JOSE, LEANA LOUISSE D.
BSN 2B
Postpartum Complications
CORNELL NOTES ON NCM109 MODULE 3
KEYS
POSTPARTAL HEMORRHAGE
 Any blood loss from the uterus greater
than 500 ml within a 24-hour period
UTERINE ATONY
Relaxation of the uterus
 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 haemorrhage
 Endometritis
 Prolonged use of magnesium sulfate or
other tocolytic therapy
LACERATIONS
 Small lacerations or tears of the birth
canal are common and may be
considered a normal consequence of
childbearing.
 Large lacerations, however, can cause
complications.
CERVICAL LACERATIONS
 Usually found on the sides of the cervix,
near the branches of the uterine artery.
VAGINAL LACERATIONS
Easier to assess than cervical lacerations, because
they are easier to view.
PERINEAL LACERATIONS
First degree
 Vaginal mucous membrane and skin of
NOTES
Early within the first 24 hours
Late after 24 hours-6 weeks
Causes:
 Uterine atony
 Lacerations
 Retained placental fragments
 Uterine inversion
 Dic
Management
 Attempt uterine massage
 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.
 Iv oxytocin
 10-40 u/1000 ml plr
 Duration of action: 1 hour
If cannot remain contracted
Methylergonovine maleate (methergine)
 Given im q2-4hrs x 5 doses
 Causes increased blood pressure
Carboprost tromethamine (hemabate)
May be given every 15-90 mins x 8 doses
Rectal misoprostol
 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
 Hysterectomy or suturing
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
 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 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 24-48 hrs can lead to tss.
Management
 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
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 be detected by ultrasound.
 Abrupt discharge, large amount of blood
 Usually the uterus is not fully contracted
upon palpation.
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.
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.
PUERPERAL INFECTION
 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)
 The risk of infection is greater if tissue
edema and trauma are present.
ENDOMETRITIS
Infection of the endometrium, the lining of the
uterus
 Fever manifests on 3rd-4th day pp, t
>38c, chills, loss of appetite, general
malaise
 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.
 Blood serum sample: hcg  placenta is still present
 Large fragments  bleeding will be apparent in the immediate
postpartal period
 Small fragments  bleeding may not be detected until postpartum
day 6-10
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
Causes:
 Small retained placental fragment
 Mild endometritis
 Accompanying problem such as uterine myoma
Management:
 Oral methylergonovine 0.2mg qid
 Oral antibiotic for endrometritis
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 of
discomfort
 Administer a mild analgesic as ordered for pain relief.
 Ice pack  prevent further bleeding
 Incision and ligation under local anesthesia.
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
Management
 Antibiotics determined by culture of lochia
 Oxytocic agent such as methergin
 Additional fluid
  Wbc is normally elevated during  Analgesics
postpartum  Walking
 Uterus is not well contracted and painful  Infection control measures
to touch
 May feel strong afterpains, lochia
usually dark brown and has foul odor
INFECTION OF THE PERINEUM  May remove perineal sutures to allow for draining, packing
Episiorrhapy  portal of entry  Systemic or topical antibiotic
 Localized infection, pain, heat, feeling of  Analgesics
pressure  Sitz bath
 Slough, purulent drainage  Infection control measures

PERITONITIS  Rigid abdomen, abdominal pain, high fever, rapid pulse,

Infection of the peritoneal cavity, usually occurs  Vomiting, and the appearance of being acutely ill
as an extension of endometritis.  Note that uterus is well-contracted, and abdomen is soft.
 One of the gravest complications of  Paralytic ileus
childbearing and is a major cause of Management
death from puerperal infection.  Ngt, iv fluids or tpn
 Abscess may form in the cul-de-sac of  Analgesics
douglas.  Antibiotics
MASTITIS Management
Infection of the breast  Antibiotics
 May occur as early as the seventh  Breastfeeding is continued, keeping the breast emptied helps to
postpartal day or not until the baby is prevent growth of bacteria
weeks or months old  Manual expression
 Usually unilateral  Cold/ice compress pain relief
 Epidemic mastitis may be bilateral  Warm/hot compress reduce inflammation and edema
 Painful, swollen, and reddened  Good supportive bra
 Fever accompanies these first symptoms
within hours, and
 Breast milk becomes scant.

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
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
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:
Post partal hemorrhage occurs early within first 24hrs, then uterine atony occurs when the uterus fails to contract after
the delivery of the baby. Lacerations is a wound that occurs when skin, tissue, and/or muscle is torn or cut open and cervical
laceration is risk for STI. There are four grades of tear that can happen in perineal laceration, with a fourth-degree tear being the
most severe. Retained placental fragments naman is a rare complication of labor, yet can potentially cause severe morbidity and
discomfort. The subinvolution happens naman when uterus does not return to its normal size, and perineal hematoma is usually
caused by a ruptured or bleeding vein while purperal infection also known as a postpartum infection. Then there’s endometritis
which is an inflammation of the inner lining of the uterus or endometrium. Peritonitis is risk for peritoneal dialysis while mastitis is
caused by a blocked milk duct leading to inflammation or by a bacterial infection. Baby blues or posprtum blues are feelings of
sadness a woman may have in the first few days after having a baby then a dramatic drop in hormones (estrogen and progesterone)
in your body may contribute to postpartum depression while postpartum psychosis is a serious mental health illness that can affect
someone soon after having a baby.

JOSE, LEANA LOUISSE D.

BSN 2B

The High Risk Newborn

CORNELL NOTES ON NCM109 MODULE 4

KEYS NOTES
ALTERED BIRTH WEIGHT AGA - APPROPRIATE FOR GESTATIONAL AGE 10TH-90TH
PERCENTILE
 SGA - SMALL FOR GESTATIONAL AGE BELOW 10TH PERCENTILE
LGA - LARGE FOR GESTATION AGE ABOVE 90TH PERCENTILE
ALTERED GESTATIONAL AGE COLORADO/LUBCHENCO INTRAUTERINE GROWTH CHART
 LOW BIRTH WEIGHT (LBW) INFANTS – UNDER 2500 G
 VERY LOW BIRTH WEIGHT – 1000-1500 G
 EXTREMELY VERY LOW BIRTH WEIGHT – 500-1000G
SMALL FOR GESTATIONAL AGE  MALNUTRITION
 INTRAUTERINE GROWTH  ADOLESCENT PREGNANCY
RESTRICTION (IUGR)  PLACENTAL ANOMALY – MOST COMMON
 FAILED TO GROW AT THE  SYSTEMIC DISEASES THAT DECREASE UTERINE
EXPECTED RATE IN UTERO. PERFUSION
 SMOKING, NARCOTIC USE
 INTRAUTERINE INFECTION- RUBELLA, TOXOPLASMOSIS
LARGE FOR GESTATIONAL AGE ASSESSMENT:
 ALSO TERMED MACROSOMIA UNUSUALLY LARGE UTERUS FOR GESTATIONAL AGE
 APPEARS DECEPTIVELY DIFFICULTY OR PROLONGED LABOR  SHOULDER DYSTOCIA
HEALTHY, BUT IMMATURE AT BIRTH:
DEVELOPMENT  IMMATURE REFLEXES, SIGNS OF PREMATURITY
 MOTHERS WITH GDM OR ARE  EXTENSIVE BRUISING OR BIRTH INJURY
OBESE  CAPUT SUCCEDANEUM, CEPHALHEMATOMA, MOLDING
 MULTIPARITY
OTHER CONDITIONS ASSOCIATED WITH COMPLICATIONS:
LGA:  BRUISING, POLYCYTHEMIA  CARDIOVASCULAR
 TRANSPOSITION OF THE GREAT DYSFUNCTION
VESSELS  HYPOGLYCEMIA (low sugar)
 BECKWITH SYNDROME
 OMPHALOCELE
(a birth defect of the abdominal (belly)
wall.)
PRETERM INFANT COMPLICATIONS:
 A LIVE BORN INFANT BORN ANEMIA OF PREMATURITY
BEFORE THE END OF 37 WEEKS  (a low serum EPO level)
GESTATION KERNICTERUS
ASSESSMENT:  A type of brain damage that can result from high levels of bilirubin in
 BALLARD SCORE OR MATURITY a baby's blood.)
SCALE PERSISTENT PATENT DUCTUS ARTERIOSUS (PDA)
 A persistent opening between the two major blood vessels leading
from the heart.
PERIVENTRICULAR/INTRAVENTRICULAR HEMORRHAGE,
INTRACRANIAL HEMORRHAGE
 A disease process that primarily affects the premature newborn infant
born at less than 33 weeks of gestation.
RESPIRATORY DISTRESS SYNDROME (RDS)
 Caused by the baby not having enough surfactant in the lungs.
RETINOPATHY OF PREMATURITY (ROP)
 An eye disease that can happen in premature babies.
NECROTIZING ENTEROCOLITIS (NEC)
 Most common gastrointestinal (GI) medical/surgical emergency
occurring in neonates.
POSTTERM INFANT POSTTERM SYNDROME:
- A LIVE BORN INFANT BORN  DRY, CRACKED, ALMOST LEATHERLIKE SKIN FROM LACK
AFTER THE 42 WEEKS AOG OF FLUID
 ABSENCE OF VERNIX
 AF LESS THAN USUAL, MAY BE MECONIUM-STAINED
LONG FINGERNAILS
COMPLICATIONS:
MECONIUM ASPIRATION
 When a baby is stressed and gasps while still in the womb, or soon
after delivery when taking those first breaths of air.
HYPOGLYCEMIA

TRANSIENT TACHYPNEA OF THE
NEWBORN (TTN)
 RESPIRATORY RATE THAT
REMAINS AT 80-120 BPM BEYOND
1 HOUR
 AFTER BIRTH.
CAUSE: RETAINED LUNG FLUIDS
APNEA
 A PAUSE IN RESPIRATIONS
LONGER THAN 20 SECONDS WITH
ACCOMPANYING BRADYCARDIA.
RESPIRATORY DISTRESS SYNDROME
(RDS)
HYALINE MEMBRANE DISEASE
 MOST INFANTS WHO DEVELOP
RDS HAVE DIFFICULTY
INITIATING RESPIRATIONS AT
BIRTH.
 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
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
 Low blood sugar
IMPAIRED THERMOREGULATION
 A known complication of many of the diagnoses commonly seen
among patients in a PM&R practice.
POLYCYTHEMIA, DEHYDRATION
 An apparent rise of the erythrocyte level in the blood caused by loss
of body fluids, such as through burns, dehydration, and stress.
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 (O2 as needed)
 PEAKS AT 36HOL THEN FADES, USUALLY ENDS AT 72HOL
RISK FACTORS:
 PRESENCE OF INFECTION
 HYPERBILIRUBINEMIA (yellow discoloration of the eyes and
skin, called jaundice.)
 HYPOGLYCEMIA (low blood sugar)
 HYPOTHERMIA (low temperature)
 GENTLY STIMULATE THE INFANT TO BREATHE AGAIN
 CLOSE MONITORING, DOCUMENT DURATION X
EPISODE/MIN
AFTER RESUSCITATION:
 LOW BODY TEMPERATURE
 NASAL FLARING
 STERNAL AND SUBCOSTAL RETRACTIONS
 TACHYPNEA (MORE THAN 60 BPM) (increased RR)
 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
MANAGEMENT
 SURFACTANT REPLACEMENT
 ENDOTRACHEAL ADMINISTRATION
 MECHANICAL VENTILATOR
 OXYGEN ADMINISTRATION
 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

MECONIUM ASPIRATION SYNDROME
(MAS)
 AN INFANT MAY ASPIRATE
MECONIUM EITHER IN UTERO OR
WITH THE FIRST BREATH AT
BIRTH.
ASSESSMENT
 MECONIUM STAINED AF
 DIFFICUFTY 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
SUDDEN INFANT DEATH SYNDROME
(SIDS)
 SUDDEN UNEXPLAINED DEATH IN
INFANCY.
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
 PEAK AGE OF INCIDENCE: 2-4
MONTHS OLD
HEMOLYTIC DISEASE OF THE NEWBORN
HEMOLYSIS  HYPERBILIRUBINEMIA
 MOST COMMON CAUSE: ABO
INCOMPATIBILITY
 ABO INCOMPATIBILITY
 SUPPORTIVE CARE: KEEP THERMOREGULATED, PROVIDE
HYDRATION AND NUTRITION
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
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.
 DO NOT 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
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%
DIAGNOSTICS: TB, B1, B2
 THERAPEUTIC MANAGEMENT
 INITIATION OF EARLY FEEDING
 PHOTOTHERAPY
 EXCHANGE TRANSFUSION
PHOTOTHERAPY
  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
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
PUSEDEMATOUS EYELIDS
 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
 CAUSED BY VASOCONSTRICTION OF IMMATURE RETINAL
BLOOD VESSELS D/T DELIVERY OF HIGH
CONCENTRATION OF OXYGEN.
 ROP SCREENING ROUTINE FOR PREMATURE BABIES.
PREVENTION
 ERYTHROMYCIN EYE PROPHYLAXIS THERAPEUTIC
MANAGEMENT
 INDIVIDUALIZED DEPENDING ON ORGANISM CULTURED
 GONOCOCCI (a bacterium which causes gonorrhoea) –
CEFTRIAXONE, PENICILLIN
 CHLAMYDIA (STI)– ERYTHROMYCIN EYE OINTMENT
 STANDARD AND CONTACT PRECAUTION
 EYE IRRIGATION WITH NSS USING STERILE MEDICINE
 DROPPER OR BULB SYRINGE, ADMINISTERED LATERALLY
TO
 PREVENT CROSS-CONTAMINATION
JOSE, LEANA LOUISSE D.
BSN 2B

Physical and Developmental Disorders

CORNELL NOTES ON NCM109 MODULE 5

KEYS NOTES
PHYSICAL AND DEVELOPMENT DISORDERS OF THE GASTROINTESTINAL SYSTEM
ANKYLOGLOSSIA  ABNORMAL RESTRICTION OF THE TONGUE CAUSED BY AN
 TONGUE-TIED ABNORMALLY TIGHT FRENULUM
 SURGICAL INTERVENTIONN TO RELEASE
CLEFT LIP  MORE PREVALENT AMONG BOYS THAN GIRLS,
 FAILURE OF MAXILLARY AND SIGNIFICANTLY HIGHER INCIDENCE IN ASIAN POPULATION,
MEDIAN NASAL PROCESSES LOWER INCIDENCE IN AFRICAN-AMERICAN POPULATION
(DEVELOPS DURING WEEKS 9-12  FACTORS SUCH AS VIRAL INFECTION OR FOLIC ACID
OF INTRAUTERINE LIFE) TO DEFICIENCY
FUSE, RANGING FROM A SMALL ASSESSMENT
NOTCH IN THE UPPER LIP TO A  MAY BE DETECTED IN SONOGRAM
TOTAL SEPARATION OF THE LIP  READILY APPARENT ON INSPECTION UPON BIRTH
AND FACIAL STRUCTURE UP MANAGEMENT
INTO THE FLOOR OF THE NOSE,  IN UTERO - FETAL SURGERY
WITH EVEN UPPER TEETH AND  SURGICAL REPAIR USUALLY BETWEEN WEEK 2-10 OF LIFE.
GINGIVA ABSENT.  NASAL MOLD APPARATUS TO SHAPE A BETTER NOSTRIL.
 MAY BE UNILATERAL OR  AS THE CHILD GROWS, REVISION OF THE ORIGINAL REPAIR
BILATERAL MAY BE DONE.
 HEREDITARY, TRANSMISSION
OF MULTIPLE GENES, OR
TERATOGENIC (NAMAMANA)
CLEFT PALATE ASSESSMENT
 OPENING OF THE PALATE,  DIRECT VISUALIZATION OF THE PALATE BY USING A
USUALLY ON THE MIDLINE AND TONGUE DEPRESSOR.
MAY INVOLVE ANTERIOR HARD  A CHILD WITH CLEFT PALATE MUST BE ASSESSED FOR
PALATE, THE POSTERIOR SOFT OTHER CONGENITAL ANOMALIES.
PALATE OR BOTH. MANAGEMENT
 PALATE PROCESS CLOSES AT  EARLY REPAIR INCREASES SPEECH DEVELOPMENT, BUT
WEEKS 9-12 OF INTAUTERINE MAY RESULT IN A SECOND-STAGE REPAIR AS THE CHILD
LIFE. GROWS.
 USUALLY OCCURS IN  SOFT PALATE REPAIR 3-6 MONTHS OLD; HARD PALATE
CONJUNCTION WITH CLEFT LIP. REPAIR 15-18 MONTHS OLD.
TRACHEOESOPHAGEAL ATRESIA AND ASSESSMENT
FISTULA  MUST BE RULED OUT IN ANY INFANT BORN TO A WOMAN
WITH HYDRAMNIOS.
 ATRESIA – AN ORIFICE OR  USUALLY BORN PRETERM D/T HYDRAMNIOS.
PASSAGE IN THE BODY IS  EXAMINE CAREFULLY FOR OTHER CONGENITAL
CLOSED OR ABSENT. ANOMALIES, SUCH AS VACTERL SYNDROME (VERTEBRAL,
 FISTULA – ABNORMAL OR ANAL, CARDIAC, TRACHEOESOPHAGEAL, RENAL AND LIMB
SURGICALLY MADE PASSAGE ANOMALIES)
BETWEEN A HOLLOW OR  FIRST FEEDING  INFANT WILL COUGH, BECOME
TUBULAR ORGAN AND THE CYANOTIC, AND DOB.
BODY SURFACE.  COPIOUS AMOUNTS OF MUCUS THAT NEWBORNS APPEAR
 ESOPHAGEAL ATRESIA - TO BE BLOWING BUBBLES.
OBSTRUCTION OF THE  A CATHETER CANNOT BE PASSED THROUGH THE INFANT’S
ESOPHAGUS ESOPHAGUS TO THE STOMACH, OR STOMACH CONTENTS
CANNOT BE ASPIRATED.
FIVE TYPES:  FLAT-PLATE RADIOGRAPH WILL REVEAL DISTENDED
A. THE ESOPHAGUS ENDS IN A STOMACH, D/T AIR PASSING FROM TRACHEA TO
 BLIND POUCH; THERE IS A
TRACHEOESOPHAGEAL
FISTULA BETWEEN THE DISTAL
PART OF THE ESOPHAGUS AND
THE TRACHEA.
B. THE ESOPHAGUS ENDS IN A
BLIND POUCH; THERE IS NO
CONNECTION TO THE TRACHEA.
C. A FISTULA IS PRESENT
BETWEEN AN OTHERWISE
NORMAL ESOPHAGUS AND
TRACHEA.
D. THE ESOPHAGUS ENDS IN A
BLIND POUCH. A FISTULA
CONNECTS THE BLIND POUCH
OF THE PROXIMAL ESOPHAGUS
TO THE TRACHEA
E. THERE IS A BLIND END PORTION
OF THE ESOPHAGUS. FISTULAS
ARE PRESENT BETWEEN BOTH
WIDELY SPACED SEGMENTS OF
THE ESOPHAGUS AND THE
TRACHEA
OMPHALOCELE
 PROTRUSION OF ABDOMINAL
CONTENTS THROUGH THE
ABDOMINAL WALL AT THE
POINT OF THE JUNCTION OF THE
UMBILICAL CORD AND
ABDOMEN.
GASTROSCHISIS
 SIMILAR TO OMPHALOCELE,
BUT ABDOMINAL ORGANS ARE
NOT CONTAINED BY A
MEMBRANE BUT SPILL FREELY
FROM ABDOMEN.
INTESTINAL OBSTRUCTION
- STENOSIS – NARROWING
- ANTICIPATED IF MOTHER HAD
HYDRAMNIOS DURING
PREGNANCY.
ESOPHAGUS AND STOMACH.
 BARIUM SWALLOW
 ESOPHAGEAL ENDOSCOPY
MANAGEMENT
 “E” SURGERY TO PREVENT DEVELOPMENT OF PNEUMONIA,
DEHYDRATION OR ELECTROLYTE IMBALANCE.
 ANTIBIOTICS
 GASTROSTOMY TO EMPTY SECRETIONS AND PREVENT
REFLUX TO LUNGS
 CLOSE MONITORING POST-OP FOR FLUID AND AIR LEAKS,
USUALLY ON POST-OP DAY 7-10 WHEN SUTURES DISSOLVE.
PROGNOSIS
 DEPENDS ON EXTENT OF THE REPAIR NECESSARY, THE
CONDITION OF THE CHILD AT THE TIME OF SURGERY, AND
THE PRESENCE OR ABSENCE OF OTHER CONGENITAL
ANOMALIES.
 HIGH MORTALITY RATE D/T ASSOCIATED CONGENITAL
ANOMALIES, LBW ASSOCIATED WITH TRACHEAL
ABNORMALITY.
 HERNIATED CONTENTS ARE USUALLY INTESTINES, BUT
MAY INCLUDE STOMACH AND LIVER.
 USUALLY COVERED AND CONTAINED BY THIN LAYER OF
AMNION AND CHORION WITH UC PROTRUDING FROM THE
EXPOSED SAC.
 DEFECT LESS THAN 4CM = HERNIA OF THE UMBILICAL
CORD
 GREATER THAN 10CM =TRUE OMPHALOCELE
ASSESSMENT
 DIAGNOSED DURING PRENATAL SONOGRAM
 ELEVATED MATERNAL SERUM ALPHAFETOPROTEIN
(MSAFP)
 IF NOT, DETECTED ON INSPECTION UPON BIRTH.
MAKE SURE TO DOCUMENT THE GENERAL APPEARANCE
AND ITS SIZE IN CENTIMETERS UPON BIRTH.
MANAGEMENT
 SURGERY WITHIN 24 HOURS BEFORE THE THIN MEMBRANE
RUPTURES OR BECOMES INFECTED.
 SMALL – ONE-STAGE REPAIR IS POSSIBLE.
 LARGE – PROSTHETIC PATCH REPAIR
 SILASTIC POUCH TERMED “SILO”
 OVER THE NEXT 5-7 DAYS, BOWEL IS GRADUALLY
RETURNED TO THE ABDOMEN.
 TPN TO SUPPLY NUTRITION
ASSESSMENT MANAGEMENT
 MORE THAN 30 ML OF GASTRIC  KEEP ON NPO
CONTENTS CAN BE ASPIRATED  OGT/NGT
FROM THE NEWBORN AT BIRTH INSERTION TO
 THE INFANT PASSES NO LOW SUCTION
MECONIUM OR MAY PASS ONE OR OPEN TO
STOOL AND THEN NOT PASS AIR
ANYMORE.  IV
 ABDOMEN BECOMES REPLACEMENT
DISTENDED AND TENDER. OF FLUIDS,
 AS IT PROGRESSES, THE INFANT ELECTROLYTE
MAY VOMIT THAT IS NOT SOUR S
SMELLING. VOMITUS MAY BE  SURGICAL
 GREEN OR BLACK. REPAIR OF THE
 PAIN EVIDENCED BY HARD, OBSTRUCTION
FORCEFUL, INDIGNANT CRYING;
PULLING THE LEGS UP AGAINST
THE ABDOMEN.
 INCREASED RR AS DIAPHRAGM
IS PUSHED UP.
 ABDOMINAL FLAT-PLATE
RADIOGRAPH OR SONOGRAM
WILL REVEAL NO AIR BELOW
THE LEVEL OF OBSTRUCTION.
 BARIUM ENEMA OR BARIUM
SWALLOW TO GREATER
VISUALIZE THE POINT OF
OBSTRUCTION.
DIAPHRAGMATIC HERNIA ASSESSMENT
 PROTRUSION OF AN UPON BIRTH:
ABDOMINAL ORGAN (USUALLY  RESPIRATORY DIFFICULTY DUE TO COMPRESSION OF
STOMACH OR INTESTINE) LUNGS BY ABDOMINAL ORGAN
THROUGH A DEFECT IN THE  ABDOMEN APPEARS GENERALLY SUNKEN
DIAPHRAGM INTO THE CHEST  ABSENT BREATH SOUNDS ON AFFECTED SIDE
CAVITY.  CYANOSIS
 USUALLY DETECTED IN UTERO  INTERCOSTAL OR SUBCOSTAL RETRACTIONS
BY SONOGRAM.  RIGHT-TO-LEFT SHUNTING THROUGH FORAMEN OVALE
 BOWEL REMOVAL VIA  MAY ALSO CAUSE PATENT DUCTUS ARTERIOSUS
FETOSCOPY. MANAGEMENT
 EMERGENCY SURGICAL REPAIR
 POSITION THE INFANT WITH HEAD ELEVATED
 KEEP ON NPO
 NGT OR GASTROSTOMY INSERTION
IMPERFURATE ANUS ASSESSMENT MANAGEMENT
- Stricture of the anus (WALANG  MAY BE DETECTED BY  KEEP ON NPO UNTIL
BUTAS ANG PWET) PRENATAL SONOGRAM SURGICAL
 INSPECTION AT BIRTH INTERVENTION IS
 OCASSIONALLY, A DONE.
MEMBRANE FILLED  IVT TO SUPPORT FLUID-
WITH BLACK ELECTROLYTE
MECONIUM CAN BE IMBALANCE,
SEEN PROTRUDING NUTRITION.
FROM THE ANUS.  TEMPORARY
 ABSENT “WINK” COLOSTOMY UNTIL
REFLEX REPAIR OF THE
 NO STOOL WILL BE IMPERFORATE ANUS IS
PASSED POSSIBLE
 ABDOMINAL
DISTENTION
 RADIOGRAPH OR
SONOGRAM
PHYSICAL AND DEVELOPMENT DISORDERS OF THE NERVOUS SYSTEM
HYDROCEPHALUS ASSESSMENT MANAGEMENT
 ABNORMAL ACCUMULATION EVIDENT IN FIRST FEW WEEKS: DEPENDS ON THE CAUSE AND
OF CSF IN THE VENTRICLES OR  FONTANELLES WIDEN EXTENT:
SUBARACHNOID SPACES. AND APPEAR TENSE  ACETAZOLAMIDE –
 COMMUNICATING  SUTURE LINES DIURETIC
HYDROCEPHALUS OR SEPARATE VENTRICULAR ENDOSCOPY
EXTRAVENTRICULAR  HEAD DIAMETER  DESTRUCTION OF
HYDROCEPHALUS IF FLUID CAN ENLARGES PORTION OF CHOROID
REACH THE SPINAL CORD. AS FLUID CONTINUES TO PLEXUS
 OBSTRUCTIVE ACCUMULATE:  REMOVAL OF TUMOR
HYDROCEPHALUS OR  SCALP BECOMES SHINY  LASER SURGERY TO
 INTRAVENTRICULAR
HYDROCEPHALUS IF THERE IS
BLOCKAGE TO SUCH PASSAGE
OOF FLUID.
 ALSO CLASSIFIED AS
CONGENITAL OR ACQUIRED
 CAUSES OF EXCESS CSF
 OVERPRODUCTION OF FLUID BY
A CHOROID PLEXUS (E.G.
TUMOR)
 OBSTRUCTION OF THE PASSAGE
OF FLUID
 INTERFERENCE WITH THE
ABSORPTION OF CSF
NEURAL TUBE DISORDERS
 Spina bifida – Latin for “divided spine
SPINA BIFIDA OCCULTA
 A BENIGN DISORDER; NO
IMMEDIATE SURGICAL
INTERVENTION NECESSARY.
MENINGOCELE
- A BIRTH DEFECT WHERE THERE
IS A SAC PROTRUDING FROM
THE SPINAL COLUMN. THE SAC
INCLUDES SPINAL FLUID, BUT
DOES NOT CONTAIN NEURAL
TISSUE.
MYELOMENINGOCELE
 A SEVERE FORM OF SPINA
BIFIDA IN WHICH THE SPINAL
CORD AND NERVES DEVELOP
OUTSIDE OF THE BODY AND
ARE CONTAINED IN A FLUID-
FILLED SAC THAT IS VISIBLE
OUTSIDE OF THE BACK AREA.
 THE SPINAL CORDS AT THE END
OF THE POINT  MOTOR AND
SENSORY
 FUNCTION IS ABSENT BEYOND
THIS POINT  LOWER MOTOR
NEURON DAMAGE.
 THE CHILD WILL HAVE
FLACCIDITY AND LACK OF
SENSATION OF LE, LOSS OF
BLADDER/BOWEL CONTROL.
 OFTEN HAVE ACCOMPANYING
TALIPES DISORDER AND
DEVELOPMENTAL HIP
DYSPLASIA.
ANENCEPHALY
 ABSENCE OF A MAJOR PORTION
OF THE BRAIN, SKULL, AND
 SCALP VEINS BECOME REOPEN THE ROUTE OF
PROMINENT FLOW OR BYPASSING
 BROW BULGES THE POINT OF
FORWARD, “BOSSING” OBSTRUCTION
 SUNSET EYES  VP SHUNT
SYMPTOMS OF INCREASED ICP  AFTER A SHUNT IS
 DECREASED RR, PR INSERTED, INFANT’S
 INCREASED TEMP, BP BED MUST BE KEPT
 HYPERACTIVE FLAT OR ELEVATED
REFLEXES ONLY 30DEGREES =
 STRABISMUS PREVENT RAPID
 OPTIC ATROPHY DRAINAGE OF CSF
 IRRITABLE, FLUID
LETHARGIC, FAILURE  ASSESS FOR SIGNS OF
TO THRIVE INCREASED ICP
 TYPICAL SHRILL, HIGH-
PITCHED CRY
 ULTRASOUND, CT SCAN
OR MRI
 TRANSILLUMINATION
 OCCURS WHEN THE POSTERIOR LAMINAE OF THE
VERTEBRAE FAIL TO FUSE.
 NOTICEABLE AS DIMPLING, ABNORMAL TUFTS OF HAIR OR
DISCOLORED SKIN AT THE POINT OF POOR FUSION.
 MENINGES COVERING THE SPINAL CORD HERNIATE
THROUGH 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 CLEAR DURA MATER.
 THE HIGHER THE MYELOMENINGOCELE IN THE CORD, THE
MORE LIKELY THAT HYDROCEPHALUS WILL ACCOMPANY
IT.
 CT SCAN/ULTRASOUND/MRI TO DIFFERENTIATE
MENINGOCELE FROM MYELOMENINGOCELE.
ASSESSMENT
 PRENATAL ULTRASOUND, FETOSCOPY, AMNIOCENTESIS,
MSAFP 
 FETOSCOPIC SURGERY.
 MAY BE BORN BY CS BIRTH TO AVOID PRESSURE AND
INJURY TO THE SPINAL CORD.
 OBSERVE FOR SPONTANEOUS MOVEMENT OF LOWER
EXTREMITIES.
 ASSESS NATURE AND PATTERN OF VOIDING AND
DEFECATION
MANAGEMENT
 MENINGOCELE/MYELOMENINGOCELE IMMEDIATE
SURGICAL INTERVENTION
 THE CHILD WITH MYELOMENINGOCELE WILL CONTINUE TO
HAVE PARALYSIS OF THE LOWER EXTREMITIES AND LOSS
OF BOWEL AND BLADDER FUNCTION AFTER SURGERY
BECAUSE THE ABSENT LOWER CORD CANNOT BE
REPLACED.
 MAY HAVE DIFFICULTY OF LABOR; THE UNDERDEVELOPED
HEAD DOES NOT ENGAGE THE CERVIX.
 MANY PRESENT AS BREECH.
 SCALP THAT OCCURS DURING
EMBRYONIC DEVELOPMENT.
MICROCEPHALY
 A CONDITION WHERE A BABY'S
HEAD IS MUCH SMALLER THAN
EXPECTED.
PHYSICAL AND DEVELOPMENT DISORDERS OF THE SKELETAL
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 seven times more
often than males.
Classification
 Acetabular dysplasia – mildest form;
femoral head remains in acetabulum.
 Subluxation – most common form;
femoral head partially displaced.
 Dislocation – femoral head not in
contact with acetabulum; displaced
posteriorly and superiorly
DEVELOPMENTAL HIP DYSPLASIA
~NURSING CONSIDERATIONS~
Respiratory Problems: Hypostatic Pneumonia
(Pneumonia)
 Usually results from the collection of
fluid in the dorsal region of the lungs
and occurs especially in those (as the
bedridden or elderly) confined to a
supine position for extended periods.
Infection and excoriation of skin
 Excoriating of skin  Skin Picking
Constipation from immobility
 Prolonged bedrest and immobility are
often associated with constipation.
Nutrition
Transportation and Positioning
ABSENT OR MALFORMED EXTREMITIES
 CHILDREN CANNOT SURVIVE WITH THIS DISORDER;
HOWEVER IF WITH INTACT MEDULLA, THE INFANT MAY
SURVIVE SEVERAL DAYS AFTER BIRTH.
CAUSES: INTRAUTERINE INFECTION (E.G. RUBELLA, CMV,
TOXOPLASMOSIS); SEVERE MALNUTRITION OR ANOXIA IN EARLY
INFANCY
 SLOWED BRAIN GROWTH THAT FALLS MORE THAN 3 TIMES
BELOW NORMAL ON GROWTH CHARTS.
 INFANT IS COGNITIVELY CHALLENGED D/T LACK OF
FUNCTIONING BRAIN TISSUE
ASSESSMENT
 Limitation in abduction of leg on the affected side.
 Asymmetry of gluteal, popliteal and thigh folds
 Audible click when abducting and externally rotating the hip on
 The affected side (ortolani’s sign)
 Apparent shortening of the femur (galeazzi’s sign)
 Waddling gait and lordosis when the child begins to walk
 Limb shorter on the affected side
 Restricted abduction of hip on affected side
MANAGEMENT
 Directed towards enlarging and deepening the acetabulum by placing
the head of the femur within the acetabulum and applying constant
pressure.
 Positioning with legs slightly flexed and abducted: Pavlik harness; spica
cast from the waist to below the knees; brace
 Surgical intervention (e.g., open reduction with casting)
 Change position frequently; raise head of mattress rather than head to
prevent flexion of the neck.
 Teach parents postural drainage and exercises for child, such as blowing
bubbles to increase lung expansion
 Encourage parents to seek immediate medical care if the child develops
congestion or cough.
 Observe for circulation to toes, pedal pulses and blanching.
 Do not let the child put small toys or food inside cast.
 Alert parents to signs of infection, such as odor.
 Protect cast edges with adhesive tape or waterproof material, especially
around perineum.
 Use diapers and plastic lining to minimize soiling of cast by feces and
urine.
 Teach parents to observe child for straining on defecation and
constipation.
 Increase fluids and fiber to prevent constipation.
 Provide small, frequent meals because of inflexibility of cast around the
waist.
 Adjust calorie intake, because less energy expenditure can lead to
obesity.
 Protect child from falling when positioned.
 Never pick up child by the bar between the legs of the cast (use two
people to provide adequate body support if necessary)
 May result from maternal drug 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 are fitted this early also, so an infant can
 handle and explore objects readily.
 Introducing a prosthesis 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  Usually amputated off early
- Presence of one or more additional
fingers or toes
SYNDACTYLY  WEBBING – Separation of digits can be done
 Two fingers or toes are fused.  BONES ARE FUSED – Cannot be fully reconstructed
CHEST DEVIATIONS
PECTUS EXCAVATUM  Decreased lung volume, heart is displaced to the left.
 Indentation of the lower portion of the
sternum.

PECTUS CARINATUM  diameter of the chest

 Sternum is displaced anteriorly,
increasing AP
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.
TALIPES DISORDER
 Latin talus (ankle) and pes (foot).
 Ankle-foot disorders popularly called
CLUBFOOT.
 pseudo-talipes d/o –d/t intrauterine
position; may be corrected via
manipulation
FOUR TYPES:
 PLANTARFLEXION – equinus or
“horsefoot” position
 DORSIFLEXION – anterior foot is
flexed towards anterior leg
 VARUS DEVIATION – foot turns in
 VALGUS DEVIATION – foot turns
out
ASSESSMENT
CLOSURE:
Sagittal suture
 Child’s head tend to grown anteriorly and posteriorly
 Only need to be observed
Coronal suture
 Orbits of the eyes become misshapen
 Exopthalmos, nystagmus, papilledema, strabismus,
 Atrophy of optic nerve with consequent loss of vision.
 Associated with syndactyly.
 Closely observe head circumference of newborns with syndactyly.
 Surgical intervention needed
 Measure head circumference on all children age 2 years or younger.
 Diagnosed by radiography or ultrasound.
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.
ASSESSMENT
 The earlier a true disorder is recognized, the better will be the
correction.
 Make a habit of straightening all newborn feet to the midline as part of
initial assessment to detect this disorder.
Therapeutic Management
 APPLICATION OF CAST – usually extends above the knee to ensure
proper correction.
 Change diapers frequently to prevent a wet diaper from touching the
cast and causing it to become soaked with urine or meconium.
 Health teaching: check infant’s toes for coldness or blueness, and how
to blanch a toenail (check for capillary refill)
 Cast is changed almost every 1 to 2 weeks
Approximately 6 weeks, cast is removed finally.
 Passive foot exercises
 Denis Browne splints
JOSE, LEANA LOUISSE D.
BSN 2B
Pediatric Illnesses
CORNELL NOTES ON NCM109 MODULE 6
KEYS
Classifications Based On Physical Sign Of Cyanosis
ACYANOTIC HEART DISEASE
 Involves heart or circulatory anomalies
that moves blood from the arterial to
the venous system
CYANOTIC HEART DISEASE
 Blood is shunted from venous to
arterial system as a result of abnormal
communication between the two
systems
 Oxygenated to unoxygenated blood
 Left-to-right shunts
VENTRICULAR SEPTAL DEFECT
 Most common type of congenital
cardiac disorder.
 An opening is present in the sputum
between the two ventricles.
 Greater pressure on left ventricle  left
to right shunt (acyanotic disorder)
ATRIAL SEPTAL DEFECT
 Abnormal communication between the
two atria  left to right shift
(acyanotic defect)
Dx:
 Doppler – enlarged right side of the
heart, increase pulmonary circulation
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
NOTES
Congenital Heart Disorder
 Oxygenated to unoxygenated blood
 Left-to-right shunts
INCREASED PULMONARY BLOOD FLOW – VSD, ASD, PDA
OBSTRUCTION TO BLOOD FLOW LEAVING THE HEART – pulmonary
stenosis, aortic stenosis, COA
MIXED BLOOD FLOW (OXYGENATED AND DEOXYGENATED BLOOD
MIXING IN THE HEART OR GREAT VESSELS) – TGA, truncus arteriosus
DECREASED PULMONARY BLOOD FLOW – tricuspid atresia, TOF
SYMPTOMS BEGIN AT AROUND 4-8 WEEKS OF AGE:
 Easy fatigue
 Loud, harsh pansystolic murmur at 3rd-4th interspace Palpable thrill
DIAGNOSIS
 Doppler or MRI – R ventricular hypertrophy, pulmonary artery
 dilatation
 ECG – R ventricular hypertrophy
MANAGEMENT
 Up to 85% close spontaneously
 Open-heart surgery before 2 y/o
ASSESSMENT
 Harsh systolic murmur over the 2nd-3rd interspace
 Fixed splitting – second heart sound auscultated as split
THERAPEUTIC MANAGEMENT
 Surgery to close the defect is done electively between 1-3 y/o.
 Without closure  Infectious endocarditis  heart failure
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
 returns to L atrium  L ventricle 
aorta  pulmonary artery.
 Increased pressure in the pulmonary
circulation  R ventricle hypertrophy
and ineffective heart action
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
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
COARCTATION OD 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
TRANSPORTATION OF GRET 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.
 Surgical intervention: ductal ligation via thoracotomy
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
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.
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
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
  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.
TRUNCUS ARTERIOSUS
 Rare defect, approximately 1%
TRICUSPID ATRESIA
 Extremely serious disorder because the
tricuspid valve is completely closed.
TETRALOGY OF FALLOT
 A number of children with this
disorder show a deletion abnormality
of chromosome 22
FOUR ANOMALIES:
 Pulmonary stenosis
 VSD (usually large)
 Dextroposition (overriding) of the
aorta
 Hypertrophy of the right ventricle
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
 There is no specific treatment for a
common cold.
Infection and inflammation of the throat
VIRAL PHARYNGITIS
procedure.
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.
No blood flow from right atrium to the right ventricle.
Instead, blood crosses patent foramen ovale into L atrium by passes
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)
ASSESSMENT
 Absent or minimal cyanosis immediately after birth, but becomes
cyanotic therafter.
 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, prevent Hypercyanotic episodes.
 Place the baby in knee-chest position
 MSO4 – generally reduces symptom
 Propanolol – 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
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
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
Sx:
  Causative agent: adenovirus
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.
TONSILLITIS
 Infection and inflammation of the
palatine tonsils.
 “Adenitis” – infection and
inflammation of the adenoid
(pharyngeal) tonsils
EPISTAXIS
 Nosebleed
  Homes that lack humidification
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.
 Sore Throat, Fever, General Malaise, Erythema On In Back Of
Pharynx And Palatine Arch, Increased Wbc
 Warm compress, gargle with warm water, wof dehydration.
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
 Sx of acute glomerulonephritis (AGN) appear in 1-2 weeks child may
be asked to come back after 2 weeks for a urine test
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 appear 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
 Bacterial tonsillitis
 Antipyretic
 Analgesic
 10-day course antibiotics such as penicillin or amoxicillin
 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
CAUSE:
 Trauma
 Strenuous exercise
 Tends to occur during respiratory illnesses
 Associated with several systemic illnesses: rheumatic fever, scarlet
Fever, measles, chicken pox.
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)
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.
CROUP
(LARYNGOTRACHEOBRONCHITIS)
 Inflammation of the larynx, trachea,
and major bronchi
 Common causative agent: viral
infection such as parainfluenza virus;
H. influenzae
ASPIRATION
 Inhalation of a foreign object into the
airway.
 Occurs most frequently in infants or
toddlers.
INFLUENZA
 Inflammation and infection of the
major airways.
BRONCHITIS
 Inflammation of the major bronchi and
trachea.
RESPIRATORY SYNCYTIAL VIRUS (RSV)
BRONCHIOLITIS
 RSV – pathogenic RNA virus that is
most common cause of bronchiolitis in
young children.
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.
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
 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.
 Caused by the orthomyxovirus influenza type A, B, or C.
 Sx: cough, fever, fatigue, aching pains, a sore throat, and often
accompanying GI symptoms such as vomiting or diarrhea.
MANAGEMENT:
 Antipyretics – acetaminophen (Tylenol) (Reduce & Prevent Fever)
 Oseltamivir (tamiflu) – children over 1 year old
 Flu vaccine
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 (reduce the thickness of mucus and make secretions in the
airways thinner.)
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

ASTHMA
 Most common chronic illness in
children
 Immediate hypersensitivity (type 1)
response
 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.
STATUS ASTMATICUS
 Child fails to respond to first-line
therapy (aerosol administration of a
bronchodilator)
 an extreme emergency
PNEUMONIA
 Hydration
 Life-threatening apnea may need mechanical ventilation.
 Ribavirin
 Isolate infants with RSV
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 suppresants 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.
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
 Infection and inflammation of the alveol
 Types: hospital-acquired and community acquired
 May be bacterial, viral or aspiration
  Pneumocystis carinii pneumonia – associated with HIV/AIDS
PNEUMOCOCCAL PNEUMONIA ASSESSMENT
 High fever (may progress to febrile seizure), nasal flaring, retractions,
 Chest pain, chills, and dyspnea, tachypnea, tachycardia
 Lung space is filled with exudates  diminished respiratory function
 Breath sounds become bronchial – air no longer or poorly enters the
 Alveoli
 Crackles – presence of fluid
 Dullness on percussion – consolidation
 Leukocytosis
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 Assessment
 Generally caused by the viruses of  Sx of URTI for first 1-2 days  low-grade fever, non-productive
upper respiratory tract infection: the cough, tachypnea.
RSVs, myxoviruses, or adenoviruses.  Diminished breath sounds and fine rales upon auscultation.
 RSV may cause apnea.
 CXR: diffuse infiltrated areas.
SYMPTOMATIC MANAGEMENT
 Anti-pyretics
 IV fluid if w/ dehydration
RHEUMATIC FEVER ASSESSMENT THERAPEUTIC MANAGEMENT
 Autoimmune disease  reaction to JONES CRITERIA (Major)  Full course is 6-8 weeks
group A beta-hemolytic streptococcal  Carditis  Maintain on bedrest during
infection  Erythema marginatum – acute phase of illness
 Inflammation  fibrin deposits on the macular rash found  Monitor VS, apical pulse
endocardium and valves, esp. mitral predominantly  Penicillin therapy; single
valve, as well as major body joints.  on the trunk IM benzathine penicillin
 Often follows an attack of pharyngitis,  Subcutaneous nodules  Oral ibuprofen – arthralgia,
tonsillitis, scarlet fever, “strep throat”,  Sydenham’s chorea – inflammation
or impetigo. sudden involuntary  Corticosteroids – if not
 Occurs most often in children 6-15 y/o, movement of the responding to ibuprofen
peak incidence at 8 y/o.  limbs  Phenobarbital, diazepam –
 Children do not develop immunity to  Polyarthritis chorea
streptococcal infections  Infections JONES CRITERIA (Minor)  Digoxin, diuretics – if heart
can recur.  Arthralgia failure is present
 Si/sx of original infection subside in a  Fever
few days, child appears well  after 1-  Hx of previous rheumatic
3 weeks, onset of rheumatic fever fever; prolonged PR interval
symptoms.  Elevated ESR, C-reactive
protein, leukocytosis
KAWASAKI DISEASE ASSESSMENT
 Mucocutaneous lymph node syndrome Subacute phase (10 days after onset)
 A febrile, multisystem disorder that  Desquamation, esp. on palms and soles
occurs almost exclusively in children  PC rises
before the age of puberty. Convalescent phase (stage II)
 The peak incidence is in boys under 4  25th-40th day
years of age. Stage III
 Vasculitis (inflammation of blood  From 40 days until ESR returns to normal
vessels) is the principal (and TREATMENT
lifethreatening) finding because it can  ASA, ibuprofen
 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
DISORDERS OF THE GASTROINTESTINAL SYSTEM
PHYLORIC 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 HISTORY TAKING:
the sphincter.
THERAPEUTIC MANAGEMENT
 Surgical or laparoscopic correction
(pyloromyotomy)
 Correct electrolyte
imbalance/dhn/starvation pre-op
 IVF PNSS or D5NSS
 NPO
 Pacifier for non-nutritive sucking
INTUSUSSCEPTION
 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
 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
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
 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 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
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
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.
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
HIRSCHSPRUNG’S DISEASE
 Aganglionic megacolon
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
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: boardlike abdomen, shallow
respirations, increased temp
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
 become noticeable between 6 and 18 months
 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 supplements
 Celiac Crisis
 Occur when child develops any type of infection
 Extreme symptoms
ASSESSMENT
 Infants who fail to pass meconium by 24 hours; abdominal distention.
  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.
 Gene abnormality on chromosome 10.
 Higher incidence among siblings.
 More often in males than in females.
URINARY TRACT INFECTION (UTI)
 Occurs more often in females than in
males.
 Ascending infection from perineum
most common, usually gramnegative
rods, such as E.Coli
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
 Symptoms may not become apparent until 6-12 mos of 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
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
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

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.
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
CHICKENPOX (Varicella)
 An infection caused by the varicella-
zoster virus. It causes an itchy rash
 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
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
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 bluewhite
center point on buccal membraine
 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
ASSESSMENT
 Low-grade fever, malaise
 In 24 hrs, rash that begins as macule  papule (6-8hrs)  vesicle 
 with small, fluid-filled blisters.
POLIOVIRUS INFECTIONS:
POLIOMYELITIS
 Polio is Greek for “gray” – the color of
the spinal cord after it atrophies from
the effect of the poliomyelitis virus.
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
DIPHTHERIA
 A serious infection caused by strains of
bacteria called Corynebacterium
diphtheriae that make toxin (poison).
 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
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 an contact precaution until all lesions are crusted.
 Complications: secondary infection of lesions, pneumonia, and
 encephalitis
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.
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
 ACTIVE ARTIFICIAL IMMUNITY: Diphtheria toxin given as part of
DTaP vaccine
 PASSIVE ARTIFICIAL IMMUNITY: Diphtheria antitoxin
 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
  IMMUNITY: Contracting the disease
gives lasting natural immunity.
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
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.
 IV antitoxin
 Penicillin or erythromycin
 Complete bedrest
 Droplet precaution
 WOF airway obstruction  ET intubation
3 Stages
CATARRHAL STAGE
 URTI symptoms, coryza, sneezing, lacrimation, cough, low grade fever
 Children are irritable and listless
 Lasts from 1-2 weeks
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
CONVALESCENT STAGE
 Gradual cessation of coughing and vomiting
 Children younger than 6 months of age: “whoop” of the cough mayCbe
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
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
HOOKWORMS
 Eggs are found in feces  enter the body through the skin  migrate to
the GI  attach themselves onto intestinal villi  they suck blood
from intestinal wall
 Great number of hookworms may result in severe anemia
 Treatment: anthelmintics, therapy for anemia
PINWORMS
 Small, white, threadlike worms live in the cecum
 At night, female pinworm travels tot 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.