Pediatric Disorders:

Module

THE ILL AND HOSPITALIZED CHILD

STRESSORS and FEARS of HOSPITALIZATION
1. Separation Stages
2. Loss of Control
3. Body Injury
4. Pain
5. Immobility
6. Punishment and Rejection

PREPARATION for HOSPITALIZATION

1. Parents eagerly seek guidance from nurses on what and how much to tell
their children about an anticipated admission. The preparation a parent
makes for a child obviously varies according to the child's age and individual
experience. No matter what the child's age, however, parents should be
encouraged to convey a positive attitude.
2. Children between 2 and 7 years of age should be told about a scheduled
ambulatory or inpatient hospitalization as many days before the procedure as
the child's age in years.
3. On the day of admission, it is important for you to discuss the preparation the
child has received to ensure that the child and family accurately understand
the child's condition and upcoming procedures.

ASSESSMENT ON ADMISSION
1. Assess each child's level of preparation for a hospitalization on admission to
the facility. Be aware of not only what the child describes orally but also what
facial expressions or nervous manifestations may be indicating.
2. Interview parents on hospital admission for a nursing history to obtain the
information needed to plan nursing care.
3. Make a note of any medication or food allergy on the child's plan of care
4. Take and record the child's temperature, pulse, and respirations. Measure
height and weight to determine overall growth and to allow for determination
of surface area, the measurement on which medication dosage is calculated.

PAIN ASSESSMENT

For children, pain is not only a hurting sensation, but it can also be a confusing
one because a child did not anticipate the pain, cannot explain its presence, and
cannot always understand its cause. Because children may have difficulty
describing pain in a manner adults can understand, it is difficult to assess the
extent of their discomfort. Both helping children describe the type and extent of
pain they are feeling and performing active interventions to relieve pain are
important nursing roles.

METHODS OF PAIN ASSESSMENT

Pain Experience Inventory
- A tool consisting of eight questions for children and eight questions for the
child's parents. It is designed to elicit the terms a child uses to denote pain
and what actions the child thinks will best alleviate the pain.
Cries Neonatal Postoperative Pain Measurement Scale
- 10-point scale on which five physiologic and behavioral variables
frequently associated with neonatal pain can be assessed and rated:
 Amount and type of crying
 Need for oxygen administration
 Increased vital signs
 Facial expression
 Sleeplessness

Comfort Behavior Scale

- A pain rating scale devised by nurses to rate pain in very young infants.
On the first part of the scale, six different categories (alertness,
calmness/agitation, crying, physical movement, muscle tone, and facial
expression) are rated from 1 to 5. Six is the lowest score (no pain), and 30
is the highest (a great deal of pain). In addition to rating physical
parameters, nurses then observe the infant for 2 minutes and rate their
evaluation of the baby's pain on an analogue (1-to-10) visual scale.

FLACC Pain Assessment

- A scale by which health care providers can rate a child's pain when a child
cannot give input, such as during circumcision. It incorporates five types of
behaviors that can be used to rate pain: facial expression, leg movement,
activity, cry.

FACES Pain Rating Scale

- This scale consists of six cartoon-like faces ranging from smiling to tearful.
Explain to the child that each face from left to right corresponds to a
person who has no hurt up to a lot of hurt the words under each face to
describe the amount of pain the face represents.

Numerical or Visual Analog Scale

- It uses a line with end points marked “0 = no pain” on the left and “10 =
worst pain” on the right. Divisions along the line are marked in units from 1
to 9. Explain to children that the left end of the line (the 0) means a person
feels no pain. At the other end is a 10, which means a person feels the
worst pain possible. The numbers 1 to 9 in the middle are for “a little pain”
to “a lot of pain.” Ask children to choose a number that best describes their
pain.

Adolescent Pediatric Pain Tool

 - It combines a visual activity and a numerical scale. On one half of the form
is an outline figure showing the anterior and posterior view of a child. To
use the tool, a child is asked to color in the figure drawing where he or she
feels pain. In addition, on the right side of the form, the child rates the pain
in reference to “no pain,” “little pain,” “medium pain,” “large pain,” and
“worst possible pain.” For a third activity, children are asked to point to or
circle as many words as possible on the form that describe their pain
(words such as horrible, pounding, cutting, and stinging)
- This is a useful tool for involving parents to talk with their child about his or
her pain. Reading the words together helps the child examine the type,
location, and level of pain he or she is experiencing. It also helps parents
to better understand what their child is experiencing.

PAIN MANAGEMENT

Non-Pharmacologic
1. Distraction - It aims at shifting a child's focus from pain to another activity or
interest.
2. Substitution of meaning - is a distraction technique to help a child place
another on a painful procedure. Children are often more adept at imagery
than adults because their imagination is less inhibited
3. Thought Stopping - a technique in which children are taught to stop anxious
thoughts by substituting a positive or relaxing thought. As with imagery, this
technique requires a great deal of practice before it is used in a painful
situation. For this technique, help the child to think of a set of positive things
about the approaching feared procedure.
4. Hypnosis - is not a common pain management technique with children but
can be very effective when a child is properly trained in the technique.
5. Magnet Therapy - is based on the belief that magnets can control or shift
body energy lines to restore health or relieve pain.
6. Music Therapy –the use of music for calming or improving well-being and can
be effective.
7. Yoga and Meditation - It offers a significant variety of proven health benefits,
such as increasing the efficiency of the heart, slowing the respiratory rate,
improving fitness, lowering blood pressure, promoting relaxation, reducing
stress, and allaying anxiety.
8. Acupuncture - involves the insertion of needles into critical positions in the
body to achieve pain relief. Although acupuncture is almost painless, children
can be very afraid of it at first because of the sight of the needles.
9. Transcutaneous Electrical Nerve Stimulation - involves applying small
electrodes to the dermatomes that supply the body portion where pain is
experienced.

Pharmacologic
1. Topical Anesthetic Cream - to reduce the pain of procedures such as
venipuncture, lumbar puncture, and bone marrow aspiration, a local
anesthetic cream or a solution of lidocaine and epinephrine is available
2. Oral Anlgesia – relatively easy to administer
3. Intramuscular Injection
4. Intravenous Administration - most rapid-acting route and the method of choice
in emergency situations.
5. Conscious Sedation - refers to a state of depressed consciousness usually
obtained through IV analgesia therapy. The technique allows a child to be
both pain-free and sedated for a procedure. Unlike with the use of general
anesthesia, protective reflexes are left intact and a child can respond to
instructions during the procedure.
6. Intranasal Administration
7. Local Anesthesia Injection
8. Epidural Analgesia - injection of an analgesic agent into the epidural space
just outside the spinal canal, it can be used to provide analgesia to the lower
body for 12 to 24 hours.

LEADING CAUSES of accidents/ injuries in children

Infancy:
 Aspiration
 Suffocation
 Fall
Toddler:
 Fall
 Drowning
 Poisoning
 Burn
Pre-schooler
 Drowning
 Motor accident
 Burn
DEVIATIONS FROM NORMAL IN THE NEWBORN

Pre-term or Low Birth Weight Infant

BACKGROUND OF THE STUDY

A preterm infant is usually defined as a live-born infant born before the end
of week 37 of gestation; another criterion used is a weight of less than 2,500
g (5 lb 8 oz) at birth. About 7% of all pregnancies end in preterm birth, and all
such infants need neonatal intensive care from the moment of birth to give
them their best chance of survival without neurologic after-effects (Petrou,
2003).

When a preterm infant is recognized by a gestational age assessment, watch

for the specific problems of prematurity, such as respiratory distress
syndrome, hypoglycemia, and intracranial hemorrhage.

Differences Between Small-for-Gestational-Age and Preterm Infants

Characteristic Small-for-Gestational-Age Infant Preterm Infant
Gestational age 24–44 wk Younger than 37 wk
Birthweight Under 10th percentile Normal for age
Congenital Strong possibility Possibility
malformations
Pulmonary problems Meconium aspiration, pulmonary Respiratory distress
hemorrhage, pneumothorax syndrome
Hyperbilirubinemia Possibility Very strong possibility
Hypoglycemia Very strong possibility Possibility
Intracranial Strong possibility Possibility
hemorrhage
Apnea episodes Possibility Very strong possibility
Feeding problems Most likely due to accompanying Small stomach capacity;
problem such as hypoglycemia immature sucking reflex
Weight gain in Rapid Slow
nursery
Future restricted Possibly always be under 10th Not likely to be restricted in
growth percentile due to poor organ growth as “catch-up” growth
development occurs
NEWBORN PRIORITIES IN FIRST DAYS OF LIFE

All newborns have eight priority needs in the first few days of life:

W - aste elimination establishment

A -dequate nourishment

T-emperature Control

E - xtrauterine circulation establishment

R- espiration initiation and maintenance

I- nfection prevention

D - evelopmental care / care that balances physiologic needs and stimulation for
best development

E - stablishment of an infant–parent relationship

These are also the priority needs of high-risk newborns. Because of small size or
immaturity or illness, fulfilling these needs, however, may require special
equipment or care measures. Not all newborns will be able to achieve full
wellness because of extreme insults to their health at birth or difficulty adjusting
to extrauterine life.

ETIOLOGY

- The exact cause of premature labor and early birth is rarely known.
- There is a high correlation between low socioeconomic level and early
termination of pregnancy.
- The major influencing factor in these instances appears to be inadequate
nutrition before and during pregnancy, as a result of either lack of money
for or lack of knowledge about good nutrition.
 Factors Associated with Preterm Birth

- Low socioeconomic level

- Poor nutritional status
- Lack of prenatal care
- Multiple pregnancy
- Previous early birth
- Race (nonwhites have a higher
incidence of prematurity than whites)
- Cigarette smoking
- Age of the mother (highest incidence
is in mothers younger than age 20)
- Order of birth (early termination is
highest in first pregnancies and in
those beyond the fourth pregnancy)
- Closely spaced pregnancies
- Abnormalities of the mother's
reproductive system, such as
intrauterine septum
- Infections (especially urinary tract
infection)
- Obstetric complications, such as
premature rupture of membranes or
premature separation of the placenta
- Early induction of labor
- Elective cesarean birt
ASSESSMENT:

- Preterm infant appears small and underdeveloped.

- Head is disproportionately large (3 cm ormore greater than chest size).
- Skin is generally unusually ruddy because the infant has little
subcutaneous fat beneath it; veins are easily noticeable, and a high
degree of acrocyanosis may be present.
- The preterm neonate, 24 to 36 weeks, typically is covered with
vernixcaseosa. However, in very preterm newborns (less than 25 weeks'
gestation), vernix is absent because it is not formed this early in
pregnancy.
- Lanugo is usually extensive, covering the back, forearms, forehead, and
sides of the face, because this amount is present until late in pregnancy.
- Both anterior and posterior fontanelles are small.
- There are few or no creases on the soles of the feet.
- The eyes of most preterm infants appear small.
- Although difficult to elicit, pupillary reaction is present.
- A preterm infant has varying degrees of myopia (near-sightedness)
because of lack of eye globe depth.
- The cartilage of the ear is immature and allows the pinna to fall forward.
The ears appear large in relation to the head.
- If tested, reflexes such as sucking and swallowing will be absent if an
infant's age is below 33 weeks; deep tendon reflexes such as the achilles
tendon reflex are also markedly diminished.
- During an examination, a preterm infant is much less active than a mature
infant and rarely cries.
- If the infant does cry, the cry is weak and high-pitched.
POTENTIAL COMPLICATIONS

Because of immaturity, preterm infants are prone to a number of specific

conditions.

1. Anemia of Prematurity - Many preterm infants develop a normochromic,

normocytic anemia (normal cells, just few in number). The reticulocyte
count is low because the bone marrow does not increase its production
until approximately 32 weeks.
2. Kernicterus - a destruction of brain cells by invasion of indirect bilirubin.
Preterm infants are more prone to the condition than term infants because
with the acidosis that occurs from poor respiratory exchange, brain cells
are more susceptible to the effect of indirect bilirubin than normally.
3. Persistent Patent DuctusArteriosus - Because preterm infants lack
surfactant, their lungs are noncompliant, so it is more difficult for them to
move blood from the pulmonary artery into the lungs. This condition leads
to pulmonary artery hypertension, which may interfere with closure of the
ductusarteriosus.
4. Periventricular/Intraventricular Hemorrhage - Preterm infants are prone
to periventricular hemorrhage (bleeding into the tissue surrounding the
ventricles) or intraventricular hemorrhage (bleeding into the ventricles);
these conditions occur in as many as 50% of infants of very low
birthweight. This occurs because preterm infants have both fragile
capillaries and immature cerebral vascular development.

NURSING DIAGNOSIS

Because a preterm infant has few body resources, both physiologic and
psychological stress must be reduced as much as possible and interventions
initiated gently to prevent depletion of resources. Close observation and analysis
of findings are essential to managing problems quickly.

1. Nursing Diagnosis: Impaired gas exchange related to immature

pulmonary functioning
 Outcome Evaluation:

Many preterm babies, particularly those under 32 weeks of age,

have an irregular respiratory pattern (a few quick breaths, a period of 5 to
10 seconds without respiratory effort, a few quick breaths again, and so
on).
There is no bradycardia with this irregular pattern (sometimes
termed periodic respirations).

2. Nursing Diagnosis: Risk for imbalanced nutrition, less than body

requirements related to additional nutrients needed for maintenance of
rapid growth, possible sucking difficulty, and small stomach.

Outcome Evaluation:

Infant's weight follows percentile growth curve; skin turgor is good;

specific gravity of urine is maintained between 1.003 and 1.030; infant has
no more than 15% weight loss in first 3 days of life and continues to gain
weight after this point.

3. Nursing Diagnosis: Risk for infection related to immature immune

defenses in preterm infant
Outcome Evaluation

Temperature is maintained at 97.6°F (36.5°C) axillary; further signs

and symptoms of infection such as poor growth or a reduced temperature
are absent
CONGENITAL HEART DEFECTS

Congenital heart disease refers to a problem with the heart's structure and
function due to abnormal heart development before birth. Congenital means
present at birth.

ACYANOTIC HEART DISEASE

Acyanotic heart disease is a broad term for any congenital heart defect in
which all of the blood returning to the right side of the heart (shunt that moves
blood from the arterial to the venous system or left-to-right shunts), passes
through the lungs and pulmonary vasculature in the normal fashion. The common
forms of acyanotic congenital heart defects are those where there is a defect in
one of the walls separating the chambers of the heart, or obstruction to one valve
or artery.

TYPES OF ACYANOTIC HEART DISEASE

1.) ATRIAL SEPTAL DEFECT

DEFINITION
-Is a form of congenital heart defect that enables blood flow between the left and
right atria via the interatrial septum.
-The interatrial septum is the tissue that divides the right and left atria. Without
this septum, or if there is a defect in this septum, it is possible for blood to travel
from the left side of the heart to the right side of the heart, or vice versa.
-This results in the mixing of arterial and venous blood, which may or may not be
clinically significant.

ETIOLOGY
The heart is forming during the first 8 weeks of fetal development. It
begins as a hollow tube, then partitions within the tube develop that eventually
become the septa (or walls) dividing the right side of the heart from the left. Atrial
septal defects occur when the partitioning process does not occur completely,
leaving an opening in the atrial septum.
Some congenital heart defects may have a genetic link, either occurring due to a
defect in a gene, a chromosome abnormality, or environmental exposure,
causing heart problems to occur more often in certain families. Most atrial septal
defects occur sporadically (by chance), with no clear reason for their
development.

SIGNS AND SYMPTOMS

 Child tires easily when  Rapid breathing.
playing.  Shortness of breath.
 Fatigue.  Poor growth.
 Sweating.

DIAGNOSIS
 Physical exam auscultation of the heart- there is a loud harsh systolic
murmur in the left sternal border at the 3 rd-4th interspaces
 Echocardiography- an atrial septal defect may be seen on color flow
imaging as a jet of blood from the left atrium to the right atrium.
 Transcranial Doppler (TCD) Bubble study- This method reveals the
cerebral impact of the ASD or PFO.
 Electrocardiogram- Individuals with atrial septal defects may have a
prolonged PR interval (a first degree heart block).
 Chest x-ray - a diagnostic test which uses invisible electromagnetic energy
beams to produce images of internal tissues, bones, and organs onto film.
With an ASD, the heart may be enlarged because the right atrium and
ventricle have to handle larger amounts of blood flow than normal.

NURSING DIAGNOSIS
 Activity intolerance  Fatigue
 Decreased cardiac output  Impaired gas exchange
 Deficient knowledge  Risk for infection
(diagnosis and treatment)

EXPECTED OUTCOMES FOR NURSING CARE PLAN

 The patient will carry out activities of daily living without weakness or
fatigue.
 The patient will maintain hemodynamic stability, and cardiac output will
remain adequate.
  The patient or her parents will verbalize understanding of the atrial septal
defect and plans for treatment.
 The patient will report that she has more energy.
 The patient will maintain adequate ventilation and oxygenation.
 The patient will remain free from signs and symptoms of infection.

TREATMENT/MANAGEMENT
 Surgery- to close the defect for children 1-3 years of age. This is to
prevent risk for infectious endocaditis and eventual heart failure.
 Cardiac catheterization- technique if the defect is small wherein the edge
of the opening of the septum is sutured.
 Open heart surgery and cardiopulmonary bypass- for large defects.

POST-OPERATIVE CARE

 Ventilator - a machine that helps your child breathe while he/she is under
anesthesia during the operation.
 Intravenous (IV) catheters - small, plastic tubes inserted through the skin
into blood vessels to provide IV fluids and important medications that help
your child recover from the operation.
 Arterial Nasogastric (NG) tube - a small, flexible tube that keeps the
stomach drained of acid and gas bubbles that may build up during
surgery.
 Heart monitor - a machine that constantly displays a picture of your
child's heart rhythm, and monitors heart rate, arterial blood pressure, and
other values.
 Closely monitor vital signs, central venous and intra-arterial pressures,
and intake and output.
 Watch for atrial arrhythmias.
 Give an antibiotic and an analgesic, as ordered.
 Provide range-of-motion exercises and coughing and deep-breathing
exercises.

PROGNOSIS
With a small to moderate atrial septal defect, a person may live a normal
life span without symptoms. Larger defects may cause disability by middle age
because of increased blood flow and shunting of blood back into the pulmonary
circulation. Some patients with ASD may have other congenital heart conditions,
such as a leaky valve.
 2.) VENTRICULAR SEPTAL DEFECT

DEFINITION
A ventricular septal defect is an abnormal opening in the wall (septum)
that divides the two lower chambers of the heart (ventricles). A Ventricular septal
defect closure is a procedure performed to correct this defect.

ETIOLOGY
The cause of VSD (ventricular septal defect) includes the incomplete
looping of the heart during days 24-28 of development. Faults with NKX2.5 gene
can cause this.
Congenital VSDs are frequently associated with other congenital conditions, such
as Down syndrome

DIAGNOSIS
Cardiac auscultation- VSD causes a pathognomonic holo- or pansystolic
murmur. Auscultation is generally considered sufficient for detecting a significant
VSD.
Ultrasound (echocardiography)

CLINICAL MANIFESTATION
 Tachypnea is typically the first presenting symptom.
 Dyspnea results in poor nursing and frequent rest during feedings
 Hepatomegaly may be present.
 The murmur of VSD is due to left-to-right shunting at the ventricular level.
Small ventricular septal defects are typically louder than larger ones. The
murmur of a VSD is heard best at the left lower sternal border.
 Right-to-left shunting at the VSD are not audible due to a small amount of
pressure difference between the right and left ventricles.
 A loud third heart sound or diastolic rumble is heard with large left-to-right
shunting due to increased flow across the mitral valve.
 A thrill is felt in many cases, particularly beyond infancy.
NURSING DIAGNOSIS
 Alteration in tissue perfusion  Weakness.
 Risk for infection  Ineffective breathing pattern
 Fatigue

SIGNS AND SYMPTOMS

 Pansystolic (Holosystolic)  Heart sounds are normal.
murmur (depending upon the  sweaty and tachypnoiec
size of the defect) (breathe faster) with feeds
 +/- Palpable thrill (palpable  easy fatigue
turbulence of blood flow).
TREATMENT/MANAGEMENT
 If the opening is SMALL- 85% closes spontaneously.
 MODERATE- cardiac catheterization, Cardiopulmonary bypass, the edges
of the septal opening is sutured.
 LARGE- (over 3 mm) open heart surgery, Silastic or Dacron patch is
sutured to occlude the space.
PRE-OPERATIVE TEACHING:
 If at all possible, it is important that the patient be free of infection prior to
going to surgery.
 If the patient is due for immunizations within a week of surgery, contact
the Congenital Heart Surgery Clinic and ask to speak to the clinic nurse
 Patients undergoing cardiac surgery frequently need blood products
 Provide emotional support to the family.
 Signing of consent.

POST-OPERATIVE TEACHING
 Watch out for the following: redness, swelling, or oozing/bleeding from
incision, fever, altered mental status, excessive fatigue, feeding/eating
problems, prolonged or worsening pain
 Avoid activities or movement for 4-6 weeks.

PROGNOSIS
This is excellent for most patients. The vast majority are able to live a
normal and unrestricted life. Re-operations for residual VSDs are now
uncommon.
 3.) PATENT DUCTUS ARTERIOSUS

DEFINITION
Is a congenital disorder in heart wherein a neonate's ductus arteriosus
fails to close after birth. The condition leads to abnormal blood flow between the
aorta and pulmonary artery, two major blood vessels surrounding the heart.
The ductus arteriosus (DA) is the vascular connection between the pulmonary
artery and the aortic arch.

ETIOLOGY
Before birth, the ductus arteriosus allows blood to bypass the baby's lungs
by connecting the pulmonary arteries (which supply blood to the lungs) with the
aorta (which supplies blood to the body). Soon after the infant is born and the
lungs fill with air, this blood vessel is no longer needed. It will usually close within
a couple of days. If the ductus arteriosus does not close, there will be abnormal
blood circulation between the heart and lungs.

RISK FACTOR
PDA is rare. It affects girls more often than boys. The condition is more
common in premature infants and those with neonatal respiratory distress
syndrome. Infants with genetic disorders, such as Down syndrome, and whose
mothers had German measles (rubella) during pregnancy are at higher risk for
PDA.

SIGNS AND SYMPTOMS

 Bounding pulse
 Fast breathing
 Poor feeding habits
 Shortness of breath
 Sweating while feeding
 Tiring very easily
 Poor growth
  Wide pulse pressure
 Murmur can be heard in upper left sternal border or under the left clavicle
(older children)
 Short grade II and III harsh systolic sound (newborn)
 Ventricle enlargement

DIAGNOSIS
 AUSCULTATION- murmur
 Echocardiogram. An echocardiogram uses sound waves to produce a
video image of the heart. This image can help doctors see the heart
chambers and evaluate how well the heart is pumping. This test also
checks the heart valves and looks for any other heart defects.
 Chest X-ray. An X-ray image helps the doctor see the condition of your
baby's heart and lungs and the amount of blood in the lungs
 Electrocardiogram (ECG). This test records the electrical activity of the
heart. This test helps diagnose heart defects or rhythm problems.
 Cardiac catheterization. This test isn't usually necessary for diagnosing a
PDA alone, but may be done to examine other congenital heart defects
found during an echocardiogram
 Cardiac computerized tomography (CT) or magnetic resonance imaging
(MRI).

TREATMENT
 PD is open because of stimulation of prostaglandins (PGE1) from the
placenta and decrease O2 of fetal blood. If PGE1 decreases and O2
increases PD is stimulated to close.
 If PD doesn’t close spontaneously IV INDOMETHACIN and ibuprofen,
prostaglandin inhibitors are given.Side effects: Decrease glomelular
filtration, impaired platelet aggregation, and diminished G.I. and Cerebral
blood flow.
 Dacron-coated staimless steel coils by interventional cardiac
catheterization (6 mos-1 yr).
 LARGE DUCTAL LIGATION
 TRANSCATHETER DEVICE CLOSURE
(Cardiomegaly and Pulmonary edema). 22 days of life, before the surgery.

Following surgical ligation of PDA, there is improving edema and less

cardiomegaly.

PROGNOSIS
Adults and children can survive with a small opening remaining in the
ductus arteriosus. Treatment, including surgery, of a larger PDA is usually
successful and frequently occurs without complications. Proper treatment allows
children and adults to lead normal lives.
 4.) COARCTATION OF AORTA

DEFINITION
Is a narrowing of the aorta, the large blood vessel that branches off your
heart and delivers oxygen-rich blood to your body. When this occurs, your heart
must pump harder to force blood through the narrow part of your aorta.
Coarctation of the aorta usually occurs beyond the blood vessels that branch off
to your upper body and before the blood vessels that lead to your lower body.
This often means you'll have high blood pressure in your arms, but low blood
pressure in your legs and ankles.

ETIOLOGY AND RISK FACTOR

The aorta carries blood from the heart to the vessels that supply the body
with blood and nutrients. If part of the aorta is narrowed, it is hard for blood to
pass through the artery.
Aortic coarctation is more common in persons with certain genetic disorders,
such as Turner syndrome. However, it can also be due to birth defects of the
aortic valves.
Aortic coarctation is one of the more common heart conditions that are present at
birth (congenital heart conditions). It is usually diagnosed in children or adults
under age 40.

SIGNS AND SYMPTOMS

BABIES WITH SEVERE COARCTATION

 Pale skin  Heavy sweating
 Irritability  Difficulty breathing
OLDER CHILDREN
 High blood pressure  Shortness of breath,
especially during exercise
  Headache  Nosebleeds
 Muscle weakness
 Leg cramps or cold feet
DIAGNOSIS/DIAGNOSTIC PROCEDURE
 HISTORY and PHYSICAL  Echocardiography
ASSESSMENT  ECG-show that you might
 The pulse in the femoral have a thickened heart
(groin) area or feet will be muscle (ventricular
weaker than the pulse in the hypertrophy).
arms or the carotid (neck).  X-ray may show an enlarged
Sometimes, the femoral pulse heart or a narrowing in the
may not be felt at all. aorta at the site of the
 The blood pressure in your coarctation. Left-sided heart
legs is usually weaker than in enlargement.
the arms. Blood pressure is  MRI- reveals the location of
usually higher in the arms the coarctation of the aorta.
after infancy. BP in arms is  MRI or MR angiography of the
20mmhg higher than in the chest may be needed in older
leg children

ASSESSMENT
 Slight Coarctation- absent of palpable femoral pulse
 Obstruction is proximal- absent of brachial pulse
 As infant grow older- leg pain on exertion due to diminish blood supply to
lower extremities

TREATMENT/MANAGEMENT
 Surgical resection of the  Cardiac catheterization and
narrow segment if there is aortography
arterial hypertension.  DACRON graft
 angioplasty  Balloon Angioplasty

NURSING DIAGNOSIS
 Fatigue  sleep deprivation secondary
 Activity intolerance to discomfort and irritability
 Ineffective breathing pattern
secondary to pulmonary
hypertension

PROGNOSIS
Coarctation of the aorta can be cured with surgery. Symptoms quickly get
better after surgery. However, there is an increased risk for death due to heart
problems among those who have had their aorta repaired. Without treatment,
most people die before age 40. For this reason, doctors usually recommend that
the patient has surgery before age 10. Most of the time, surgery to fix the
coarctation is done during infancy. Narrowing or coarctation of the artery can
return after surgery. This is more likely in persons who had surgery as a
newborn.

CYANOTIC HEART DEFECT

Definition:

 Blood is shunted from the venous to the arterial system as a result of

abnormal communication between the two
 Deoxygenated blood to oxygenated blood
 Right to left shunt

Types:

 Transposition of great artery

 Tetralogy of fallot

TRANSPOSITION OF GREAT ARTERY

Definition:

 Defect with mixed blood flow

 Aorta arises from right ventricle instead of left
 Pulmonary artery arises from left ventricle instead of right
 Atrial and ventricular septal defects occur in connection with transposition
making the entire heart one mixed circulatory system
 Large newborn(9-10lbs), more on boys
 5% of congenital anomalies

Etiology/Pathophysiology:

The pulmonary and systemic circulations function in parallel, rather than in

series. Oxygenated pulmonary venous blood returns to the left atrium and left
ventricle but is re-circulated to the pulmonary vascular bed via the abnormal
pulmonary arterial connection to the left ventricle. Deoxygenated systemic
venous blood returns to the right atrium and right ventricle where it is
subsequently pumped to the systemic circulation, effectively bypassing the lungs.
This parallel circulatory arrangement results in a deficient oxygen supply to the
tissues and an excessive right and left ventricular workload. It is incompatible
with prolonged survival unless mixing of oxygenated and deoxygenated blood
occurs at some anatomic level.
Signs and Symptoms:

 Cyanotic from birth

 No murmurs/ various murmurs

Laboratory/Diagnostic Findings:

 Echocardiography reveals enlarged heart

 ECG may or may not reveal enlarged heart
 Decreased oxygen saturation in cardiac catetherization

Management:

 Patent ductus arteriosus

 PGE administration
 Balloon atrial septal pull through operation
 Cardiac catheterization
 Arterial switch procedure (1week to 3 mos, 95%)

Nursing diagnosis:

1. Ineffective cardiopulmonary tissue perfusion related to impaired cardiac

function and increased cardiac workload.
2. Excess fluid volume related to impaired cardiac contractility and venous
congestion
3. Activity intolerance related to effects of heart failure.
4. Risks for injury related to congenital heart defect and surgery.
5. Risks for infection related to immature immune system and neonatal age.
6. Risks for imbalanced nutrition, less than body requirements.
Implementation
1. Administer supplemental oxygen.
2. Elevate head of the bed 30 to 60 degrees or have child sit upright.
3. Assess vital signs including heart rate, pulse and respirations.
Auscultate heart and lung sounds.
4. Obtain baseline weight and monitor at least daily.
5. Monitor intake and output and urine specific gravity.
6. Provide a balance of activity and rest periods.
7. Provide small and frequent meals.
8. Assesses infant's skin integrity; sensory impairments, and immune
status.
9. Implements protective measures to prevent injury caused by electrical,
thermal, chemical, or physical sources, including
 * verifying allergies,
* applying safety devices,
* ensuring prep solution does not run under
electrosurgical grounding pad,
* performing required counts, and
* using supplies and equipment within safe parameters.
Prognosis:

The child's symptoms will improve after surgery to correct the defect. Most
infants who undergo arterial switch do not have symptoms after surgery and live
normal lives. If corrective surgery is not performed, the life expectancy is months.

TETRALOGY OF FALLOT

Definition:

 Defect with decreased pulmonary blood flow

 10% of children with congenital disease
 Four anomalies: pulmonary stenosis
VSD
Dextraposition of aorta
Hypertrophy of right ventricle
 15% of children with this disorder show deletion abnormality of
chromosome22

Etiology/Pathophysiology:

 Pulmonary stenosis

A narrowing of the right ventricular outflow tract and can occur at the pulmonary
valve (valvular stenosis) or just below the pulmonary valve (infundibular
stenosis). Infundibular pulmonic stenosis is mostly caused by overgrowth of the
heart muscle wall (hypertrophy of the septoparietal trabeculae), however the
events leading to the formation of the overriding aorta are also believed to be a
cause. The pulmonic stenosis is the major cause of the malformations, with the
other associated malformations acting as compensatory mechanisms to the
pulmonic stenosis. The degree of stenosis varies between individuals with TOF,
and is the primary determinant of symptoms and severity. This malformation is
infrequently described as sub-pulmonary stenosis or subpulmonary obstruction.
 Overriding aorta

An aortic valve with biventricular connection, that is, it is situated above the
ventricular septal defect and connected to both the right and the left ventricle.
The degree to which the aorta is attached to the right ventricle is referred to as its
degree of "override." The aortic root can be displaced toward the front (anteriorly)
or directly above the septal defect, but it is always abnormally located to the right
of the root of the pulmonary artery. The degree of override is quite variable, with
5-95% of the valve being connected to the right ventricle.

 Right ventricle hypertrophy

The right ventricle is more muscular than normal, causing a characteristic boot-
shaped (coeur-en-sabot) appearance as seen by chest X-ray. Due to the
misarrangement of the external ventricular septum, the right ventricular wall
increases in size to deal with the increased obstruction to the right outflow tract.
This feature is now generally agreed to be a secondary anomaly, as the level of
hypertrophy generally increases with age.

 Ventricular septal defect

A hole between the two bottom chambers (ventricles) of the heart. The defect is
centered around the most superior aspect of the ventricular septum (the outlet
septum), and in the majority of cases is single and large. In some cases
thickening of the septum (septal hypertrophy) can narrow the margins of the
defect.

Signs and Symptoms:

 May not exhibit high degree of cyanosis immediately

 Bluish tint
 Polycythemia
 Severe dyspnea
 Growth restriction
 Clubbing of fingers
 Fainting
 Hypoxic episode (tet spell)
 Cognitive challenge

Laboratory/Diagnostic Findings:

 Increased Hg, Hct

 Echocardiography shows enlarged chamber of right heart
  Echocardiography shows decrease size in pulmonary artery and reduced
blood flow through lungs.
 ECG shows enlarged chamber of right heart
 Cardiac catheterization and angiography evaluate extent of defect
 Polycythemia
 Reduced oxygen saturation

Management:

 Propranolol
 Administer oxygen
 Knee chest position
 Blalock taussig
 Brock procedure

Nursing diagnosis:

1. Decreased cardiac out put related to structural defect.

2. Activity intolerance related to imbalance between oxygen supply and
demand.
3. Altered growth and development related to inadequate oxygen, nutrients
to tissue and social isolation.
4. High risk for infection related to debilitated physical status.
5. Altered family process related to having a child with a heart condition.
6. High risk for injury (complications) related to cardiac condition and
therapies.
Implementation
1. Administer supplemental oxygen.
2. Elevate head of the bed 30 to 60 degrees or have child sit upright.
3. Assess vital signs including heart rate, pulse and respirations.
Auscultate heart and lung sounds.
4. Allow time for frequent of rest.
5. Help child to select activities appropriate to age, condition and
capabilities.
6. Avoid extremes of environmental temperature.
7. Provide well balanced highly nutritive diet.
8. Avoid contact with infected persons.
9. Discuss with parents their fears regarding child symptoms.
10. Encourage family to participate in care of child while hospitalized.
11. Encourage family to include others in child’s care to prevent their own
exhaustion.
Prognosis:

Most cases can be corrected with surgery. Babies who have surgery usually do
well. Ninety percent survive to adulthood and live active, healthy, and productive
lives. Without surgery, death usually occurs by the time the person reaches age
20.

Patients who have continued, severe leakiness of the pulmonary valve may need
to have the valve replaced.

Regular follow-up with a cardiologist to monitor for life-threatening arrhythmias

(irregular heart rhythms) is recommended

TRANSPOSITION OF GREAT ARTERIES

TETRALOGY OF FALLOT
OVERRIDING OF AORTA
Acute Rheumatic Fever

Background of Case
- Autoimmune disease that occurs as a reaction to a group A beta-
hemolytic streptococcal infection
- Follows attack of pharyngitis, tonsillitis, scarlet fever, “strep throat”, or
impetigo
- Inflammation from immune system will lead to fibrin deposits on
endocardium and valves , and body joints

Etiology
- group A beta-hemolytic streptococcal infection (GABS)

Laboratory findings
1. High ESR
2. Anemia, leucocytosis
3. Elevated C-reactive protein
4. ASO titre >200 Todd units.(Peak value attained at 3 weeks,then comes
down to normal by 6 weeks)
5. Anti-DNAse B test
6. Throat culture-GABHstreptococci
7. ECG- prolonged PR interval, 2nd or 3rd degree blocks, ST-depression, T-
inversion
8. 2D Echo cardiography- valve edema,mitral regurgitation, LA & LV
dilatation, pericardial effusion, decreased contractility

Signs and Symptoms

 Major:
1. Subcutaneous nodules
2. Pancarditis
3. Arthritis
4. Chorea
5. Erythema marginatum

 Minor
1. Fever
2. Arthralgia
3. Previous rheumatic fever attacks
4. All that is stated in the laboratory findings

(Using Jones Criteria)*the presence of 2 MAJOR criteria or of 1 MAJOR and 2

MINOR criteria indicates a high probability of acute rheumatic fever, if supported
by evidence of Group A streptococcal infection
NANDA Problems
1. Nursing Diagnosis: Risk for non-adherence to drug therapy related to
knowledge deficit about importance of long-term therapy
Outcome Evaluation: child takes oral penicillin daily; absence of symptoms
of throat infection; vital signs are within age-acceptable parameters.
2. Nursing Diagnosis: Situational low-esteem related to chorea movements
secondary to rheumatic fever
Outcome Evaluation: child expresses frustration with inability to control
movements; continues to feed and dress self with help as needed.
Children may have difficulty feeding themselves because of chorea. They
may be also be emotionally unstable and cry easily. Emphasize the
transitory nature of the chorea; stress that is frustrating to have to be fed
and to be unable to use your hands meaningfully, but that is lack of
coordination will pass without permanent effects. Provide toys and games
that do not require fine coordination, because it may be frustrating to try to
do something such as move checkers or chessmen on a board (a typical
low activity game). Children with chorea who are on bed rest may need to
have bedrails padded so they do not injure themselves with thrashing
movements.

Nursing and Medical Management

1. Bed Rest
2. Monitor vital signs
3. Penicillin Therapy/ single intramuscular injection of benzathine penicillin
4. Oral ibuprofen
5. Corticosteroids: SE- Hirsutism, Cushing’s Syndrome
6. Phenobarbital and Diazepam

Prognosis
- Rheumatic fever can recur whenever the individual experience new GABH
streptococcal infection, if not on prophylactic medicines
- Good prognosis for older age group & if no pancarditis during the initial
attack
- Bad prognosis for younger children & those with pancarditis with valvar
lesions
KAWASKI DISEASE (Mucocutaneous lymph node syndrome)
Definition:
 A febrile disease  The incidence is higher in late
 Multisystem disorder almost winter and spring
exclusively in children before  Unknown cause
the age of puberty.  Develops in genetically
 The peak incidence is in boys predisposed clients
under 4 years old

Etiology/Pathophysiology:
 Unknown Etiology
 Pathophysiology
1. After the infection (upper 6. The inflammation of the
respiratory infection) blood vessels (Vasculitis)
2. Altered immune function leads to:
occurs  Aneurysms
3. Increase in the antibody  Platelet accumulation
production  Formation of Thrombi
4. Creates circulating immune  Obstruction in the heart
complexes that bind and blood vessels
5. to the endothelium and
cause inflammation
Signs and Symptoms:
• High fever( 102 to 104⁰F [39 • Strawberry tongue and red,
to 40⁰C]) Does Not Respond cracked lips
toAntipyretic • Rashes occur(diaper area)
• Child acts lethargic/irritable • Cervical lymph node become
• May have reddened and enlarged
swollen hands & feet • Internal lymph nodes swell
• Bulbar mucous membrane of • May develop abdominal pain,
the eyes become inflamed anorexia and diarrhea
(Conjunctivitis) • Joints may swell and
redden(simulating arthritic
process)
Laboratory/Diagnostic Findings:
 WBC and ESR are both elevated

Progression of the Disease:

10 days after onset(subacute phase)
• The skin desquamates (palms • Aneurysms may form in
and soles) coronary arteries(CHA)
• Platelet count rises (increased • Sudden death from
clotting necrosis of distal accumulating thrombi or
body cells, particularly in the rupture of an aneurysm
fingertips) (MOST DANGEROUS
PHASE)
25 days after onset (Convalescent Phase)
• Begins @ about the 25th day and last until 40 days

STAGE III last from 40 days until ESR returns to normal

Management:
 Administration of acetysalicylic acid or ibuprofen (dec I & PA)
 Abciximab – platelet receptor inhibitor specific for KD
 IV immune globulin can also be administed (reduce immune response)
 Coronary artery bypass surgery (CAD from stenosis of the Coronary
Arteries)
NOTE: *Steriods  CONTRAINDICATED (increase aneurysm formation)*

Nursing diagnosis:
1. Conjunctivitis: "L & R eye redness and yellow drainage" (Doesn't need
evidence. This IS the evidence)

2.Gingivitis: "Gum irritation M/B redness and swelling at upper and lower gums"

3.Rash: "Impaired Skin Integerity at bilateral hands M/B red rash with exfoliation"

4."Impaired Skin Integrity at bilateral feet M/B red rash with exfoliation"

5.Hand edema: "Impaired Tissue Integrity M/B 2+ pitting edema at bilateral

hands"

6.Foot edema: "Impaired Tissue Integrity M/B 3+ pitting edema at bilateral feet"

Joint inflammation: "Pain M/B warmth, redness and swelling at bilateral knees
and pt. states 6/10 pain on 0-10 P/S"
Implementation

Monitoring
1. Monitor pain level and child’s response to analgesics.
2. Institute continual cardiac monitoring and assessment for complications;
report arrhythmias.
o Take vital signs as directed by condition; report abnormalities.
o Assess for signs of myocarditis (tachycardia, gallop rhythm, chest
pain).
o Monitor for heart failure (dyspnea, nasal flaring, grunting,
retractions, cyanosis, orthopnea, crackles, moist respirations,
distended jugular veins, edema).
Closely monitor intake and output, and administer oral and I.V fluids as
ordered.
Monitor hydration staus by checking skin turgor, weight, urinary output,
specific gravity, and presence of tears.
 Observe mouth and skin frequently for signs of infection.

Supportive care
1. Allow the child periods of uninterrupted rest. Offer pain medication
routinely rather than as needed during stage I. Avoid NSAIDS if the child
is in aspirin therapy.
2. Perform comfort measures related to the eyes.
o Conjunctivities can cause photosensitivity, so darken the room,
offer sunglasses.
o Apply cool compress.
o Discourage rubbing the eyes.
o Instill artificial tears to soothe conjunctiva.
3. Monitor temperature every 4 hours. Provide sponge bath if temperature
above normal.
4. Perform passive range of motion exercises every 4 hours while the child is
awake because movement may be restricted.
5. Provide quiet and peaceful environment with diversional activities.
6. Provide care measures for oral mucous membrane.
o Offer cool liquids like ice chips and ice pops.
o Use soft toothbrush only.
o Apply petroleum jelly to dried, cracked lips.
7. Provide skin measures to improve skin integrity.
o Avoid use of soap because it tends to dry skin and make it more
likely to breakdown.
o Elevate edematous extremities.
o Use smooth sheets.
o Apply emollients to skin as ordered.
o Protect peeling of skin, observe for signs of infection.
8. Offer clear liquids every hour when the child is awake.
9. Encourage the child to eat meals and snack with adequate protein.
10. Infuse I.V fluids through a volume control device if dehydration is present,
and check the site and amount hourly.
11. Explain all procedures to the child and family.
12. Encourage the parents and child to verbalize their concerns, fears, and
questions.
13. Practice relaxation techniques with child, such as relaxation breathing,
guided imagery, and distraction.
14. Prepare the child for cardiac surgery or thrombolytic therapy if
complications develop.
15. Keep the family informed about progress and reinforce stages and
prognosis.
Prognosis:
A large majority of children who develop Kawasaki disease recover within
two weeks and experience no long-lasting effects. As many as 25 percent of
sufferers may develop heart problems, but that percentage drops dramatically to
below 5 percent with quick treatment. Only about 1 percent of cases prove fatal,
but because that possibility exists, you must know what symptoms to watch for
and what steps to take to prevent immediate and future complications.
Infective Endocarditis
Endocarditis is inflammation and infection of the endocardium or valves of the
heart. It may occur in a child without heart disease but more commonly occurs as
a complication of congenital heart disease such as tetralogy of Fallot, VSD, or
coarctation of the aorta.
Bacteria or other infectious substance can enter the bloodstream during certain
medical procedures, including dental procedures, and travel to the heart, where it
can settle on damaged heart valves. The bacteria can grow and may form
infected clots that break off and travel to the brain, lungs, kidneys, or spleen.

Etiology: Streptococci of the viridans type

Pathophysiology: A high-velocity flow through a stenotic or incompetent valve

or an abnormal communication between systemic and pulmonary circulations
causes turbulence downstream from the opening. This turbulence damages or
denudes the endothelium, to which platelets and fibrin adhere, and a small,
sterile" nonbacterial thrombotic endocardial lesion" forms. In addition, indwelling
intravascular catheters in the right heart may directly traumatize the endocardium
or valvular endothelium. Circulating bacteria and inflammatory cells adhere to
and grow in these thrombi, forming infected vegetation. Infection may occur on
the wall, where the turbulent jet strikes, or downstream, near the orifice, where
the flow eddies. Once vegetation forms, the constant blood flow may result in
embolization to virtually any organ in the body. A brisk immunologic response is
produced.

Manifestation:
 Paleness
 Anorexia
 weight loss
 Chills
 Arthralgia
 Sweating at night
 murmur become audible
 petechiae in conjunctiva
 RUQ abdominal pain
Laboratory Test
 CBC count: Anemia is present in 70-90% of patients and is usually
normocytic and normochromic. Leukocytosis is noted in 20-30% of
patients.
 ESR and C-reactive protein level: The ESR is elevated in almost all
patients except for those with congestive heart failure (CHF), renal failure,
and disseminated intravascular coagulation (DIC). The mean ESR is 55
mm/h. The C-reactive protein, although nonspecific, is elevated in most
patients but decreases with successful treatment. Levels of C-reactive
protein may be used to monitor response to antibiotic therapy..
 Urinalysis may reveal proteinuria (50-60%) and/or microscopic hematuria
(30-50%).

Treatment
Prophylactic administration
antibiotic
Penicillinase-resistant
penicillin (Nafcillin) UNIPEN
via IV (cvc)

Nursing Diagnosis:
 Decreased cardiac
output related to
congenital structural
disorder
 Ineffective tissue
perfusion related to
inadequate cardiac
output
Prognosis:
The prognosis of bacterial endocarditis varies with the etiologic agent. Infection
by a penicillin-sensitiveStreptococcus, diagnosed early, has a cure rate of almost
100%. Because many infections are diagnosed late or due to resistant
organisms, the average mortality rate is approximately 20-25%.
UTI- Urethritis
Background:
Urethritis is inflammation of the urethra. The main symptom is dysuria, which is
painful or difficult urination.

Etiology:
>gonococcocal urethritis
Other causes include:
 Adenovirus  Mycoplasma genitalium
 Uropathogenic Escherichia  Reiter's syndrome
coli (UPEC)  Trichomonas spp.
 Herpes simplex  Ureaplasma urealyticum

Signs and symptoms/ Clinical Manifestations:

>In men- purulent discharge >Dysuria
>Frequency

Labs and Diagnostics:

>Culture and sensitivity testing

Nursing Management:
>Removal of etiologic agent- by >Sitz bath
administering doctor-prescribed >Increases fluid intake
systemic and topical antibiotics >Advise client to avoid coitus

NANDA problems:
Impaired Urinary elimination r/t irritation and inflammation of the urethral mucosa
Acute pain r/t irritation and inflammation of the urethral mucosa

Prognosis:
With the correct diagnosis and treatment, urethritis usually clears up without any
complications.
However, urethritis can lead to permanent damage to the urethra (scar tissue
called urethral stricture) and other urinary organs in both men and women.
UTI: Cystitis
Background:
Is a term that refers to urinary bladder inflammation that results from any one of a
number of distinct syndromes. It is most commonly caused by a bacterial
infection in which case it is referred to as a urinary tract infection

Etiology:
>gram negative bacteria (E. coli, Klebsiella, Enterobacter, Proteus)
>Candida spp.
>Chlamydia trachomitis, Trichomonas vaginalis, Neiseria gonorrhea

Signs and symptoms/ Clinical Manifestations:

>change in voiding habits >voiding in small amounts
>burning pain on urination (dysuria) >incomplete bladder emptying
>frequency >hematuria
>urgency

Labs and Diagnostics:

>urine culture
>dipstick test

Nursing Management:
>Inhibit bacterial growth- give adequate
instructions about antibiotics therapy and dietary
and activity restrictions.
>Advice patient to Modify Diet- dietary changes
needed to keep urine acidic and to reduce bladder
irritation by avoiding spicy foods, caffeinated and
alcoholic beverages
> Advice patient to Increase fluid intake- to flush
urinary system
>Prevent complications- educate client about inc manifestations that might result
from infection of the upper UT

NANDA problems:
Impaired Urinary elimination r/t irritation and inflammation of the bladder mucosa
Acute pain r/t irritation and inflammation of the bladder and mucosa

Prognosis:
The prognosis for recovery from uncomplicated cystitis is very good. With proper
treatment, the infection usually clears up quickly. In many cases, the condition
may reoccur. However, it can be treated in essentially the same way each time it
appears. More complicated infections in men may be difficult to treat if antibiotics
are not able to clear up the problem.
Enuresis (bed wetting)

 Background
 Enuresis is an involuntary passage of urine past the age when a
child should be expected to have attained bladder control

 Etiology
 Unclear
 Possible causes: anatomical malformation of kidneys and bladder;
lack of Anti-diuretic hormone secretion;
mental disorder

 Classification according to time of urine

passage
 Nocturnal- at night
 Diurnal- at morning

 Major types
 Primary- occurs when the child never
establish bladder control
 Secondary- occurs when a person acquires bladder control for the
past 6 months then having relapses and started bed wetting.

 Clinical Findings
 5-7 years old
 Most common in boys

 Laboratory and Diagnostic Findings

 Abnormal ECG patterns
 IVP
 VCUG
 UTz
 Management
 If the cause is stress; stress modification is recommended
 Limit fluids after dinner
 Administration of synthetic Anti-diuretic hormone
 Desmopressin
 Nursing Management
 Urge parents to exercise common sense
 Caution parents of children with sickle-cell anemia not to restrict
fluid because sickling of RBC is increased in case of dehydration
 Advise bladder stretching exercises by drinking lots of water and
trying not to void as long as possible to increase functional size of
the bladder
  Prognosis
 Good if readily prevented
Acute Glomerulonephritis

 Background
Acute Glomerulonephritis is the sudden inflammation of the
glomeruli of the kidney.

 Etiology
 History of recent infection to Group A Beta-Hemolytic
Streptococcus such as: tonsillitis, otitis media, strep throat and
impetigo
 Tissue damage from complement fixation reaction in the
glomeruli

 Clinical Findings
 B- oys
 R- ecent respiratory infection (7-14days)
 A- ges 5-10
 S- pring and winter seasons
 S- trep infection

 Signs and Symptoms

 H- ematuria
 E- dema Periorbital area
 L- ow grade fever
 P-roteinuria
 V-omiting
 A- norexia
 H- eadache
 A-bdominal pain

 Laboratory and Diagnostic Findings

 CXR & UTz- hepatocardiomegaly, pulmonary edema
 ECG- Galloping HR, T wave inversion, prolong P-R interval,
orthopnea

 Urinalysis: RBC casts, WBC, epithelial cells, hyaline and granules

are present; Increase CRea and BUN
 Blood analysis:
↑Antistreptolysin O

Albumin
Serum Complement
Hct & Hgb
RBC Sedimentation
 Nursing Management
 Bed rest  Weighing
 Diet: ↑ Protein;  I & O monitoring
↓Sodium or DAT with
normal sodium content
 Health teachings
 Positioning semi
fowlers
 Digitalis
 Oxygen therapy
  Nursing Diagnosis
 Situational low self-esteem related to feelings of responsibility for
onset of serious illness.

 Prognosis
 Good if readily prevented

Nephrotic Syndrome
 Background
 Nephrotic syndrome is an abnormal loss of protein in urine
involving immunologic mechanism that may be caused by
hypersensitivity to an antigen-antibody reaction or an immune
process.

 Etiology
 hypersensitivity to an antigen-antibody reaction

 Pediatric Nephrotic Syndrome

1. Congenital- autosomal recessive disorder (rare)

2. Secondary- as progression of glomerulonephritis, sickle cell anemia

or SLE
3. Idiopathic- primary; acquired; common

 Classification of NS according to Membrane

Destruction
 Minimal Change Nephrotic Syndrome
 Focal Segmental Glomerulosclerosis
 Membranoproliferative glomerulonephritis

 Signs and Symptoms

 P- roteinuria
 I- ncrease blood lipid
 D- ecrease serum albumin
 E- dema Periorbital area and abdomen
(ascites)

 Laboratory and Diagnostic Findings

 + Proteinuria
 Entirely albumin
 Minimal Hematuria
 ↑ RBC sedimentation
 Dx Pocedure: RENAL BIOPSY

 Management
  Supportive-Symptomatic (no cure)
FOCUS: Reducing proteinuria and edema
 Meds: Corticosteroids
IV Methylprednisone: until diuresis w/o protein loss
Oral Prednisone: SE- halt growth and suppress
adrenal gland secretion

 Keeping child free from infection

 Instruct parents to test the first urine of the day
for protein. Approx. 1x a wk.
 Instruct to alternate drug therapy
If diuretics are necessary WOF: tendency for Hypo-K
 Diet: may need to ↑ K & K-supplementation
 Albumin Infusion
 If prednisone resistant (w/ FGS & MPGN):
 cyclophosphamide (anti-neoplastic)
 Mycophenolate
 Cyclosporine

**Rationale: NS is an autoimmune disorder

**Nsg. Consideration: Should take with adequate fluid intake to avoid
bladder irritation and bleeding.

 Nursing Diagnosis
 Imbalance nutrition less than body requirements related to poor
appetite, restricted diet and protein loss

 Prognosis
 MCNS- responds to steroids
 FGS & MPGN- 2 relapses at irregular intervals for several years
Hemolytic-Uremic Syndrome

 Background
 Hemolytic-Uremic Syndrome is the inflammation of glomerular
arterioles because of occlusion with particles of fibrin and platelets.

 Etiology
 Recent E. coli GI infection

 Clinical Findings
 Summer
 6 mos. – 4 years
 Transient diarrhea→ severe fluid
loss and bowel wall
necrosis
 Fever → stupor and hallucination
 Oliguria → proteinuria, hematuria and protein casts
 Edema
 Pale
 Petichiae → thrombocytopenia

 Laboratory and Diagnostic Findings

 ↑ BUN and Creatinine

 Management
 Symptomatic Approach
 FOCUS: to maintain heart and kidney function
 Oliguria- Peritoneal dialysis
 Anemia- Blood transfusion

 Nursing Management
 Educate parents about the need for P.D.
 Ensure parents understand the importance of follow up care.

 Prognosis
 Good
Bladder Exstrophy- Epispadia Complex

Background:
Bladder exstrophy-epispadia complex is a congenital abnormality in which part of
the urinary bladder is present outside the body. It is rare, occurring once every
30,000 live births with a 2:1 male:female ratio. The diagnosis involves a spectrum
of anomalies of the lower abdominal wall, bladder, anterior bony pelvis, and
external genitalia. It occurs due to failure of the abdominal wall to close during
fetal development and results in protrusion of the posterior bladder wall through
the lower abdominal wall.
Etiology:
The cause of bladder exstrophy is maldevelopment of the lower abdominal wall,
leading to a rupture which causes the bladder to communicate with the amniotic
fluid.

Signs and symptoms / Clinical manifestations:

The typical manifestations of exstrophy-epispadias complex are:
 bladder everted through a midline lower abdominal wall defect
 widening of the pubic symphysis
 epispadias in males (dorsal cleft in the penis, exposing the urethral mucosa)
 the anus and vagina appear anteriorly displaced
 The testicles may be undescended.
 Bifid clitoris in females, with a short "urethral strip" indistinguishable from
bladder mucosa.
The spectrum of disease extends from spade penis and epispadias on one hand,
to exstrophy with cloaca (also known as cloacal exstrophy).

Nursing Management:
 In neonates with exstrophy and epispadias, initiate general supportive
care appropriate for the overall condition and associated anomalies.
 Institute parenteral nutrition early for patients with cloacal exstrophy.
 Place clean plastic wrap over the bladder plate. Avoid moistened or
impregnated gauze, which is irritating to the delicate bladder mucosa. Mist
tents may be used to protect exposed tissue.
 Start antibiotic therapy with doctor’s order after delivery and continue
through the early postoperative period.
 Daily prophylactic antibiotic therapy may be continued in the weeks after
bladder closure. Surgeon's philosophy on this matter varies.
 Infections may be related to poor emptying and are to be prevented in light
of the high incidence of vesicoureteral reflux. Institute latex precautions
due to high incidence of latex sensitization in patients with exstrophy-
epispadias complex.
NANDA problems:
Impaired urinary elimination r/t anatomical malformation of the bladder and
ureters
Risk for infection r/t broken skin

Prognosis:
Even with successful surgery, patients may have long-term problems with
 incontinence
 urinary reflux (see Vesicoureteral_reflux)
 repeated urinary tract infections
 bladder adenocarcinoma
 colonic adenocarcinoma
 sexual dysfunction
 pain
 uterine prolapse
Polycystic Kidney Disease
Background:
It occurs in humans and some other animals. PKD is characterized by the
presence of multiple cysts (hence, "polycystic") in both kidneys. The cysts are
numerous and are fluid-filled resulting in massive enlargement of the kidneys.
The disease can also damage the liver,pancreas, and in some rare cases,
the heart and brain. The two major forms of polycystic kidney disease are
distinguished by their patterns of inheritance.
Polycystic Kidney Disease is the most common genetic, life threatening disease
affecting an estimated 12.5 million people worldwide

Etiology:
It is an autosomal recessive trait, and both parents must have carried the gene.

Signs and symptoms/ Clinical Manifestations:

>ESRD
>Uremia (when renal nephrons are destroyed and renal function deteriorates)
>UTI (bec of distorted renal archithecture)
>hyponatremia (PKD tends to waste Na+)

Labs and Diagnostics:

Urinalysis (hema/proteinuria)
CBC (low Hct and Hgb)
Cerebral angiography ((+) aneurysm)

Nursing Management:
1) Aggressive control of HPN
2) Inc sodium intake (but if + HPN, dietary sodium is restricted)
3) Dialysis or renal transplant (if ESRD develops)
4) Genetic counseling (bec of hereditary nature of disease)

NANDA problems:
Pain (acute) related to compression of tissues, trauma to structures from calculi,
inflammation, and infection

Prognosis:
Many infants and children with recessive PKD die from hapatic fibrosis, which
obstructs blood flow and causes bile buildup in the liver. Its symptoms are
enlargement of the liver and the spread of a fibrous connective tissue over the
liver. Those who survive into their 20s may develop splenic, pancreatic, and
vascular problems. Children with recessive PKD often have smaller than average
stature.
Hydronephrosis

Background:

Hydronephrosis is distension and dilation of the renal pelvis calyces, usually

caused by obstruction of the free flow of urine from the kidney, leading to
progressive atrophy of the kidney. In case of hydroureteronephrosis, there is
distention of both the ureter and the renal pelvis and calices

Etiology:

Hydronephrosis is the result of several abnormal pathophysiological occurrences.

Structural abnormalities of the junctions between the kidney, ureter, and bladder
that lead to hydronephrosis can occur during fetal development. Some of these
congenital defects have been identified as inherited conditions, however the
benefits of linking genetic testing to early diagnosis have not been
determined. Other structural abnormalities could be caused by injury, surgery, or
radiation therapy.
Compression of one or both ureters can also be caused by other developmental
defects not completely occurring during the fetal stage such as an abnormally
placed vein, artery, or tumor. Bilateral compression of the ureters can occur
during pregnancy due to enlargement of the uterus. Changes in hormone levels
during this time may also affect the muscle contractions of the bladder, further
complicating this condition.
Sources of obstruction that can arise from other various causes include kidney
stones and blood clots.
The obstruction may be either partial or complete and can occur anywhere from
the urethral meatus to the calyces of the renal pelvis.
Hydronephrosis can also result from the reverse flow of urine from the bladder
back into the kidneys. This reflux can be caused by some of the factors listed
above as well as compression of the bladder outlet into the urethra by prostatic
enlargement or impaction of feces in the colon, as well as abnormal contractions
of bladder muscles resulting from neurological dysfunction or other muscular
disorders.

Signs and symptoms/ Clinical Manifestations:

 onset of intense flank or back pain radiating to the groin,

 nausea, vomiting,
 Sweating.
 Colicky pain
 Blood seen in the urine.
 Chronic hydronephrosis
 weakness,
 malaise
If electrolyte abnormalities occur because the kidneys are unable to regulate
sodium, potassium, and calcium, there may be heart rhythm
disturbances and muscle spasms.

Labs and Diagnostics:

The following laboratory tests may be ordered depending upon what potential
diagnosis is being considered.
 Urinalysis to look for blood, infection or abnormal cells
 Complete blood count (CBC) may reveal anemia or potential infection
 Electrolyte analysis may be helpful in chronic hydronephrosis since the kidneys
are responsible for maintaining and balancing their concentrations in the blood
stream.
 BUN (blood urea nitrogen), creatinine and glomerular filtration rate (GFR) are
blood tests that help assess kidney function.

…Imaging Studies
CT scan of the abdomen can be performed to evaluate the kidney anatomy and
make the diagnosis of hydronephrosis. It also may allow the health care
practitioner to look for the underlying cause including kidney stones or structures
that are compressing the urinary collecting system. Depending upon the situation
and the health care practitioner's concerns, the CT may be done with or without
contrast dye injected into a vein, and with or without oral contrast (that the patient
drinks) to outline the intestine. Most commonly, for kidney stones, neither oral nor
intravenous contrast is needed.
Ultrasound is another imaging study that can be done to look for hydronephrosis.
The quality of the test depends upon the skill of the ultrasonographer to evaluate
the structures in the abdomen and retroperitoneum. Ultrasound is also useful
inwomen who are pregnant where radiation concerns exist.
Intravenous pyelography (IVP) has mostly been replaced by CT scanning but
does have a role in diagnosing some patients and its use is now limited.
KUB X-rays (an X-ray that shows the kidney, ureter, and bladder) are used by
some urologists to classify a kidney stone as radiodense or radiolucent and may
use KUB X-rays to determine if the stone is able to migrate down the ureter into
the bladder.

Nursing Management:
1) Asses:
Pain
Urine input& output
Palpate kidney
Urine for labs (spec gravity, albumin, glucose, and edema)
2) Intervention:
Administer fluids (hourly fluid replacement)
Watch out for pain and reduced U.O.
Avoid urinary infections(keep urine bag above not touching the floor)

NANDA problems:
Impaired urinary elimination r/t obstruction (mechanical or anatomical)
Risk for infection r/t urinary stasis

Prognosis:
Left untreated, bilateral obstruction (occurring to both kidneys rather than one)
has a poor prognosis
Wilm’s Tumor

Background:
Wilm’s Tumor or nephroblastoma is cancer of the kidneys that typically
occurs in children, rarely in adults. Its common name is an eponym, referring to
Dr. Max Wilms, the German surgeon (1867–1918) who first described this kind of
tumor.
Approximately 500 cases are diagnosed in the U.S. annually. The majority
(75%) occurs in otherwise normal children; a minority (25%) is associated with
other developmental abnormalities. It is highly responsive to treatment, with
about 90% of patients surviving at least five years.

Etiology:
Wilms tumor may arise in 3 clinical settings, the study of which resulted in
the discovery of the genetic abnormalities that lead to the disease. Wilms tumors
can arise sporadically, can develop in association with genetic syndromes, or can
be familial. Although some of the molecular biology of Wilms tumor is coming to
light, the exact cellular mechanisms involved in the etiology of the tumor are still
being investigated.

Signs and symptoms/ Clinical Manifestations:

...More common findings:
 Palpable abdominal mass
 Gross Hematuria (onset: 9 mos), Flank pain, Fever , Weight loss,
Cachexia fatigue, HPN, amyloidosis, thromblophlebitis,
anemia,erythrocytosis, hypercalcemia, abnormal serum liver profile,
elevated ESR,
…Less frequent findings:
 Peripheral neuropathy, inferior vena cava obstruction, priapism, variocele,
hydronephrosis (if tumor blocks ureteropelvic junction)

Labs and Diagnostics:

Plasma erythropoietin, renin, chorionic gonadotropin ang prostaglandin are
elevated
IV Pyelogram
UTZ
CT Scan
Nephrotomography

Nursing Management:
PRE- OP: Inc fluid intake if indicated, emotional support
POST-OP:
V/S, WOF signs of hemorrhage, pneumothorax
NANDA problems:
Anxiety r/t threat of death
Risk for injury
Interrupted family process r/t expensive treatments
Knowledge deficit of the disorder and therapy

Prognosis:
Tumor-specific loss-of-heterozygosity (LOH) for chromosomes 1p and 16q
identifies a subset of Wilms' tumor patients who have a significantly increased
risk of relapse and death. LOH for these chromosomal regions can now be used
as an independent prognostic factor together with disease stage to target
intensity of treatment to risk of treatment failure. Genome-wide copy number and
LOH status can be assessed with virtual karyotyping of tumor cells (fresh or
paraffin-embedded). The overall prognosis with surgical removal is positive. Early
removal tends to promote positive outcomes.
Hypertrophic Pyloric Stenosis

A condition that causes severe vomiting in the few months of life. There is
narrowing (stenosis) of the opening from the stomach to the intestines, due to
enlargement (hypertrophy) of the muscle surrounding this opening (pylorus),
which spasms when the stomach empties. It is uncertain whether there is a real
congenital narrowing or whether there is a functional hypertrophy of the muscle
which develops few weeks of life.
Hypertrophic pyloric stenosis may also cause almost complete gastric
outlet obstruction. It affects 1 of 250 infants and is common among males by a
4:1 ratio, particularly firstborn males. It occurs most often between 3 to 5 weeks
of age and rarely after 12 weeks.

Etiology
There is no known etiology of pyloric stenosis, but a genetic component is
likely because siblings and offspring of affected people are at increased risk.
Proposed mechanisms include lack of neuronal nitric oxide synthase and
abnormal innervations of the muscular layer. Infants exposed to certain
macrolide antibiotics in the first few weeks of life are at significantly increased
risk.

Clinical Findings
- Olive shaped mass - Narrowed pyloric outlet in
palpated on the upper GI series
epigastrium. - Hypokalemic,
- Palpable or even visible hypochloremic metabolic
peristaltic waves alkalosis in blood
- Thickened pylorus in chemistry
ultrasound - Hypovolemia
- Hyperaldosteronism

Signs and Symptoms

- Progressive worsening - Crying without tears and
non-bile stained projectile less wet or dirty diapers
vomiting (dehydration)
- Poor feeding - Constant hunger
- Weight loss - Belching
- Colic
Laboratory and Diagnostic procedures
- Ultrasound ( most common diagnostic exam)
- Upper gastro-intestinal series ( most common confirmatory diagnostic
exam)
- Blood chemistry and arterial blood gases

Nursing Management
- Immediate fluid replacement (dehydration and electrolyte imbalances)
 - Oral atropine
- If the client undergoes surgery, secure consent and properly educated
the client’s parents and guardians about the procedure.
- If the client has an ostomy, clean the stoma properly and regularly, and
educated the client’s parents and guardians in how to clean the stoma.

Nursing Diagnosis
- Fluid volume deficit
- Imbalanced nutrition less than body requirement
- Risk for aspiration

Prognosis
If intervention and surgery are immediately done, good prognosis is
accomplish.
 CLEFT LIP (CL) AND/ OR CLEFT PALATE (CP)
Cleft lip and cleft palate are facial malformations that occur during
embryonic development and can constitute a severe disability to the affected
individual. Cleft lip, also known as cheiloschisis, and cleft palate, also known
as palatoschisis, are types of abnormal developments of the face during
pregnancy - they are types of clefting congenital deformities. They can occur
together as cleft lip and palate.

Before birth, there are natural

structures that form in the body and
then join together (fuse). A cleft is a
non-fusion of these structures - a
fissure or a gap. In this case, the gap
(cleft) occurs in the upper lip, the
palate (roof of the mouth), or both.
When just one side of the lip is
affected it is called a unilateral cleft;
a bilateral cleft affects both sides.
According to the National Institutes
of Health (NIH), USA, about 1 in
every 700 newborns has a cleft lip
and/or cleft palate. The National
Health Service (NHS), UK says the
incidence is 1 in 600.

ETIOLOGY
Researchers believe that most cases of cleft lip and cleft palate are caused by an
interaction of genetic and environmental factors. In many babies, a definite cause
isn't discovered.
 Genetic factors. Either the mother or the father can pass on genes that cause
clefting, either as an isolated defect or as part of a syndrome that includes
clefting as one of its signs. In some cases, babies inherit a gene that makes them
more likely to develop a cleft, and then an environmental trigger actually causes
the cleft to occur.
 Environmental factors. Fetal exposure to cigarette smoke, alcohol, certain
medications, illicit drugs and certain viruses have been linked to the development
of a cleft.

Other risk factors:

Several factors may increase the likelihood of a baby developing a cleft lip and
cleft palate.
 Family history. Parents with a family history of cleft lip or cleft palate face a
higher risk of having a baby with a cleft.
 Race. Cleft lip and palate are most common in American Indian and Asian
children. Black children are least likely to have a cleft.
 Sex. Males are twice as likely to have a cleft lip with or without cleft palate. Cleft
palate without cleft lip is more common in females.
 Environmental factors. Exposure in early pregnancy to cigarette smoke, alcohol
or illicit drugs may put a baby at higher risk of developing a cleft.
 Maternal obesity. Obesity in the mother is associated with a slightly increased
risk of cleft lip and palate.

PATHOPHYSIOLOGY
During embryonic development the lateral and medial tissues forming the
upper lip palates fuse between weeks 7 and 8 of gestation; the palatal tissues
forming the hard and soft palates fuse between weeks 7 and 12 gestation. Cleft
lip and cleft palate result when these tissues fail to fuse.

MANIFESTATIONS
Clinical manifestations

a. Cleft lip and cleft palate are readily apparent at birth. Careful physical
assessment should be performed to rule out other midline birth defects. Palpate
the palate with the fingers to check for defects.
b. Cleft lip and cleft palate appear as incomplete or complete defects, and may
be unilateral or bilateral.

Laboratory and diagnostic study findings.

Obstetric ultrasound will reveal cleft lip while the infant is in utero at 18 to 20
weeks of gestation can identify a cleft in a fetus.

COMPLICATIONS

Children with cleft lip with or without cleft palate face a variety of challenges,
depending on the type and severity of the cleft.
 Feeding difficulties. One of the most immediate concerns after birth is feeding.
While most babies with cleft lip can breast-feed, a cleft palate can make sucking
difficult or cause gagging or nasal regurgitation. Your health care team will
discuss feeding strategies with you, such as using a special bottle nipple or a
small artificial palate (obturator) that fits into the roof of the mouth.
 Ear infections and hearing loss. Babies with cleft palate are especially
susceptible to middle ear infections. Over time, repeated ear infections can
damage hearing, but hearing loss may resolve with treatment. It's important for
children with cleft palate to be evaluated regularly by an audiologist or an ear,
nose and throat doctor. Most children with clefts have tubes inserted in their ears
to drain fluids and help prevent infections.
 Dental problems. If the cleft extends through the upper gum, tooth development
will likely be affected. A pediatric dentist should monitor tooth development and
oral health from an early age.
 Speech difficulties. Because both the lip and palate are used in forming
sounds, the development of normal speech can be affected. A speech
pathologist can evaluate your child and provide speech therapy.
 Psychological challenges. Children with clefts may face social, emotional and
behavioral problems due to differences in appearance and the stress of intensive
medical care. A psychologist and a social worker can help you and your child
deal with the stresses your family encounters.
NURSING MANAGEMENT
Assess for problems with feeding, breathing parental bonding, and speech.
Provide child and family teaching.

Ensure adequate nutrition and prevent aspiration.

a. Provide special nipples or feeding devices (eg, soft pliable bottle with soft
nipple
with enlarged opening) for a child unable to suck adequately on standard
nipples.
b. Hold the child in a semi-upright position; direct the formula away from the
cleft and toward the side and back of the mouth to prevent aspiration.
c. Feed the infant slowly and burp frequently to prevent excessive swallowing
of air and regurgitation.
d. Stimulate sucking by gently rubbing the nipple against the lower lip.

Feeding bottle for infant with Cleft lip and cleft palate.

Support the infant’s and parents’

emotional and social adjustment.
a. Help facilitate the family’s
acceptance of the infant by
encouraging the parents to
express their feelings and
concerns and by conveying
 an attitude of acceptance b. Emphasize the infant’s positive
toward the infant. aspects and express optimism
regarding surgical correction
.

Provide preoperative care.

a. Depending in the defect and the child’s general condition, surgical
correction of the cleft lip (cheiloplasty ) usually occurs at 1 to 3 months
of age; repair of the cleft palate (palatoplasty) is usually performed
between 6 and 18 months of age. Repair of the cleft palate may require
several stages of surgery as the child grows.
b. Early correction of cleft lip enables more normal sucking patterns and
facilitates bonding. Early correction of cleft palate enables development
of more normal speech patterns.
c. Delayed closure or large defects may require the use of orthodontic
appliances.
d. The responsibilities of the nurse are to:
1. Reinforce the physician’s explanation of surgical procedures.
2. Provide mouth care to prevent infection.

Provide postoperative care.

a. Assess airway patency and vital signs; observe for edema and respiratory
distress.
b. Use a mist tent, if prescribed, to minimize edema, liquefy secretions, and
minimize distress.
c. Position the child with cleft lip on her back, in an infant seat, or propped on
a side to avoid injury to the operative site; position the child with a cleft
palate on the abdomen to facilities drainage.
d. Clean the suture line and apply an antibacterial ointment as prescribed to
prevent infection and scarring. Monitor the site for signs of infection.
e. Use elbow restraints to maintain suture line integrity. Remove them every 2
hours for skin care and range-of-motion exercises.
f. Feed the infant with a rubber-tipped medicine dropper, bulb syringe, Breck
feeder, or soft bottle-nipples, as prescribed, to help preserve suture
integrity. For older children, diet progresses from clear fluids; they should
not use straws or sharp objects.
g. Attempt to keep the child from putting tongue up to palate sutures.
h. Manage pain by administering analgesic as prescribed.

NURSING DIAGNOSIS
 Altered nutrition : less than body requirements related to physical defect
 Risk for altered parenting related to infant with a highly visible physical
defect
  Risk for trauma of the surgical site related to surgical procedure,
dysfunctional swallowing
 Altered nutrition: less than body requirements related to difficulty eating
following surgical procedure
 Pain related to surgical procedure
 Altered family processes related to child with a physical defect,
hospitalization
PROGNOSIS
Although treatment may continue for several years and require several
surgeries, most children with a cleft lip and palate can achieve normal
appearance, speech, and eating. However, some people may have a continued
speech problem that needs further therapy.
CLEFT LIP/ CLEFT PALATE MIND MAP
ESOPHAGEAL ATRESIA WITH TRACHEOESOPHAGEAL FISTULA
. A rare congenital malformation that is believed to result from failed separation of
the esophagus and trachea by a septum that forms in the 4 th week of gestation.
The esophagus ends in a blind pouch and is accompanied by
Tracheoesophageal Fistula.

ETIOLOGY AND INCIDENCE • C- ardiovascular,

• T-racheo
The cause of esophageal atresia • E-sophageal
and TEF is unknown. • R-enal
• 1:2000 to 1:1500 live births. • L-imb abnormalities
• Happens in both sexes.
• EA/TEF is often present in • Low birth weight babies.
VATER or VATERL • And high incidence in
syndromes premature infants
• V-ertebral
• A-norectal

TYPES:
 Type A (7.7%): Esophageal atresia in which both segments of the
esophagus end in blind pouches. Neither segment is attached to the
trachea.
 Type B (0.8%): Esophageal atresia with tracheoesophageal fistula in
which the upper segment of the esophagus forms a fistula to the trachea.
The lower segment of the esophagus ends in a blind pouch. This condition
is very rare.
 Type C (86.5%): Esophageal atresia with tracheoesophageal fistula, in
which the upper segment of the esophagus ends in a blind pouch (EA)
and the lower segment of the esophagus is attached to the trachea (TEF).
 Type D (0.7%): Esophageal atresia with tracheoesophageal fistula, in
which both segments of the esophagus are attached to the trachea. This
is the rarest form of EA/TEF.
 Type H (4.2%): Tracheoesophageal fistula in which there is no
esophageal atresia because the esophagus is continuous to the stomach.
Fistula is present between the esophagus and the trachea.
PATHOPHYSIOLOGY
SIGN AND SYMPTOMS
• Excessive salivation or drooling
• Three C’s OF TEF
• C-hoking
• C-oughing
• C-yanosis
• Apnea
• Increased respiratory distress after feeding
• Abdominal distention

DIAGNOSTIC EXAM
• Esophageal Atresia- maternal polyhydramnios.
• Determined by radiographic studies
• A size 10 or 12 French catheter passed through the nose meets an
obstruction (esophageal atresia) approximately 4" to 5" (10 to 12.5 cm)
distal from the nostrils. Aspirate of gastric contents is less acidic than
normal.
• Chest X-ray demonstrates the position of the catheter and can also show
a dilated, air-filled upper esophageal pouch, pneumonia in the right upper
lobe, or bilateral pneumonitis. Both pneumonia and pneumonitis suggest
aspiration.
• Abdominal X-ray shows gas in the bowel in a distal fistula (type C) but
none in a proximal fistula (type B) or in atresia without fistula (type A).
• Cinefluorography allows visualization on a fluoroscopic screen. After a
size 10 or 12 French catheter is passed through the patient’s nostril into
the esophagus, a small amount of contrast medium is instilled to define
the tip of the upper pouch and to differentiate between overflow aspiration
from a blind end (atresia) and aspiration due to passage of liquid through
a tracheoesophageal fistula.

COMPLICATIONS
 The infant may breathe saliva and other secretions into the lungs, causing
aspiration pneumonia, choking, and possibly death.
 Other complications may include:
 Feeding problems
 Reflux (the repeated bringing up of food from the stomach) after
surgery
 Narrowing (stricture) of the esophagus due to scarring from surgery
 Tracehomalacia – weakness in the tracheal wall that occurs when a
dilated proximal pouch compresses the trachea in early fetal life.
 Prematurity may complicate the condition.
 THERAPEUTIC/NURSING MANAGEMENT

• Keep infant warm and oxygenated

• Keep infant supine with the HOB elevated to keep gastric secretions from
entering the lungs
• NGT aspirate every 5 to 10 minutes to keep the keep the proximal pouch
clear
• Intravenous IV fluids are essential
• Surgical repair: Ligation of the fistula and end-to-side anastomosis of the
atresia.

NURSING DIAGNOSIS

 Impaired gas exchange and ineffective airway clearance related to

Respiratory distress/ EA& TEF
 Risk for aspiration related to infants immature gag and cough reflex
 Risk for imbalanced nutrition: less than body requirements related to
inability to take in oral feedings
 Risk for infection related to aspiration or seepage of stomach secretions
on the lungs
 Risk for impaired skin integrity related to gastrostomy tube insertion site.

PROGNOSIS
Surgery to correct esophageal atresia is usually successful, with
survival rates close to 100 percent in otherwise healthy infants after the
condition is corrected. Postoperative complications may include difficulty
swallowing, since the esophagus may not contract efficiently, and
gastrointestinal reflux, in which the acidic contents of stomach back up
into the lower part of the esophagus, possibly causing ulcers.
BACKGROUND OF THE DISEASE

Intussusception- the invagination of one portion of the intestine into another,

usually occurs in the second half of the first year of life.

ETIOLOGY
<1 year old-occurs for Idiopathic reasons
>1 year old-a “lead point” on the intestine likely cues the invagination
Meckel’s diverticulum-a polyp, hypertrophy of Peyer’s patches (lymphatic tissue
of the bowel that increases in size with viral diseases) or bowel tumors. The point
of the invagination is generally at the juncture of the distal ileum and proximal
colon.

SIGNS AND SYMPTOMS

Assessment:
 Suddenly draw up their legs and cry and they vomit
 After the peristaltic wave, they are symptom free and play happily
 (Approx. 15 min.) Same phenomenon of intense abdominal pain strikes
again
 Vomitus will begin that contains bile bec. the obstruction is invariably
below the ampulla of Vater (the point in the intestine where bile empties
into the duodenum
 (Approx. 12 hrs.)blood appears into the stool and possibly in vomitus
(currant jelly appearance)
 The abdomen becomes distended as the bowel above the
intussusceptions distends.
DIAGNOSTIC TEST

The presence of intussusceptions is confirmed by ULTRASOUND or CT scan

MANAGEMENT
 Surgical Emergency
 Instillation of a water soluble sol’n, barium enema or air (pneumatic
insufflation) into the bowel or surgery to reduce invagination.
 After this type of reduction, children must observe for 24 hrs. because
some children will have recurrence of the intussusceptions.

NURSING DIAGNOSIS
 Pain related to abnormal abdominal peristalsis
 Risk for deficient fluid volume related to bowel obstruction
 Risk for impaired parenting related to infant’s illness
BACKGROUND OF THE DISEASE
Hirschsprung’s Disease-is absence of ganglionic innervations to the muscle of
a section of the bowel. In most instances, the lower portion of the sigmoid colon
just above the anus. The absence of nerve cells means there are no peristaltic
waves in this section to move fecal material through the segment of the intestine.

ETIOLOGY
Assessment:
 If infants fail to pass
meconium by 24
hours of age
 Increasing
abdominal
distention
 History of
constipation or
intermittent
constipation and
diarrhea

 What is the duration of the constipation? (It may have been a

problem from birth)
 What do parents mean
constipation? (Children do not have
a bowel movement more than 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)

Normal Hirschsprung Disease

If a gloved finger is inserted into the With aganglionic disease, the rectum is
rectum of a child with true constipation, the empty because fecal material cannot pass
examining finger will touch hard, caked into the rectum through the obstructed
stool. portion.
DIAGNOSTIC TEST
 A barium enema is generally ordered to substantiate the diagnosis. The
barium will outline on x-ray film the narrow, nerveless portion and the
proximal distended portion of the bowel

 Biopsy of the affected segment to show the lack of innervations or by

anorectal manometry (a technique to test the strengthor innervations of
the internal rectal sphincter by inserting a balloon catheter into the rectum
and measuring the pressure exerted against it.

MANAGEMENT

SOAVE PULL THROUGH OPERATION

Repair of aganglionic megacolon involves dissection and removal of affected
section, with anastomosis of the intestine (termed a pull-through operation)
Two stage surgery:
 Temporary colostomy

 Bowel repair at 12 to 18 months of age

*After the final surgery, the children should have functioning, normal bowel. In the
few instances in which the anus is deprived of nerve endings, a permanent
colostomy will established.

NURSING DIAGNOSIS
 Constipation related to reduced bowel function
 Imbalanced nutrition, less than body requirements, related to reduced
bowel function
BACKGROUND OF THE DISEASE
Anorectal Malformation-are birth
defects (problems that happen as a
fetus is developing during
pregnancy). With this defect, the
anus and rectum (the lower end of
the digestive tract) do not develop
properly. "Ano" refers to the anus
(the opening at the end of the large
intestine through which stool passes
when a baby has a bowel
movement) "Rectal" refers to the
rectum (the area of the large
intestine just above the anus)

With an anorectal malformation, several abnormalities can occur, including the

following:
 a membrane may be present over  the rectum may connect to a part
the anal opening of the urinary tract or the
 the rectum may not connect to the reproductive system through an
anus (imperforate anus) abnormal passage called a fistula
Diagnostic test: Abdominal ultrasound/sonography and xray

MANAGEMENT
Treatment may depend on the ff:
 the extent of the problem
 the overall health of the baby and the medical history
 parental opinion and preference
 the opinion of the physicians involved in the baby's care
 expectations for the course of the disease
The majority of babies with anorectal malformation will need to have surgery to
correct the problem. The type and number of operations necessary depends on
the type and extent of abnormality the baby has, including the following:
 Narrow anal passage - Babies who have the type of malformation that
causes the anal passage to be narrow may not need an operation. A
procedure known as anal dilatation may be done periodically to help
stretch the anal muscles so stool can pass through it easily. However, if
the anal opening is positioned wrongly, an operation may be neeeded to
correctly relocate the anal opening.
 Anal membrane - Babies with this type of malformation will have the
membrane removed during surgery. Anal dilatations may need to be done
 afterward to help prevent any narrowing of the anal passage that is
present.
 Lack of rectal/anal connection, with or without a fistula -These babies may
need a series of operations in order to have the malformation repaired.

IMPERFORATE ANUS

Imperforate Anus is stricture of anus. It is

congenital (present from birth) defect in
which the opening to the anus is missing or
blocked.

Etiology/ cause
The problem is caused by abnormal
development of the fetus. In week 7 of
intrauterine life, the upper bowel elongates
to pouch and combine with a pouch
invaginating form the perineum

Clinical findings
 It is a relatively common condition that occurs in about 1 out of 5,000
infants.
 Most common in boys

Sign and symptoms

 Anal opening very near the  Stool passes out of the

vaginal opening in girls vagina, base of penis,
 Missing or misplaced opening scrotum, or urethra
to the anus  Swollen belly area
 No passage of first stool
within 24 - 48 hours after birth

Diagnostic/ laboratory
 Prenatal sonogram, Radiograph

Assessment
 Inspection of the newborn’s anal region
 May be revealed because a membrane filled with black meconium
  No wink reflex in the anal area (touching the skin near the rectum should
make it contact)
 Inability to insert rubber catheter into the
rectum

Nursing management
 Anastomosis, Colostomy

NANDA problems
 Imbalanced nutrition, less than body
requirements, related to bowel obstruction
and inability for oral intake
 Impaired tissue integrity at rectum related to
surgical incision
 Risk for impaired parenting related to difficulty in bonding with infant ill
from birth

GASTRO ESOPHAGEAL REFLUX

DISEASE

Gastro esophageal reflux disease is a

condition in which the liquid content of the
stomach regurgitates (backs up or refluxes)
into the esophagus. The liquid can inflame
and damage the lining of the esophagus
although visible signs of inflammation occur
in a minority of patients

Etiology/ cause
 Neuromuscular disturbance in which the cardiac sphincter and the lower
portion of the esophagus spasm and allow easy regurgitation of gastric
contents into the esophagus

 Incompetent cardiac sphincter

 Maybe related to hiatal hernia

Clinical findings
 Starts within 1 week after birth
 Regurgitation starts after feeding

Sign and symptoms

 Effortless vomiting not  heartburn, regurgitation, and
projectile nausea.
  Ulcers, strictures, esophageal
cancer
 Inflammation of larynx and
throat
Diagnostic and laboratory
 Endoscopy (fiberoptic
endoscopy) esophagography
 Esophageal ph testing
 X-ray
Nursing management
 Formula or breast milk with
rice cereal
 Upright position while eating
and an hour after eating
 Laparoscopic or surgical
myotomy (narrowing of the
esophageal sphincter)
 Inflammation and infection of
lungs
 Fluid in the sinuses and
middle ears
 Examination of throat and
larynx
 Esophageal manometry- used
to measure the strength of
the esophageal sphincter
 Ranitidine
 Omeprazole
 Avoid acidic, fatty and
alcoholic foods
 Eat small portion of foods

NANDA problems
Risk for imbalanced nutrition, less than body requirements, related to
regurgitation of food with esophageal reflux

CONSTIPATION

Difficulty of passing hardened stools, may occur in children of

any age

Cause/ etiology
 Lack of fluid intake
 High fiber meals

Clinical findings
 Distressing to children (painful, and may have anal fissures)

 May experience abdominal pain from force of intestinal contractions

 Large and firm stool

Sign and symptoms

 Hard with discomfort in defecating
  Anal fissures (may cause blood in
stool)
 Abdominal pain

Diagnostic and laboratory findings

 Blood occult test (for sign of
bleeding)

Nursing management
 Increase fluid intake
 Diet high in fiber
 Privacy in bathroom
 Determine the cause of stress

NANDA problems

Constipation related to pain from anal fissure and hardened stool

DIARRHEA

Frequent bowel evacuation or the passage of abnormally soft of liquid feces

Etiology/cause
 Caused by virus which is the major
cause of infant gastroenteritis

 Common viral pathogens : rotavirus,

adenovirus

 Common bacterial pathogens ;

campylobacter jejuni, salmonella, giardia
lamblia and clostridium difficile

 Acute associated by infection

 Chronic associated with malabsorption and inflammatory cause

Sign and symptoms

 Frequency- unlimited number

 Color- green
 Effort of expulsion- effortless; may be
explosive
 pH- less than 7 (acidic)
 Odor- sweet or foul
 Occult blood- positive; blood may be overt
  Reducing saubstances- positive

Assessment (mild diarrhea)

 Anorectic and irritable  Warm skin

 Episodes of diarrhea 2-10  Dry mouth
loose watery  Rapid pulse
 With fever (38.4-39)

Assessment (severe diarrhea)

 39.5-40 temperature  Depressed fontanelle, sunken

 Pulse and respiration are eyes and poor skin turgor
weak and rapid  Elevated hemoglobin and
 Pale and cool skin hematocrit because of
 May appear apprehensive, dehydration
listless and lethargic  Loss in body weight

Therapeutic management

 Oral rehydration solution

 Rest the GI tract
 Breastfeeding
 Zinc administration (zinc deficiencies)
 Antibiotic therapy

NANDA problems

Deficient fluid volume related to loss of fluid through diarrhea

Risk for impaired skin integrity related to presence of diarrheal stool on skin

APPENDICITIS

Appendicitis is a condition characterized by inflammation of the

appendix. It is classified as a medical emergency and many cases require
removal of the inflamed appendix, either by laparotomy or laparoscopy.
Untreated, mortality is high, mainly because of peritonitis and shock

 First visible during week 8

 Function Unknown
 Most likely caused by luminal obstruction

ETIOLOGY:

 Fecal material
  Parasite

Signs and symptoms

For the most part symptoms related to disturbed function of bowels. Pain
first, vomiting next and fever last has been described as classic presentation of
acute appendicitis. Pain starts mid abdomen, and except in children below 3
years, tends to localize in right iliac fossa in a few hours. This pain can be elicited
through various signs. Signs include localized findings in the right iliac fossa. The
abdominal wall becomes very sensitive to gentle pressure (palpation). Also, there
is severe pain on suddenly releasing a deep pressure in lower abdomen rebound
tenderness. In case of a retrocecal appendix, however, even deep pressure in
the right lower quadrant may fail to elicit tenderness (silent appendix), the reason
being that the cecum, distended with gas, prevents the pressure exerted by the
palpating hand from reaching the inflamed appendix. Similarly, if the appendix
lies entirely within the pelvis, there is usually complete absence of the abdominal
rigidity. In such cases, a digital rectal examination elicits tenderness in the
rectovesical pouch. Coughing causes point tenderness in this area (McBurney's
point) and this is the least painful way to localize the inflamed appendix. If the
abdomen on palpation is also involuntarily guarded (rigid), there should be a
strong suspicion of peritonitis requiring urgent surgical intervention.

Diagnostics

Diagnosis is based on patient history (symptoms) and physical

examination backed by an elevation of neutrophilic white blood cells. Histories
fall into two categories, typical and atypical. Typical appendicitis usually includes
abdominal pain beginning in the region of the umbilicus for several hours,
associated with anorexia, nausea or vomiting. The pain then "settles" into the
right lower quadrant, where tenderness develops. Atypical histories lack this
typical progression and may include pain in the right lower quadrant as an initial
symptom. Atypical histories often require imaging with ultrasound and/or CT
scanning.[23] A pregnancy test is vital in all women of child bearing age, as
ectopic pregnancies and appendicitis present with similar symptoms. The
consequences of missing an ectopic pregnancy are serious, and potentially life
threatening. Furthermore the general principles of approaching abdominal pain in
women (in so much that it is different from the approach in men) should be
appreciated.

Blood Test Most patients suspected of having appendicitis would be asked to do

a blood test. 50% of the time, the blood test may be normal, so it is not fool proof
in diagnosing appendicitis.
Two form of blood tests are commonly done: FBC (Full blood count) or CBC
(Complete blood count), is an inexpensive and commonly requested blood test. It
involves measuring the blood for its richness in red blood cells as well as the
number of the various white blood cell constituents in it. The number of white
cells in the blood is a usually less than 10,000 cells per cubic millimeter. An
abnormal rise in the number of white blood cells in the blood is a crude indicator
of infection or inflammation going on in the body. Such rise is not specific to
appendicitis alone. If it is abnormally elevated, with a good history and
examination findings pointing towards appendicitis, the likelihood of having the
disease is higher. In pregnancy, there may be a normal elevation of white blood
cells, without any infection present.
CRP is an acronym for Cryo-Reactive Proteins. It is an acute phase response
protein produced by the liver in response to any infection or inflammatory
process in the body. Again, like the FBC, it is not a specific test. It is another
crude marker of infection or inflammation. Inflammation at ANY site can lead to
the CRP to rise. A significant rise in CRP with corresponding signs and
symptoms of appendicitis is a useful indicator in the diagnosis of appendicitis.It is
said that if CRP continues to be normal after 72 hours of the onset of pain, it is
likely that the appendicitis will resolve on its own without intervention. A
worsening CRP with good history is a sure signal fire of impending perforation or
rupture and abscess formation

Urine Test: Urine test in appendicitis is usually normal. It may however show
blood if the appendix is rubbing on the bladder, causing irritation A urine test or
urinalysis is compulsory in women, to rule out pregnancy in appendicitis, as well
to help ensure that the abdominal pain felt and thought to be acute appendicitis is
not in fact, due to ectopic pregnancy.

X – Ray In 10% of patients with appendicitis, plain abdominal x-ray may

demonstrate hard formed feces in the lumen of the appendix (Fecolith). It is
agreed that the finding of Fecolith in the appendix on X – ray alone is a reason to
operate to remove the appendix, because of the potential to cause worsening
symptoms. In this respect, a plain abdominal X-ray may be useful in the
diagnosis of appendicitis, though plain abdominal x- ray is no longer requested
routinely in suspected cases of appendicitis. An abdominal X – ray may be done
with a barium enema contrast to diagnose appendicitis. Barium enema is whitish
toothpaste like material that is passed up into the rectum to act as a contrast. It
will usually fill the whole of the large bowel. In normal appendix, the lumen will be
present and the barium fills it up and is seen when the x-ray film is shot. In
appendicitis, the lumen of the appendix will not be visible on the barium film.

NURSING MANAGEMENT

The treatment begins by keeping the patient from eating or drinking in

preparation for surgery. An intravenous drip is used to hydrate the patient.
Antibiotics given intravenously such as cefuroxime and metronidazole may
be administered early to help kill bacteria and thus reduce the spread of
infection in the abdomen and postoperative complications in the abdomen
or wound.
 NANDA PROBLEMS

IMBALANCED NUTRITION ,LESS THAN BODY REQUIREMENTS

RELATEDTO MALABSORPTION OF FOOD

PROGNOSIS

 Most appendicitis patients recover easily with surgical treatment, but

complications can occur if treatment is delayed or if peritonitis occurs.
Recovery time depends on age, condition, complications, and other
circumstances, including the amount of alcohol consumption, but usually
is between 10 and 28 days. For young children (around 10 years old), the
recovery takes three weeks.
 The real possibility of life-threatening peritonitis is the reason why acute
appendicitis warrants speedy evaluation and treatment. The patient may
have to undergo a medical evacuation. Appendectomies have
occasionally been performed in emergency conditions (i.e., outside of a
proper hospital), when a timely medical evaluation was impossible.

INFLAMMATORY BOWEL DISEASE

ULCERATIVE COLITIS- inflammation of distal colon and rectum

Common manifestation: Diarrhea and malnutrition
Complication: Hemorrhage from bowel perforation, peritonitis or formation of
fistula between bowel and loops
CROHN’S DISEASE – inflammation of segments of the intestine which involves
terminal ileum
COBBLE STONE- colon wall becomes thickened and inflamed.
Assessment: Diarrhea and steatorrhea develops, melena, recurring fever, growth
failure
Diagnostic/Laboratory procedure:
-colonoscopy
- Barium enema
- biopsy
Management: Enteral and Parenteral nutrition
High protein, carbohydrate and vitamin diet
Drugs: prednisone (corticosteroid), sulfasilizine (azulfidine sulfamide and salicylic
acid), azathioprine (imuran immunosuppressive agent), monoclonal antibodies
(infiximab)

PEPTIC ULCER DISEASE

A peptic ulcer may be referred to as a gastric, duodenal or esophageal

ulcer depending on its location. A person who has a peptic ulcer, depending on
its location. A person who has an peptic ulcer has peptic ulcer has an peptic
ulcer disease. A peptic ulcer is an excavation (hollowed-out area) that forms in
the mucosal wall of the stomach, in the pylorus (the opening between the
stomach and duodenum) in the duodenum (the first part of small intestine) or in
the esophagus. Erosion of a circumscribed area of mucous membrane is the
cause. This erosion may extend as deeply as the muscle layers or through the
muscle of the peritoneum. Peptic ulcers are more likely to be in duodenum than
in the stomach. Chronic gastric ulcers tend to occur in the lesser curvature of the
stomach, near the pylorus. Peptic ulcer disease occur with the greatest
frequency in people between 40 and 60 years of age. It is relatively uncommon in
women of childbearing age but it has been observed in children and infant. In
addition, excessive secretion of HCI in the stomach may contribute to the
formation of peptic ulcers and stress may also be a contributing factor. The
ingestion of milk and caffeinated beverages, smoking and alcohol also may
increase HCl. Stress and eating spicy food may make peptic ulcer worse. Some
other factors like genetic tendency, NSAIDS use and cigarettes can be
associated.

ETIOLOGIC AGENT: Helicobacter pylori

ASSESSMENT:
Neonate: hematemesis (blood in vomitus), Melena (blood in stool), rupture ulcer
leads to respiratory distress, abdominal distention, vomiting, cardiovascular
collapse (if extensive).
Toddler: Anorexia and vomiting
Pre-school: local pain: mild, severe, colicky or continous.
School-aged: gnawing or aching on epigastric area, vomiting, epigastric
tenderness.
Laboratory procedure: fiberoptic endoscopy – most reliable diagnostic test to
confirm peptic ulcer disease.

Treatment management: children: Cimetidine (Targamet)

Adult: Amoxicillin/Clarythromycin (Biaxin)
Nursing Dx: Pain r/t ulceration in intestinal tract

NECROTIZING ENTEROCOLITIS
BACKGROUND
– most commonly occurring gastrointestinal emergency in preterm
infants
– leading cause of emergency surgery in neonates
– overall incidence: 1-5% in most NICU’s
– most common in VLBW preterm infants
• 10% of all cases occur in term infants
ETIOLOGY
• W –with Infections
• I - ischemia
• P - premature
• E – enteral feeding
• S – shock

SIGNS AND SYMPTOMS: PUNASAN mo nah

• P – period of apnea
• U – undigested milk of > 2ml
• N – not normal BP
• A – aw! Stool = positive occult blood
• S – stomach not full empty
• A – abdomen distended
• N – not stabilized temperature

LABORATORY/DX
• MEASUREMENT OF ABDOMINAL GIRTH IS INCREASED
• XRAY

NURSING MANAGEMENT
• BREAST FEEDING IS DISCONTINUED OR FORMULA FEEDINGS
• IV OR TOTALPARENTERAL NUTRITION IS MAINTAINED
• HANDLE THE ABDOMEN GENTLY TO LESSEN THE POSSIBILITY OF
PERFORATION
• TEMPORARY COLOSTOMY TO PROVIDE BOWEL FUNCTION

PROGNOSIS

• Typical recovery from NEC if medical, non-surgical treatment succeeds,

includes 10–14 days or more without oral intake and then demonstrated
ability to resume feedings and gain weight. Recovery from NEC alone may
be compromised by co-morbid conditions that frequently accompany
prematurity. Longterm complications of medical NEC include bowel
obstruction and anemia.
• Despite a significant mortality risk, long-term prognosis for infants
undergoing NEC surgery is improving, with survival rates of 70-80%.
"Surgical NEC" survivors are at-risk for complications including short
bowel syndrome, and neurodevelopmental disability.
CELIAC DISEASE
Sensitivity or Abnormal immunologic response to protein, particulary the
gluten factor of protein found in grains, wheat, rye, oats and barley.

STEATORRHEA- bulky, foul-smelling, fatty stools

Deficiency on Fat-soluble vitamins ADEK (vitamins are not absorbed because fat
is not absorbed)

ASSESSMENT:
Characteristics: Anorexic, irritable, appears skinny, splindly extremities, wasted
buttocks but face is plump and well-rounded
Clinical symptoms: bulky stools, malnutrition, distended abdomen, anemia
between 6-18 months of age

Diagnostic/laboratory test:
- glucose tolerance test- poor absorption
- stool analysis- increase of antibodies
- serum analysis of antibodies – IgA antiglandin antibodies
- endoscopy – biopsy for intestinal mucosa

Treatment Management:
- gluten free diet for life
- water soluble forms of vitamin A and D
- iron folate for anemia

Nursing Diagnosis : imbalance nutrition less than body requirements r/t

malabsorption of food

LACTOSE INTOLERANCE
Lactose intolerance is the inability to digest and absorb lactose (the sugar
in milk) that results in gastrointestinal symptoms when milk or food products
containing milk are consumed. Also caused by reduced or absent activity of
lactase that prevents the splitting of lactose. Lactase deficiency may occur for
one of the three reasons, congenital, secondary or developmental.
Assessment: Abdominal pain, diarrhea and flatulence
Diagnostic/Laboratory procedure: Breath test, blood glucose, stool acidity test
and intestinal biopsy
Management:
- dietary changes- reducing amount of lactose in diet
- avoidance of milk-containing product
- lactase enzyme- caplets or tablets of lactase are available to take with
milk-containing foods.
LEAD POISONING

Lead poisoning (also known as plumbism, colica Pictonum, saturnism,

Devon colic, or painter's colic) is a medical condition caused by increased
levels of the heavy metal lead in the body. Lead interferes with a variety of body
processes and is toxic to many organs and tissues including the heart, bones,
intestines, kidneys, and reproductive and nervous systems. It interferes with the
development of the nervous system and is therefore particularly toxic to children,
causing potentially permanent learning and behavior disorders. Symptoms
include abdominal pain, confusion, headache, anemia, irritability, and in severe
cases seizures, coma, and death.

ETIOLOGY

Routes of exposure to lead include contaminated air, water, soil, food, and
consumer products. Occupational exposure is a common cause of lead
poisoning in adults. One of the largest threats to children is lead paint that exists
in many homes, especially older ones; thus children in older housing with
chipping paint are at greater risk. Prevention of lead exposure can range from
individual efforts (e.g. removing lead-containing items such as piping or blinds
from the home) to nationwide policies (e.g. laws that ban lead in products or
reduce allowable levels in water or soil).
Elevated lead in the body can be detected by the presence of changes in blood
cells visible with a microscope and dense lines in the bones of children seen on
X-ray. However, the main tool for diagnosis is measurement of the blood lead
level; different treatments are used depending on this level. The major treatments
are removal of the source of lead and chelation therapy (administration of agents
that bind lead so it can be excreted).
Humans have been mining and using this heavy metal for thousands of years,
poisoning themselves in the process. Although lead poisoning is one of the
oldest known work and environmental hazards, the modern understanding of the
small amount of lead necessary to cause harm did not come about until the latter
half of the 20th century. No safe threshold for lead exposure has been
discovered—that is, there is no known amount of lead that is too small to cause
the body harm.

Signs and symptoms

Lead poisoning can cause a variety of symptoms and signs which vary
depending on the individual and the duration of lead exposure. Symptoms are
nonspecific and may be subtle, and someone with elevated lead levels may have
no symptoms.Symptoms usually develop over weeks to months as lead builds up
in the body during a chronic exposure, but acute symptoms from brief, intense
exposures also occur Symptoms from exposure to organic lead, which is
probably more toxic than inorganic lead due to its lipid solubility, occur
rapidly.Poisoning by organic lead compounds has symptoms predominantly in
the central nervous system, such as insomnia, delirium, cognitive deficits, tremor,
hallucinations, and convulsions.
The classic signs and symptoms in children are loss of appetite, abdominal pain,
vomiting, weight loss, constipation, anemia, kidney failure, irritability, lethargy,
learning disabilities, and behavior problems.
Diagnosis

Blood film examination may reveal basophilic stippling of red blood cells (dots in
red blood cells visible through a microscope), as well as the changes normally
associated with iron-deficiency anemia (microcytosis and
hypochromasia).However, basophilic stippling is also seen in unrelated
conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin)
and folate deficiencies.
Exposure to lead also can be evaluated by measuring erythrocyte protoporphyrin
(EP) in blood samples EP is a part of red blood cells known to increase when the
amount of lead in the blood is high, with a delay of a few weeks.Thus EP levels in
conjunction with blood lead levels can suggest the time period of exposure; if
blood lead levels are high but EP is still normal, this finding suggests exposure
was recent.However, the EP level alone is not sensitive enough to identify
elevated blood lead levels below about 35 μg/dL.Due to this higher threshold for
detection and the fact that EP levels also increase in iron deficiency, use of this
method for detecting lead exposure has decreased.
Blood lead levels are an indicator mainly of recent or current lead exposure, not
of total body burden. Lead in bones can be measured noninvasively by X-ray
fluorescence; this may be the best measure of cumulative exposure and total
body burden. Fecal lead content that is measured over the course of a few days
may also be an accurate way to estimate the overall amount of childhood lead
intake. This form of measurement may serve as a useful way to see the extent of
oral lead exposure from all the diet and environmental sources of lead.

NANDA PROBLEMS
SITUATIONAL LOW SELF ESTEEM REALATED TO CHILDS POISONING
NURSING MANAGEMENT
 Child’s BLL >10g/dL
 Provide educational interventions to the
parent/caregiver.
 Communicate assessments and interventions to the health care provider
 Monitor timeliness and levels of follow-up blood lead tests
 Initiate appropriate interventions if level rises
 Provide ongoing evaluation to
see that BLLs decline and
outcome measures are
achieved.
PROGNOSIS
 Outcome is related to the extent and duration of lead exposure.Effects of
lead on the physiology of the kidneys and blood are generally reversible;
its effects on the central nervous system are not. While peripheral effects
in adults often go away when lead exposure ceases, evidence suggests
that most of lead's effects on a child's central nervous system are
irreversible. Children with lead poisoning may thus have adverse health,
cognitive, and behavioral effects that follow them into adulthood.
Omphalocele - Is a protrusion of abdominal contents through the abdominal wall
at the point of the junction of the umbilical cord and the abdomen.
The herniated organs are usually the intestines, but they may include the
stomach and liver. Usually covered and contained by a thin transparent layer of
amnion and chorion with the umbilical cord protruding from the exposed sac.

ETIOLOGY
This condition occurs because at approximately weeks 6-8 of intrauterine life, the
fetal abdominal contents, are extruded from the abdomen into the base of the
umbilical cord.
Normally at 7-10 weeks when the abdomen has enlarged sufficiently, the
intestines return to the abdomen. Omphalocele occurs when the abdomen fails to
return the usual way.

Fetal omphalocele may occur in conjunction with other conditions, including

cardiac or genitourinary abnormalities, neural tube defects or twisted intestines,
as well as the genetic defects trisomy 13 or 18. In addition, omphalocele may
also be associated with Beckwith-Wiedermann Syndrome or Pentalogy of
Cantrell. For this reason, fetuses with omphalocele are carefully evaluated to rule
out these abnormalities

SIGNS AND SYMPTOMS

An omphalocele can be clearly seen, because the abdominal contents stick out
(protrude) through the belly button area.
There are different sizes of omphaloceles. In small ones, only the intestines stick
out. In larger ones, the liver or spleen may stick out of the body as well.

DIAGNOSTICS

The diagnosis of omphalocele is confirmed by ultrasound. Because of the

increased risk of an associated anomaly, a targeted ultrasound will be performed
by a perinatologist. Omphaloceles can be associated with
some chromosomal abnormalities (up to 30 percent)
so an amniocentesis may be offered. An ultrasound of your baby's heart (fetal
echocardiogram) may also be recommended.

These babies will be monitored closely throughout the pregnancy. Ultrasounds

will be done every two to four weeks to assess how well the fetus is growing, the
amniotic fluid volume and fetal well-being. You will be instructed on daily fetal
movement counting at about 26 weeks' gestation. Non-stress tests (a recording
of the baby's heart rate while you are sitting and pressing a button each time the
baby moves) may be scheduled at around 32 weeks' gestation.

Biophysical profiles (BPP) may also be scheduled weekly. The BPP is an

ultrasound that monitors amniotic fluid volume, the baby's breathing movements,
and movements of the extremities along with the nonstress test. Also Elevated
AFP (Alpha-feto protein) may be an indicative of omphalocele.

The method of delivery will be discussed as the time gets closer. The method of
delivery is dependent on the size of the omphalocele. If the size is quite large
and especially if the liver is involved, the doctor may prefer to do a cesarean
section to avoid the risk of injury to the liver. Otherwise, the preferred method of
delivery is vaginal.
Other reasons to do a C-section for a baby with an omphalocele include those
reasons that would affect a routine pregnancy. Labor may be induced or allowed
to start on its own.

TREATMENT

Omphaloceles are repaired with surgery, although not always immediately. A sac
protects the abdominal contents and allows time for other more serious problems
(such as heart defects) to be dealt with first, if necessary. To fix an omphalocele,
the sac is covered with a special man-made material, which is then stitched in
place. Slowly, over time, the abdominal contents are pushed into the abdomen.
When the omphalocele can comfortably fit within the abdominal cavity, the man-
made material is removed and the abdomen is closed. Sometimes the
omphalocele is so large that it cannot be placed back inside the infant's
abdomen. The skin around the omphalocele grows and eventually covers the
omphalocele. The abdominal muscles and skin can be repaired when the child is
older to achieve a better cosmetic outcome.

PROGNOSIS

Complete recovery is expected after surgery for an omphalocele. However,

omphaloceles often occur with other birth defects. How well a child does
depends on which other conditions the child also has.
If the omphalocele is identified before birth, the mother should be closely
monitored to make sure the unborn baby remains healthy. Plans should be made
for careful delivery and immediate management of the problem after birth. The
baby should be delivered in a medical center that is skilled at repairing
omphaloceles. The baby's outcome is improved if he or she does not need to be
taken to another center for further treatment.
Parents should consider screening their unborn baby for other genetic problems
that are associated with this condition.

NURSING DIAGNOSIS:
 Impaired skin integrity related to protrusion in the umbilicus
 Imbalanced nutrition: less than body requirements
 Risk for constipation
 Risk for infection
Gastroschisis - Gastroschisis (also called paraomphalocele) represents a
congenital defect characterized by a defect in the anterior abdominal wall through
which the intestinal contents freely protrude. There is no overlying sac and the
size of the defect is usually less than 4 cm. The abdominal wall defect is located
at the junction of the umbilicus and normal skin, and is almost always to the right
of the umbilicus

ETIOLOGY

High-risk pregnancies such as those complicated by infection, young maternal

age, smoking, drug abuse, or anything that contributes to low birth weight can
increase the incidence of gastroschisis, which is more frequent in newborns who
are small for gestational age. Whether the intrauterine growth retardation can
facilitate the apparition of gastroschisis or the abdominal wall defect impairs fetal
growth is not clear yet.

A change in paternity (childbearing with different fathers) has been implicated as

a risk factor in a recent study, suggesting that the immune system of the mother
may play a role in the development of gastroschisis.

Gastroschisis as a stand-alone congenital defect is usually inherited in

an autosomal recessive manner. It may begin as a sporadic mutation, can be
associated with non-genetic congenital disorders, but has also been observed to
be autosomal dominant.

The malformation is slightly more frequent in males than females. The frequency
of gastroschisis is associated with young maternal age, and low number of
gestations. This abnormality is seen in ratio of 1:10,000 and is usually detected
before birth.
It has been reported that the incidence of gastroschisis has increased in recent
years.

SIGNS AND SYMPTOMS

> Lump in the abdomen

> Intestine sticks through the abdominal wall near the umbilical cord

DIAGNOSTICS

Physical examination of the infant is enough for the health care provider to
diagnose gastroschisis. The baby will have problems with movement and
absorption in the gut, because the unprotected intestine is exposed to irritating
amniotic fluid.
The mother may have shown signs of too much amniotic fluid (polyhydramnios).
A prenatal ultrasound often identifies the gastroschisis.

TREATMENT

If gastroschisis is found before birth, the mother will need special monitoring to
make sure her unborn baby remains healthy. Plans should be made for careful
delivery and immediate management of the problem after birth.
Treatment for gastroschisis is surgery to repair the defect. A surgeon will put the
bowel back into the abdomen and close the defect, if possible. If the abdominal
cavity is too small, a mesh sack is stitched around the borders of the defect and
the edges of the defect are pulled up. Over time, the herniated intestine falls back
into the abdominal cavity, and the defect can be closed.
Other treatments for the baby include nutrients by IV and antibiotics to prevent
infection. The baby's temperature must be carefully controlled, because the
exposed intestine allows a lot of body heat to escape.

PROGNOSIS

Current advances in surgical techniques and intensive care management for

neonates have increased the survival rate to 90%, in adequate settings. The
possibility of prenatal diagnosis either through echosonogram or any other
method available allows the mother to be referred to an adequate center where a
caesarean section or induced natural birth can be performed before term (as
natural birth is recommended and just as safe as with a normal baby), preferably
within 2 weeks of term, and allow the immediate surgery to be performed on the
newborn.
The general procedure for gastroschisis is to simply tuck the protruding organs
back into the opening and apply a belly band pressure until the wound heals
itself. New advances have been pioneered in repairing the protruding bowel by
placing a protective "silo" around the intestine outside the abdomen, then slowly
pressuring the herniated intestine into the abdominal cavity. This new procedure
allows for the bowel to return to its intended shape and location without further
traumatizing the infant's viscera with undue internal pressure. The main cause for
lengthy recovery periods in patients is the time taken for the infants' bowel
function to return to normal.
The morbidity is closely related to the presence of other malformations and
complications of the wound or the intestine. Patients frequently require more than
one surgery.
NURSING DIAGNOSIS

 Impaired skin integrity related to protrusion in the abdomen

 Imbalanced nutrition: less than body requirements
 Risk for constipation
 Risk for infection
BACKGROUND

Biliary Atresia - is a rare condition in newborn infants in which the common bile
duct between the liver and the small intestine is blocked or absent. If
unrecognized, the condition leads to liver failure, as the liver is still able to
conjugate bilirubin, and conjugated bilirubin is unable to cross the blood-brain
barrier.

ETIOLOGY

The cause of biliary atresia is UNKNOWN. The two types of biliary atresia
appear to be a “fetal” form, which arises during fetal life and is present at the time
of birth, and a “perinatal” form, which is more typical and does not become
evident until the second to fourth week of life.

An important fact is that biliary atresia is not an inherited disease. Cases of biliary
atresia do not run in families; identical twins have been born with only one child
having the disease. Biliary atresia is most likely caused by an event occurring
during fetal life or around the time of birth.

SIGNS AND SYMPTOMS

Newborns with this condition may appear normal at birth. However, jaundice (a
yellow color to the skin and mucous membranes) develops by the second or third
week of life. The infant may gain weight normally for the first month, but then will
lose weight and become irritable, and have worsening jaundice.
Other symptoms may include:
 Dark urine  Pale or clay-colored stools
 Enlarged spleen  Slow growth
 Floating stools  Slow or no weight gain
 Foul-smelling stools

DIAGNOSTICS

 The health care provider will perform a physical exam, which includes feeling
the patient's belly area. The doctor may feel an enlarged liver.

Tests to diagnose biliary atresia include:

 Abdominal x-ray cholescintigraphy, to help
 Abdominal ultrasound determine
 Blood tests to check total and whether the bile ducts and
direct bilirubin levels gallbladder are working properly
 Hepatobiliary iminodiacetic acid  Liver biopsy to determine the
(HIDA) scan, also called severity of cirrhosis or to rule out
other causes of jaundice
 X-ray of the bile ducts (cholangiogram)

TREATMENT

Surgery - If biliary atresia appears to be the cause of the jaundice in the

newborn, the next step is surgery. At the time of surgery the bile ducts can be
examined and the diagnosis confirmed. For this procedure, the infant is sedated.
While the infant is asleep, the surgeon makes an incision in the abdomen to
directly examine the liver and bile ducts. If the surgeon confirms that biliary
atresia is the problem, a Kasai procedure will usually be performed on the spot.

The Kasai Procedure

Biliary Atresia occurs within the first two
months of life when there is a blockage
of the bile duct connecting the liver to
the gut. Eventually the blockage will
cause a buildup of bile in the liver that
leads to damage and scarring of the
liver cells, and if untreated, this scarring
will cause liver failure and the need for
liver transplantation. The Kasai
operation attempts to reconstruct the
bile duct with a loop of intestine. In the
Kasai procedure the small intestine is
attached to the liver directly so that the
bile may drain. The Children's Hospital
sees six to ten new patients with biliary
atresia every year and the Kasai
procedure is the most effective treatment available.
While the Kasai procedure allows some children who would otherwise not be
able to live normal healthy lives return to normal growth and activities, most
patients with this disease will still eventually need a Liver transplant.

Liver transplant. If the Kasai procedure is not successful, the infant usually will
need a liver transplant within the first 1 to 2 years of life. Children with the fetal
form of biliary atresia are more likely to need liver transplants—and usually
sooner—than infants with the typical perinatal form. The pattern of the bile ducts
affected and the extent of damage can also influence how soon a child will need
a liver transplant. (More about liver transplantation follows.)

PROGNOSIS

Timely Kasai portoenterostomy (e.g. < 60 postnatal days) has shown better
outcomes. Nevertheless, a considerable number of the patients, even if Kasai
portoenterostomy has been successful, eventually undergo liver transplantation
within a couple of years after Kasai portoenterostomy.
Recent large volume studies from Davenport et al. (Ann Surg, 2008) show that
age of the patient is not an absolute clinical factor affecting the prognosis. In the
latter study, influence of age differs according to the disease etiology—i.e.,
whether isolated BA, BASM (BA with splenic malformation ), or CBA(cystic biliary
atresia).
It is widely accepted that corticosteroid treatment after a Kasai operation, with or
without choleretics and antibiotics, has a beneficial effect on the postoperative
bile flow and can clear the jaundice; but the dosing and duration of the ideal
steroid protocol have been controversial ("blast dose" vs. "high dose" vs. "low
dose"). Furthermore, it has been observed in many retrospective longitudinal
studies that steroid does not prolong survival of the native liver or transplant-free
survival. Davenport at al. also showed (hepatology 2007) that short-term low-
dose steroid therapy following a Kasai operation has no effect on the mid- and
long-term prognosis of biliary atresia patients.

NURSING DIAGNOSIS

 Neonatal Jaundice
 Imbalanced nutrition: less than body requirements
 Impaired skin integrity
 Delayed development
BACKGROUND

Cirrhosis - is a condition in which the liver slowly deteriorates and malfunctions

due to chronic injury. Scar tissue replaces healthy liver tissue, partially blocking
the flow of blood through the liver. Scarring also impairs the liver’s ability to
control infections remove bacteria and toxins from the blood process nutrients,
hormones, and drugs
make proteins that regulate blood clotting produce bile to help absorb fats—
including cholesterol—and fat-soluble vitamins A healthy liver is able to
regenerate most of its own cells when they become damaged. With end-stage
cirrhosis, the liver can no longer effectively replace damaged cells. A healthy liver
is necessary for survival.

ETIOLOGY

Cirrhosis in children often stems from a wide variety of liver disorders, including
(but certainly not limited to):
 Hepatitis B and C  Bile duct diseases:
 Autoimmune hepatitis  Biliary artresia
 Inherited diseases:  Sclerosing cholangitis
 Glycogen storage disease  Congenital hepatic fibrosis
 Tyrosinemia  Choledochal cysts
 Wilson disease  Drugs and toxins:
 Alpha1-antitrypsin deficiency  Isoniazid
 Cystic fibrosis  Methotrexate
 Excess vitamin A
 Fatty liver disease

SIGNS AND SYMPTOMS

As the disease progresses, bile flow is blocked or stopped, and jaundice (yellow
skin or eyes) appears. The same bile pigment, bilirubin, which is responsible for
the yellow skin tones of jaundice can turn urine dark. Bleeding and bruising can
occur more easily and take longer to heal. Other later symptoms, some due to
complications, include:

 Reddened palms  Water retention and swelling in

 Loss of body hair the legs and abdomen
 Enlarged liver  Vomiting blood
 Enlarged spleen  Itching
 Appearance of thin, purplish-red,  Abdominal infections
spidery looking blood vessels on  Forgetfulness or confusion
the skin, especially around the  Tremors
navel  Inability to fully process drugs
 Enlarged, twisted, thin-walled that can rupture and lead to life-
blood vessels called varices in threatening bleeding
the esophagus and/or stomach  Liver cancer

DIAGNOSTICS

 Blood Tests – to assess how well the liver is working and determine a cause
 CT Scan, Ultrasound, MRI or Liver/Spleen Scan to identify changes in the
liver
 Liver Biopsy – analyzing a sample of liver tissue removed via a thin needle
inserted into the liver

TREATMENT

In general, cirrhosis cannot be cured or reversed. Treatment for cirrhosis

depends on the cause of the disease and whether complications are present.
The goals of treatment are to slow the progression of scar tissue in the liver
and prevent or treat the complications of the disease. Hospitalization may be
necessary for cirrhosis with complications.

A liver transplant is considered when complications cannot be controlled by

treatment. Liver transplantation is a major operation in which the diseased liver is
removed and replaced with a healthy one from an organ donor. A team of health
professionals determines the risks and benefits of the procedure for each patient.
Survival rates have improved over the past several years because of drugs that
suppress the immune system and keep it from attacking and damaging the new
liver.

PROGNOSIS

When the complications developed are not controlled with the help of the
treatment, liver transplant is recommended. Liver transplant dramatically
improves the cirrhosis of the liver prognosis. Cirrhosis life expectancy is about 15
to 20 years when cirrhosis is detected during the initial stage. Life expectancy
decreases to about 6 to 10 years, when cirrhosis is detected in second stage. But
these patients have enough time and can opt for liver transplant. They have
various treatment options and medicines which can help control the
advancement of the disease. When cirrhosis of the liver is diagnosed during the
last stage, the life expectancy is very poor, about 1-3 years, depending upon the
patient's overall health, prompt use of advanced treatment, etc.

The Child-Pugh Classification

The Child-Pugh classification is a scoring system which helps determine the

cirrhosis of the liver prognosis. Here, scoring is based upon several factors:
albumin, ascites, total bilirubin, prothrombin time, and encephalopathy, as
follows:

Name of the Factor Score: 1 Point Score: 2 Score: 3

Points Points
Serum Albumin (g/dL) Higher than 3.0 - 3.5 Lower than 3.0
3.5
Serum Bilirubin (mg/dL) Lower than 2.0 2.0 - 3.0 Higher than
3.0
Prothrombin time 1 - 4 4-6 Higher than
(seconds) 6.0
Ascites None Moderate Severe
Encephalopathy None Mild Severe

The three classes are formed and their scores are:

 Class A - score of 5 - 6
 Class B - score of 7 - 9
 Class C - score higher than 9
 Patients with a score of 10 or more (in the Class C category): Have a
prognosis with 1 year survival being about 50%.
 Patients with Class A or B: Have a better prognosis of 5-years, with a
survival rate of 70%- 80%.
 Refractory ascites, albumin < 3.2 gm/l, and an episode of SBP
(spontaneous bacterial peritonitis): A one-year survival of 50% or less.
Studies show that liver cirrhosis affects men slightly more often than women and
each year, thousands of people die because of liver cirrhosis. I hope you find the
above information regarding cirrhosis of the liver prognosis helpful. With healthy
diet, exercises and healthy eating habits, you may succeed in keeping deadly
diseases away.

NURSING DIAGNOSIS:

 Excess fluid volume related to compromised regulatory system

 Impaired skin integrity
HERNIAS

 It is a protrusion of a portion of an organ or organs through an abnormal

opening.
 The danger from herniation arises when the organ protruding through the
opening is constricted to the extent that circulation is impaired or when the
protruding organs enroach on and the impair the function of other
structures.

Incarcerated hernia – a hernia that cannot be reduced easily

Strangulated hernia – a hernia in which the blood supply to the herniated organ
is impaired.

Types of Hernia
DIAPHRAGMATIC HERNIA

A diaphragmatic hernia is a birth defect in which there is an abnormal opening in

the diaphragm, the muscle that helps you breathe. The opening allows part of the
organs from the belly (stomach, spleen, liver, and intestines) to go up into the
chest cavity near the lungs.
CAUSES
A diaphragmatic hernia is caused by the improper joining of structures during
fetal development. As a result, the abdominal organs such as the stomach, small
intestine, spleen, part of the liver, and the kidney appear in the chest cavity. The
lung tissue on the affected side is thus not allowed to completely develop.
Congenital diaphragmatic hernia is seen in 1 out of every 2,200 to 5,000 live
births. Most affect the left side. Having a parent or sibling with the condition
slightly increases your
risk.

SIGNS AND SYMPTOMS

 Mild to severe respiratory  Bluish colored skin due to lack
distress within a few hours of oxygen
after birth  Abdomen generally appears
 Tachypnea, tachycardia sunken
 Cyanosis  May lead to R to L shunting
 Absent breath sound in through the foramen ovale in
affected area the heart and can cause
patent ductus arteriosus
DIAGNOSTIC TESTS
 Chest Ultrasonography – may excessive amounts of
show abdominal organs in the amniotic fluid
chest cavity  Fetoscopy
 Pelvic Ultrasonography (for
mother) – may show

NURSING MANAGEMENT
Pre-operative:
1. Reduce stimulation – environmental/ care activities
2. Prompt recognition, resuscitation and stabilization
3. Maintain suction, oxygen and IV fluids
4. Positioning – head up
5. Administer medication as ordered.

Post-operative;
1. Carry out routine post operative care and observation
2. Relieve pain and provide comfort
3. Support family because this is a critical illness

THERAPEUTIC MANAGEMENT
 Supportive treatment of respiratory distress and correction of acidosis,
possible use of endotracheal intubation, GI decompression
 Surgical reduction of hernia and repair of defect
 - if the defect in the diaphragm is large, an insoluble
polymer(Teflon) patch may be used in reconstruction.
- in infant, abdominal incision may not be closed, it is covered by silicon
elastomer (Silastic) and left to be closed at a later date after the abdomen has
grown.

NURSING DIAGNOSIS
 Risk for ineffetive airway clearance related to displaced bowel
 Risk for imbalanced nutrition related, less than body requirements related
to NPO status

PROGNOSIS
 Congenital diaphragmatic hernia is a very serious disorder. The outcome
of surgery depends on how well your baby's lungs have developed.
Usually the outlook is very good for infants who have enough lung tissue.
 With advances in neonatal and surgical care, survival is now greater than
80%.

HIATAL HERNIA
Hiatal hernia is a condition in which a portion of the stomach protrudes upward
into the chest, through an opening in the diaphragm. The diaphragm is the sheet
of muscle that separates the chest from the abdomen. It is used in breathing.

CAUSES
The cause is unknown, but hiatal hernias may be the result of a weakening of the
supporting tissue. Increasing age, obesity, and smoking are known risk factors in
adults.
Children with this condition are usually born with it (congenital). It is often
associated with gastroesophageal reflux in infants.
Hiatal hernias are very common, especially in people over 50 years old. This
condition may cause reflux (backflow) of gastric acid from the stomach into the
esophagus.

SIGNS AND SYMPTOMS

 Dysphagia  Frequent unexplained
 Failure to thrive respiratory problem
 Vomiting  May cause gastric volvulus
 Neck contortions and obstruction
 Heartburn
DIAGNOSTIC TESTS
 Barium swallow x-ray
 Esophagogastroduodenoscopy (EGD)

NURSING MANAGEMENT
1. Positioning – a baby can be kept in an upright position to help prevent the
condition from reoccurring.
 2. Give medications as ordered. Medication to reduce acid secretion may be
helpful.

THERAPEUTIC MANAGEMENT
 Pharmacologic treatment
 Surgical treatment – laparoscopic surgery

NURSING DIAGNOSIS
 Pain related to indigestion of food
 Imbalanced nutrition, less than body requirements related to limiting of
foods

PROGNOSIS
Most symptoms are alleviated with treatment.

UMBILICAL HERNIA
Umbilical hernias are especially common in infants of African descent, and occur
more in boys. They involve protrusion of intraabdominal contents through a
weakness at the site of passage of the umbilical cord through the abdominal wall.
These hernias often resolve spontaneously. Umbilical hernias in adults are
largely acquired, and are more frequent in obese or pregnant women. Abnormal
decussation of fibers at the linea alba may contribute.

CAUSES
An umbilical hernia in an infant occurs when the muscle through which blood
vessels pass to feed the developing fetus doesn't close completely.
Umbilical hernias are common in infants. They occur slightly more often in
African Americans. Most umbilical hernias are not related to disease. However,
umbilical hernias can be associated with rare conditions such as
mucopolysaccharide storage diseases, Beckwith-Wiedemann syndrome, and
Down syndrome.

SIGNS AND SYMPTOMS

 Noted by inspection and palpation of the abdomen
 About 1 to 2 cm (1/2 to 1inch) in diameter but may be as big as an orange.
 There is a soft swelling over the belly button that often bulges when the
baby sits up, cries, or strains. The bulge may be flat when the infant lies
on the back and is quiet.

DIAGNOSTIC TESTS
 Ultrasonography
 The doctor can find the hernia during a physical exam.

NURSING MANAGEMENT
1. Discourage use of home remedies such as belly bands, coins
 2. Encourage parents to spongebath the child until they for postoperative
visit and until the dressing is removed.

THERAPEUTIC MANAGEMENT
 No treatment of small defects
 Operative repair if persists to age 4 to 6 year or if defect is > 1.5-2.0 cm by
age 2
 Strangulation requires immediate attention
 Herniorrhaphy

NURSING DIAGNOSIS
 Pain related to the protrusion of intra abdominal organs.

PROGNOSIS
Most umbilical hernias get better without treatment by the time the child is 3 - 4
years old. Those that do not close may need surgery. Umbilical hernias are
usually painless.

INGUINAL HERNIA
An inguinal hernia is a condition in which intra-abdominal fat or part of the small
intestine, also called the small bowel, bulges through a weak area in the lower
abdominal muscles. An inguinal hernia occurs in the groin—the area between the
abdomen and thigh. This type of hernia is called inguinal because fat or part of
the intestine slides through a weak area at the inguinal ring, the opening to the
inguinal canal. An inguinal hernia appears as a bulge on one or both sides of the
groin. An inguinal hernia can occur any time from infancy to adulthood and is
much more common in males than females. Inguinal hernias tend to become
larger with time.

CAUSES

The two types of inguinal hernia have different causes.

Indirect inguinal hernia. Indirect inguinal hernias are congenital hernias and are
much more common in males than females because of the way males develop in
the womb. In a male fetus, the spermatic cord and both testicles—starting from
an intra-abdominal location—normally descend through the inguinal canal into
the scrotum, the sac that holds the testicles. Sometimes the entrance of the
inguinal canal at the inguinal ring does not close as it should just after birth,
leaving a weakness in the abdominal wall. Fat or part of the small intestine slides
through the weakness into the inguinal canal, causing a hernia. In females, an
indirect inguinal hernia is caused by the female organs or the small intestine
sliding into the groin through a weakness in the abdominal wall.
Indirect hernias are the most common type of inguinal hernia. Premature infants
are especially at risk for indirect inguinal hernias because there is less time for
the inguinal canal to close.
Direct inguinal hernia. Direct inguinal hernias are caused by connective tissue
degeneration of the abdominal muscles, which causes weakening of the muscles
during the adult years. Direct inguinal hernias occur only in males. The hernia
involves fat or the small intestine sliding through the weak muscles into the groin.
A direct hernia develops gradually because of continuous stress on the muscles.
One or more of the following factors can cause pressure on the abdominal
muscles and may worsen the hernia:
 sudden twists, pulls, or  straining on the toilet because
muscle strains of constipation
 lifting heavy objects  weight gain
 chronic coughing

SIGNS AND SYMPTOMS

 a small bulge in one or both sides of the groin that may increase in size
and disappear when lying down; in males, it can present as a swollen or
enlarged scrotum
 discomfort or sharp pain—especially when straining, lifting, or exercising—
that improves when resting
 a feeling of weakness or pressure in the groin
 a burning, gurgling, or aching feeling at the bulge

TESTS
 family history taking
 physical examination

NURSING MANAGEMENT
Keep the suture line dry and free of urine or feces to prevent infection.

THERAPEUTIC MANAGEMENT
 Herniorrhaphy (Hernioplasty, Hernia repair) is a surgical procedure for
correcting hernia. A hernia is a bulging of internal organs or tissues, which
protrude through an abnormal opening in the muscle wall. Hernias can
occur in the abdomen, groin, and at the site of a previous surgery.
 An operation in which the hernia sac is removed without any repair of the
inguinal canal is described as a 'herniotomy'.
 When herniotomy is combined with a reinforced repair of the posterior
inguinal canal wall with autogenous (patient's own tissue) or
heterogeneous (like steel or prolene mesh) material it is termed
Hernioplasty as opposed to herniorrhaphy in which no autogenous or
heterogeneous material is used for reinforcement.

PROGNOSIS
Inguinal hernia repair is a routine operation with very few risks. Without an
operation, the hernia will get bigger, become more painful and could lead to
complications, such as a strangulated hernia. Surgery will get rid of the hernia
and prevent you from having any serious complications. After having the
operation, you should be able to go home the same day or the day after.

MALROTATION AND VOLVOLUS

Malrotation of the intestines results when the intestinal rotation and fixation that
occurs during pregnancy fails to occur. This normally happens in the 4 th and 12th
weeks of fetal life. In the 4th fetal week, the entire bowel is basically a straight
tube with the superior mesenteric artery (SMA). During the course of pregnancy,
the bowel rotates in place to the left of the SMA at the ligament of Treitz. In
normal rotation and fixation of the intestines, the bowel has plenty of room to
function normally. In malrotation, the primary concern becomes volvulus, or
twisting of the intestine that causes obstruction and death to that part of the gut.
Accidental bodily movements, unusual effort, abnormal peristaltic movement
(digestive wavelike motion of the intestines) or distention of the intestine can
bring on this volvulus.

CAUSES
The cause of intestinal malrotation is disruption in the normal embryological
development of the bowel. Clinical features depend on the stage of disruption
and are discussed as follows. A full understanding of normal development aids in
understanding the etiology of malrotation.

SIGNS AND SYMPTOMS

 Intermittent vomiting  Distention
 Recurrent abdominal pain  Lower GI bleeding

DIAGNOSTIC TESTS
 Upper GI series

THERAPEUTIC MANAGEMENT
 Laparotomy
 Untwisting by performing sigmoidoscopy and placing rectal tube, monitor
for signs of bowel ischemia for 2-3 days, if no improvement, consult
surgery for laparotomy (sigmoid resection and primary anastamosis)
 Transduodenal band of ladd is divided

PROGNOSIS
Younger patients have higher rates of morbidity and mortality. In infants, the
mortality rate ranges from 2-24%. The presence of necrotic bowel at surgery
increases the mortality rate by 25 times for infants, and the presence of other
anomalies increases the risk by 22 times. A report of 25 years' experience
demonstrated congenital cardiovascular disease in 27.1% of patients with
intestinal malrotation; those patients had a morbidity rate of 61.1% after intestinal
malrotation surgery.
Meckel's Diverticulum
 Meckel's diverticulum, a congenital diverticulum, is a small bulge in the
small intestine present at birth. It is a vestigial remnant of the omphalomesentric
duct http://en.wikipedia.org/wiki/Omphalomesenteric_duct(also called the vitelline
duct or yolk stalk), and is the most frequent malformation of the gastrointestinal
tract. It is present in approximately 2% of the population, with males more
frequently experiencing symptoms.
Meckel's diverticulum is located in the distal ileum, usually within about 60-
100 cm (2 feet) of the ileocecal valve. It is typically 3-5 cm long, runs
antimesenterically and has its own blood supply. It is a remnant of the connection
from the yolk-sac to the small intestine present during embryonic development.
Rule of 2s: 2% (of the population). 2 feet (from the ileocecal
valve). 2 inches (in length). 2% are symptomatic. 2 types of common ectopic
tissue (gastric and pancreatic). 2 years is the most common age at clinical
presentation. 2 times more boys are affected.

Symptoms
 The majority of people afflicted with Meckel's diverticulum
are asymptomatic. If symptoms do occur, they typically appear before the
age of two.
 painless rectal bleeding
 black tarry stool
 intestinal obstruction
 severe pain in upper abdomen
 bloating stomach
 it is followed by volvulus and intussusception

Diagnosis
 Technetium-99m (99mTc) pertechnetate scan - detects gastric mucosa
 Colonoscopy
 Screenings for bleeding disorders
 Angiography

Treatment
 Surgical resection –done in conditions such as bleeding, strangulation of
bowel, bowel perforation or bowel obstruction.
 Appendicectomy/ laparotomy – for asymptomatic meckel’s diverticulum
with acute abdomen; prevents complication.
Prognosis
 Once a complication arises and surgery is required, the operative mortality
and morbidity rates have both been estimated at 12%. The cumulative
long-term risk of postoperative complications in this cohort was found to
be 7%. If the Meckel diverticulum is removed as an incidental finding, the
risk of mortality and morbidity and long-term complications are much less
(1%, 2%, and 2%, respectively).
 As many as 5% of complicated Meckel diverticulum contain malignant
tissu
Short bowel syndrome
It is also called short gut syndrome or simply short gut. It is
a malabsorption disorder caused by the surgical removal of the small intestine, or
rarely due to the complete dysfunction of a large segment of bowel. Most cases
are acquired, although some children are born with a congenital short bowel. It
usually does not develop unless more than two thirds of the small intestine have
been removed.
Signs and symptoms
 Abdominal pain  Complications – deficiencies
 Diarrhea and steatorrhea (oily in Vitamin A, D, E, K,
or sticky stool, which can be and B12, calcium, magnesium
malodorous) , iron, folic acid, and zinc.
 Fluid retention Also,
 Weight loss anemia, hyperkeratosis (scali
 Malnutrition ng of the skin), easy bruising,
 Fatigue muscle spasms, poor blood
clotting, and bone pain
appears.
Laboratory/Diagnostic Tests
 Blood chemistry tests (such  Small intestine x-ray
as albumin level)  Vitamin levels in the blood
 Complete blood count (CBC)
 Fecal fat test
Treatments
 Anti-diarrheal medicine (e.g. loperamide, codeine)
 Vitamin, mineral supplements and L-Glutamine powder mixed with water
 H2 blocker and proton pump inhibitors to reduce stomach acid
 Lactase supplement (to improve the bloating and diarrhoea associated
with lactose intolerance)
 Parenteral nutrition (PN or TPN for total parenteral nutrition - nutrition
administered via intravenous line).
 Nutrition administered via gastrostomy tubes

Surgical procedure
 Bianchi procedure - where the
bowel is cut in half and one
end is sewn to the other
 Serial Transverse
Enteroplasty(STEP)—where
the bowel is cut and stapled in
a zigzag pattern
 Small intestine transplant
 Intestinal lengthening and
tapering
Prognosis
 There is no cure for short bowel syndrome. In newborn infants, the 4-year
survival rate on parenteral nutrition is approximately 70%. In newborn
infants with less than 10% of expected intestinal length, 5 year survival is
approximately 20%. Some studies suggest that much of the mortality is
due to a complication of the TPN, especially chronic liver disease.
 Although promising, small intestine transplant has a mixed success rate,
with postoperative mortality rate of up to 30%. One-year and 4-year
survival rate are 90% and 60%, respectively.
HERNIAS

Pictures of different hernias

MECKEL’S DIVERTICULUM
 Red Blood Cell Disorders

I. Aplastic Anemia

BACKGROUND OF THE STUDY

Aplastic anemia results from depression of

hematopoietic activity in the bone marrow. The
formation and development of WBCs, platelets, and RBCs can all be
affected.

a) Congenital aplastic anemia (Fanconi's syndrome) is inherited as an

autosomal recessive trait. Child is born with a number of congenital
anomalies.
b) Acquired aplastic is a decrease in bone marrow production. The child is
exposed excessively to radiation, drugs, or chemicals known to cause bone
marrow damage. (sulfonamides, arsenic (contained in rat poison), hydantoin,
quinine, insecticides chemotherapeutic drugs).

ASSESSMENT:

1. Low RBC count - child appears pale, fatigues easily, and has
anorexia.
2. Reduced Platelet - (thrombocytopenia), the child bruises easily or has
petechiae (pinpoint, macular, purplish-red spots caused by
intradermal or submucous hemorrhage). excessive nosebleeds or
gastrointestinal bleeding.
3. Decreased WBCs (leukopenia), a child may contract an increased
number of infections and respond poorly to antibiotic therapy.

MANAGEMENT

The ultimate therapy for aplastic anemia is stem cell

transplantation.
 If a donor cannot be located, the disease is managed by procedures to
suppress T lymphocyte-dependent autoimmune responses with
antithymocyte globulin (ATG) or cyclosporine or transfusion of new blood
elements.

NURSING DIAGNOSIS

Risk for injury related to ineffective blood clotting mechanisms secondary to

inadequate platelet formation

OUTCOME EVALUATION:

Child exhibits no ecchymotic skin areas, gingival bleeding, or epistaxis; stools are
negative for occult blood.

Inadequate platelet formation interferes with blood coagulation, placing a child at

risk for bleeding.

PLAN OF CARE:

Some techniques for reducing bleeding due to inadequate platelet formation

include:

 Limit the number of blood-drawing procedures; combine samples

whenever possible; use a blood pressure cuff instead of a tourniquet to
reduce the number of petechiae.
 Apply pressure to any puncture site for a full 5 minutes before applying a
bandage.
 Minimize use of adhesive tape to the skin (pulling for removal may tear the
skin and cause petechiae).
 Pad side and crib rails to prevent bruising.
 Protect intravenous sites to avoid numerous reinsertions.
 Administer medication orally or by intravenous infusion to minimize the
number of injection sites.
 Assess diet for foods that the child can chew without irritation (e.g., avoid
toast crusts).
 Urge the child to use a soft toothbrush.
 Check toys for sharp corners, which may cause scratches. Urge the child
to be careful with paper, because paper cuts can bleed out of proportion to
their size.
 Assess the need for routine blood pressure determinations. Tight cuffs
could lead to petechiae.
 Distract the child from rough play; suggest stimulating but quiet activities
to minimize risk of injury.
  Keep a record of blood drawn; do not draw extra amounts “just in case” so
children do not become more anemic.

II. Iron Deficiency Anemia

BACKGROUND OF THE STUDY

RBCs are both small in size (hypocytic) and pale (hypochromic) due to the
stunted hemoglobin.
The most common anemia of infancy and childhood, occurring when the
intake of dietary iron is inadequate.
Children are at high risk for iron-deficiency anemia because they need
more daily iron in proportion to their body weight to maintain an adequate
iron level than do adults.

ETIOLOGY:
1. Infants - Infants of low birthweight have fewer iron stores than those born
at term because iron stores are laid down near the end of gestation.
Because low-birthweight infants grow rapidly and their need for RBCs
expands accordingly, they will develop an iron-deficiency anemia before 5
to 6 months. As a preventive measure, they are given an iron supplement
beginning at about 2 months of age.
2. Children – (older than 2 years) This results from gastrointestinal tract
lesions such as polyps, ulcerative colitis, Crohn's disease, protein-induced
enteropathies, parasitic infestation, or frequent epistaxis.
3. Adolescent – (girls) can become iron deficient because of frequent
attempts to diet and overconsumption of snack foods low in iron. Without
sufficient iron, their body cannot compensate for the iron lost with
menstrual flow.

ASSESSMENT:
a) Pallor
b) Pale mucous membranes
c) Infants may show poor muscle tone and reduced
activity.
d) Generally irritable from fatigue
e) The heart may be enlarged, and there may be a soft systolic
precordial murmur as the heart increases its action, attempting to
supply body cells with more oxygen.

MANAGEMENT:

a) Sources of gastrointestinal bleeding must be ruled out.

 b) Diet must be rich in iron and should contain extra vitamin C, as this
enhances iron absorption.
c) An iron compound such as ferrous sulfate for 4 to 6 wks to improve RBC
formation and replace iron stores.

NURSING DIAGNOSIS:

Imbalanced nutrition, less than body requirements, related to inadequate

ingestion of iron

OUTCOME EVALUATION:

Parents report child's dietary intake includes iron-rich foods; parents administer
ferrous sulfate as prescribed; serum iron levels increase to normal by 6 months.

PLAN OF CARE:

a) When planning care for an infant with iron-deficiency anemia, it is helpful

to minimize the child's activities to prevent fatigue, particularly at mealtime,
as a fatigued child will not be able to eat, let alone eat iron-rich foods.
b) Counsel parents on measures to improve their child's diet, such as adding
iron-rich foods while decreasing milk intake to maintain iron levels and
prevent recurring anemia. If the child is not fond of meat, suggest parents
substitute cheese, eggs, green vegetables, or fortified cereal. Because
iron-rich foods are often expensive, remind parents that these items are
important and that they should not substitute less expensive, high-
carbohydrate foods.
c) Before iron therapy is started, alert parents to possible side effects, such
as stomach irritation. If oral iron is not tolerated or if there is a doubt the
child will take it, an iron-dextran injection (Imferon) can be given
intramuscularly. Imferon stains the skin and is extremely irritating unless it
is given by deep Z-track intramuscular injection.
d) Of all age groups, adolescents tend to do the least well with taking
medicine consistently. Help them plan a daily time for taking their iron
supplement with a medication reminder chart. At first, they may reject this
as childish, but assure them that everyone needs these charts. Review
with them the iron-rich foods they will need to eat daily. An iron
supplement is effective only if taken with iron-rich foods.
e) After 7 days of iron therapy, a reticulocyte count is usually done. If
elevated, this means the child is now receiving adequate iron and the
rapid proliferation of new erythrocytes is correcting the anemia. Iron
medication must be taken for at least 4 to 6 weeks after the RBC count is
normal to rebuild iron levels in the blood. In some children, maintenance
the
III. Folic Acid Deficiency

BACKGROUND OF THE STUDY

- A deficiency of folic acid combined with vitamin C.

- Megaloblastic arrest, or inability of RBCs to mature past an early stage,
may occur in the first year of life from the continued use of infant food
containing too little folic acid or from an infant drinking goat's milk, which
tends to be deficient in folic acid.
- Treatment is daily oral administration of folic acid.

IV. Pernicious Anemia

BACKGROUND OF THE STUDY

a) Vitamin B12 (Cobalamin) is necessary for maturation of RBCs.

b) Deficiency or inability to use the Vitamin B12, found primarily in foods of
animal origin, including both cow's milk and breast milk.
c) An adolescent may be deficient in vitamin B12 if he or she is on a long-
term, poorly formulated vegetarian diet.
d) For absorption of vitamin B12 from the
intestine, an intrinsic factor must be present in
the gastric mucosa.

ASSESSMENT
- The child appears pale, anorexic, and irritable, with chronic diarrhea.
- The tongue appears smooth and beefy red due
to papillary atrophy.
- In children, neuropathologic findings such as
ataxia, hyporeflexia, paresthesia and a positive
Babinski reflex are less noticeable than in
adults.

MANAGEMENT
- If the anemia is caused by a B12-deficient diet, temporary injections of
B12 will reverse the symptoms.
- If the anemia is caused by lack of the intrinsic factor, lifelong monthly
intramuscular injections of B12 may be necessary.
-
V. Sickle Cell Anemia

BACKGROUND OF THE STUDY

The presence of abnormally shaped (elongated)

RBCs.

An autosomal recessive inherited disorder on the beta chain of hemoglobin;

the amino acid valine takes the place of the normally appearing glutamic
acid.

1. Sickle-cell crisis - term used to denote a sudden, severe onset of sickling.

- Occurs when a child has an illness causing dehydration or a respiratory
infection that results in lowered oxygen exchange and a lowered arterial
oxygen level, or after extremely strenuous exercise (enough to lead to
tissue hypoxia).
- Laboratory reports reveal a hemoglobin level of only 6 to 8 g/100 mL.
Bilirubin and reticulocyte levels are increased.
2. Sequestration Crisis – may occur when there is splenic sequestration of
RBCs or severe anemia occurs due to pooling and increased destruction of
sickled cells.
3. Hyperhemolytic Crisis – occurs when there is increased destruction of
RBCs.
4. Aplastic Crisis – manifested by severe anemia due to a sudden decrease
in RBC production.

ASSESSMENT

- Hemoglobin electrophoresis is used to diagnose sickle-cell

anemia at birth.
- Stasis of blood and infarction may occur in any body part,
leading to local disease.
- Some infants have swelling of the hands and feet (a hand–foot syndrome)
probably caused by aseptic infarction of the bones of the hands and feet.
- A chest syndrome with symptoms similar to pneumonia may occur.
- Liver may become enlarged from stasis of blood flow.
- Kidneys may have subsequent scarring and kidney function may be
decreased.
- Sclerae are generally icteric (yellowed) from release
of bilirubin from destruction of the sickled cells.
 MANAGEMENT

1. Pain relief -
Acetaminophen
(Tylenol) may be
adequate pain
relief for some
children; for
others, a narcotic analgesic such as intravenous morphine may be needed.
2. Hydration - intensive intravenous fluid replacement therapy. Tissue hypoxia
leads to acidosis. The acidosis must be corrected by electrolyte replacement.
3. Prevention - Blood transfusion (usually packed RBCs)
may be necessary to maintain the hemoglobin above 12
g/dL (termed hypertransfusion). Hydroxyurea, an
antineoplastic agent that has the potential to increase the
production of hemoglobin F (fetal hemoglobin), can be
used in children with sickle-cell disease to increase their
overall hemoglobin level.

Stem cell transplantation is possible for the child who does

not respond to usual therapies.

VI. Thalassemia

BACKGROUND OF THE STUDY

Autosomal recessive associated with abnormalities of the beta chain of adult

hemoglobin (HgbA). It occurs most frequently in the Mediterranean population,
they also occur in children of African and Asian heritage.

1. Thalassemia Minor (Heterozygous Beta-Thalassemia)

- It is a mild form of this anemia that produces both defective beta
hemoglobin and normal hemoglobin. Because there is some normal
production, the RBC count will be normal, but the hemoglobin
concentration will be decreased 2 to 3 g/100 mL below normal levels.
 The blood cells are moderately hypochromic and microcytic because
of the poor hemoglobin formation.
- Children may have no symptoms other than pallor.
- They require no treatment, and life
expectancy is normal. They should not
receive a routine iron supplement because
their inability to incorporate it well into
hemoglobin may cause them to accumulate
too much iron.
2. Thalassemia Major (Homozygous Beta-
Thalassemia)
- Also called Cooley’s anemia or
Mediterranean anemia.
- Unable to produce normal beta
hemoglobin.
- Child shows symptoms of anemia: pallor,
irritability, and anorexia
ASSESSMENT
- Bone pain
- As bone marrow becomes hyperactive, this results in a characteristic
change in the shape of the skull
- The base of the nose may be broad and flattened; the eyes may be
slanted with an epicanthal fold, as in Down syndrome.

MANAGEMENT
Digitalis, diuretics, and a low-sodium diet
Transfusion of packed RBCs every 2 to 4 weeks

VII. Polycythemia Vera

 An increase in the number of rbcs

 Occurs as a compensatory response to insufficient oxygenation of the
blood in order to help supply more oxygen to body cells.
 Plethora (marked reddened appearance of the skin) occurs because of
the increase in total RBC volume.
 The RBC count may be as high as 7 million/mm3. Hemoglobin levels
may be as high as 23 g/100 ml.
 Exchange transfusion to reduce the RBC count may be necessary.
Disorders of the White Blood Cells

Neutropenia

-is the reduced number of white blood cells.

-neutrophils make-up 50-70% of circulating white blood cells and serve as the
primary defense against infections by destroying bacteria in the blood.

-as nursing management, the nurse must maintain aseptic technique when
interacting with the patient to prevent transmission of organisms and protect the
client from infection. (e.g. proper hand washing)

-Causes: maybe response therapy with some drugs: 6-mercaptopurine or

nitrogen mustard

: Possible side effect of Phenytoin sodium (DILANTIN), Chloramphenicol

or Chloropromazine.

-Treatments: would be WBC transfusion and

Prophylactic Antibiotics.

-Neutropenia is identified thru complete blood

count.

Neutrophilia

-Increased number of white blood cells

(total number increase, immature cells > mature neutrophils) “Left Shift”

-Usually in response to infection or inflammation

-Treatment: Antibiotic therapy to eliminate infectious organisms.

Eosinophilia

-Increased number of eosinophils

-allergic or atopic diseases are the most common causes, especially those of the
respiratory or integumentary systems.

-A sign of a disorder

-Treatment: is directed to underlying cause

-Prednisone can also be taken.

Facial Granuloma w/ Eosinophilia

Lymphocytosis

-Increased number of lymphocytes

-In adults, absolute lymphocytosis is

present when the absolute lymphocyte
count is greater than 4000 per microliter, in
older children greater than 7000 per
microliter and in infants greater than 9000 per microliter[2

-Normally occurs in pre-school period, when there is a marked predominance of

lymphocytes in relation to neutrophils

-Elevated in childhood illnesses: pertussis, infectious mononucleosis and

lymphocytic leukemia

-Treatment is directed to underlying condition.

-Lymphocytosis is identified thru Complete Blood Count.

Leukemia

-is the uncontrolled malignant proliferation of white blood cells within a an

unknown cause affecting all blood.

-this is most common in children.

Types:

Acute Lymphocytic (Lymphoblastic) Leukemia is characterized by a

rapid increase in the numbers of immature blood cells.

Chronic leukemia is characterized by the excessive build up of relatively

mature, but still abnormal, white blood cells. Typically taking months or
years to progress, the cells are produced at a much higher rate than
normal cells, resulting in many abnormal white blood cells in the blood.

-Treatment:
 A ntibiotic

B one marrow aspiration/ Blood

tansfusion

C hemotheraphy

-Nursing Care:

Check early signs of infection

Use good hand washing technique

(universal precaution)

Provide nutritional intake ( increase

calorie, protein, iron)

Protect from injury

Promote rest and comfort

Provide realistic feedback on child’s appearance

Alopecia r/t chemotherapy

Bone marrow aspiration

Disorders of Blood Coagulation in Children

Platelets are very necessary for blood coagulation, so disorders that limit
the number of platelets limit the effectiveness of this process. A normal platelet
value is 150,000/mmз. Thrombocytopenia [decreased platelet count] is defined
as a platelet count of less than 40,000/mmз. Thrombocytopenia often leads to
purpura or blood seeping from blood vessels into the skin.

1. Purpura

 Hemorrhagic rash or small hemorrhages in superficial layer of skin

Has 2 types:

a. Idiopathic Thrombocytopenic Purpura {ITP}

 Decrease number of  Result = increase rate of

circulating platelets with platelet destruction
presence of adequate  Occurs 2 weeks after viral
megakaryocyte infection {rubella, rubeola,
 Cause is unknown varicella, URTI}

Assessment:

 Miniature petichiae  Epistaxis

 Ecchymosis – Legs  Bleeding into joints

Lab studies

 Thrombocytopenia
 Less than 20,000/mm³ with normal number of megakaryocytes

Management:

 Oral prednisone  Acetaminophen administration

 Intravenous immunoglobulin  Vaccinated against viral
{IVIG} diseases of childhood
 Platelet transfusion
b. Henoch-Schönlein Syndrome

 Anaphylactoid purpura  More frequently on boys

 Hypersensitivity reaction to an
allergen
 Caused by increase vessel
permeability
 Occurs between 2-8 years old
 Mild infection before outbreak
of symptoms
 Runs for 4-6 weeks

Assessment:

 Purpural rush {buttocks,  Abdominal pain

posterior thighs and extensor  Vomiting
surface of the arms and legs,  Blood in stools
tips of the ear}
 Joints are tender and swollen

Lab studies

 Normal platelet count

 Sedimentation rate, WBC, eosinophil are elevated

Management

 Oral costicosteroid therapy

 Mild analgesics
 Assessment of urine of protein and glucose presence
Nursing Diagnoses:

 Health seeking behaviors related to injury-prevention measures

 Risk for compromised family coping related to diagnosis of child’s illness

2. Disseminated Intravascular Coagulation {DIC}

 Acquired disorder of blood clotting

Assessment

 Uncontrolled bleeding  Toes and fingers are pale,

 Ecchymoses and petichiae cyanotic, mottled and feel cold
Lab studies

 Thrombocytopenia  Prolong prothrombin and

 Large platelets on blood partial thromboplastin times
smear  Low serum fibrinogen levels
 Elevated fibrin split products

Management

 IV heparin administration
 Fresh plasma, platelets, fibrinogen infusion

Nursing Diagnosis:

 Deficient knowledge about blood clotting disorder related to its paradoxical

nature
  Prognosis:
 Prognosis varies depending on the underlying disorder, and the extent of
the intravascular thrombosis (clotting). The prognosis for those with DIC,
regardless of cause, is often grim: Between 10% and 50% of patients will
die. DIC with sepsis (infection) has a significantly higher rate of death than
DIC associated with trauma.

3. Hemophilia

 Inherited disorder of blood coagulation

a. Hemophilia A {Factor VIII Deficiency}

 Caused by factor VIII deficiency

{antihemophilic factor}

 Transmitted as a sex linked recessive trait

Assessment

 Epistaxis is common
 Severe bleeding may also occur into the gastrointestinal tract, peritoneal
cavity or central nervous system
Infant Become active
{crawl, climb, walk}

Lower extremities
Become heavily
Undergoes
bruised
circumcision
Soft tissue
bleeding

Painful hemorrhage
Bleeds excessively into joints
after circumcision
Swollen and
warm
First time to
Damage to Severe loss of
Recognize the
Synovial joint mobility
disease
membrane
Lab studies

 Platelet count and prothrombin time are normal

 Thromboplastin generation test is abnormal

Management

 Administration of Factor VIII {fresh whole blood, fresh/frozen plasma}

 Administration of Desmopressin {DDAVP}

*child must be identified as having hemophilia before undergoing surgery

Nursing Diagnoses:

 Pain related to joint infiltration by blood

 Risk for interrupted family processes related to fears regarding child’s
prognosis and long term nature of illness

b. Von Willebrand’s Disease

 referred as angiohemophilia  affect both sexes

 factor VIII deficiency, inability  blood vessels cannot constrict
of platelets to aggregate  bleeding time is prolonged
 inherited autosomal dominant
disorder

Assessment

 Epistaxis
 Unusual heavy menstrual flow
Management

 Factor VIII replenishment

 Administration of DDAVP
c. Christmas Disease {Hemophilia B, Factor IX Deficiency}

 cause by factor IX deficiency

 15% of people having hemophilia have this form

Management

 Concentrate of Factor IX

d. Hemophilia C {Factor XI Deficiency}

 plasma thromboplastin
antecedent deficiency
 caused by factor XI deficiency
 occurs in both sexes
 symptoms are generally mild
compared to Factor VIII and
IX deficiency
Management

 Administration of DDAVP
 Transfusion of fresh blood or plasma

Prognosis:

 Near normal lifestyle with treatment, but with need to avoid injury.
 Advances in treatment over the last three decades have permitted a near-
normal lifestyle and life-span for many individuals with hemophilia.
 Deaths from Hemophilia: 1,681 deaths for coagulation defects (NHLBI
1999)

Estimated mortality rate for Hemophilia from prevalence and deaths

statistics:

 Deaths: 1,681 (USA annual deaths calculated from this data: 1,681 deaths
for coagulation defects (NHLBI 1999))

 Incidence: 20,000 (USA prevalence calculated from this data: 20,000

people in the United States (NHLBI)

8.4% (ratio of deaths to prevalence).

 I. UPPER RESPIRATORY DISORDER

A. Acute Nasopharyngitis

Description/ Background Study

The common cold (also known
as nasopharyngitis, acute viral rhinopharyngitis, acute
coryza, or a cold) is a viral infectious disease of the
upper respiratory system, caused primarily
by rhinoviruses and corona viruses. Common
symptoms include a cough, throat, runny, and fever.
There is currently no known treatment that shortens the duration; however,
symptoms usually resolve spontaneously in 7 to 10 days, with some symptoms
possibly lasting for up to three weeks.
The common cold is the most frequent infectious disease in humans with
the average adult contracting two to four infections a year and the average child
contracting between 6–12. Collectively, colds, influenza, and other infections with
similar symptoms are included in the diagnosis of influenza-like illness. They may
also be termed upper respiratory tract infections (URTI).

Etiology
More than 200 viruses are known to cause the symptoms of the common cold.

 Rhinoviruses:
 Coronaviruses:
 Enteroviruses,
 Other viruses: Adenoviruses, orthomyxoviruses (including influenza A
and B viruses), paramyxoviruses (eg, PIV), RSV, EBV, and hMPV account
for many URIs. Varicella, rubella, and rubeola infections may manifest as
a nasopharyngitis before other classic signs and symptoms develop. The
remainder of URI pathogens are not identified but are presumed to be
viral. This group represents greater than 30% of common colds in adults.

Patophysiology
The common cold virus is transmitted mainly from contact with saliva or
nasal secretions of an infected person, either directly, when a healthy person
breathes in the virus-laden aerosol generated when an infected person coughs or
sneezes, or by touching a contaminated surface and then touching the nose or
eyes.
 Symptoms are not necessary for viral shedding or transmission, as a
percentage of asymptomatic subjects exhibit viruses in nasal swabs.It is
generally not possible to identify the virus type through symptoms, although
influenza can be distinguished by its sudden onset, fever, and cough
The major entry point for the virus is normally the nose, but can also be
the eyes (in this case drainage into the nasopharynx would occur through
the nasolacrimal duct). From there, it is transported to the back of the nose and
the adenoid area. The virus then attaches to a receptor, ICAM-1, which is located
on the surface of cells of the lining of the nasopharynx. The receptor fits into a
docking port on the surface of the virus. Large amounts of virus receptor are
present on cells of the adenoid. After attachment to the receptor, virus is taken
into the cell, where it starts an infection.[7] Rhinovirus colds do not generally
cause damage to the nasal epithelium. Macrophages trigger the production
ofcytokines, which in combination with mediators cause the symptoms. Cytokines
cause the systemic effects. The mediator bradykinin plays a major role in causing
the local symptoms such as sore throat and nasal irritation.
The common cold is self-limiting, and the host's immune system effectively
deals with the infection. Within a few days, the body's humoralimmune response
begins producing specific antibodies that can prevent the virus from infecting
cells. Additionally, as part of the cell-mediated immune
response, leukocytes destroy the virus through phagocytosis and destroy
infected cells to prevent further viral replication. In healthy, immune competent
individuals, the common cold resolves in seven days on average.

Manifestations
Signs and symptoms of acute nasopharyngitis include:
 Sore throat  Muscle weakness
 Runny nose  Uncontrollable shivering
 Nasal congestion  Loss of appetite
 Sneezing  low grade fever
 Sometimes accompanied by  cervical lymph nodes may be
'pink eye' swollen
 Muscle aches  edematous and inflamed
 Fatigue mucous membrane
 Malaise  constricting airway space
 Headaches causing difficulty of breathing

Laboratory and diagnostic tests
No explicit diagnostic test exists to isolate the specific organism responsible
for the common cold. Consequently, diagnosis rests on the typically mild,
localized, and afebrile upper respiratory symptoms. Despite infection, white blood
cell counts and differential are within normal limits. Diagnosis must rule out
allergic rhinitis, measles, rubella, and other disorders that produce similar early
symptoms. A temperature higher than 100° F (37.8° C), severe malaise,
anorexia, tachycardia, exudate on the tonsils or throat, petechiae, and tender
lymph glands may point to more serious disorders and require additional
diagnostic tests.

 Cold & Flu: Home Testing:

o Home Fever Tests
o Home Ear Infection Test Kits
o Home Flu Tests
o Home Strep A Tests

Treatment
Cough relief
Cough suppression may increase comfort when cough is severe or when it
prevents sleep. The following agents may reduce cough in the setting of a
URI.26 The risk-to-benefit ratio for using cough and cold medicines in children
younger than 2 years requires careful consideration because serious adverse
events, including fatalities, have been reported with the use over-the-counter
preparations in young children.29 Since 2008, many nonprescription cough and
cold product labels state "do not use" in children younger than 4 years.

 Antihistamine and decongestants: Cough associated with the common

cold may be treated with a first-generation antihistamine combined with a
decongestant (eg, brompheniramine with pseudoephedrine). Inhaled
ipratropium: An anticholinergic, inhaled ipratropium may be useful in
postinfectious cough (3-8 wk after the onset of the URI) in adults.
 Inhaled steroids: These agents may be considered in postinfectious cough
(3-8 wks after URI onset),
 Dextromethorphan: This is a centrally acting cough suppressant and it
may be considered for the treatment of postinfectious cough in adults if
other medications fail. Additional data are required to permit evidence-
based recommendations for the use of central-acting antitussives in URI-
related cough in children.
 Peripherally acting cough suppressants: While these medications may
have a role in bronchitis, they may have limited efficacy in relieving cough
associated with URI.
  Guaifenesin: As an expectorant, guaifenesin is intended to mobilize
secretions. However, consistent data regarding its effectiveness in
reducing discomfort from cough associated with URIs are scarce.
 Long-acting inhaled beta-agonists: Beta-agonists are not thought to be
helpful in URI-related cough, including that due to pertussis. Nonsteroidal
anti-inflammatory drugs: They may be used to reduce discomfort due to
cough. Avoid aspirin in children with viral illness because aspirin is
associated with Reye syndrome.

Nursing Management
There are currently no medications or herbal remedies which have been
conclusively demonstrated to shorten the duration of illness. Treatment
comprises symptomatic support usually via analgesics for fever, headache, sore
muscles, and sore throat.
Symptomatic
Treatments that help alleviate symptoms include
simple analgesics and antipyretics such as ibuprofen and acetaminophen
/paracetamol. Evidence does not show that cough medicine is any more effective
than simple analgesics and is not recommended for use in children due to a lack
of evidence supporting its effectiveness and the potential for harm.
Symptoms of a runny nose can be reduced by a first generation
antihistamine, however it can cause drowsiness and other side effects.
Anticholinergics such as Ipratropium nasal spray can reduce the symptoms
of runny nose with less side effects, however it is a prescription drug.
One study has found chest vapor rub to be effective at providing some
symptomatic relief of nocturnal cough, congestion, and sleep difficulty.
Getting plenty of rest, drinking fluids to maintain hydration,
and gargling with warm salt water, are reasonable conservative measures.
Evidence for encouraging the active intake of fluids in acute respiratory infections
is lacking, as is the use of heated humidified air. Saline nasal drops may help
alleviate nasal congestion.

Prognosis

 A common cold may last up to 14 days, with symptoms averaging 7-11

days in duration.
 Fever, sneezing, and sore throat typically resolve early, whereas cough
and nasal discharge are among the symptoms that last longest.
  Attendance at daycare may affect the duration of symptoms in young
children. In one study, the duration of viral URI ranged from 6.6 days for 1-
to 2-year-old children in home care to 8.9 days for children younger than 1
year who were in daycare. Young children in daycare were more likely to
have protracted respiratory symptoms lasting more than 15 days .
 Most patients with influenza recover within a week, although cough,
fatigue, and malaise may persist for up to 2 weeks. For newborns, elderly
persons, and patients with chronic medical conditions, the flu may be life
threatening. More than 200,000 people are hospitalized because of
complications of the flu, with 0.36 deaths occurring per 100,000 patients
each year.
The common cold is generally mild and self-limiting

B. Tonsillitis

Background Study

Tonsillitis is an inflammation of the tonsils, the

fleshy clusters of tissue on both sides of the back of
the throat that fight off germs that enter the body
through the mouth. The tonsils become enlarged and
red, and have a yellow or white coating.

Most types of tonsillitis are contagious, spreading from person to person

by contact with the throat or nasal fluids of someone who is infected. Tonsillitis
symptoms include a sore throat, fever, swollen glands in the neck, and trouble
swallowing.

Etiology/ Patophysiology
The most common causes of tonsillitis are the common cold viruses
(adenovirus, rhinovirus, influenza, coronavirus, respiratory syncytial virus). It can
also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus,
or HIV. The second most common causes are bacterial. The most common
bacterial cause is Group A β-hemolytic streptococcus (GABHS), which
causes strep throat. Less common bacterial causes include: Staphylococcus
aureus, Streptococcus pneumoniae, Mycoplasma pneumoniae,Chlamydia
pneumoniae, pertussis, Fusobacterium, diphtheria, syphilis, and gonorrhea.
Under normal circumstances, as viruses and bacteria enter the body
through the nose and mouth, they are filtered in the tonsils. Within the
 tonsils, white blood cells of the immune system mount an attack that helps
destroy the viruses or bacteria, and also causes inflammation and fever. The
infection may also be present in the throat and surrounding areas, causing
inflammation of the pharynx. This is the area in the back of the throat that lies
between the voice box and the tonsils.
Tonsillitis may be caused by Group A streptococcal bacteria, resulting
in strep throat. Viral tonsillitis may be caused by numerous viruses ] such as
the Epstein-Barr virus (the cause of infectious mononucleosis) or adenovirus.
Sometimes, tonsillitis is caused by an infection of spirochaeta and treponema, in
this case called Vincent's angina or Plaut-Vincent angina.

Manifestations

Tonsillitis Symptoms

 Sore throat
 Difficulty feeding (in babies)
 Pain with swallowing
 Fever
 Headache
 Abdominal pain
 Nausea and vomiting
 Cough
 Hoarseness
 Runny nose
 Redness of the tonsils and throat
 Tenderness in the glands of the neck (swollen lymph glands)
 White patches on the tonsils
 Redness of the eyes
 Rash
 Ear pain (nerves that go to the back of the throat also go to the ear)

Laboratory and diagnostic tests

The health care provider will look in the mouth and throat for swollen
tonsils. The tonsils are usually red and may have white spots on them. The
lymph nodes in the jaw and neck may be swollen and tender to the touch.

Tests that may be done include:

 Blood count
 Mononucleosis test
  Rapid strep test
 Throat swab culture

Treatment

If bacteria such as strep are causing the tonsillitis, antibiotics are given to
cure the infection. The antibiotics may be given once as a shot, or taken for 10
days by mouth.

If antibiotic pills are used, they must be taken for the entire amount of time
prescribed by the doctor. DO NOT stop taking them just because the discomfort
stops, or the infection may not be cured.

Other treatments include:

 Drink cold liquids or suck on popsicles
 Drink fluids, especially warm (not hot), bland fluids
 Gargle with warm salt water
 Suck on lozenges (containing benzocaine or similar ingredients) to reduce
pain (these should not be used in young children because of the choking
risk)
 Take over-the-counter medications, such as acetaminophen (Tylenol)
or ibuprofento reduce pain and fever. Do NOT give a
child aspirin. Aspirin has been linked toReye syndrome.

Some people who have repeated infections may need surgery to remove the
tonsils (tonsillectomy).

Complications of untreated strep tonsillitis may be severe. Children with

tonsillitis related to strep throat or pharyngitis should generally be kept home
from school or day care until they have been on antibiotics for 24 hours. This
helps reduce the spread of illness.

Complications
 Blocked airway from swollen tonsils
 Dehydration from difficulty swallowing fluids
 Kidney failure
 Peritonsillar abscess or abscess in other parts of the throat
 Pharyngitis - bacterial
 Post-streptococcal glomerulonephritis
 Rheumatic fever and related cardiovascular disorders
Nursing Management

Kids with tonsillitis need plenty of nourishment and rest. If swallowing so

painful that eating is difficult, try serving liquids and soft foods, like soups,
milkshakes, smoothies, ice pops, or ice cream.
Make sure that your child drinks lots of fluids and gets plenty of rest, and
take his or her temperature regularly. Use a nonprescription pain reliever, such
as acetaminophen or ibuprofen, for throat pain. Don't give aspirin or other
products that contain aspirin, though, because these can put kids at risk for Reye
syndrome, an illness that can have serious complications.

Keep your sick child's drinking glasses and eating utensils separate, and
wash them in hot, soapy water. All family members should wash their hands
frequently.

If your child starts antibiotic therapy for strep, throw out his or her
toothbrush and replace it with a new one.

Management

Tonsillectomy is surgery to remove the tonsils. These glands are at the

back of your throat. Often, tonsillectomy is done at the same time
as adenoidectomy, surgery to remove the adenoid glands.

Description

Your child will be given general anesthesia before surgery. They will be asleep
and pain free.
 The surgeon will insert a small tool into your child’s mouth to prop it open.
 The surgeon then cuts or burns away the tonsils. The doctor will control
bleeding, and the cuts heal naturally without stitches.

Your child will stay in the recovery room after surgery until they are awake and
can breathe easily, cough, and swallow. Most children go home several hours
after this surgery.

Preoperative

Careful history taking is needed to evaluate for the following:

 Bleeding disorders or wish to avoid transfusion

 Anesthesia intolerance
 Obstructive sleep apnea
 Regarding admission planning, insurance plans are increasingly
disallowing inpatient admission for tonsillectomy or adenoidectomy.
Children who should be admitted are those with obstructive sleep apnea,
those with significant comorbid disease such as hypotonia or neuromotor
delays, and those younger than 3 years.

Postoperative
A sore throat will persist for around two weeks after the operation.
Most patients do not feel like swallowing anything during the first few days
after surgery. Patients should try to get as much fluid down as possible, as
it will help speed recovery. Very cold drinks will help bring down swelling.
Ice cream, frozen yogurt and other dairy products are not recommended
because they leave a film in the mouth that is difficult to
swallow. Sorbet and popsicles, on the other hand, are recommended.
Additionally, Slushies are particularly helpful for sore throats, especially
when sugar-free.
Pain following the procedure is significant and may include a
hospital stay.[7] Recovery can take from 10 up to 20 days, during
which narcotic analgesics are typically prescribed. Patients are
encouraged to maintain diet of liquid and very soft foods for several days
following surgery. Rough textured, acidic or spicy foods may be irritating
and should be avoided. Proper hydration is very important during this time,
since dehydration can increase throat pain, leading to a vicious circle of
poor fluid intake.
At some point, most commonly 7–11 days after the surgery (but
occasionally as long as two weeks (14 days) after), bleeding can occur
when scabs begin sloughing off from the surgical sites. The overall risk of
bleeding is approximately 1%–2% higher in adults. Approximately 3% of
adult patients develop significant bleeding at this time. The bleeding might
naturally stop quickly or else mild intervention (e.g., gargling cold water)
could be needed (but ask the doctor before gargling because it might
bruise the area of the skin that has been cauterized). Otherwise, a
surgeon must repair the bleeding immediately by cauterization, which
presents all the risks associated with emergency surgery (primarily the
administration of anesthesiaparticularly on a patient whose stomach may
not be empty).
Generally speaking, tonsils will be removed if a patient needs
antibiotics to be prescribed six times a year for tonsilitis, and the general
practitioner's recommendation is based on how the quality of life will be
 improved after the operation. Tonsillectomies can be performed while the
patient is actually suffering from tonsillitis, however this increases the risk
of bleeding

Prognosis
Tonsillitis usually gets better on its own within a few days. Treating the
symptoms of sore throat and fever will make the patient more comfortable. In
cases where the fever lasts for more than forty-eight hours or reaches a
temperature of more than 102°F (38°C) the patient should be seen by a doctor.
Any medication that has been prescribed should be taken until all of it has
been taken. Patients sometimes stop taking their medications when they feel
better, but though the symptoms may have cleared up, the infection may not
have been cured. The infection may spread to other parts of the upper
respiratory (breathing) system. The ears and sinuses are especially subject to
such infection. In rare cases, much more serious conditions, such as rheumatic
fever (see rheumatic fever entry) or pneumonia (see pneumonia entry) may
develop.

C. Pharyngitis

Background Study
Pharyngitis is very common but rarely
serious. Most cases clear up on their own after
three to ten days and require no therapy other
than pain relievers to ease the discomfort. Rarely,
though, tissues may swell considerably and
obstruct breathing - a life-threatening condition.
In addition, strep throat (caused by streptococcal bacteria) requires
antibiotics to prevent complications, including rheumatic fever, a condition that
can permanently damage the heart valves.
Diphtheria is a rare but serious bacterial variety of pharyngitis.
Pharyngitis appears in three forms - nonexudative, exudative, and ulcerative:
Nonexudative - although group A streptococci may cause nonexudative
pharyngitis, viruses are by far the most common causative agents of this group.
Exudative - group A streptococcus is the most common bacterial cause of
exudative and nonexudative pharyngitis. Beta-hemolytic streptococci in groups C
and G have also been associated with exudative pharyngitis and tonsillitis.
Ulcerative - coxsackievirus A and herpes virus are the most common cause of
ulcerative pharyngitis. Vincent's angina due to fusobacteria and poor oral hygiene
may also cause ulcerative pharyngitis that is associated with malaise and low-
grade fever. The most common finding is a unilateral tonsillar ulceration with a
gray necrotic membrane.

Etiology/ Patophysiology
This is most often viral in origin. Importantly, group A streptococcal
pharyngitis must be recognized because serious complications may follow
untreated disease.

 Causes of viral pharyngitis

o Adenovirus, which may also cause laryngitis and conjunctivitis
o Influenza viruses
o Coxsackievirus
o HSV
o EBV (infectious mononucleosis)
o Cytomegalovirus
 Causes of bacterial pharyngitis
o Group A streptococci (approximately 15% of all cases of
pharyngitis)
o Group C and G streptococci
o N gonorrhoeae
o Arcanobacterium (Corynebacterium) hemolyticum
o Corynebacterium diphtheriae
o Atypical bacteria (eg, M pneumoniae, C pneumoniae): Absent lower
respiratory tract disease, the clinical significance of these
pathogens is uncertain.
o Anaerobic bacteria

Manifestations
Sore throat
Red throat
Lump in throat feeling
Fever
Headache
Swollen glands
Swollen neck lymph glands
Tender neck lymph glands
 Difficulty swallowing
Pain swallowing
Breathing difficulty

Laboratory and diagnostic tests

Your health care provider will perform a physical exam and look at your throat.
A rapid test or throat culture to rule out strep throat may be done. Additional
laboratory tests may be done depending on the suspected cause.

 GABHS rapid antigen detection test

Rapid antigen detection test for group A beta-hemolytic streptococci.

o This is the preferred method for diagnosing GAS infection in the

emergency department because of difficulties with culture follow-
up.
o Only patients with a high clinical likelihood of GAS pharyngitis
should be tested. Patients with a Centor score of 0-1 should be
treated symptomatically without testing.
o Antigens are specific, but sensitivities vary. Children with a negative
antigen test should have a follow-up culture unless the antigen
being used in the office has been shown to be as sensitive as a
culture.9
o The use of a GABHS rapid antigen detection test can decrease the
use of unnecessary antibiotics in pediatric patients when used
properly.
o Adults do not need follow-up culture after a negative antigen test
because of the low incidence of GAS in this population.
 Throat culture
o This is the criterion standard for diagnosis of GAS infection (90-
99% sensitive). Although less expensive than the rapid antigen
detection test, it is not be the best test to use in the emergency
department because of difficulty with follow-up. The guidelines that
recommend cultures for GAS screening are aimed at office-based
practices and not the emergency department.
o Patients can be treated up to 9 days after onset of symptoms to
prevent acute rheumatic fever, so immediate antibiotic therapy is
not crucial if patients can be easily contacted for follow-up should a
culture become positive.
 Mono spot is up to 95% sensitive in children (less than 60% sensitivity in
infants).
  Peripheral smear may show atypical lymphocytes in infectious
mononucleosis.2
 Perform gonococcal culture, as indicated by history.
 A complete blood count (CBC), erythrocyte sedimentation rate (ESR), and
C-reactive protein have a low predictive value and usually are not
indicated.
Imaging Studies

 Imaging studies generally are not indicated for uncomplicated viral or

streptococcal pharyngitis.
 Lateral neck film should be taken in patients with suspected epiglottitis or
airway compromise.
 Soft tissue neck CT can be used if concern for abscess or deep-space
infection exists; however, peritonsillar abscess is almost always a clinical
diagnosis. Imaging is rarely needed for diagnosis.

Procedures

 The procedure for a throat swab is to vigorously rub a dry swab over the
posterior pharynx and both tonsils, obtaining a sample of exudate. If any
exudate is obtained, then transport it dry (not in a liquid medium).

Treatment
If your doctor suspects that you have a sore throat caused by bacteria, he
or she will prescribe an antibiotic. But if your sore throat is caused by a virus,
there is no medicine that will cure it -- it will go away on its own. Cool air and
humidity are suggested to relieve symptoms. In the meantime, your doctor may
recommend gargling with salt water and taking an over the counter pain reliever
such as acetaminophen (Tylenol) or ibuprofen (Advil, Motrin). Children under 18
should not take aspirin as a pain reliever, because of the risk of a rare but
serious illness called Reye's syndrome.

Lifestyle

 Rest
 Drink lots of fluid. Water and warm broths are better than soft drinks
 Avoid drinking alcohol
 Gargle several times per day with ½ tsp. of salt in a glass of warm water
 Try throat lozenges (do not give to a child under 3 years old due to choking
hazard).
Medications
If your sore throat is caused by a bacterial infection, your doctor will prescribe an
antibiotic. Penicillin or, if you have an allergy to penicillin, erythromycin are most
commonly prescribed.

In children with early colds, begin acetaminophen or ibuprofen in an appropriate

dose on a regular schedule (every 4 hours) during the waking hours.

Other symptomatic treatments may be used if they appear to be helpful. These

include:

 Topical and systemic decongestants (neo-synephrine, pseudoephedrine);

decongestants may cause excitability.
 Antihistamine (especially at bedtime). Antihistamine may cause
drowsiness.
 Mucoevacuants (guafenesin)

Children should never be given aspirin because of the danger of it causing brain
damage. (Reyes syndrome)

Antibiotics do not shorten a cold, reduce the severity of the illness, or prevent
secondary bacterial complications.

Consider consulting your doctor :

 If the child develops a "second fever" later in the course of the cold.
 If the nasal symptoms and cough are no better or worsen after 10-14
days.
 If the child complains of ear pain (or the young child pulls at the ear).

Prognosis

 Viral pharyngitis typically resolves in 1-2 weeks.

 In patients with penicillin-sensitive streptococcal pharyngitis, symptomatic
improvement is expected within 24-72 hours after the start of treatment.
The clinician should be aware of potential complications. Treatment
failures are common and mainly attributed to poor adherence, antibiotic
resistance, and untreated close contacts. A chronic carrier state may
develop with group A streptococcal infection. Eradicating the pathogen is
difficult in these cases; however, carriers without active symptoms are
unlikely to spread group A streptococci, and they are at low risk for
 developing rheumatic fever. The risk of mortality is significant in patients
who progress to streptococcal toxic shock syndrome, which is
characterized by multiorgan failure and hypotension.
 With infectious mononucleosis from EBV, complete resolution of
symptoms may take up to 2 months. Acute symptoms rarely last more
than 4 months. EBV typically remains dormant throughout the patient's
life. Reactivation of
 the virus is not usually symptomatic.

D. Retropharyngeal abscess

Background Study

Retropharyngeal abscesses are deep neck space

infections that can pose an immediate life-threatening
emergency, with potential for airway compromise and other
catastrophic complications.
The retropharyngeal space is located immediately
posterior to the pharynx (nasopharynx, oropharynx, hypopharynx), larynx, and
trachea. The visceral (buccopharyngeal) fascia, which surrounds the pharynx,
trachea, esophagus, and thyroid, forms the anterior border of the retropharyngeal
space. Bounded posteriorly by the alar fascia, the retropharyngeal space is
bounded laterally by the carotid sheaths and parapharyngeal spaces. It extends
superiorly to the base of the skull and inferiorly to the mediastinum at the level of
the tracheal bifurcation.

Etiology/Patophysiology
The retropharyngeal space can become infected in two ways. Infection
can either spread from a contiguous area or the space can be directly inoculated
from penetrating trauma. The "classic" retropharyngeal abscess observed in
pediatric patients occurs when an upper respiratory infection (URI) spreads to
retropharyngeal lymph nodes, forming chains in the retropharyngeal space on
either side of the superior constrictor muscle.

Sources of infection can include pharyngitis, tonsillitis, adenoiditis,

adenitis, otitis, sinusitis, and other infections (ie, nasal, salivary, dental).
Degeneration/suppuration of these nodes leads to abscess formation. Infectious
sources (eg, osteomyelitis of the spine) also can spread directly anteriorly from
the prevertebral space.
Of specific interest is the group of lateral retropharyngeal nodes at the base of
the skull that bear the name of French anatomist Henri Rouviere. These
Rouviere nodes are typically not of great clinical interest, but as the primary
lymphatic drainage of the nasopharynx, they can become significant in cases
of nasopharyngeal cancer. They are also pertinent to the discussion of
retropharyngeal abscess, as they can suppurate and lead to a retropharyngeal
abscess.

Penetrating trauma can also be involved in retropharyngeal space

infection. Accidental lacerations are not uncommon in children who run and fall
down after they have placed a sharp object in their mouths. Foreign bodies (for
example, fishbones) have been implicated in penetrating trauma to the
retropharyngeal space. Iatrogenic causes of inoculation to this space include
instrumentation with laryngoscopy, endotracheal intubation, surgery, endoscopy,
feeding tube placement, and dental injections and procedures.
Complications of retropharyngeal abscesses are secondary to mass
effect, rupture of the abscess, or spread of infection. The most urgent
complication involves the abscess expanding against the pharynx or trachea,
causing airway compression. Rupture of the abscess can cause aspiration of
pus, resulting in asphyxiation or pneumonia. The infection can spread, resulting
in inflammation and destruction of adjacent tissues. Spread of the infection to the
mediastinum can result in mediastinitis, purulent pericarditis and tamponade,
pyopneumothorax, pleuritis,empyema, or bronchial erosion.

Spread of the infection laterally can involve the carotid sheath and cause
jugular vein thrombosis or carotid artery rupture. Posterior spread of infection can
result in osteomyelitis and erosion of the spinal column, causing vertebral
subluxation and spinal cord injury. The infection itself can evolve into necrotizing
fasciitis, sepsis, and death.

Hence, accurate and prompt treatment and intervention for presumed

retropharyngeal abscess is crucial to prevent significant untoward sequelae.
Clinical Findings

History

 Patients with a retropharyngeal abscess present with constitutional

complaints such as fever, chills, malaise, decreased appetite, and
irritability.
 Patients may complain of a sore throat, difficulty swallowing (dysphagia),
pain on swallowing (odynophagia), jaw stiffness (trismus), or neck
stiffness (torticollis). Small children with torticollis tend to hold their neck in
a non-neutral position and do not turn their head from side to side.
 Patients may also complain of muffled voice, the sensation of a lump in
the throat, and/or pain in the back and shoulders upon swallowing.
 Difficulty breathing may be an ominous complaint that portends impending
airway obstruction.
 Patient history is not always straightforward. Signs and symptoms
can include fever (74%), sore throat (47%), dysphagia (38%), trismus
(36%), decreased appetite (22%), voice change (18%), odynophagia
(17%), neck pain (15%), irritability (11%), and difficulty breathing (8%).
 The course of pharyngeal abscess can be insidious.
o Sometimes an upper respiratory illness can precede symptoms by
weeks.
o Many patients do not recall (or parents are not aware of) incidences
of penetrating trauma.
o Maintain a high index of suspicion, especially in patients with upper
respiratory illnesses that do not appear to resolve in a normal
course or with conventional therapy.
Physical

 Most patients with a retropharyngeal abscess are febrile. Some appear

toxic and irritable.
 Cervical lymphadenopathy, usually unilateral, is the most common
physical finding in these patients.
 Patients may have decreased or painful range of motion of their necks or
jaws.
 A neck mass or tenderness may be appreciated.
 These patients may present with a muffled "hot potato" voice (dysphonia).
 Patients in respiratory distress or those who present with stridor or
drooling have potential airway compromise and should be immediately
triaged as such.
  Address vascular complications in the physical examination.
o Jugular vein thrombophlebitis may manifest as tender induration at
the anterior sternocleidomastoid border, vocal cord paralysis, or
sepsis of an unknown source. It may also be asymptomatic.
o Carotid artery rupture can be heralded by sentinel bleeding from
the ear, nose, or mouth.
o Ecchymosis may be detected in the lateral neck.
Causes

 Most retropharyngeal space infections are spread from various sources in

the upper respiratory tract due to the retropharyngeal lymph nodes.
The lymphadenitis can form a cellulitis, which suppurate and become an
abscess.
o Possible predisposing infections can include pharyngitis, tonsillitis,
otitis, adenitis, adenoiditis, sinusitis, and nasal, salivary, and dental
infections.
o Retropharyngeal infections are also spread from contiguous
spaces, such as the parapharyngeal space (eg, abscesses),
submandibular space, or prevertebral space (eg, osteomyelitis).
 The retropharyngeal space can also be directly inoculated secondary to
penetrating trauma.
o Running and falling down with a sharp object in the mouth is not
unusual in children. Because parents may be unaware of these
predisposing events, diagnosis is even more elusive.
o Foreign bodies (for example, fishbones) can become lodged in the
posterior pharynx. Although this can happen in the pediatric age
group, a foreign body lodged in the posterior pharynx is also a
cause of abscess formation in adults.
 Deep space infections can be iatrogenic secondary to instrumentation of
the upper respiratory tract. All of the following can predispose to abscess
formation:
o Laryngoscopy
o Endoscopy
o Esophagoscopy
o Feeding tube insertion
o Endotracheal intubation
o Head and neck surgery
o Dental procedures
o Injections
 Risk factors may include low socioeconomic status, poor oral hygiene,
immune disfunction (including HIV, diabetes, and immunosuppression)
  Bacteria are often polymicrobial, with gram-positive organisms and
anaerobes predominating, but gram-negative bacteria have also been
isolated. The source is usually oropharyngeal flora.
o The most common cause is group A beta-hemolytic streptococci.
Other nonhemolytic streptococci can be present. Staphylococcus
aureus is also fairly common. The most common anaerobes
areBacteroides species.
o Other causative agents include Haemophilus
parainfluenzae and Veillonella, Peptostreptococcus,
Fusobacterium, and Eikenella species.
o The incidence of beta-lactamase production is high. One study
noted 22% beta-lactam resistance.
o Suspect mycobacterium tuberculosis, B henselae, and coccidiosis
in patients who may be predisposed (immunosupression, recent
immigrants), especially if they are not responding to more
conventional therapy.
o Another consideration when evaluating these patients is the
possibility of Lemierre syndrome (septic thrombophlebitis of the
internal jugular vein from a head and neck infection (eg,
retropharyngeal abscess). This infection is classically associated
with the Fusobacterium necrophorum, an anaerobic, gram-negative
rod

Laboratory/ Diagnostic tests

Laboratory Studies

 Complete blood count

o The mean white blood cell (WBC) count in one study was 17,000,
with a range of 3100-45,900.
o WBC counts in 18% of the patients were less than 8000; thus, a
normal WBC count does not rule out the diagnosis of
retropharyngeal abscess.
o In a study in Germany, the mean WBC (±standard deviation was
14,700 [±10,500]), with a range from 200-114,000.
 Blood cultures are indicated before administration of intravenous
antibiotics, but culture results may be negative in as many as 82% of
retropharyngeal abscess cases.
 A culture of pus, aspirated at the time of surgical drainage of the
retropharyngeal abscess, can grow one or more organisms 91% of the
time.
  C-reactive protein
o In one study of adults and children with deep cervical space
infections, patients with C-reactive protein level greater than 100
had longer hospital stays.
o In a German study, mean (±standard deviation) C-reactive protein
level was 15.7 (±12.9), with a range from 0.0-74.
Imaging Studies

 Lateral neck radiography

o Widening of the retropharyngeal soft tissues was observed in 88%
of patients with retropharyngeal abscess in a series that defined
soft tissue swelling as more than 7 mm at C2 and more than 14 mm
at C6. Most authors define retropharyngeal soft tissue swelling as
more than 7 mm at C2 and more than 22 mm at C6; thus, lateral
neck radiographs may be considerably less sensitive for detecting
retropharyngeal abscess than this study indicates.
o Generally, the anteroposterior diameter of the prevertebral soft
tissue space in children should not exceed that of the contiguous
vertebral bodies.
o In addition to showing widening of the prevertebral space, the
lateral neck radiograph rarely may show a gas-fluid level, gas in the
tissues, or a foreign body.

 CT scan of the neck

o A CT scan of the neck with intravenous contrast is very useful in
the diagnosis and management of retropharyngeal abscess.
Retropharyngeal abscess appears as a hypodense lesion in the
retropharyngeal space with peripheral ring enhancement. Other
findings on CT scan include soft-tissue swelling, obliterated fat
planes, and mass effect.
o Obtain a CT scan of the neck with intravenous contrast when the
findings on the lateral neck radiograph are equivocal or if the
clinical suspicion for retropharyngeal abscess is high in patients
with negative findings on lateral neck radiograph. Lateral neck
radiographic findings may be misleading, especially in young
children.
o A CT scan of the neck with intravenous contrast also may be useful
if the radiographic findings are positive because the CT scan can
differentiate between retropharyngeal abscess and cellulitis. The
 CT scan also shows the extent of the retropharyngeal abscess and
its relation to the great vessels, which is very helpful to the surgeon.
o CT scan of the neck can also differentiate between retropharyngeal
abscess and retropharyngeal lymphadenopathy in children, which
may help the ear, nose, and throat (ENT) surgeon decide whether
to treat with intravenous antibiotics alone or intravenous antibiotics
plus surgical drainage.
 A chest radiograph is indicated to look for aspiration pneumonia and
mediastinitis.
 An MRI with gadolinium enhancement may demonstrate a retropharyngeal
abscess, but this modality has not been used widely.
 Ultrasonography may demonstrate the presence of a retropharyngeal
abscess, but its use has not yet been clarified.
Procedures

 Nasopharyngolaryngoscopy
o A review of the literature did not reveal a role for
nasopharyngolaryngoscopy use in the diagnosis of retropharyngeal
abscess.
o Safety of this procedure in the setting of retropharyngeal abscess is
unclear.
o Nasopharyngolaryngoscopy has been performed preoperatively in
2 adults; no reports of its use in children exist.
 Endotracheal intubation
o Securing the airway may be required if the patient with
retropharyngeal abscess is exhibiting signs of impending upper
airway obstruction. Endotracheal intubation may be attempted, but
it may be difficult because of distortion of the upper airway.
o Prophylactic intubation for a patient with retropharyngeal abscess
but without respiratory distress generally is not indicated unless an
interhospital transfer is planned.
 If a patient with signs of upper airway obstruction cannot be intubated, a
surgical or needle cricothyrotomy may be required.
 A tracheostomy may be required as definitive airway management in
patients with retropharyngeal abscess and respiratory distress.
Treatment
Prehospital Care

 Supplemental oxygen and attention to upper airway patency are the

essential components of prehospital care in patients with suspected
retropharyngeal abscess.
 If a child exhibits respiratory distress, the sniffing position may be
beneficial.
 Occasionally, endotracheal intubation or cricothyrotomy may be required if
the patient exhibits signs of upper airway obstruction.

Emergency Department Care

ED management of retropharyngeal abscess includes attention to the airway,
fluid resuscitation if necessary, antibiotic treatment, and preparation for an
emergency operation. Frequent vital sign checks and continuous oxygen
saturation monitoring are essential.

 Airway management
o Apply supplemental oxygen. In young children, this can be
completed in a nonthreatening way by letting the parent direct blow-
by oxygen at the child's face.
o Endotracheal intubation may be required if the patient has signs of
upper airway obstruction. It may be difficult because of upper
airway swelling.
o Cricothyrotomy (surgical or needle) may be required in the patient
with upper airway obstruction who cannot be intubated.
Tracheostomy may be required for definitive airway management.
 Intravenous fluids are required if the patient is dehydrated because of
fever and difficulty swallowing.

Medications
The goals of pharmacotherapy are to eradicate the infection, to reduce
morbidity, and to prevent complications. Intravenous broad-spectrum antibiotic
coverage is indicated in the treatment of retropharyngeal abscess.

Antibiotics

Gram-positive organisms (including beta-lactamase producing), gram-

negative organisms, and anaerobes must be covered. penicillin and oxacillin,
second- or third-generation cephalosporin and clindamycin, penicillinase-
resistant penicillin combined with either clindamycin or metronidazole, or third-
generation cephalosporin in combination with clindamycin, nafcillin, or both (triple
therapy).

In a review of retropharyngeal infections in children by Wald, the

recommendation was to add vancomycin or linezolid to the regimen in patients
not responding to clindamycin, and in patients who present with severe disease,
in order to cover MRSA

Prognosis
It is important to get immediate medical help. This condition can lead to blockage
of the airway, which can be life-threatening. With prompt treatment, you can
make a full recovery.
E. Epistaxis

Background Study
Epistaxis, or nosebleed, is a common pediatric complaint.
Most incidents are rarely life threatening but cause significant
parental concern.1 Most nosebleeds are benign, self-limiting, and
spontaneous but may also be recurrent. Many uncommon causes
are also noted.
Epistaxis can be divided into 2 categories, anterior bleeds
and posterior bleeds, based on where the bleeding originates.

Etiology/ Patophysiology
Ninety per cent of epistaxis in children originates from Little’s
area in the anterior part of the nose, often being either idiopathic or the result of
trauma. Idiopathic epistaxis forms the most common aetiological category (Table
I).
Although bleeding may occur spontaneously, it often results from forceful
nose blowing and sneezing which increases arterial and venous pressure in the
vascularised nasal septum, which usually accompanies allergic rhinitis,
viral/bacterial URIs and trauma/sepsis secondary to foreign bodies. Posterior
epistaxis is uncommon in children and is usually the result of bleeding disorders,
inflammatory disorders or neoplasms. Persistent or recurrent epistaxis should
raise the suspicion of bleeding disorders or neoplasms, necessitating further
investigation.
Nosebleeds are due to the rupture of a blood vessel within the richly perfused
nasal mucosa. Rupture may be spontaneous or initiated by trauma. Nosebleeds
are reported in up to 60% of the population with peak incidences in those under
the age of ten and over the age of 50 and appear to occur in males more than
females. An increase in blood pressure (e.g. due to general hypertension) tends
to increase the duration of spontaneous epistaxis. Anticoagulant medication and
disorders of blood clotting can promote and prolong bleeding. Spontaneous
epistaxis is more common in the elderly as the nasal mucosa (lining) becomes
dry and thin and blood pressure tends to be higher. The elderly are also more
prone to prolonged nose bleeds as their blood vessels are less able to constrict
and control the bleeding.
The vast majority of nose bleeds occur in the anterior (front) part of the
nose from the nasal septum. This area is richly endowed with blood vessels
(Kiesselbach's plexus). This region is also known as Little's area. Bleeding
farther back in the nose is known as a posterior bleed and is usually due to
rupture of the sphenopalatine artery or one of its branches. Posterior bleeds are
often prolonged and difficult to control. They can be associated with bleeding
from both nostrils and with a greater flow of blood into the mouth.

Laboratory and diagnostic tests

For the most part, laboratory studies are not needed for first-time or infrequent
recurrences with a good history of nose picking or trauma to the nose.

 If significant blood loss, leukemia, or malignancy is suspected or if

recurrent bleeding occurs, perform a CBC count with differential.
 If a coagulopathy is suspected, perform CBC count and obtain
prothrombin time (PT)/activated partial thromboplastin time (aPTT) and
bleeding time.
Direct visualization with a good directed light source, nasal speculum (see image
below), and nasal suction should be sufficient in most patients

Treatment
Medical Care
Initial treatment begins with direct pressure by squeezing the nostrils
together for 5-30 minutes straight, without frequent peeking to see if the bleeding
is controlled. Usually only 5-10 minutes is required.
 Patients should keep their heads elevated but not hyperextended because
hyperextension may cause bleeding into the pharynx and possible aspiration.
This maneuver works more than 90% of the time.
If bleeding is caused by excessive dryness in the home (eg, from radiator
heating), patients may benefit from the following care options:

 Humidify the air with a cool mist vaporizer in the bedroom.

 Alternately, a metal basin of water may be placed on top of a radiator to
humidify the ambient air.
 Nasal saline sprays are useful. Oxymetazoline (Afrin) may also be used,
with fewer cardiac adverse effects. These agents should only be used for
3-5 days at a time to avoid rhinitis medicamentosa and tachyphylaxis.
 The physician may consider local application of bacitracin or petrolatum
ointment directly to the Kiesselbach area with a cotton applicator to
prevent further drying (studies recommend 2 wk).
 If direct pressure is not sufficient, gauze moistened with epinephrine at a
ratio of 1:10,000 or phenylephrine (Neo-Synephrine) may be placed in the
affected nostril to help vasoconstrict and achieve hemostasis.

Diet
While bleeding is occurring and the assessment is in process, the child
should remain nothing by mouth (NPO). Once bleeding is controlled, a full diet
can be started.
Activity
Patients with a simple controlled bleed may resume regular activity;
however, instruct individuals not to forcefully blow or pick their noses. For a few
days, avoiding contact sports or activities that may directly traumatize the nose is
probably prudent.

No medications are required for simple epistaxis. An antibiotic with

staphylococcal coverage (eg, oral cephalexin, intravenous cephazolin) or
antistaphylococcal penicillin (eg, orla dicloxacillin, intravenous nafcillin) is
required for patients sent home or admitted with anterior or posterior packing in
place.

Antibiotic agents
Antibiotics with staphylococcal and streptococcal coverage are required if
nasal packing is placed. The oral route is used most commonly because most
patients are treated on an outpatient basis. If the patient requires admission,
initially use intravenous medications. Continue all antibiotics until the packing is
removed

Management

How do you stop the common nosebleed?

Most people who develop nose bleeding can handle the problem without the
need of a physician if they follow the first aid recommendations below:

1. Pinch all the soft parts of the nose together between your thumb and index
finger.
2. Press firmly toward the face - compressing the pinched parts of the nose
against the bones of the face.
3. Lean forward slightly with the head tilted forward. Leaning back or tilting
the head back allows the blood to run back into your sinuses and throat
and can cause gagging or inhaling the blood.
4. Hold the nose for at least five minutes. Repeat as necessary until the nose
has stopped bleeding.
5. Sit quietly, keeping the head higher than the level of the heart. Do not lay
flat or put your head between your legs.
6. Apply ice (wrapped in a towel) to nose and cheeks.

Surgical Care
Cauterization of an identified small bleeding area (only one side should be
cauterized at a time to avoid possible septal perforation)

 Can be performed with silver nitrate sticks

 Caution advised not to burn the entire septum or cause perforation (septal
perforation is a risk)
 Performed in only one nostril at a time
 Used very judiciously; must avoid nasal tissues other than the bleeding
site of septum
 Presents risk of nasal stenosis of the vestibule
Nasal packing items and procedures

 Quarter-inch strips of gauze impregnated with petroleum jelly, layered with

the use of bayonet forceps (see images below)
 Bayonet forceps.
 Vaseline gauze packing.

 Oxycel cotton with bacitracin, which dissolves and does not have to be
removed, preferred by some (especially helpful in patients with leukemia)
 Merocel or other tamponlike packing (see image below) that expands
when water is injected into it
Expandable (Merocel) packing (dry).

 Epistat, Rapid Rhino, or other balloon inflation catheter (see image below)
Epistat anterior and/or posterior nasal catheter.

 Ligation of vessels
 Angiographic embolization

Prognosis
With a little patience and pressure, almost all uncomplicated anterior
nosebleeds respond to simple first-aid measures. Even the rare nosebleed that
requires a doctor's care usually can be treated successfully with cauterization,
packing or other options. Even severe posterior nosebleeds can be controlled
with appropriate first-aid measures at home.
Some people who have excessive bleeding, multiple medical problems or
who are taking anticoagulant medications may need to be hospitalized for
treatment of a nosebleed.

F. SINUSITIS

 Sinuses are hollow air spaces in the human body. In relation to the
respiratory system, each sinus cavity has an opening into the nose for free
exchange of air and mucus and is joined with the nasal passages by a
continuous mucous membrane lining. The maxillary (behind the cheek)
and ethmoid (between the eyes) sinuses are small but present at birth.
The child’s sinus cavities are not fully developed until 20 years of age,
which makes the child vulnerable to sinus infection. Sinusitis is an
infection of the sinus cavities.
Etiology:

 It occurs as a secondary infection in older children when streptococcal,

staphylococcal, or H. influenzae organisms spread from the nasal cavity.

Pathophysiology
The ostiomeatal complex (OMC) is believed to be the critical anatomic structure
in sinusitis and is entirely present, although not at full size, in newborns. Present
within the middle meatus, the OMC is composed of the uncinate process,
infundibulum ethmoidalis, hiatus semilunaris, ethmoid bulla, and frontal recess.
Although obstruction of the OMC has not been proven to be the primary source
for pediatric sinusitis, changes occurring in the anterior ethmoids are known to
impair drainage through the OMC, resulting in chronic maxillary sinusitis and,
occasionally,frontal sinusitis.

The normal metachronous movement of mucous toward the natural ostia of the
sinuses and eventually to the nasopharynx can be disrupted by mucosal
inflammation. This most commonly occurs secondary to routine viralupper
respiratory tract infections (URTIs) or nasal allergies and the host response to
these insults. In addition, many other predisposing factors to chronic disease
exist, including allergic rhinitis, anatomical abnormalities,gastroesophageal
reflux (GER), immune deficiency, and disorders of ciliary function.

S/S:

 fever,
 a purulent nasal discharge
 headache,
 tenderness over the affected sinus.

Diagnostic Test:

 A nose and throat culture will identify the infectious organism.

Treatment:

 for acute sinusitis consists of an:

o antipyretic for fever
o an analgesic for pain
o an antibiotic for the specific organism involved.

 Oxymetazoline hydrochloride (Afrin), supplied as nose drops or a nasal

spray, shrinks the edematous mucous membranes and allows infected
material to drain from the sinuses.
 To avoid a rebound effect, this type of nasal spray should be used for only 3
days at a time; otherwise, it actually causes more nasal congestion than was
present originally.
 Warm compresses to the sinus area may encourage drainage and relieve
pain.
 Some children need acetaminophen (Tylenol) for pain.

Patient Education

 Child should not dive.

 Child should not travel by airplane.
 Urge parent to eliminate triggers in the home (dust, smoking)
 Have all members of the family treated, if indicated.

Prognosis of Sinusitis: Sinusitis can be acute (going on less than four

weeks), subacute(4-12 weeks) or chronic (going on for 12 weeks or more)

.
G. LARYNGITIS

Laryngitis: Laryngitis is an inflammation of the mucous membrane lining

the larynx which is located in the upper part of the respiratory tract

CAUSES

Viral infection - common cause of acute laryngitis

Allergies

Larynx cancer

ent coughing (see Severe cough)

Chlamydia pneumoniae - laryngitis
Chemical poisoning -- Acrylic acid - laryngitis
Common cold

-hemolytic streptococcus
Haemophilus influenzae
Streptococcus pneumoniae
Rhinovirus - laryngitis
Tumour

Influenza
cal
 Tuberculosis
Barrett's esophagus - Laryngitis
Moraxella catarrhalis infection - laryngitis
infection

underlying disorder, such as pneumonia or tuberculosis

Postnasal drip

polyps
see Coughing spasms)
Smoking
see Alcohol use)

Signs and Symptoms

 Hoarseness
 Loss of voice
 Sore throat
 Difficulty swallowing
 Lump in throat feeling
 Fever
 Symptoms of laryngitis can vary, depending on the severity and also the cause.
The most common, and obvious, symptom is
 Impaired speech, ranging from a raspy hoarseness to the total loss of ability to
speak, except at a whisper.
 Dry, sore throat
 Coughing
 Sensation of swelling in the area of the larynx
 Cold or flu-like symptoms
 Swollen lymph glands in the throat, chest, or face
 Sensation of a lump in the throat or constant need to clear the throat
 Difficulty breathing
 Difficulty singing
 Difficulty eating
 Treatment List for Laryngitis

 Symptomatic treatment
 Resting the voice
 Steam inhalation
 Analgesics
 Voice rest
 Antibiotics, Antifungal, Antacid medication
 Throat lozenges
 Warm liquids
 Cool mist humidifier
 Cessation of smoking, alcohol
 Speech therapy

Prognosis of Laryngitis:

It is a minor ailment and clears up on its own within a few days or weeks.

H. CROUP (LARYNGOTRACHEOBRONCHITIS)

 Croup (inflammation of the larynx, trachea, and major bronchi) is one of the
most frightening diseases of early childhood for both parents and children.
 parainfluenza virus. In previous years, the most common cause wasH.
influenzae.

Assessment:

 children typically have only a mild upper respiratory tract infection at bedtime.
 Temperature is normal or only mildly elevated.
 During the night, they develop a barking cough (croupy cough),
 inspiratory stridor
 marked retractions.
 They wake in extreme respiratory distress.
 The larynx, trachea, and major bronchi are all inflamed.

Therapeutic Management

 to run the shower or hot water tap in a bathroom until the room fills with
steam, then keep the child in this warm, moist environment.
 cool moist air with a corticosteroid such as dexamethasone, or racemic
epinephrine, given by nebulizer, can reduce inflammation and produce
effective bronchodilationto open the airway
 Intravenous therapy may be prescribed to keep the child well hydrated.
  Maintain accurate intake and output records and test urine specific gravity
to ensure that hydration is adequate.

I. EPIGLOTTITIS

 Epiglottitis is inflammation of the epiglottis (the flap of tissue that covers

the opening to the larynx to keep out food and fluid during swallowing).
 It occurs most frequently in children from 2 to about 7 years of age .
 Epiglottitis can be either bacterial or viral in origin. H. influenzae type B
has been replaced as the most common bacterial cause of the disorder by
pneumococci, streptococci, or staphylococci. Echovirus and respiratory
syncytial virusalso can cause the disorder.

Assessment:
 Symptoms begin as those of a mild upper respiratory tract infection.
 After 1 or 2 days, as inflammation spreads to the epiglottis,
 the child suddenly develops severe inspiratory stridor
 a high fever
 hoarseness
 a very sore throat.
 difficulty swallowing that he or she drools saliva
 child may protrude the tongue to increase free movement in the pharynx.

If a child's gag reflex is stimulated with a tongue blade, the swollen and inflamed
epiglottis can be seen to rise in the back of the throat as a cherry-red structure. It
can be so edematous, however, that the gagging procedure causes complete
obstruction of the glottis and respiratory failure. Therefore, in children with
symptoms of epiglottitis (dysphagia, inspiratory stridor, cough, fever, and
hoarseness), never attempt to visualize the epiglottis directly with a tongue blade
or obtain a throat culture unless a means of providing an artificial airway, such as
tracheostomy or endotracheal intubation, is readily available. This is especially
important for the nurse who functions in an expanded role and performs physical
assessments and routinely elicits gag reflexes.

Diagnostic Test:

 leukocytosis (20,000 to 30,000 mm3), with the proportion of neutrophils

increased.
 A blood culture to evaluate for septicaemia
 ABGs to evaluate respiratory sufficiency may be ordered.

Therapeutic Management:

 Children need moist air to reduce the epiglottal inflammation.

 If cyanosis is present, they need oxygen.
  An antibiotic, such as a second-generation cephalosporin (e.g.,
cefuroxime).
 Because they can't swallow, children need intravenous fluid therapy to
maintain hydration.
 They may need a prophylactic tracheostomy or endotracheal intubation to
prevent total obstruction, although it is often difficult to intubate children
with epiglottitis because the tube cannot be passed beyond the
edematous epiglottis.
 After antibiotic therapy begins, the epiglottal inflammation recedes rapidly.
By 12 to 24 hours, it has reduced enough that the airway may be
removed.
 Antibiotic administration will continue for a full 7 to 10 days.
 Siblings of the ill child may be prescribed prophylactic antibiotic therapy to
prevent them from developing the same symptoms.

Nursing Diagnoses and Related Interventions

Nursing Diagnosis:
Ineffective airway clearance related to edema and constriction of airway

Outcome Evaluation:
Respiratory rate is below 22 breaths/min; no cyanosis is present; PO2 is 80 to
100 mm Hg; SaO2 is over 95%.
Attach a sensor for pulse oximetry monitoring and remain constantly with a child
with croup, not only to observe closely for increasing respiratory distress but also
to reduce the child's anxiety. Take vital signs as often as every 15 minutes,
because extreme restlessness and thrashing, increased stridor, increased heart
and respiratory rates, and cyanosis are symptoms of oxygen deprivation. In
some children, it is difficult to distinguish between fright from the newness of the
experience (and their sense of their parents' fright) and the anxiety that comes
from oxygen deprivation. Keep a continuous record of vital signs and activity as a
way to demonstrate increasing respiratory rate and restlessness. ABGs may be
obtained to assess for sufficient oxygenation if pulse oximetry is not being used.
A tracheostomy or endotracheal intubation along with oxygen therapy may be
necessary if symptoms do not diminish. (It is difficult to intubate children with
croup because of the severe respiratory tract edema.)
Laryngospasm with total occlusion of the airway can occur when a child's gag
reflex is elicited or when the child is crying. Therefore, do not elicit a gag reflex in
any child with a croupy, barking cough, and provide comfort to prevent crying.
Croup is a frightening disease for parents because their child is suddenly ill with
severe symptoms. When the severe symptoms disappear by morning, parents
may feel foolish they rushed to a hospital with the child in the middle of the night.
Assure them that their initial judgment was correct. When they brought the child
in, he or she was seriously ill. Parents may be reluctant to see their child
discharged in the morning until they are convinced that he or she is now well
enough to go home (Box 40.10).

TABLE 40.5 Comparison of Laryngotracheobronchitis (Croup) and

Epiglottitis

Assessment Laryngotracheobronchitis Epiglottitis

Causative Usually viral Usually pneumococci or
organism streptococci
Usual age of 6 mo–3 yr 3–6 yr
child
Seasonal Late fall and winter None
occurrence
Onset pattern Preceded by upper respiratoryPreceded by upper
infection; cough becomes worse respiratory infection;
at night suddenly very ill
Presence of Low grade Elevated to about 103°F
fever
Appearance Retractions and stridor; prolonged Drooling; very ill-appearing;
inspiratory phase of respirations; neck hyperextended to
not very ill-appearing breathe. (Do not attempt to
view enlarged epiglottis, or
immediate airway obstruction
can occur.)
Cough Sharp, barking Muffled cough
Radiographic Lateral neck radiograph showing Lateral neck radiograph
findings subglottal narrowing showing enlarged epiglottis
Possible Asphyxia due to subglottic Asphyxia due to supraglottic
complications obstruction obstruction

II. LOWER RESPIRATORY DISORDER

A. Influenza

- involves inflammation and infection of the trachea and bronchi, caused by

orthomyxoviruses types A, B, and C. The virus attaches to and penetrates
respiratory epithelial cells where viral replication occurs, which results in the
destruction of the host cell.

- can be transmitted through direct contact such as kissing, touching or holding

hands with an infected person, indirect contact, and droplet when a person
coughs or sneezes.
SIGNS/SYMPTOMS

• Sore throat • Vomiting

• Cough • Diarrhea
• Aching pains • Chills and shakes
• Fatigue • Loss of appetite
• Fever

DIAGNOSTIC PROCEDURES

 nasopharyngeal or nasal swab, and nasal wash or aspirate. Samples

should be collected within the first 4 days of illness.
 Routine serological testing for influenza
 some respiratory samples should be tested by both rapid tests and by viral
culture. The collection of some respiratory samples for viral culture is
essential for determining the influenza A subtypes and influenza A and B
strains causing illness, and for surveillance of new strains that may need
to be included in the next year's influenza vaccine.

MANAGEMENT

Antipyretic suh as acetaminophen (Tylenol) are given to reduce fever. A new

antiviral drug, Oseltamivir (TamiFlu), is given to children above 1 year of age at
the first sign of illness, to halt virus replication. An influenza vaccine must also be
readministered yearly.

DIAGNOSIS

1. Fluid Volume Deficit: Related to fever, increased secretions, decreased

appetite, possible vomiting/diarrhea
2. Imbalanced Body Temperature (Fever): Related to influenza
3. Altered Nutrition: Less Than Body Requirements: Related to decreased
appetite
4. Acute Pain: Related to influenza (body aches, possible chest pain, headache,
etc)

PROGNOSIS

Most people recover fully from the flu. But some develop serious complications.
Complications can include life-threatening conditions such as pneumonia.
B. Bronchitis

- inflammation of the major bronchi and trachea

- one of the more common illnesses affecting preschool and school-age
children
 - Causative agents include the influenza viruses, adenovirus, and
Mycoplasma pneumonia

SIGNS/SYMPTOMS

• Fever • Nasal congestion

• Cough • Crackles/rales
• Sore throat • Malaise
DIAGNOSTIC PROCEDURES

 Chest X-Ray
 Complete Blood Count (CBC)
Test
 History and Physical Exam
 Sputum Smear Examination
 Lung Function Tests
 X-Ray
MANAGEMENT
• Analgesic and antipyretic agents - are used to control fever, myalgias, and
arthralgias.
• Bronchodilators
• Antibiotics
• Antivirals

DIAGNOSIS

Ineffective airway clearance related to excessive, thickened mucous secretions

PROGNOSIS

In an average, healthy person, acute bronchitis typically clears up quickly on its own or
with antibiotic treatment. Some people, including the elderly, infants, smokers or people
with heart or lung disorders, are at higher risk of developing pneumonia from acute
bronchitis.

C. Bronchiectasis

- Greek bronchion, meaning windpipe, and ektasis, meaning stretched

- dilatation of bronchi with destruction of elastic walls
- due to acute/chronic infection or inflammation, anatomic airway obstruction
- chronic dilatation and plugging of the bronchi
- may follow pneumonia, aspiration of a foreign body, pertussis, or asthma
- often associated with cystic fibrosis

SIGNS/SYMPTOMS

- Chronic, productive cough

- Occasional hemoptysis
- Wheezing/stridor in infants
- Shortness of breath

MANAGEMENT

• Antibiotics
• Bronchodilators - indicated when bronchial hyperreactivity is evident, used to
improve ciliary beat frequency and, thus, facilitate mucus clearance
• Chest physiotherapy: Manual and mechanical interventions such as chest
percussion, vibration, postural drainage
DIAGNOSIS

1. Impaired gas exchange related to ventilation–perfusion inequality

2. Ineffective airway clearance related to bronchoconstriction, increased mucus
production, ineffective cough, bronchopulmonary infection, and other
complications
3. Ineffective breathing pattern related to shortness of breath, mucus,
bronchoconstriction and airway irritants
4. Self-care deficits related to fatigue secondary to increased work of breathing and
insufficient ventilation and oxygenation
5. Activity intolerance due to fatigue, hypoxemia, and ineffective breathing patterns
6. Ineffective coping related to reduced socialization, anxiety, depression, lower
activity level, and the inability to work
7. Deficient knowledge about self-management to be performed at home.

PROGNOSIS

Early recognition and adequate treatment can help control bronchiectasis and decrease
symptoms. Life- long awareness of the need for treatment may allow people with
bronchiectasis to minimize complications and maximize life expectancy.

The outlook depends upon the underlying reason for developing bronchiectasis.
Congenital causes of bronchiectasis, like cystic fibrosis, may have a worse prognosis
than acquired diseases.

D. Status Asthmaticus

- When children fail to respond and an attack continues

- Caused by:
• viral respiratory illness
• following exposure to a potent allergen or irritant
• after exercise in a cold environment
• history of endotracheal intubation and mechanical ventilation
• frequent emergency department visits
• poor adherence to the medical regimen

SIGNS/SYMPTOMS

• Chest tightness
• Hyperexpanded chest, and accessory muscles (sternocleidomastoid and
intercostal muscles) are used
• Audible wheezing
• Rapidly progressive shortness of breath
• Tachypnea/tachycardia
• Dry cough
DIAGNOSTIC PROCEDURES

- CBC count and differential to evaluate for infectious causes (eg, pneumonia, viral
infections such as croup), allergic bronchopulmonary aspergillosis, and Churg-Strauss
vasculitis

- arterial blood gas (ABG) value to assess the severity of the asthma attack and to
substantiate the need for more intensive care. The 4 stages of blood gas progression in
persons with status asthmaticus are as follows:

 The first stage is characterized by hyperventilation with a normal partial pressure

of oxygen (PO2).
 The second stage is characterized by hyperventilation accompanied by
hypoxemia (ie, a low partial pressure of carbon dioxide [PCO2] and low PO2).
 The third stage is characterized by the presence of a false-normal PCO2;
ventilation has decreased from the hyperventilation present in the second stage.
This is an extremely serious sign of respiratory muscle fatigue that signals the
need for more intensive medical care, such as admission to the ICU and,
probably, intubation with mechanical ventilation.
 The last stage is characterized by a low PO2 and a high PCO2, which occurs with
respiratory muscle insufficiency. This is an even more serious sign that mandates
intubation and ventilatory support.

- chest radiograph to evaluate for pneumonia, pneumothorax, congestive heart failure,

and signs of chronic obstructive pulmonary disease, which would complicate the
patient's response to treatment or reduce the patient's baseline spirometry values

MANAGEMENT

- Ipratropium treatment
- Oxygen therapy
- Fluid replacement
- Antibiotics

DIAGNOSIS

1. Risk for suffocation related to bronchospasm, mucous secretion and edema

2. Risk for fluid volume deficit related to difficulty taking fluids, insensible losses from
hypoventilation and diaphoresis

3. Risk for injury related to hypoventilation and dehydration

PROGNOSIS
In general, unless a complicating illness such as congestive heart failure or chronic
obstructive pulmonary disease is present, with appropriate therapy status asthmaticus
has a good prognosis. A delay in initiating treatment is probably the worst prognostic
factor. Delays can result from poor access to health care on the part of the patient or
even delays in using steroids. Patients with acute asthma should use steroids early and
aggressively.

E. Respiratory Syncytial Virus Bronchiolitis

- most common cause of bronchiolitis in young children

- can be transmitted through: direct contact, indirect contact, and droplet

In the community setting, a number of factors have been associated with increased risk
of acquiring RSV disease, including the following:

- Childcare attendance
- Older siblings in preschool or school
- Crowding, lower socioeconomic status
- Exposure to environmental pollutants (eg, cigarette smoke)
- Multiple birth sets (especially triplets or greater)
- Minimal breastfeeding

SIGNS/SYMPTOMS

 Fever (typically low-grade)

 Cough
 Tachypnea
 Cyanosis
 Retractions
 Wheezing
 Rales
 Sepsislike presentation or apneic episodes (in very young infants)

DIAGNOSTIC PROCEDURES

- CBC count, serum electrolytes, urinalysis, and oxygen saturation measurement. The
CBC count may reveal a normal or mildly elevated WBC count and an elevated
percentage of band forms. Blood cultures, although obtained frequently, are rarely
positive for pathogenic bacteria.

- An arterial blood gas may be indicated if carbon dioxide retention is a concern.

- tests can be performed on samples of secretions obtained by washing, suctioning, or

swabbing the nasopharynx. Secretions can be analyzed for virus in the laboratory by
culture and/or antigen revealing techniques.
- Chest radiography is frequently obtained in children with severe RSV infection. Chest
radiography typically reveals hyperinflated lung fields with a diffuse increase in
interstitial markings. In 20-25% of cases, focal areas of atelectasis and/or pulmonary
infiltrate are also noted.

MANAGEMENT

• Supportive treatment
• Isolation
• Ribavirin, antiviral

PROGNOSIS

Children hospitalized secondary to RSV infection typically recover and are discharged in
3-4 days. High-risk infants remain hospitalized longer and have higher rates of ICU
admission and mechanical ventilation.

Infants hospitalized due to RSV infection have higher rates of subsequent wheezing
than age-matched controls not hospitalized for this condition over the next 10 or more
years. Whether RSV leads to alterations of airways and/or immune responses that
contribute to these subsequent events or is just a marker for abnormal airways is still
not completely understood.

F. PNEUMONIA

DESCRIPTION

 Infection and inflammation of alveoli. It occurs at a rate of 2-4 children in 100.

Most common cause of pulmonary death in infants younger than 48 hours.

ETIOLOGY

 It maybe of bacterial origin (pneumococcal, streptococcal or chlamydial) or viral

(RSV).
 Aspiration of lipid or hydrocarbon substances also causes pneumonia.

TYPES

1. PNEUMOCOCCAL PNEUMONIA
The onset of pneumococcal pneumonia is abrupt and follows an upper
respiratory tract infection. In infants, pneumonia tends to remain
bronchopneumonia with poor consolidation. In older children, pneumonia may
localize in a single lobe, and consolidation may occur.

 MANIFESTATION
- High fever
- Nasal flaring
- Retractions
- Chest pain
- Chills
- Dyspnea
- Tachypnea
- Tachycardia
- Diminished respiratory function
- Bronchial breath sounds

 LABORATORY
- Chest X ray
- Leukocytosis

 TREATMENT
- Antibiotics: Ampicillin or third generation cephalosphorins
- Amoxicillin clavulanate (Augmentin) maybe prescribed for penicillin-
resistant organisms
- Antipyretic: Acetominaphin (febrile)

 MANAGEMENT
- Intravenous therapy
- Humidified oxygen

 NURSING MANAGEMENT
- Turning and repositioning to avoid pooling of secretions
- Chest physiotherapy
 NURSING DIAGNOSIS
- Ineffective airway clearance
- Impaired gas exchange
- Acute pain
- Risk for infection
- Risk for fluid volume deficit
2. CHLAMYDIAL PNEUMONIA

Most often seen in newborns up to 12 weeks of age because the chlamydial

organism is contracted from the mother’s vagina during birth.

 MANIFESTATION
- Nasal congestion
- Sharp cough
- Failure to gain weight
- Tachypnea
- Wheezing and rales on auscultation
 LABORATORY
- Elevated level of immunoglobulin IgG and IgM antibodies
- Peripheral eosinophilia
- Specific antibody to C. trachomatis
 TREATMENT
- Macrolide antibiotic: erythromycin

3. VIRAL PNEUMONIA

Generally caused by the viruses of the upper respiratory tract infection (RSV,
myxovirus or adenovirus).

 MANIFESTATION
- Begins as an upper respiratory tract infection
- Low grade fever
- Nonproductive cough
- Tachypnea
- Diminished breath sounds
- Fine rales
 LABORATORY
- Chest X ray: diffuse infiltrated areas
 MANAGEMENT
- Rest
- Antipyretic (febrile)
- Intravenous fluid
4. MYCOPLASMAL PNEUMONIA

Occurs more frequently in children in children over 5 years of age and more often
during winter.

 MANIFESTATION
- Fever
- Cough
- Feels ill
- Enlarged cervical lymph nodes
- Persistent rhinitis
 TREATMENT
- Erythromycin: for children younger than 8 years old

5. LIPID PNEUMONIA

Caused by the aspiration of an oily or lipid substance. It is much less common

than it was once because children are not given oil-based tonics anymore.

 MANIFESTATION
- Initial coughing spell at time of aspiration
- Period of symptomless
- Chronic cough
- Dyspnea
- General respiratory distress
 LABORATORY
- Chest X ray: densities at affected site
 TREATMENT
- Antibiotic therapy if secondary bacterial infection has occurred
 MANAGEMENT
- Surgical resection of lung portion
-
6. HYDROCARBON PNEUMONIA

Common household products like furniture, polish, cleaning fluids causes

childhood poisoning which results to hydrocarbon pneumonia.

 MANIFESTATION
- Nausea and vomiting
- Drowsy
 - Cough
- Increased and dyspneic respirations
- Increased percussion sound
- Rales
 MANAGEMENT
- Supplemental oxygen: cool, moist air
- Antipyretic (febrile)
- Positioning
- Chest physiotherapy

G. ATELECTASIS

DESCRIPTION

 The collapse of lung alveoli. It may occur in children as a primary or

secondary condition.

TYPES

1. PRIMARY ATELECTASIS

Occurs in newborns who do not breathe with enough respiratory strength at birth
to inflate lung tissue or whose alveoli are so immature or lacks in surfactant. This
is seen most commonly in immature and with CNS damage. It may occur when
infants have mucus or meconium plugs in the trachea.

 MANIFESTATION
- Irregular respirations
- Nasal flaring
- Apnea
- Respiratory grunt
 - Cyanosis

2. SECONDARY ATELECTASIS

Occurs in children when they have respiratory tract obstruction that prevents air
from entering a portion of the alveoli. The causes of obstruction in children
include mucus plugs that may occur with chronic respiratory distress or aspiration
of foreign objects.

 MANIFESTATION
- Asymmetry of chest
- Decreased breath sounds on affected side
- Tachypnea
- Cyanosis
 LABORATORY
- Chest X ray: collapsed alveoli
 MANAGEMENT
- If atelectasis is caused by foreign object: bronchoscopy is performed to
remove the object.
- If atelectasis is caused by mucus plug: moving out or expectoration of
mucus

 NURSING MANAGEMENT
- Make sure that chest is kept free from pressure to allow full lung
expansion
- Check clothing and make sure it is loose and nonbinding
- Make sure that child’s arm are not position across the chest because
weight can interfere with deep inspiration
- Place in a semi-fowler’s position because it lowers abdominal contents
and increases chest space
- Increase humidity of the environment to prevent further bronchial plugging
- Suction and chest physiotherapy
 NURSING DIAGNOSIS
- Ineffective airway clearance
- Impaired gas exchange
- Ineffective breathing pattern
- Risk for volume deficit

H. PNEUMOTHORAX

 DESCRIPTION AND ETIOLOGY

 Presence of atmospheric air in the pleural space. In children, it usually occurs
when air seeps from ruptured alveoli and collects in the pleural cavity. It can also
occur when external puncture wounds allow air to enter the chest.
 MANIFESTATION
- Tachypnea
- Grunting respirations
- Flaring of the nares
- Cyanosis
- Absent or decreased breath sounds
 LABORATORY
- Chest X Ray: darkened area of the air-filled fluid space
 TREATMENT
- Oxygen therapy: relieve respiratory distress
- Thoracotomy catheter or needle with low-pressure suction with water
sealed drainage: remove accumulated air
 NURSING DIAGNOSIS
- Ineffective breathing pattern
- Risk for trauma or suffocation
- Deficient knowledge

I. TUBERCULOSIS

 DESCRIPTION AND ETIOLOGY

 A highly contagious pulmonary disease. It is caused by Mycobacterium
tuberculosis. The mode of transmission is inhalation of infected droplets. The
incubation period is 2-10 weeks.
 MANIFESTATION
- Fever
- Hemoptysis
- Sweating
 LABORATORY
- Tuberculin test
- Mantoux test: 5-10 mm of induration is positive
- Sputum test
 TREATMENT
- Isoniazid
- Rifampicin
- Para-aminosalicylic acid ( PAS)
- High protein, calorie and pyridoxine diet
 MANAGEMENT
 - Periodic chest x rays
- BCG vaccine
- Prophylactic isoniazid
 NURSING DIAGNOSIS
- Ineffective airway clearance
- Risk for impaired gas exchange
- Risk for spread of infection

J. CYSTIC FIBROSIS

 DESCRIPTION AND ETIOLOGY

 The disorder is inherited as an autosomal recessive trait. It occurs approximately
in 1 in 2500 live births. It occurs most commonly in Caucasian children and rarely
in black or Asian children. All newborns can be screened at birth by a simple heel
puncture blood sample for the disorder.


 MANIFESTATION
 PANCREAS INVOLVEMENT

The acinar cells of the pancreas normally produce lipase, trypsin and amylase,
enzymes that flow into the duodenum to digest fat, protein and carbohydrate.
With Cystic Fibrosis, these enzyme secretions become so thickened that they
plug the ducts, there is such a back pressure in the acinar cells that they become
atrophied and then are no longer capable of producing the enzymes.

Without pancreatic enzymes in the duodenum, children cannot digest fat, protein
and some sugars. The child’s stool become large, bulky and greasy
(steatorrhea). The intestinal flora increases because of the undigested food;
when combined with fat in the stool, gives the stool an extremely foul odor. The
bulk of feces in the intestine leads to a protuberant abdomen. Because children
are benefiting from only about 50% of the food they ingest, they show signs of
malnutrition – emaciated extremities and loose, flabby folds of skin on their
buttocks. The fat soluble vitamins, particularly A, D and E, cannot be absorbed
because fat is not absorbed, so children develop symptoms of low levels of these
vitamins.

In approximately 10% of children with CF, the meconium may be so thick,

because pancreatic enzymes are lacking, that it obstructs the intestine. The
newborn develops abdominal distention with no passage of stool. Rectal
 prolapsed from straining to evacuate hard stool is another common findings in
infants with CF.

 LUNG INVOLVEMENT

Thickened mucus pools in the bronchioles. Pockets of infection then begin in these
secretions. Secondary emphysema occurs because air cannot be pushed past the
thick mucus on expiration, when all bronchi are narrower than they are on
inspiration. Bronchiectasis and pneumonia occur. Respiratory acidosis may
develop because obstruction interferes with the ability to exhale carbon dioxide.
Atelectasis occurs as a result of absorption of air from alveoli behind blocked
bronchioles. The child fingers become clubbed because of the inadequate
peripheral tissue perfusion. The anterior-posterior diameter of the chest becomes
enlarged.

 SWEAT GLAND INVOLVEMENT

If CF is not diagnosed by a screening blood sample at birth, it can be diagnosed by

documenting the chromosomal abnormality, or by ht history and the combination of
the abnormal concentration of chloride in sweat, the absence of pancreatic
enzymes in the duodenum, the presence of immunoreactive trypsinogen in the
blood and pulmonary involvement.

CF may be suspected in newborn when a newboern losses the normal amount of

weight at birth but then, the infant cannot make use of the fat in milk, does not gain
it back at the usual time of 7 to 10 days and perhaps not until 4 to 6 weeks of age.
Chromosome analysis or analysis of serum immunoreactive trypsin in the stool,
which is elevated because obstruction in the pancreas occurs as early as during
fetal life, confirms the diagnosis.

Children who are not diagnosed at birth may be seen in a health care setting at
about 1 month of age because of a feeding problem. Using only about 50% of their
intake because of the poor digestive function, they are always hungry. This cause
them to eat so ravenously they tend to swallow air. This leads to colic or abdominal
distention and vomiting. The appearance of typical CF stools is an important
finding because children with simple colic do not show these changes in stool
consistency.

Respiratory infections develop at 4 to 6 months of age. Even at this early stage of

the disease, wheezing and rhonchi may be heard on chest auscultation.

By the time a child with CF is a preschooler, a cough is a prominent finding. On

percussion, the chest is hyperresonant, reflecting the emphysema present. Rales
and rhonchi are heard. Clubbing of the fingers may already be apparent. It is rare
for a child to go undiagnosed beyond this time because the symptom of the illness
have become so persistent and evident.

 LABORATORY
- Sweat testing: a level of more than 60 mEq/L chloride in children is
diagnostic of CF.
- Duodenal analysis: alaysis of duodenal secretions for detection of
pancreatic enzymes reveals the extent of the pancreatic involvement.
- Stool analysis: stool may be collected and analyzed for fat content and
lack of trypsin, although description of the large greasy appearance
maybe all that is necessary.
- Pulmonary testing: Chest radiograph generally confirm the extent of
pulmonary involvement. It is done to determine if atelectasis and
emphysema are oresent.
-
 MANAGEMENT
- Therapy for children with CF consists of measures to reduce the
involvement of the pancreas, lungs and sweat glands.
- Diet: high sodium