to
various stimuli RAST test or radioallergosorbent test

Any of these stimuli can trigger a hyperactive allergic response which Medical management
produces:
Short acting
1. Inflammation of the respiratory tract
bronchodilators
2. Bronchoconstriction, and
Anticholinergic ipratropium bromide
3. Hypersecretion of mucus
Mast cell inhibitors
Etiology
Medical management
Extrinsic asthma
Corticosteroids.
→ Allergic asthma
Leukotriene blockers: zileuton
Symptoms
diminish the mediator action of leukotrienes.
the inhalation of a specific allergen like pollen, dust, smoke, powder
Antibiotics
Intrinsic asthma
Oxygen therapy
Non allergic asthma - same manifestations of airway obstruction - response to
Magnesium sulphate: IV
an unidentified or non specific factor in the environment.
administration of drug have shown bronchodilating effect.
❖Triggered by:
Heliox: a mixture of helium and oxygen can be given in case of breathing Abdominal cramps or pain
difficulty.
Loss of appetite
Methylxanthines: such as theophylline: it works by relaxing the muscles
around the airway. Fever

Nursing management Signs of dehydration

*Assessment: history and PE Nursing interventions

Ineffective airway clearance related to bronchospasm and mucosal edema. Give oral rehydration solutions (ORS)

Monitor respiratory rate How to prepare:

Administer humidified oxygen. Keep NPO. 6 level teaspoons of sugar and half a level teaspoon of salt into 1 liter (about 4
cups) of clean, boiled, and cooled water.
Maintain IV line.
Give the solution in small, frequent sips from a cup or spoon until tno longer
Administer medication as prescribed. thirsty.

Nebulization. Nursing interventions

Positioning Diet:

Nursing diagnosis Continue feeding your child with bland, starchy items like rice, cereal, and
crackers.
Ineffective Airway Clearance related to bronchoconstriction, increased mucus
production, ineffective cough, possible bronchopulmonary infection. Avoid: sugary drinks

Ineffective Breathing Pattern related to chronic airflow limitation. Seek Medical Management if

Impaired Gas Exchange related to chronic pulmonary obstruction Shows signs of dehydration.
abnormalities due to destruction of alveolar capillary membrane.
Has severe or worsening abdominal pain.
Imbalanced Nutrition: Less Than Body Requirements related to increased
work of breathing, air swallowing, drug effects with resultant wasting of Has fever.
respiratory and skeletal muscles.
Has blood or pus in their stool.
Activity Intolerance related to compromised pulmonary function, resulting in
Severe or lasts for an extended period.
shortness of breath and fatigue.
Is very young (infants under 3 months with diarrhea need immediate medical
Disturbed Sleeping Pattern related to hypoxemia and hypercapnia.
care).
Acute Gastroenteritis in pediatric(Diarrhea)
Types of diarrhea
Definitions and Terms:
Intractable diarrhea of infancy 3months occur in infancy in the first few
Acute Gastroenteritis (AGE): months of life persistent longer than two weeks with no pathogens is
refractory to treatment of a heterogeneous syndrome with high mortality
inflammation of the stomach and intestines
Gastroenteritis
Diarrhea: the frequent passage of unformed liquid
Rotavirus is the most common cause of severe gastroenteritis
Dysentery: blood or mucus in stools
Gastroenteritis
If caused by Rotavirus;
If cause by:
low grade fever
Salmonella, compylobacter organism bacteria(less than 1 year)
Malaise
colicky pain
nausea
bloody diarrhea
vomiting
Fever
[Link] diarrhea: in children < than 5
drowsiness, confusion
If cause by Parasites
(life threaten septicemia persist 2-3 weeks)
Less common, parasites such as giardia and cryptosporidium
Etiology: Viral
Symptoms of acute diarrhea
70-85% in developed countries
Watery stools
Rotavirus: represent of all pediatric AGE hospitalizations
Vomiting
Presentation: Complications

Mild or moderate fever Dehydration

Vomiting followed by watery diarrhea Excessive loss of fluids and minerals (electrolytes) from the body&
Electrolyte deficiency
Diarrhea persisting for 5-7 days
Kidney failure& Acid base imbalance with acidosis
Etiologies:
Shock occur when dehydration progress to the point circulatory impaired
Bacterial
Physical Examination
Campylobacter, Salmonella, Shigella, E. coli, Yersinia, Clostridium difficile
Cool extremities.
Presentation:
Anterior fontonellae markedly depressed and eyes were sunken.
High fevers
Blood pressure 45/30 mm Hg, difficult to obtain.
Shaking
The pulse 160 beats/min, with weak pulsation.
chills
Temperature 39°C, skin turgor markedly decreased.
Bloody bowel movements (dysentery)
The tongue and buccal mucosa were dry.
Abdominal cramping & fecal leukocytes
Respiratory deep. The weight 9 kg.
Etiologies:
Laboratory Investigation
Parasitic
➤ Careful history(travel, blood in stool, water, contact with birds, recent
Giardia and Cryptosporidium <10% of cases antibiotics, fever, vomiting
Presentation: ➤ Stool analysis:
Watery stools ➤ Foul smell stool means malabsorption
Low-grade fever ➤ Neutrophil in stool indicated bacterial infection
Causes & High risk groups ➤ Eosinophil means parasitic infection
Contaminated water& food ➤ gross Blood in stool means shigella and campylobacter
Poor hygiene > CBC
Nutritional deficiency > Electrolyte
Poor sanitation Treatment
Increase frequency in infancy Aim of treatment:
Immune deficient individuals [Link] fluid and electrolyte imbalance
Malnutrition [Link]
Travel to endemic areas [Link] fluid therapy
Lack of breast feeding 4. Reintroduction adequate diet
Exposure to unsanitary conditions Management
Poor maternal education. Symptom management
Sign & Symptoms Correction of underlying causes If the cause is found to be a medication,
lactose intolerance
Nausea & Vomiting
Oral rehydration, a person with diarrhea needs to continue to eat to maintain
Diarrhea
adequate caloric intake as well as meeting the needs of increase fluids
Loss of appetite
ORS Composition
Fever
Oral rehydration solutions (ORS) have sugar, salt and water to be easily
Headaches absorbed in the gut. Used in case vomiting and dehydration

Abdominal pain 5-10 ml every minute by syringe or NGT 10 ml/kg

Abdominal cramps Composition of ORS

➤ Sodium Chloride Severe and forceful cough

➤Tri-Sodium Citrate (bicarbonate) Environmental factors Slum dwellers Street children

➤ Potassium Chloride IV drug abuser

➤ Glucose Malnutrition

Treatment Clinical manifestations

-Early feeding reduces illness duration and improves nutritional outcome. *Pulmonary Symptoms

Cereal, cooked vegetable and meats persistent cough, potentially with blood-tinged sputum or phlegm,

Formula fed infants chest pain

-Restart feeding once the rehydration phase is complete (ideally in 2-4 h). Systemic symptoms fever,

- Fatty foods and foods high in simple sugars should be avoided. unexplained weight loss

-Lactose-free formulas are unnecessary; night sweats

Treatment loss of appetite,

Antidiarrheals fatigue,

Antiemetics are recommended general feeling of being unwell.

Probiotics (e.g. Lactobacillus) alter the Clinical Spectrum - Pulmonary TiBB

composition of gut flora and assist in restoring Lesions of Secondary TB

normal gut function Progressive Primary Disease

Antimicrobials Complicated Ghon focus

C difficile- & start metronidazole Poor disease

Cholera-tetracycline containment at the point of entry; infants and severely immune-compromised

individuals are particularly vulnerable.
Giardia-metronidazole
Clinical Spectrum - Pulmonary TB
Cryptosporidium-metronidazole
Airway obstruction with "check valve" effect
Nursing Management
➤ Hyperinflation (ball valve effect) of left lung
Goals of treatment
Pleural effusion
Maintain adequate hydration
Follows rupture of subpleural focus
Maintain appropriate nutrition
Hypersensitivity tuberculoproteins to
Prevent spread infection
Asymptomatic (minor), Fever, cough, dyspnea, pleuritic chest pain
Tuberculosis in Children
Adult-type disease
Transmission
At 8-10 yr of age
Inhalation of air borne mucus
Associated with an excessive and poorly regulated immune response
droplet nuclei 1-5 micron in diameter
Any child with cavitary disease is infectious (as infectious as an adult sputum
Cough 3000 droplet nuclei smear-positive case) and should be regarded as a potential source case.

Sneeze up to 1 million droplet nuclei Symptoms - Pulmonary TB

10-200 droplets can cause TB infection Primary complex - mild fever, anorexia, weight loss, decreased activity, cough

Droplet nuclei can stay airborne for up to 72 hours in dark, damp rooms Progressive primary complex - high grade fever, cough, expectoration and
(sunlight kills them) hemoptysis - cavity and ulceration of bronchus

Chance of transmission increases with Endobronchial TB - wheeze, fever, troublesome cough, dyspnea, cyanosis.

Extensive infiltrates / cavity Wheezing child not responding to bronchodilators, less than 2 yrs age

Copious production of thin sputum Symptoms

Cough (2 weeks) Closeness of contact

▸ Fever (2 weeks) Sputum smear result of index case (if known) -

Night sweats (drenching) Timing of contact children usually develop TB

Weight loss or poor weight gain If no source case is identified

➤ Malaise and fatigue - A standard dose of 5 tuberculin units (TU0.1 ml) of PPD

Loss of appetite Tuberculin Skin Test (TST)

Shortness of breath Interpretation

Chest pain > 5 mm

Diagnosis of TB in childrem Immunocompromised

Clinical judgment - based on exposure history & clinical features HIV-infected children

2 Tuberculin Skin Test (TST) severely malnourished;

3 Chest x-ray (CXR) Immunosuppressed patients

4 Bacteriologic confirmation Organ transpints

Definitions in treatment of TB in childrem In presence of history of close contact,

Presumptive pediatric TB Findings suggestive of TB Persons with nodular or fibrotic changes on chest
X-ray (old healed TB)
Children with persistent fever and/or cough,
Patients with organ transplants, and other
loss of weight (loss of > 5% body weight as compared to highest weight
recorded) >10 mm

No weight gain in last 3 months and or In all other children (whether they have received BCG vaccination or not)

History of contact with infectious TB cases. Persons with clinical conditions that place them at high risk

Clinically diagnosed TB Children less than four years of age, or children and adolescents exposed to
adults in high-risk categories
Based only on X-ray / Bacteriology
>15mm
Drug resistant TB
Persons with no known risk factors for TB
Monoresistance: resistance to one 1st anti-TB drug only
False Positive
Poly-drug resistance (PDR) resistance to more than one first-line ATD, other
than both INH and Rifampicin. Caused by atypical tuberculous mycobacteria

Multi-drug resistant (MDR) Previous administration of BCG vaccine.

Extensively-drug resistant (XDR) TB. When the injected area is touched, causing swelling & itching

Suspected TB in IMCI Allergic reaction or hypersensitivity

Common clinical presentations to suspect TB in children: Infection at the site of test

Cough, including severe pneumonia not improving False negative result

Weight loss or failure to gain weight, including severe malnutrition Recent TB infection (less than 8-10 weeks)

Fever Recent Viral infection (EBV, measles, HIV, mumps, chicken pox)

* Lymph node enlargement Recent Live Viral Vaccine (3 weeks gap mandatory)

Especially if symptoms persist (>2 weeks) without improvement following Chronic renal failure, Liver failure

other appropriate therapies Hodgkin's disease, Lymphomas, Leukemia

broad-spectrum antibiotics for pneumonia; or Corticosteroid therapy/steroid use

anti-malarial treatment for fever; or Immunological compromised state (malnutrition)

nutritional rehabilitation for malnutrition CXR

Exposure History
Persistent opacification in the lung together with enlarged hilar or sub-carinal Psychological Support
lymph glands.
Empowerment
A miliary pattern of opacification children is highly suggestive of TB.
Resource Connection
Adolescents:

Large pleural effusions and apical infiltrates with cavity formation being the
most common forms of presentation (similar to adults). MEASLES

Diagnosis of TB WHAT IS MEASLES?

Smear Test: AFB Measles is an acute viral infectious disease

Staining Highly contagious viral illness

The acid-fast bacilli will stain bright red, and the background will stain blue. Is a very contagious (easily spread) infection that causes a rash all over your
body. It is also called rubeola or red measles.
Reagents used in the procedure include Ziehl-Neelsen carbolfuchsin solution,
1% acid alcohol, and methylene blue solution Measles Virus

Aims of Treatment of TB in children [Link] (RNA) or ribonucleic acid,

To cure the patient of TB [Link] antigenic type

2 prevent death from TB disease 3. Rapidly inactivated by heat, sunlight, acidic pH, ether and trypsin

Prevent its late effects Mode of transmission

Prevent relapse of TB Measles can be spread by

5 prevent dt & transmission of dr Direct contact

6 reduce transmission of TB to others Airborne and indirect contact less common

7 achieve all this with minimal toxicity Respiratory droplets

Drug Resistance – Definitions Touch a surface or object contaminated with the virus and then touch your
eyes, nose, or mouth (indirect)
Drug Redistant TB: Mycobacterium tuberculosis bacilli resistant to at least
one of the 1st line anti TB drugs, INH, RMP, Pyrazinamide or Ethambutol Clinical Features

Multidrug Resistant TB: Mtb resistant to INH and RMP 1. Incubation period 10-12 days

Extensively Resistant TB: Mtb resistant at least to INH, RMP plus any 2. Early symptom 2-4 days & increase in fever to 39.4°C to 40.6°C cough,
resistance to fluroqunolones and injectable anti TB drugs. coryza, conjunctivitis Koplik spots (rash on mucous membranes)

Nursing Interventions 3. Rash 2-4 days after prodrome, 14 days after exposure persists 5-6 days
begins on face and upper neck maculopapular, becomes confluent
Infection Control & Prevention
3. Recovery: fades in order of appearance
Airborne Precautions:
Measles complications
Personal Protective Equipment (PPE)
Corneal scarring causing blindness Vitamin A deficiency
Source Control
(Common)
Screening
Encephalitis
Reporting
Older children, adults
Respiratory Support & Monitoring
0.1% of cases
Assess Respiratory Status
Chronic disability
Administer Oxygen
Pneumonia & Diarrhea (Common)
Provide Airway Clearance
Diarrhea common in developing countries
Sputum Samples
Pneumonia 5-10% of cases, usually bacterial
Patient & Family
Measles Complications
Support
Other complications:
Education
[Link] media 7%
[Link] 0.6-0.7% Isolation until 5th of rash

3. Death 0.2% Kept on bed until fever & cough subsides

Measles Laboratory Provide dim light, clean eye lid, irrigate affected eye with saline

Diagnosis Encourage more fluid intake during fever.

[Link] of measles virus from urine, nasopharynx, blood, throat Increase humidity (for children) of the room to relieve cough

[Link] rise in measles IgG by any standard serologic assay (e.g., ΕΙΑ, Nursing Care:
ΗΙ)
Relieve itching of skin (for children) by tepid bath & soothing lotion
3. Positive serologic test for measles IgM antibody
Immune serum or gamma-globuline may be given to modify illness & reduce
PREVENTION complication

MMR Vaccine Antibacterial therapy given for treatment of complication (e.i. respiratory
infection & gastroenteritis).
1. First dose of MMR at 12-15 months

2. 12 months is the minimum age 3.2nd dose of MMR at 4-6 years

4.2nd dose may be given any time at least 4 weeks after the 1st dose

5. May boost antibody titers in some persons

MMR Vaccine Indication

1. All children 12 months of age and older

2. Susceptible adolescents and adults without documented evidence of

immunity

3. All persons who work within medical facilities should have evidence of
immunity to measles

NOTE:***YOU CAN CONSIDERED TO BE IMMUNE TO MEASLES

ONLY IF YOU RECEIVED 2 DOSES OF MEASLES VACCINE.

Vaccine Contraindications and Precautions

1. History of anaphylactic reactions to neomycin

2. History of severe allergic reaction to any component of the vaccine

3. Pregnancy

4. Immunosuppression

5. Moderate or severe acute illness

6. Recent blood product

7. Personal or family (i.e. sibling or parent) with history of seizures of any

etiology.

Incubation Period

A person with measles can spread the virus to others for about eight days,
starting four days before the rash appears and ending when the rash has been
present for four days.

TREATMENT AND NURSING INTERVENTION

SUPPORTIVE CARE:

[Link] FLUIDS (IV)

[Link] to control fever & pain

[Link] to treat secondary infection from bacteria

4. Vit. A

Nursing Care: