NURSING CARE OF A FAMILY WHEN A CHILD HAS AN Transmission – Based Precautions

INFECTIOUS DISORDER
Incubation period – is the time between the invasion
of an organism and the onset of symptoms of
infection.
Koplik Spots – a small white spots with a bluish white
center on an erythematous background.
Mode of transmission – refers to whether the
infection is spread by direct or indirect contact.
1. Standard Precaution / Universal Precaution
 Use at all times
 Do not know how has the infection, the
patient or the nurse
 Hand hygiene or handwashing before and
after contact with patient
 PPE: gloves, gown, goggles, face mask
2. Airborne Transmission

Portal of entry – refers to the opening through which
a pathogen can enter a child’s body.
Portal of Exit – is the route by which an organism
leaves an infected child’s body to be spread to others.
Airborne precaution include:
Prodromal period – is the time between the beginning
of a nonspecific symptoms.
Reservoir – is the container or place in which the
organism grows and reproduce.
Septicemia – is a serious bloodstream infection.
Susceptible host – a person susceptible to infection.
3. Droplets transmission
Vectors – are living organisms that can transmit
infectious diseases between humans or from animals
to humans.
Stages of Infection Definitions
1. Incubation Rapid replication of
pathogenic
microorganism without
recognizable signs and
symptoms
2. Prodromal The appearance of the
first set of signs and Droplet Precaution include:
symptoms that is non-
specific.
3. Acute/Clinical Signs Stage where patient
and Symptoms experience the greatest
impact of the disease
4. Contact Transmission
process.
Pathognomonic signs
and symptoms are
present.
4. Convalescent If proper health is given,
patient can survive.
Containment of the
infection.
5. Recovery Progressively eliminating
the pathognomonic
microorganism.
Vital Exanthems
 Suspended in the air that can be inhaled
 Examples; Measles, TB, Varicella
 Use standard precaution plus the airborne
precaution
 Standard Precaution
 Use of N95 mask
 Negative pressure room with 6-12 air
exchanges
 Always close door
 Limit transportation of client
 Infect less than 3 feet
 Microorganism that can settle down on
surface
 Examples: Streptococcal pharyngitis, Sepsis,
Scarlet Fever, Pertussis (Whooping cough),
Pneumonia, Parvovirus 19 (fifth disease),
influenza, Diphtheria (pharyngeal), Epiglotitis,
Rubella (German Measleas), Mumps,
Meningitis, Mycoplasma Pneumonia,
Adenovirus
 Standard precaution
 Face mask
 Visitor should be 3 feet away
 Examples: MRSA, Respiratory infections, Skin
infections, Wound Infections, Eye infections,
Enteric-diarrhea
Contact Precaution include:
 Standard Precaution
 Wear gloves
 Other PPEs: goggles, face mask, gown
  Viruses cause childhood exanthems (skin
rashes). Each of these diseases has specific
symptoms, characteristics lesions, and a
specific distribution or pattern to the rash that
allows it to be identified.
Exanthem Subitumn (Roseola Infantum)
 Causative subitum: human herpesvirus 6
(HHV-6)
 Incubation period: 6 to 10 days
 Period of communicability: during febrile
period
 Mode of transmission: unknown
 Immunity: contracting the disease offers
lasting natural immunity; no vaccine is
available
Assessment:
 The first symptom is fever (101 degree to 105
degree F[38.3 – 40.6 degree C]). The fever will
fall abruptly after 3 to 5 days.
 There may be associated cervical adenopathy
with mild injection of the pharynx.
 A distinctive rash of discrete, rose-pink
macules approximately 2 to 3 mm in size
appears. The lesions occur most prominently
on the trunk, fade on pressure, and last 1-
2days.
 The children have no accompanying coryza
(upper respiratory symptoms), conjunctivitis,
or cough.
 The condition is diagnosed based on the
history with the hallmask appearance of a
rash appearing immediately after the sharp
decline in fever
Therapeutic Management:
 Treatment focuses on measures to reduce the
fever with acetaminophen (Tylenol) or
ibuprofen (Motrin) if the child is over 6
months.
 If an infant should develop this exanthema in
the hospital, follow standard infection
precautions.
Rebulla (german measles)
 Causative agent: rubella virus
 Incubation period: generally 14 days within a
range of 12 – 23 days
 Period off communicability: 7 days before to
approximately 7 days after the rash appears.
 Mode of transmission: direct an d indirect
contact with droplets
 Immunity: contracting the disease offers
lasting natural immunity; a high rubella
antibody titer reveals infection has occurred.
 Active artificial immunity: attenuated live
virus vaccine (e.g., MMR vaccine)
 Passive artificial immunity: immune serum
globulin is considered or pregnant women
exposed to the virus.
Assessment:
 The rash is characterized by a discrete pink-
red moculopapular rash that begins on the
ace and then spreads downward to the trunk
and extremities.
 In older children and adolescents, the disease
has a 1-5 days prodromal period, during
which children have a low-grade ever,
headache, malaise, anorexia, mild
conjunctivitis, upper respiratory symptoms,
and lymphadenopathy such as those in the
suboccipital, postauricular, and cervical
chains.
 The fever with rubella is not marked, although
arthritis(joint pain) with effusion into the
joints occurs in some children on the second
or third day and lasting as long as 5-10 days.
Therapeutic Management:
 Children need comort measures ffor the rash
and an antipyretic such as acetaminophen
(Tylenol) or ibuprofen (motrin) or ffever or
joint pain.
 If a child develops rebulla while in the
hospital, follow droplet precautions for 7 days
after the onset of the rash in addition to
standard infection precautions.
 If a woman contracts rebulla while pregnant,
it can cause extensive congenital
malformation in the fetus. It is important that
girls are immunized against rebulla before
they reach childbearing age.
 The MMR vaccine is administered at age 1
year and again at age 4 years to expand
protection. MMR vaccine is not
recommended in pregnancy because it is a
live viral vaccine.
Measles (Rubeola)
 Causative agent: measles virus
  Incubation period: 8-12 days from time o
exposure to onset of any symptoms with a
range from 7-21 days.
 Period of communicability: 4 days before the
rash to 4 days ater the rash appears
 Mode of transmission: direct contact with
droplets or airborne spread
 Immunity: contracting the disease offers
lasting natural immunity
 Active artificial immunity: attenuated live
measies vaccine (e.g., MMR)
 Passive artificial immunity: immune serum
globulin
Assessment:
 Measles is an acute febrile viral illness
associated with cough, coryza (clear nasal
discharge), and conjunctivitis (the “three Cs”)
with a confluent maculopapular,
erythematous rash, which starts behind the
ear and spreads to the feet over a course o 3-
6 days.
 Koplik spots, or small white spots with a
bluish white center on an erythematous
background, are seen in the oral mucosa
opposite the buccal mucosa efore symptoms
appear. Koplik spots then develop on the
buccal mucosa and are a hallmark symptom
because they are unique to measles. Koplik
spots look like raised papules on an
erythematous bbase. Any rash on mucosa
surfaces is called an enanthem.
Therapeutic Management:
 Children with measles need comfort measures
for the rash and an antipyretic for the fever.
 Applying a lubricating jelly or an emollient
(e.g.,A&D ointment) to the area below the
nose may help prevent excoriation.
 The use of buckwheat honey in children older
than 1 year off age may be helpful with the
cough.
 Photophobia is an accompanying symptoms,
so drawing the curtains or wearing sunglass is
a comfort measure.
 If a child is hospitalized, follow airborne
precautions for the duration of the illness on
addition to standard infection precaution.
Chickenpox (Varicella)
• Causative agent: varicella-zoster virus (VZV)
• Incubation period: 10 to 21 days with the most
common incidence at 14 to 16 days following
exposure (Kroger, 2015)
• Period of communicability: 1 day before the
rash to 5 to 6 days after its initial appearance,
when all the vesicles have crusted
• Mode of transmission: highly contagious; spread
by direct or indirect contact of saliva or open
vesicles
• Immunity: contracting the disease offers lasting
natural immunity to chickenpox; however,
because VZV is latent, it causes herpes zoster
(shingles) when it is reactivated at a later time
• Active artificial immunity: attenuated live virus
vaccine
• Passive artificial immunity: children who are
immunosuppressed, such as those with leukemia
or HIV/AIDS, or those who are being treated with
corticosteroids are offered varicella-zoster
immune globulin (VZIG) within 72 hours of
exposure to help prevent or modify disease
symptoms
Assessment:
 In children, the rash occurs first accompanied
by a low-grade fever and malaise.
 The lesions of varicella present as a macule,
papule, and vesicle all appearing at the same
time, starting on the trunk and progressing
outward to the arms, face, legs, and mucosal
surfaces including the genitalia.
 When the lesion is in the healing stage, there
is a characteristic black crust. The hallmark is
a 2- to 3-mm vesicle on an erythematous
base. The lesions appear in crops, with each
new lesion moving through progressive
stages. Usually, all four stages of lesions
(macule, papule, vesicle, and crust) may be
present at the same time.
Therapeutic Management:
 The rash of varicella is very pruritic and so it is
important to decrease scratching to reduce
infection.
 Topical oatmeal-based creams along with an
antihistamine such as diphenhydramine
(Benadryl) can reduce the pruritus, and an
antipyretic such as acetaminophen (Tylenol)
can reduce the fever.
  The development of Reye syndrome has been
associated with aspirin use during varicella
and influenza viral illnesses, so caution
parents to avoid aspirin and instead use
acetaminophen or ibuprofen to control fever.
 Acyclovir (Zovirax), an antiviral, may be
prescribed to reduce the number of lesions
and shorten the course of the illness.
 During hospitalization due to a complication
of varicella infection, standard infection
precautions along with airborne and contact
precautions are adhered to until all lesions are
crusted. Children may return to school as
soon as all the lesions are crusted as the
crusted lesions are not infectious.
Herpes Zoster
 Herpes zoster is a reactivation of the VZV. The
herpes viral family has viral latency, which
means that once you develop varicella, the
virus lies latent in the posterior dorsal root
ganglia. The reactivation of the VZV occurs
during aging as well as during times of
immunosuppression.
 The first manifestations are paresthesia and
pain with subsequent groups of vesicular
lesions in different stages of healing along a
dermatomal distribution.
 Treatment for herpes zoster includes
analgesia for pain and measures to reduce
pruritus.
 Acyclovir, which inhibits viral DNA synthesis,
may be effective at limiting the disease but
should be started within 72 hours of the start
of the rash.
Smallpox (Variola)
• Causative agent: smallpox virus
• Incubation period: 7 to 17 days with a mean of 12
days
• Period of communicability: The child is contagious
for 24 hours before the onset of the rash and remains
contagious until all lesions are dried which can take up
to 4 weeks.
• Mode of transmission: airborne transmission.
 Patients with smallpox develop a febrile
prodrome not seen in varicella.
 The lesions of smallpox may resemble those
of varicella, the lesions of smallpox are similar
in the same stage of disease and all the
smallpox lesions progress at the same rate.
 The pustular lesions are firm and deeply
embedded in the skin dermal layer. In the
crusting phase, the lesions of smallpox are
contagious.
 Smallpox is a serious illness; its mortality rate
is greater than 30% , and it can be spread
readily by direct contact with an infected
person or indirect contact with a fomite.
 Disease symptoms can be modified by
administration of disease specific vaccinia
immune globulin (VIG) with experimental
drugs in development.
 Antibiotics may be used to prevent secondary
infection of lesions.
 Oxygen or other measures to support
respiratory and cardiac function should be
provided as necessary.
 There is a severe prodrome phase for this
disease with a high fever from 102° to 104°F
(38.9° to 40.0°C) and symptoms that include
headache, abdominal pain, malaise, and
severe fatigue.
 Within 24 hours of symptoms starting, skin
lesions develop on the face, spreading down
the body to the forearms, trunk, and legs. The
face and distal extremities are the most
frequently affected.
 The lesions start as macules and then
progress to papules, vesicles, and firm
pustules by the seventh day.
Erythema Infectiosum (“Fifth Disease”)
• Causative agent: parvovirus B19
• Incubation period: most common between 4 to 14
days, with an outside window of 21 days
• Period of communicability: uncertain
• Mode of transmission: respiratory tract secretion,
blood transfusion, vertical transmission from mother
to baby
• Immunity: none
Assessment:
 The classic presentation starts with mild
systemic symptoms, which can include a fever
in 15% to 30%, headache, and malaise. This is
 present for 7 to 10 days before the child
develops a “slapped cheek” appearance with
erythema of the cheeks with circumoral
pallor.
 Following this rash, a maculopapular, lacy-
appearing rash on the arms, thigh, and
buttocks may appear. This can fade and
become more intense depending on the
child’s activity level and environmental
changes, which includes sunlight and ambient
room temperature.
 Other presentations of this virus include a
petechial, papular purpuric stocking and glove
distribution or a mild respiratory illness
without rash.
Therapeutic Management:
 Treatment is typically supportive, with
antipyretics and analgesics and comfort
measures for the rash.
 Use droplet precautions in a hospital.
 Children can return to school as soon as the
rash appears because they are no longer
infectious after this point.
NONPOLIO ENTEROVIRUSES
• Causative agent: member of the enteroviral family
• Incubation period: most common is between 3 to 6
days, with hemorrhagic conjunctivitis having a shorter
incubation of 24 to 72 hours
• Period of communicability: uncertain
• Mode of transmission: respiratory tract secretion,
fecal–oral, vertical transmission from mother to baby
at the time of birth; possibly breastfeeding
• Immunity: none
There are over 90 serotypes (members of the same
viral family) with three members of enteroviral family:
numbered enteroviruses, echoviruses, and
coxsackievirus. More recently, the virus was
reclassified into enterovirus A, B, C, and D based on
their genetics and their phenotypes. As a group, there
are several common manifestations from these
viruses including:
• Nonspecific viral illness
• Respiratory illness (coryza, pharyngitis, stomatitis,
pneumonia, pleurodynia, bronchitis)
• Skin infections (hand, foot, and mouth disease)
• Gastrointestinal illness (gastroenteritis, pancreatitis,
and hepatitis)
• Eye infections (hemorrhagic conjunctivitis, uveitis)
• Neurologic disease (aseptic meningitis, encephalitis,
acute flaccid paralysis)
• Genitourinary illness (orchiditis)
• Heart disease (myocarditis)
• Muscular manifestations (myositis)
Coxsackievirus Infections
 Coxsackievirus A6 and A16 are associated
with hand-foot-mouth disease with distinctive
erythematous papules mainly on the hands
and feet but occasionally on the buttocks and
oral ulcers in the pharynx.
 It is associated with high fever and anorexia,
which can lead to dehydration.
 Herpangina is also caused by a coxsackie virus
and is associated with fever, anorexia,
difficulty swallowing, sore throat, headache,
abdominal pain, and vomiting.
 The small lesions associated with herpangina
are generally discrete pinpoint grayish vesicles
or ulcers appear on the tonsillar fauces, soft
palate, and uvula.
 Children need a bland, soft diet or
nonirritating liquids when they have the
mouth lesions.
 If a child is hospitalized, follow contact
precautions for the duration of the illness in
addition to standard infection precautions.
Poliovirus Infections: Poliomyelitis (Infantile
Paralysis)
• Causative agent: poliovirus
• Incubation period: Nonparalytic polio—3 to 6 days.
Paralytic polio is commonly 7 to 21 days with a range
of 3 to 35 days.
• Period of communicability: greatest shortly before
and after onset of clinical symptoms, when virus is
present in the throat (1 to 2 weeks after the onset of
illness and in feces (3 to 6 weeks); however, the virus
is contagious as long as it is present in the feces.
• Mode of transmission: respiratory secretions and
feces
• Immunity: Contracting the disease causes active
immunity against the one strain of virus causing the
illness.
• Active artificial immunity: inactivated polio virus
(IPV) vaccine
• Passive artificial immunity: none
Assessment:
 The symptoms of paralytic polio include fever,
headache, nausea, vomiting, abdominal pain,
constipation, and malaise initially followed by
a period of no symptoms.
 Less than 1% will go on to paralysis with
areflexia and bulbar symptoms such as
difficulty swallowing and respiratory muscle
involvement.
 Sensation remains intact and the disease is a
motor paralysis.
 In 25% to 40% of patients, a postpolio
syndrome can occur 15 to 40 years after polio
infection, presenting as weakness and pain
affecting the muscles and joints that were
most affected with the original infection.
Therapeutic Management:
 Treatment for nonparalytic poliomyelitis is
bed rest with antipyretics.
 There is no antiviral known to treat any form
of polio.
 Supportive care is given depending on
symptoms. If the respiratory muscles are
involved, long-term ventilation may be
necessary.
 Physical therapy is needed to prevent
contracture and promote strength during the
recovery period.
Herpesvirus Infections
 Herpesviruses (HSV) infections are common,
potentially life threatening, and are caused by
both HSV-1 and HSV-2.
 They can be found as primary mucocutaneous
infection, an acute infection of the ganglia, or
in a latent form, reactivated form or a
recurrent infection.
 HSV-1 is more commonly found acutely in the
oral region as herpetic gingivostomatitis and
in the chronic recurrent form as herpes
labialis. HSV-2 is more commonly found in the
genital region as both an acute or recurrent
infection.
• Causative agent: herpes simplex, type 1 or type
2 virus
• Incubation period: 2 days to 2 weeks, average of
6 days
• Period of communicability: greatest early in the
course of the infection
• Mode of transmission: direct contact with
persons with active lesions or persons shedding
the virus asymptomatically
• Immunity: Herpes viruses like VZV have viral
latency, so patients can have recurrent infections.
There is currently no vaccine available
Acute Herpetic Gingivostomatitis
 Acute herpetic gingivostomatitis is most
common in children from 6 months to 5 years
but can be seen in older children.
 In the initial infection, there is a sudden onset
of pain, drooling, anorexia, and a significant
fever as high as 105°F (40.6°C). Their gumline
is also swollen, reddened, and bleeds easily.
White, shallow ulcers with red borders appear
on the gum, lips, buccal mucosa, tongue,
palate, perioral skin, and, less commonly, on
the tonsillar pillars. The anterior cervical
lymph nodes are usually enlarged and tender.
The disease runs its course in 5 to 14 days.
 Children will need an antipyretic to reduce
fever and soft, nonirritating, acidfree foods to
reduce irritation.
 Popsicles, ice milk, and Jell-O are soothing
against inflamed mucous membranes.
 Oral acyclovir can be used to shorten the
course of illness.
 Use contact precautions with hospitalized
children to avoid contact with lesions.
Although usually mild, the disease can
become serious, especially in infants and
children where the lack of fluid intake leads to
dehydration.
Warts (Verrucae)
  The papillomavirus most commonly cause skin
manifestation but can cause both genital and
oral malignancies.
 HPV infect the conjunctiva, oral cavity,
respiratory tract, genital tract, and the skin.
 The incubation period varies from 3 weeks to
8 months, but the average is 3 months.
 The mode of transmission is likely direct
contact as there is little evidence to suggest
indirect transmission by fomites.
 Warts appear as flesh-colored, dirty-
appearing papules that generally occur on the
dorsal surface of the hands.
 There are several treatment options including
over-the-counter preparations with a salicylic
acid solution. Carbon dioxide snow, liquid
nitrogen, electrodessication, laser, and
cryotherapy are other methods also available
for removal, but these methods are painful
and rarely necessary.
 Anogenital warts in young children, like HSV
lesions, can be a mark of sexual maltreatment
 Certain strains of HPV can cause vaginal,
vulvar, and cervical cancer in women, penile
cancer in men, as well as anal or
oropharyngeal cancers in both sexes.
Rabies
 Rabies causes an acute encephalitis that is
fatal and caused by Lyssavirus genus, which
includes rabies virus (RABV). RABV infections
number over 59,000 people worldwide and is
most common in poor countries. The
domestic dog causes most rabies worldwide
due to lack of vaccination.
• Causative agent: RABV
• Incubation period: average is 1 to 3 months
but can range from days to years
• Period of communicability: 3 to 5 days
before the onset of symptoms through the
course of the disease
• Mode of transmission: the bite of a rabid
animal; rarely through saliva from an infected
animal being transferred to an open lesion on
a child’s skin
• Immunity: Contracting the disease
apparently offers active immunity, but few
people have ever survived the illness to verify
this.
• Active artificial immunity: human diploid cell
rabies vaccine
• Passive artificial immunity: rabies immune
globulin (RIG)
 Any warm-blooded animal can contract
rabies. Any mammal can be infected with the
virus and unprovoked attacks are suggestive
of a rabid animal. Rodents (squirrels, mice, or
rats) seldom carry the RABV virus. Infection
with RABV causes a rapidly progressive
central nervous system infection.
Assessment:
 After the long incubation period of the virus,
children begin to show prodromal signs of
malaise, fever, anorexia, nausea, sore throat,
drowsiness, irritability, and restlessness.
 The clinical manifestations include anxiety,
radicular pain pruritus, hydrophobia,
dysautonomia, and in some patients,
paralysis. The disease almost always leads to
death with a history of only four survivors of
rabies.
 When children try to drink, they experience
violent contractions of the muscles of the
mouth leading to drooling of saliva. This
phenomenon gives the disease its former
name: hydrophobia (“water fear”). As
symptoms progress, children will become
comatose. Peripheral vascular collapse and
death can follow as quickly as 5 or 6 days
later.
Therapeutic Management:
 Once the disease process begins, rabies is
almost invariably fatal, so the key is
prevention of the active process.
 The healthcare provider must know if there
have been rabid animals found in the
community; however, if the bite seems
unprovoked, rabies vaccine and RIG should be
given.
 The decision to immunize and use prophylaxis
should be done after contact with the local
department of health and/or an infectious
disease specialist.
 Following any bite or close exposure to bats,
prophylaxis should be initiated as soon as
possible and, if the animal is unknown, or
suspected to have rabies, there should be no
delay in prophylaxis treatment.
  Prophylaxis is twofold. The child receives
human rabies vaccine immediately along with
the administration of RIG (20 IU/kg) into the
area of the bite with the remainder of the RIG
administered in an intramuscular (IM)
injection. The immediate administration of
RIG provides antibodies against the RABV
while administering the rabies vaccine allows
the child to begin additional antibody
formation so that by the time the RABV from
the bite begins to have an effect (2 to 6 weeks
after the bite), the child has developed
sufficient antibodies to combat it and prevent
the illness.
OTHER INFECTIONS TRANSMITTED BY ANIMAL
VECTORS
 Animal vectors can transmit viruses and
bacteria to human hosts. For example, mice
and rats are reservoirs of the bacteria
Leptospira. The bacteria can be transmitted to
humans by the infected animal’s urine, and it
can pass to humans via damaged skin or
mucosa. The transmission of viruses and
bacteria by animal vectors is not uncommon,
and it is important to take a careful travel
history as well as a history of any exposure to
animals.
Hantavirus Pulmonary Syndrome Infection
 The hantavirus is a member of the arbovirus
group and can cause two different diseases—
hantavirus pulmonary syndrome (HPS), with a
mortality rate of 60%, and hemorrhagic fever
with renal syndrome (HFRS), with a mortality
rate of 12%. The virus infects rodents.
 HPS has an incubation period between 1
to 6 weeks. In HPS, there is prodrome of
no more than 5 days, characterized by
fever, chills, cough, myalgia,
gastrointestinal symptoms of diarrhea,
and vomiting and headache.
 One to 3 days after the onset of
respiratory symptoms, capillary leak
develops in the lung resulting in
pulmonary edema and hypoxemia after
cough and dyspnea. Hypotension leads to
cardiac dysfunction and subsequent
death.
 HFRS has an incubation of 3 weeks with a
range of 10 days to 6 weeks. The clinical
manifestations depend on the type of
hantavirus. There are usually five phases:
(a) febrile phase, (b) hypotension, (c)
oliguria, (d) polyuria, and (e)
convalescence.
 At present, no antiviral medication
immunotherapy or vaccines are approved
for the treatment of hantavirus. The
treatment is supportive, but prevention is
key. Rodent control is the best
prevention, and rodents should be kept
out of the house. Campers need to avoid
rodent-infested areas.
Zika Virus Disease
 The yellow fever mosquito is one of the
world’s most deadly animals, causing yellow
fever, Zika virus, dengue, and chikungunya
viral infections.
 These mosquitos lay their eggs in any
containers that can hold water, including
cups, tree holes, bowls, discarded tires, flower
pots, cans, and clogged rain gutters.
 They are daytime biters with peak feeding
activity 2 hours before sunrise and 2 hours
after sunset. Aedes aegypti is the main vector,
but transmission of the virus via the Aedes
albopictus appears possible.
 The relationship of microcephaly to active
Zika viral infection in pregnant women has
been established, and the CDC recommends
testing of all pregnant women who have
traveled to counties with active infection.
 The incubation period is thought to be less
than 1 week. The symptoms of Zika virus
infection include fever, arthralgia,
conjunctivitis, eye pain, myalgia, rash, and
headache.
 To prevent infection with Zika virus, the nurse
should screen potential blood donors and
advise the use of condoms after travel to
countries with known Zika viral infections.
Stress that the use of insect repellants with a
maximum of 30% N, N-diethyl-meta-
toluamide (DEET) for infants and children can
help prevent mosquito bites.
West Nile Virus Disease
  The transmission of arbovirus occurs between
arthropods and their hosts, which are usually
small mammals or birds.
 Infected mosquitoes or ticks transmit the
virus to humans, with person-to-person
transmission occurring from organ transplant
or blood transmission.
 The majority of clinical disease is
asymptomatic. The symptomatic
manifestations include fever, arthralgia, and
myalgia.
 The neuroinvasive form of West Nile virus is
uncommon and includes encephalitis,
meningitis, and acute flaccid paralysis. The
symptoms of encephalitis and meningitis
include mental confusion, lethargy,
photophobia, headache, muscle weakness,
and coma, leading to death.
 There is no evidence-based therapy for the
disorder, except for supportive measures to
maintain function; however, ribavirin and
intravenous immunoglobulin (IVIG) have been
used to reduce symptoms. Commercially
available West Nile virus–specific
immunoglobulin M (IgM) antibodies in either
serum or cerebrospinal fluid is the current
way to establish the diagnosis. The antibodies
can be found 3 to 8 days after illness onset
and persists for 1 to 3 months at the
minimum. Therefore, positive results may
reflect past rather than current infection. If
the testing was done before 8 days of illness,
there may be an absence of West Nile virus–
specific IgM antibodies and repeat testing
may be needed. There is also currently no
vaccine for this condition.
Mumps (Epidemic Parotitis)
• Causative agent: mumps virus
• Incubation period: usually 16 to 18 days with an
outside range from 12 to 25 days
• Period of communicability: communicable for 5 days
from onset of the swollen parotid gland
• Mode of transmission: direct contact with
respiratory droplets
• Immunity: Contracting the disease gives lasting
natural immunity.
• Active artificial immunity: attenuated live mumps
vaccine in combination with measles and rubella
(MMR)
• Passive artificial immunity: mumps immune globulin
Assessment:
 If the disease occurs, it begins with fever,
headache, anorexia, and malaise. About one
third of infections are subclinical, and
therefore, no swelling of the parotid gland is
noted.
 Mumps cause a parotid gland enlargement
without skin erythema in the majority of
patients. This enlargement will obscure the
angle of jaw and therefore is helpful from
differentiating it from submaxillary adenitis
(inflammation of lymph nodes). The best
method of differentiation is to place a hand
along the child’s jawline. If the major amount
of swelling is above the hand, it is probably
mumps. Fever typically occurs early and is
accompanied by anorexia and inability to
open the mouth (trismus). The swelling will
resolve in 5 to 7 days. Boys may also develop
testicular pain and swelling (orchitis) after
puberty, and this complication is more likely
as an adult or adolescent. Sterility is a rare
complication of the orchitis.
Therapeutic Management:
 Supportive care is key including pain control
and fever control with acetaminophen or
nonsteroidal anti-inflammatory and a soft
bland diet.
 If a child is hospitalized, follow droplet
precautions in addition to standard infection
precautions. Some parents worry that
because their child had swelling only on one
side, their child will develop mumps on the
opposite side in the future. One attack of
mumps gives lasting immunity, so the child
will not contract the disease again. If a child
does appear to have contracted mumps twice,
the diagnosis was probably confused with
cervical adenitis at one occurrence.
Epstein–Barr Infectious Mononucleosis
• Causative agent: Epstein–Barr virus (EBV)
• Incubation period: Incubation period in adults and
adolescents is 30 to 50 days with a shorter incubation
period in children
• Period of communicability: occurs during direct
contact with saliva by individuals who are
symptomatic or asymptomatic but shedding the virus
• Mode of transmission: direct contact and through
blood transfusions
• Immunity: Most of the time, one episode gives
lasting immunity; however, EBV is latent and can
reactivate and cause a milder clinical presentation. No
vaccination is available.
Assessment:
 The classic symptoms of EBV infection include
several days of prodromal symptoms of
anorexia, chills, and malaise with fever in 90%
and enlargement of the cervical nodes and
tonsils.
 Pharyngitis with palatal petechial and
periorbital edema and found with
splenomegaly is present in about 5%. If the
mesenteric lymph nodes enlarge, children
may experience abdominal pain so sharp that
it simulates appendicitis.
Therapeutic Management:
 Children with infectious mononucleosis
should be treated for pain and fever with
acetaminophen or nonsteroidal anti-
inflammatory agents.
 The child should be encouraged to rest when
fatigued, and all contact sports should be
avoided for at least 4 weeks after the onset of
infection. It can take 3 months for the child to
return to his or her baseline fitness.
 The nurse should stress fluid intake with cool,
nonacidic fluids and soft, nonirritating foods.
It can interfere with the completion of school
work and normal activities. The nurse can
support the child or adolescent by listening to
them about talk about the effect this illness
has on their lives.
Bacterial Infections
Bacteria are independent, living organisms with a
nucleus that contains both DNA and RNA. They
reproduce by fission, in which one cell enlarges and
duplicates itself and then divides into two equal parts.
They occur in three main shapes: spheres (cocci), rods
(bacilli), and spirals (spirochetes). Types of bacteria
can be distinguished after they are fixed onto a
laboratory slide and then stained. Bacteria that stain
violet are said to be gram-positive organisms and
those that stain red are gram-negative organisms.
Those that cannot be decolorized with acid after being
stained are acid-fast. Different bacteria from the same
family can act differently. In the case of streptococcus,
they have an M protein surrounding their cell wall.
Some of the M protein produce pyogenic exotoxins,
which are toxins that act as super antigens. When this
happens, disease symptoms arise from the bacteria
and the effect of the exotoxins on the body. Tetanus,
botulism, exotoxin producing staphylococcus and
streptococcus, and diphtheria are examples of
diseases caused by the systemic spread of toxins
produced by bacteria.
STREPTOCOCCAL DISEASES
Streptococci, which are gram-positive organisms, are
found normally in the respiratory, alimentary, and
female genital tracts. There are more than 120
serotypes or genotypes of group A β-hemolytic
streptococci or Streptococcus pyogenes. S. pyogenes
or Lancefield group A streptococcus are responsible
for mild infections like impetigo, tonsillitis, or scarlet
fever; however, they can also produce severe
infections such as toxic shock syndrome or necrotizing
fasciitis. S. pyogenes (β-hemolytic streptococci, group
A) is responsible for strep throat and scarlet fever,
and this is treated due to the risk of nonsuppurative
complications of rheumatic fever and
glomerulonephritis. A βhemolytic, group B
streptococcal infection can be contracted from vaginal
secretions at birth; when newborns become infected
with this bacteria, they can die from sepsis,
pneumonia, or meningitis. The manifestations of
group A streptococcal infections include erysipelas,
cellulitis, pneumonia, endocarditis, pericarditis,
osteomyelitis, sepsis, bacteremia, and toxic shock
syndrome.
Scarlet Fever
• Causative agent: β-hemolytic streptococci, group A
• Incubation period: 2 to 5 days for streptococcal
pharyngitis
• Period of communicability: greatest during acute
phase of respiratory illness; 1 to 7 days
• Mode of transmission: direct contact from a person
with the disease and large droplets, not fomites or
household pets
• Immunity: One episode of disease gives lasting
immunity to scarlet fever toxin. No vaccination is
available.
Assessment:
 Scarlet fever occurs most commonly in
school-age children, peaking in the 7- to 8-
year-old age group.
 Symptoms of streptococcal pharyngitis begin
abruptly and include fever, sore throat,
headache, chills, a rapid pulse, and malaise.
As the disease progresses, the production of
exotoxins SpeA, SpeC, and SSA causes a rash
that appears 12 to 48 hours after the onset of
the pharyngeal symptoms. The skin rash
typically is red with pinpoint lesions that
blanch on pressure and feel as rough as
sandpaper. They tend to be densest on the
trunk and very prominent in skin folds
(Pastia’s sign). The rash persists for
approximately 1 week. It desquamates or
peels off in fine flakes.
 The tonsils appear inflamed and enlarged and
are usually covered with white exudate. The
palate may be covered with reddened
punctiform (pinpoint) lesions and perhaps
scattered petechiae. The tongue, during the
first 2 days of the illness, is white and appears
furry. By day 3, papillae enlarge and protrude
through the white coat, giving the tongue a
“white strawberry” appearance.
 A “strawberry tongue” is a hallmark symptom
of scarlet fever and helps to differentiate the
disease from other rashes or pharyngeal
infections. A positive rapid strep test or
positive throat culture is the diagnostic test of
choice.
Therapeutic Management:
 Children with scarlet fever usually recover
without sequela once penicillin is
administered.
 Children may need an analgesic and
antipyretic, such as acetaminophen (Tylenol)
or children’s ibuprofen (Motrin) for pain and
fever.
 They need a soft or liquid diet until the pain
from the pharyngitis improves. Comfort
measures are important for the rash. Because
the underlying cause of the illness is a
streptococcal infection, a course of antibiotics
is prescribed.
Impetigo
• Causative agent: β-hemolytic streptococcus, group A
or S. aureus including MRSA
• Incubation period: 7 to 10 days for impetigo
• Period of communicability: from outbreak of lesions
until lesions are healed
• Mode of transmission: direct contact with lesions
• Immunity: none
 It is common to see several children in a
family with identical impetigo lesions because
it is spread by direct contact. An underlying
scabies infection can cause impetigo due to
infection from scratching with nails
Assessment:
 Impetigo involves the top layer or epidermal
layer of the skin and is generally characterized
by honey-colored crusts with local erythema.
It is usually caused by either S. aureus or by
group A hemolytic streptococci. The lesions
are found most commonly on the face and
extremities. They are often seen as secondary
infections of insect bites or in children who
have body piercings. If the impetigo is
extensive, children may have local lymph
node enlargement.
Therapeutic Management:
 Localized disease is treated with mupirocin
(Bactroban) ointment for 7 to 10 days or with
retapamulin (Altabax) for children over 9
months twice a day (bid) for 5 days. The use
of oral antibiotic that cover both
staphylococcus and streptococcus is reserved
for extensive impetigo.
Cat-Scratch Disease
• Causative agent: Bartonella henselae bacteria which
is slow growing
• Incubation period: usually 1 to 2 weeks with a range
of 7 to 60 days
• Period of communicability: unknown
• Mode of transmission: bite or scratch from more
commonly a kitten rather than a cat
• Immunity: one episode of disease gives lasting
immunity; no passive artificial immunity
 Cat-scratch disease occurs most commonly in
preschool children because children at that
age play roughly with cats or pick them up
and so receive scratches. At the time, the
child contracts the disease, the cat does not
appear ill. The first symptom is a single skin
papule or pustule at the site of inoculation
which precedes the lymphadenopathy by 1 to
2 weeks (range of 5 to 50 days). A Bartonella-
infected lymph node will usually resolve over
a period of 4 to 6 weeks without treatment,
and 10% to 25% will eventually drain
spontaneously. Other forms of this disease
includes Parinaud oculoglandular syndrome,
which presents clinically with preauricular
lymphadenitis and a follicular conjunctivitis as
well as 1 to 2 weeks of fever with nonspecific
symptoms.
STAPHYLOCOCCAL INFECTIONS
Furunculosis/Carbunculosis (Abscesses or Boils)
 A furuncle is a staphylococcal infection of a
single hair follicle, and a carbuncle has
multiple hair follicles with openings. A single
or multiple yellow pustule forms at the site.
There is localized redness, pain, and edema of
the surrounding skin. As these enlarge, they
may need an incision and drainage to drain
the pus. The nurse should educate the family
and child to never press an abscess to rupture
the lesions. The use of antibiotics after an
incision and drainage is controversial and
depends on the size of carbuncle.
Cellulitis Cellulitis
 is staphylococcal inflammation of the dermal
and subcutaneous layers of skin. It can occur
anywhere on the body and there will be
warmth, tenderness, and erythema at the
area of cellulitis. The treatment is a systemic
antibiotic that will cover both staphylococci
and streptococci.
Scalded Skin Disease
 Staphylococcal scalded skin syndrome (Ritter
disease) is a staphylococcal infection seen in
infants. Newborns develop rough-textured
skin and general erythema, especially on
areas that encounter friction. Large bullae
(vesicles) filled with clear fluid form. The
epidermis separates in large sheets and
desquamates, leaving a raw, red, glistening,
and scalded-looking surface. This is called
Nikolsky sign.
Diphtheria
• Causative agent: Corynebacterium diphtheriae
(Klebs–Löffler bacillus)
• Incubation period: 2 to 5 days with a range of 1 to
10 days
• Period of communicability: In untreated persons,
the organism is contagious from nares, throat, skin,
and eyes for 2 to 6 weeks following infection; 48
hours after initiation of antibiotics in treated children
and adults.
• Mode of transmission: direct contact or indirect
contact droplets
• Immunity: Contracting the disease gives lasting
natural immunity.
• Active artificial immunity: diphtheria toxin given as
part of diphtheria, tetanus, and pertussis (DTaP)
vaccine
• Passive artificial immunity: diphtheria antitoxin
Assessment:
 Diphtheria bacilli invade and grow in the
nasopharynx of children and produce an
exotoxin that causes massive cell necrosis and
inflammation.
 The endotoxin promotes bacilli growth and
causes the infected cells form a characteristic
gray membrane on the nasopharynx. This may
extend up into the nose and down into the
major bronchi, causing a purulent nasal
discharge and a brassy cough. The toxin is
absorbed from the membrane surface and
spreads systemically by the bloodstream to
 affect major organs, such as the heart and
nervous system.
 If untreated, myocarditis with heart failure
and conduction disturbances may occur.
Central nervous system involvement can
include severe neuritis with paralysis of the
diaphragm and pharyngeal and laryngeal
muscles.
 Diphtheria can also form skin lesions aside
from the usual presentation of respiratory
infections.
Therapeutic Management:
 Treatment involves a single dose of equine
antitoxin based on clinical suspicion.
 In addition, children are given penicillin or
erythromycin intravenously. Complete bed
rest is crucial during the acute stage of the
illness.
 Droplet precautions must be followed until
cultures are negative.
 Children need careful observation at all times
to prevent airway obstruction.
Whooping Cough (Pertussis)
• Causative agent: Bordetella pertussis
• Incubation period: 5 to 21 days
• Mode of transmission: highly contagious by direct or
indirect contact
• Period of communicability: greatest in catarrhal
(respiratory illness) stage; eliminates contagiousness
within 5 to 7 days of treatment, but it continues for
weeks in the untreated patient
• Immunity: contracting the disease offers lasting
natural immunity
• Active artificial immunity: pertussis vaccine given as
part of DTaP vaccine
• Passive artificial immunity: pertussis immune serum
globulin
Assessment:
 The disease can primarily manifest as a mild
rhinitis with a mild cough to persistent cough
illness or to the classic pertussis disease.
Classic pertussis manifests itself in three
steps: the catarrhal stage, the paroxysmal
stage, and the convalescent stage.
The catarrhal stage begins with upper respiratory
symptoms such as coryza, sneezing, lacrimation,
cough, and a low-grade fever, symptoms subtle
enough they may at first be mistaken for those of
a common cold. This first period lasts 1 to 2
weeks.
The paroxysmal stage lasts from 2 to 6 weeks.
During this time, the cough changes from a mild
one to paroxysmal, involving 5 to 10 short, rapid
coughs, followed by a rapid inspiration, which
causes the hallmark “whoop” or high-pitched
crowing sound of whooping cough. Children are in
obvious distress while coughing. They may
become cyanotic or red faced, and their nose may
drain thick, tenacious mucus. They often vomit
after a paroxysm of coughing, and they feel
exhausted afterward from the effort.
During the convalescent stage, there is a gradual
cessation of the coughing and vomiting. Pertussis
is diagnosed by its striking symptoms, although in
children younger than 6 months of age, the
“whoop” of the cough may be absent, making it
more difficult to diagnose.
Therapeutic Management:
 Infants younger than 3 months with
pertussis are generally admitted to the
hospital for at least 48 hours to see how
the disease course is progressing and to
monitor for complications from
paroxysms, particularly nutritional intake
and oxygen levels.
 As a rule, frequent small meals are
vomited less than larger meals and so
should be encouraged. A full 10-day
course of erythromycin or azithromycin
may be prescribed because these drugs
have the potential to shorten the period
of communicability and may shorten the
duration of symptoms.
 Droplet precautions are used until 5 days
after a child starts antibiotic therapy.
 Complications of pertussis include
alkalosis and dehydration caused by
vomiting and pneumonia, atelectasis, or
emphysema from plugged bronchioles.
Epistaxis, subconjunctival and
 subarachnoid bleeding, or seizures from
asphyxia as a result of severe paroxysms
of coughing may also occur.
 Infants with pertussis may be admitted to
a healthcare facility for observation
because they become dehydrated or may
have such tenacious secretions that they
need airway suction.
Prevention
The current recommendation is to immunize the
pregnant woman from 27 weeks to 36 weeks of
gestation to maximize maternal antibody transfer to
the fetus and reduce the risk of pertussis to the
newborn. Cohorting of young infants and making sure
that all caretakers are immunized is another method
of risk reduction to the young infant. All children
should be immunized in infancy with DTaP and a
booster dose given at 11 to 12 years of age.
Anthrax
• Causative agent: Bacillus anthracis, a bacteria
• Incubation period: 1 to 7 days (inhalational), 1 to 12
days (cutaneous), 1 to 7 days (gastrointestinal)
• Mode of transmission: originally contracted from
contact with the feces of infected cows or sheep; not
transmissible from person to person
• Types of immunity: unstudied
• Active artificial immunity: At present, the anthrax
vaccine is not used in children but is available for
adults 18 to 65 years of age who work with anthrax in
the lab, certain vets who handle animals or animal
products contaminated with anthrax, and only some
members of the military.
• Passive artificial immunity: not available
Anthrax is an acute infectious disease that is
contracted from exposure to the anthrax bacteria or
its spores. As the organism grows inside the human
body, a toxin is produced that causes the bulk of the
symptoms. Children may present with any of the
three clinical forms: cutaneous, inhalational, or
gastrointestinal. Inhalational anthrax has a mortality
rate of over 90%. It begins with a brief prodromal
period of flulike symptoms, followed shortly by
dyspnea, severe systemic shock, and marked evidence
of mediastinal widening and pleural effusion on X-ray.
Because it can be fatal and spreads through coughing,
anthrax has been proposed as bacteria that could be
used in bioterrorism. Cutaneous anthrax is
characterized by a skin lesion that begins as a papule
and then passes through a vesicle stage, to a painless
depressed black eschar. Fever, malaise, headache,
and regional swollen lymph nodes may accompany
the skin lesion.
Gastrointestinal anthrax is contracted by eating
undercooked meat infected with the organism. The
child develops severe abdominal pain, fever, bloody
diarrhea, and septicemia (blood infection). The
mortality rate for this form is about 25%. If exposed to
anthrax, prophylaxis with ciprofloxacin (Cipro) for
those older than 18 years of age and doxycycline for
younger patients are the drugs of choice. Drug
therapy is continued for 60 days because of the
potential persistence of and difficulty in killing spores.
Tetanus (Lockjaw)
• Causative agent: C. tetani
• Incubation period: 3 days to 3 weeks • Period of
communicability: none
• Mode of transmission: direct or indirect
contamination of a closed wound
• Immunity: development of the disease gives lasting
natural immunity
• Active artificial immunity: tetanus toxoid contained
in DTaP vaccine
• Passive artificial immunity: TIG
 Tetanus occurs worldwide causing an acute,
spastic paralytic illness caused by neurotoxin
produced by Clostridium. It is a highly fatal
disease if untreated and is caused by an
anaerobic, spore-forming bacillus found in soil
and the excretions of animals. It enters the
body through an open wound.
 If the wound is deep, such as a stab wound,
where the distal end of the wound is shut off
from an oxygen source, tetanus bacilli begin
to reproduce. The organism may also enter
through a burn site, which crusts, thus
creating an anaerobic environment. As the
bacilli grow, they produce exotoxins that
cause the disease symptoms by affecting the
motor nuclei of the central nervous system.
  The onset of the disease occurs gradually over
1 to 7 days with severe muscle spasm
stimulated by external stimuli and autonomic
dysfunction causing arrhythmias, tachycardia,
and diaphoresis. The entrance site of the
bacillus does not appear infected (no pus or
reddened area is present unless a secondary
infection also exists). After the incubation
period, the exotoxins have developed to such
an extent, however, that they are capable of
disrupting the nervous system.
Assessment:
The first symptoms that are noticeable are stiffness of
the neck and jaw (lockjaw). Within 24 to 48 hours,
muscular rigidity of the trunk and extremities
develops. The back becomes arched (opisthotonos),
the abdominal muscles are stiff and board-like, and
the face assumes an unusual appearance, with
wrinkling of the forehead and distortion of the
corners of the mouth (a “sardonic grin” sign). Any
stimulation, such as a sudden noise, a bright light, or a
touch, causes painful, paroxysmal spasms. The
sensorium is clear throughout the course of the
disease, so the child is aware of the pain associated
with the muscle spasms. As these spasms begin to
include the larynx, respiratory obstruction and death
by asphyxiation can occur.
Therapeutic Management:
A child needs to be cared for in a quiet, stimulation-
free room with total parenteral nutrition, sedation,
and a muscle relaxant to prevent aspiration from
muscle spasms. If the wound is filled with necrotic
tissue, it may be debrided to ensure no secondary
infections arise. The first line of treatment is human
tetanus immune globulin (TIG) with parenteral
penicillin G or oral or intravenous metronidazole
(Flagyl) administration to decrease the vegetative
forms of C. tetani. A child may need to be intubated
and mechanical ventilation begun to maintain
respiratory function.
Prevention:
Prevention Tetanus is a serious disease, but it can be
prevented through active immunization and suitable
booster immunizations. Children routinely receive
tetanus immunization as part of routine DTaP
immunization with a booster dose at school age;
thereafter, they should receive a booster dose every
10 years. At the time of a wound, the wound site
should be cleaned well with soap and water and a
suitable antiseptic.
Lyme Disease
• Causative agent: Borrelia burgdorferi, a spirochete •
Incubation period: 3 to 30 days
• Period of communicability: not communicable from
one person to another
• Mode of transmission: deer tick
• Active artificial immunity: none available; Lyme
vaccine discontinued
• Passive artificial immunity: immune globulin
 Lyme disease is caused by a spirochete, B.
burgdorferi, which is transmitted by a tick
frequently carried on deer.
 Almost immediately after a tick bite, an
erythematous papule is noticeable at the site,
which spreads over the next 3 to 30 days (the
incubation period) to become a large, round
ring with a raised swollen border (erythema
chronicum migrans).
 This is followed by systemic involvement that
can lead to cardiac, musculoskeletal, and
neurologic symptoms. Cardiac involvement
may be so severe that it includes heart block
from atrioventricular conduction
abnormalities.
 Neurologic symptoms commonly include stiff
neck, headache, and cranial nerve palsy.
Musculoskeletal symptoms include painful
swollen arthritic joints, particularly in the
knee.
 Amoxicillin is administered to symptomatic
children less than 8 years old, whereas
doxycycline is given to those older than 8
years of age. Encourage parents to inspect the
skin of children who have been playing in
wooded areas for tick bites to help identify
the disorder before debilitating symptoms
occur.
TIPS FOR AVOIDING EXPOSURE TO LYME DISEASE
• Wear protective clothing when hiking or playing in
wooded areas, such as long sleeves, high necklines,
and long slacks. Tuck bottom of slacks into socks or
boots.
• Wear light-colored clothing so any tick present on
clothing can be readily observed.
• Inspect the skin daily and thoroughly for ticks after
hiking or playing in wooded areas.
• Remove any ticks found with tweezers placed at the
head of the tick, pulling gently and steadily for several
seconds. The tick mouth takes a while to release their
hold.
• Report any area of inflammation that might be a tick
bite to a healthcare provider for early diagnosis.
Rocky Mountain Spotted Fever
• Causative agent: Rickettsia rickettsii
• Incubation period: 3 to 12 days
• Period of communicability: not communicable from
one person to another
• Mode of transmission: wood, dog, or rabbit tick
• Active artificial immunity: Rocky Mountain spotted
fever (RMSF) vaccine is not available.
 Most tick infections occur between April and
October; however, ticks can bite in the winter
with 9% of infections in New York, New
Jersey, and Pennsylvania reported in the
winter. The initial presentation is nonspecific
and includes malaise, nausea, vomiting, and
myalgia. The reported clinical presentation of
RMSF is a triad rash, fever, and tick bite
history; however, this occurs in fewer than
60% of children. The others reported a
prominent reddened area at the site of the
tick bite. In 2 to 8 days, a blanching pink
macular rash on the ankles, wrists, or
forearms develops, eventually spreading to
the palms, soles, arms, legs, and trunk but
tending to spare the face. The classic
petechial rash will develop by 5 to 6 days and
is a sign of advanced disease. The child will
also have abdominal pain that mimics
appendicitis, diarrhea, gastroenteritis,
conjunctiva redness, and periorbital and
peripheral edema. A persistent headache and
fever (as high as 104°F [40°C]) with mental
confusion can also occur.
 In late-stage disease, untreated children will
develop central nervous system involvement
including a meningoencephalitis (stiff neck
and seizures) and renal failure, with signs of
cardiac and pulmonary failure including
pneumonia.
 First-line therapy is with doxycycline for 7 to
10 days and should be initiated within the first
5 days of the appearance of symptoms.
Children are generally admitted for initiation
of treatment and as they improve are
discharged home. Caution parents to finish
the full course of therapy to ensure disease
eradication and to prevent the risk of
complications.
Roundworms (Ascariasis)
Ascaris lumbricoides are generally asymptomatic
infections but when there is an extensive parasite
load, malnutrition and gastrointestinal symptoms
result. With an incubation period of 8 weeks, the
nurse must obtain a history of travel to
underdeveloped countries. The roundworm parasite
lives in the intestinal tract. Larvae, which hatch from
the ingested eggs, penetrate the intestinal wall and
enter the circulation. From there, they may migrate to
any body tissue. Children develop a loss of appetite
and nausea and vomiting. Intestinal obstruction may
occur from a mass of roundworms in the intestine.
Ascariasis can be prevented by the sanitary disposal of
feces to prevent contamination of the soil. There are
several treatment options: (a) a single dose of
albendazole with food, (b) nitazoxanide twice a day
for 3 days, or (c) a single dose of ivermectin (off-label
use and not to be used in children less than 15 kg).
Enterobiasis (Pinworms)
Giardia lamblia, a flagellated protozoa, is the most
common intestinal parasitic infection in the United
States with transmission occurring from ground water
contamination and untreated surfaces that are
contaminated. The peak of the disease occurs in the
early summer through the fall. Transmission occurs
through the fecal–oral route and occurs from fecal
contaminated water and stool. Transmission can
occur from person to person or from person to
animal. The child ingests the cysts of the organism,
and the cysts develop in the intestine into the mature
form of the organism. Ingestion of as little as 10 cysts
has been associated with illness. It is contagious as
long as the infected person still has excreted cysts.
The disease can be asymptomatic or, in symptomatic
people, associated with diarrhea, weight loss,
abdominal cramps, bloating, and weight loss. The
diagnosis is made through DFA assays as well as
specific EIA with DFA being the recommended test by
the CDC. According to the 2015 Red Book,
metronidazole (Flagyl), nitazoxanide (Alinia, Nizonide),
and tinidazole (Tindamax) are the drugs of choice in
pediatric patients, with metronidazole being the least
expensive. Nitazoxanide is approved over 1 year of
age, whereas tinidazole is approved over 3 years of
age. Treatment of asymptomatic carriers is not
recommended for well children living in a household
with well people. Prevention measures include hand
washing for more than 20 seconds, improved
sanitation at day care, adequate chlorination of pool
and drinking water, and camping water
decontamination.
Tinea Capitis
Tinea capitis is a dermatophytic fungal infection of the
scalp which can present one of four ways: (a) a patchy
alopecia with short 2 to 4 mm broken-off hair shafts,
(b) a well demarcated scaling erythematous patch in
circular area, (c) a yellow crusting, perifollicular
erythema of scalp which has heavy hair loss, or (d) a
kerion or boggy circular area of hair loss which is the
result of an inflammatory response to the fungus.
The child must be treated with oral antifungal such as
griseofulvin (Gris-PEG) or terbinafine (Lamisil) and
topical shampoo such as selenium sulfide (Selsun
Shampoo), ketoconazole (Nizoral shampoo), and
ciclopirox (Loprox Shampoo) applied two to three
times a week. Adolescents should be cautioned not to
consume alcohol while taking any oral antifungal
medications as they are metabolized by the liver and
can cause nausea and vomiting. Safety of the drug
during pregnancy is not established. Caution children
to avoid strong sunlight during griseofulvin therapy
because photosensitivity may occur.
Tinea Cruris
Tinea cruris (jock itch) is a brownish to erythematous,
well-demarcated patch on the groin, inner thighs, and
scrotum. The patch can sometimes have central
clearing and may have a papular or vesiculopapular
border. The area is pruritic and may result from
moisture, close-fitting garments, and obesity. The
incubation period is from 1 to 3 weeks. Local
application of an antifungal agent for 4 to 6 weeks is
needed, and the use of corticosteroids in the area
should be avoided.
Tinea Pedis
Tinea pedis (athlete’s foot) produces pruritic, pinpoint
vesicles with fissuring between the toes and on the
plantar surface of the foot. It is treated with
antifungal agent such as clotrimazole (Lotrimin).
Tinea Corporis
Tinea corporis is a superficial, well-demarcated, mildly
erythematous, ring-like infection of the epidermal
layer of the skin characterized by slightly scaly central
clearing and raised papular borders. It starts as a
papular lesion and spreads over several days. It is
called ringworm due to its circular shape (Fig. 43.14).
The incubation period is 1 to 3 weeks. The lesions are
confused with granuloma annulare and nummular
eczema. Topical antifungal treatment should be
applied to the affected area for 1 week following
complete clearing of the lesion.
NURSING CARE OF A FAMILY WHEN A CHILD HASA
GASTROINTESTINAL DISORDER
Beriberi – tingiling and numbness of extremities, heart
palpitations, exhaustion
Dehydration – excessive fluid loss
Gastroesophageal reflux – is the regurgitation of
stomach secretions into the esophagus through the
lower esophageal sphincter
Inguinal hernia – is a protrusion of a secretion of the
bowel into the inguinal ring
Insensible loss – is the amount of body fluid lost daily
that is not easily measured, from the respiratory
system, skin, and water in the excreted stool
Intussusception – the invagination of one portion of
the intestines into another.
Keratomalacia – is an eye disorder that results from
vitamin A deficiency.
Kwashiorkor – a disease caused by protein deficiency
Liver Transplantation – is the surgical replacement of
a malfunctioning liver.
McBurney’s Point – is the name given to the point
over the right side of the abdomen that is one third of
the distance from the anterior superior iliac spine to
the umbilicus (navel).
Meckel’s Diverticulum – is an outpouching or bulge in
the lower part of the small intestine.
Necrotizing Enterocolitis – is the development of
necrotic patches in the intestine.
Nutritional Marasmus – deficiency of all food groups
Overhydration – excessive bloody fluid intake
Pellarga – is a disease caused by low levels of niacin,
also known as vitamin B-3.
Rickets – is a skeletal disorder that’s cause by a lack of
vitamin D, calcium, or phosphate.
Scurvy – is a disease resulting from a lack of vitamin C
(ascorbic acid).
Steatorrhea – or fatty stool occurs when there is too
much fat in the stool.
Volvulus – is a twisting of the intestine.
Xerophthalmia – refers to the spectrum of ocular
manifestations due to vitamin A deficiency.
Fluid, Electrolyte and acid – base imbalances
Normal pH 7.35 – 7.45
PaCO2 35 – 45 mmHg
Nral Bicarbonate (HCO3) 22 – 26
PaO2 80 – 100 mmHg
SaO2 95 – 100%
Metabolic Acidosis
 Metabolic acidosis results from diarrhea
because a great deal of sodium is lost with
stool. With metabolic acidosis, an arterial
blood gas analysis will reveal a decreased pH
(under 7.35) and a low HCO3.
Metabolic Alkalosis
 With vomiting, a great deal of hydrochloric
acid is lost. The pH will be elevated and HCO3
will be near or above 28mEq/L.
FLUID IMBALANCES
Under most circumstances, water and salt are lost in
proportion to each other, termed isotonic
dehydration. Occasionally, water is lost out of
proportion to salt, and water depletion or hypertonic
dehydration occurs. If electrolytes are lost out of
proportion to water, this is termed hypotonic
dehydration. Each of these abnormal states produces
specific symptoms.
Isotonic Dehydration
Isotonic dehydration occurs when a child’s body loses
more water than it absorbs (as with diarrhea) or
absorbs less fluid than it excretes (as with nausea and
vomiting).
Hypertonic Dehydration
When water is lost in a greater proportion than
electrolytes, hypertonic dehydration occurs. This
might occur in a child with nausea (thus preventing
fluid intake) and fever (which increases fluid loss
through perspiration); profuse diarrhea, where there
is a greater loss of fluid than salt; or renal disease
associated with polyuria such as nephrosis with
diuresis. Electrolytes such as sodium, chloride, and
bicarbonate concentrate in the blood. The red blood
cell count and hematocrit will be elevated because
the blood is more concentrated than usual.
Hypotonic Dehydration
With hypotonic dehydration, there is a
disproportionately high loss of electrolytes in
proportion to fluid loss. The plasma concentration of
sodium and chloride are low. This could result from
excessive loss of electrolytes by vomiting, from an
increased loss of salt from diuresis, or from diseases
such as adrenocortical insufficiency or diabetic
acidosis. In order to achieve an electrolyte balance,
the kidneys begin to excrete more fluid to bring the
proportion of electrolytes and fluid back in balance,
leading to a secondary extracellular dehydration.
Overhydration
Overhydration, or excessive body fluid intake, can be
as serious as dehydration. It generally occurs in
children who are receiving IV fluid and can lead to
cardiovascular and cardiac failure. When large
quantities of salt-poor fluid (hypotonic solutions) such
as tap water are ingested or are given by enema, the
body transfers water from the extracellular space into
the intracellular space to restore normal osmotic
relationships. This transfer results in intracellular
edema manifested by a headache, nausea, vomiting,
dimness and blurring of vision, cramps, muscle
twitching, and seizures. A situation in which
intracellular edema may occur is when tap water
enemas are given to a child with aganglionic disease
of the intestine.
Common Gastrointestinal Symptoms of Illness in
Children
VOMITING
 Most children with vomiting are suffering
from a mild gastroenteritis (infection) due to a
viral or bacterial organism, but other causes
of vomiting should be considered, such as
obstruction, increased intracranial pressure,
and metabolic disease. The adolescent who is
pregnant may mistake the normal nausea and
vomiting of pregnancy for an illness.
Assessment:
 Character of vomitus
 Presence of pain and abdominal cramping
 Signs of dehydration and fluid and electrolyte
imbalances.
 Signs of metabolic alkalosis
Therapeutic Management:
The treatment for vomiting related to gastroenteritis
is to:
 Give small amounts of fluid frequently as soon
as tolerated to prevent dehydration and
electrolyte imbalance.
 Clear liquids such as ginger ale, tea, and
sports drinks can be used to maintain
hydration, but they are not suitable for
rehydration.
 Oral rehydration solutions (ORS) such as
Pedialyte should be used for infants and
younger children as well as older children
with dehydration.
 Children with intractable vomiting or severe
dehydration will require IV fluids.
DIARRHEA
 Diarrhea that is acute is usually associated
with infection; chronic diarrhea is more likely
related to a malabsorptive or inflammatory
cause. Giardia lamblia is a frequent protozoan
infection that causes diarrhea. The most
common bacterial pathogens include
Campylobacter jejuni, Salmonella, Clostridium
difficile, and Escherichia coli.
Assessment:
 Character of the stools
 Presence of pain and abdominal cramping
 Signs of dehydration and fluid and electrolyte
imbalances
 Sigs of metabolic acidosis
Therapeutic Management:
 Parents can begin to offer an ORS such as
Pedialyte in small amounts on a regimen
similar to that for vomiting.
 Probiotics (dietary supplements containing
potentially beneficial bacteria or yeasts) to
change the bacterial flora of the intestine may
be administered.
 Children also may need measures to reduce
their elevated temperature.
Severe Diarrhea
 Severe diarrhea may result in dehydration and
the need for hospitalization.
Assessment:
 Infants with severe diarrhea appear obviously
ill. Rectal temperature is often as high as 103°
to 104°F (39.5° to 40.0°C).
 Both pulse and respirations are weak and
rapid, and the skin is pale and cool.
 Depressed fontanelle, sunken eyes and poor
skin turgor.
 Liquid green stool passed with explosive force
a minute.
 Severe diarrhea quickly causes a 5% to 15%
loss of body weight, which suggests severe
dehydration. Any infant who has lost 10% or
more of body weight requires immediate
treatment.
Therapeutic Management:
 Regulating electrolyte and fluid balance by
initiating oral or IV rehydration therapy and
on discovering the organism responsible for
the diarrhea.
 All children with severe diarrhea or diarrhea
that persists longer than 24 hours should have
a stool culture taken to determine if infection
is causing the diarrhea, and if appropriate, a
definite antibiotic therapy can be prescribed.
  Infants usually have a potassium depletion,
potassium is not given until it is established
that the child is not in renal failure because
giving a potassium IV when the body has no
outlet for excessive potassium can lead to
excessively high potassium levels and heart
block.
 Enough fluid must be given not only to
replace the deficit that has occurred but also
to replace the continuing loss until the
diarrhea improves.
BACTERIAL INFECTIOUS DISEASES THAT CAUSE
DIARRHEA AND VOMITING
Salmonellosis
• Causative agent: one of the Salmonella bacteria
• Incubation period: 6 to 72 hours for intraluminal
type; 7 to 14 days for extraluminal type
• Period of communicability: as long as organisms are
being excreted (may be as long as 3 months)
• Mode of transmission: ingestion of contaminated
food, especially chicken and raw eggs
Listeriosis
• Causative agent: Listeria monocytogenes
• Incubation period: variable, ranging from 1 day to
more than 3 weeks
• Mode of transmission: ingestion of unpasteurized
milk or cheeses or vegetables grown in contaminated
soil. The infection is particularly important to avoid
during pregnancy because infections during
pregnancy can lead to miscarriage or stillbirth,
prematurity, or infection of the newborn.
Shigellosis (Dysentery)
• Causative agent: organisms of the genus Shigella
• Incubation period: 1 to 7 days
• Period of communicability: approximately 1 to 4
weeks
• Mode of transmission: contaminated food, water, or
milk products
Staphylococcal Food Poisoning
• Causative agent: staphylococcal enterotoxin
produced by some strains of Staphylococcus aureus
• Incubation period: 1 to 7 hours
• Period of communicability: Carriers may
contaminate food as long as they harbor the
organism.
• Mode of transmission: ingestion of contaminated
food such as poultry, creamed foods (e.g., potato
salad), and inadequate cooking.
PROTOZOAN OR VIRAL DIARRHEA
 Most protozoan or viral diarrhea results in
loose, watery stools. The chief therapy for
these is ORS. Children who are cultured with
G. lamblia may be prescribed metronidazole
(Flagyl).
Common Disorders of the Stomach and Duodenum
GASTROESOPHAGEAL REFLUX
 Gastroesophageal reflux is the regurgitation
of stomach secretions into the esophagus
through the lower esophageal (cardiac)
sphincter. It is a normal physiologic process
that occurs throughout the day in infants,
children, and adults.
Gastroesophageal Reflux in Infants
Assessment:
 Diagnosis is informed by patient history, and
therefore, diagnostic testing is not necessary
for uncomplicated reflux. In patients with
GERD, diagnostic workup may include the
following:
• Upper GI series to look for anatomical abnormalities
such as intestinal malrotation
• pH probe (catheter inserted through the nose into
the lower esophagus) to calculate the amount of
acidic reflux into the esophagus in a 24-hour period
• Esophageal manometry to assess esophageal
motility to ensure there is normal esophageal
peristalsis
• Endoscopy to obtain biopsies to assess the degree of
esophagitis
Therapeutic Management:
  The traditional treatment of GI reflux is to
feed infants small frequent feedings of
formula thickened with rice cereal (1
tablespoon of cereal per 1 oz of breast milk or
formula).
 The infant should be held in an upright
position for 30 minutes after feedings if
possible (e.g., on the parent’s shoulder).
 Burp infant frequently when feeding and
handle the infant minimally.
Gastrointestinal Reflux in Children and Adolescents
Therapeutic Management:
 To prevent reflux, the child should avoid lying
down until 3 hours after a meal and should
sleep at night with their upper body elevated
on a foam wedge or extra pillow.
 They should avoid acidic foods such as tomato
products, citrus fruits, or spicy foods.
 Avoiding foods that delay gastric emptying
such as fatty foods, chocolate, or alcohol and
eating smaller portions may also be helpful.
 Antacid for symptom relief.
 Proto pump inhibits (Prevacid, Prilosef) and
histamine H2-receptor antagonist (Tagament,
Pepcid, Zantac) to decrease gastric secretion.
PYLORIC STENOSIS
 The pyloric sphincter is the opening between
the lower portion of the stomach and the
beginning portion of the intestine (the
duodenum). If hypertrophy or hyperplasia of
the muscle surrounding the sphincter occurs,
it is difficult for the stomach to empty, a
condition called pyloric stenosis.
Assessment:
 With this condition, at 4 to 6 weeks of age,
infants typically begin to vomit almost
immediately after each feeding. The vomiting
grows increasingly forceful until it is
projectile, possibly projecting as much as 3 to
4 ft.
 Vomitus contains gastric contents such as milk
or formula, may contain mucus and may be
blood-tinged.
 The child exhibits huger and irritability.
 An olive – shaped mass in the epigastrium just
right of the umbilicus.
 Signs for dehydration and malnutrition.
 Signs of electrolyte imbalances.
Treatment Management:
 Pyloromyotomy- an incision trough the
muscle fibers of the pylorus, may be
performed by laparoscopy.
 Lactose Intolerance – inability to tolerate as a
result of an absence of deficiency of lactase,
an enzyme found in the secretions of the
small intestine that is required for the
digestion of lactose.
PEPTIC ULCER DISEASE
 A peptic ulcer is a shallow excavation formed
in the mucosal wall of the stomach, the
pylorus, or the duodenum. They are rare
occurring in only 1% to 2% of children and
more frequently in males than females. Peptic
ulcer disease includes gastritis (irritation of
the lining of the stomach or duodenum) and is
more commonly seen in childhood.
 In infants, ulcers tend to occur in the
stomach; in adolescents, they are usually
duodenal. Such ulcers occur in a primary form
caused by infection with H. pylori bacteria and
a secondary form that follows severe stress
such as burns or chronic ingestion of
medications such as aspirin, nonsteroidal
antiinflammatory drugs (NSAIDs), alcohol,
caffeine, and smoking cigarettes.
 The small ulceration of the gastric or
duodenal lining leads to pain, blood in the
stool, and vomiting (with blood). If left
uncorrected, peptic ulcer disease can lead to
bowel or stomach perforation with acute
hemorrhage or pyloric obstruction. A chronic
ulcer condition may lead to anemia from the
constant, gradual blood loss.
Assessment:
Gastric:
 Gnawing, sharp pain in or to the left of the
mid – epigastric region occurs 30-60 minutes
after a meal (food ingestion accentuates the
pain).
 Hematemesis is more common than melena.
Duodenal:
 Burning pain occur in med-epigastric area
1 ½ to 3 hours after a meal and during the
night (often awakens the client).
  Melena is more common than
hematemesis.
 Pain is often relieved by the ingestion of
food.
Therapeutic Management:
 Children with peptic ulcer disease due to H.
pylori infection are treated with triple
therapy, a combination of medications that is
given to attempt to eradicate the bacteria
from the stomach. This treatment consists of
two antibiotics, usually amoxicillin and
clarithromycin (Biaxin), and a PPI such as
omeprazole (Prilosec). Bismuth subsalicylate
(Pepto-Bismol) is soothing and mildly
antibiotic and so may be prescribed
concurrently. Stool can be sent for H. pylori
stool antigen to check if the infection has
cleared. Children with stress ulcers can be
treated with a PPI alone.
Hepatic Disorders
• Causative agent: a picornavirus, hepatitis A virus
(HAV)
• Incubation period: 25 days on average
• Period of communicability: highest during 2 weeks
preceding onset of symptoms
• Mode of transmission: in children, ingestion of
fecally contaminated water or shellfish; day care
center spread from contaminated changing tables
• Immunity: Natural immunity: one episode induces
immunity for the specific type of virus.
Active artificial immunity: HAV vaccine (recommended
for all children 12 to 23 months of age, workers in day
care centers, and certain international travelers)
Passive artificial immunity: immune globulin
Hepatitis B
• Causative agent: a hepadnavirus; hepatitis B virus
(HBV)

 Hepatic disorders include both congenital
disorders, such as obstruction or atresia of the
biliary duct, and acquired disorders, such as
hepatitis or cirrhosis.
LIVER FUNCTION
 In infants, 1 or 2 cm of liver is readily and
normally palpable under the diaphragm on
the right side of their abdomen. An organ
essential for the normal metabolism of
carbohydrates, proteins, and fats, the liver
plays a major role in the maintenance of
normal blood sugar levels by changing glucose
to glycogen and storing it until needed by
body cells.
 fat; fibrinogen and prothrombin, substances
essential for blood clotting; heparin, a
substance necessary to keep blood from
clotting in intact vessels; and blood proteins,
which are necessary for cell growth and
repair. It destroys red blood cells and
detoxifies many harmful absorbed
substances, such as drugs.
• Incubation period: 120 days on average
• Period of communicability: later part of incubation
period and during the acute stage
• Mode of transmission: transfusion of contaminated
blood and plasma or semen; inoculation by a
contaminated syringe or needle through IV drug use;
may be spread to fetus if mother has infection in third
trimester of pregnancy
• Immunity: Natural immunity: one episode induces
immunity for the specific type of virus
Active artificial immunity: HBV vaccine (recommended
for routine immunization beginning at birth and also
to all healthcare providers)
Passive artificial immunity: specific hepatitis B
immune serum globulin
Hepatitis C, D, and E

HEPATITIS

 Hepatitis (inflammation and infection of the

liver) is caused by invasion of the hepatitis A,
B, C, D, or E virus.

Hepatitis A
  Although hepatitis A and B are the viruses
that most frequently cause hepatitis,
hepatitis C, D, and E viruses may also be
involved. Hepatitis C virus (HCV) is a single-
strand RNA virus. Transmission, as with HBV,
is primarily by blood or blood products, IV
drug use, maternal–fetal transfer, or sexual
contact. The virus produces mild symptoms
of disease, but there is a high incidence of
chronic infection with the virus.
 Hepatitis D virus (HDV), or the delta form, is
similar to HBV in transmission, although it
apparently requires a coexisting HBV
infection to be activated. Disease symptoms
Fulminant Hepatic Failure
are mild, but there is a high incidence of
fulminant hepatitis after the initial infection.
 The E form of hepatitis is enterically
transmitted similarly to hepatitis A (e.g.,
fecally contaminated water). Disease
symptoms from the E virus can range from
asymptomatic to mild to chronic liver
disease.
Assessment:
Prodromal or Anicteric Phase
 Lasts 5 to 7 days
 Absence of jaundice
 Anorexia, malaise, lethargy, easy fatigability
 Fever (especially in adolescents)
 Epigastric or right upper quadrant abdominal
pain
 Arthralgia and rashes (more likely with
Hapatitis B virus)
 Hepatomegaly
Icteric Phase
 Jaundice, which is best assessed in the sclera,
nail beds, and mucous membranes
 Dark urine and pale stools
 Pruritus
Therapeutic Management:
 Strict washing is required.
 Hospitalization is required in the event of
coagulopathy or fulminant hepatitis.
 Standard precaution during hospitalization.
 Provide a low fat, well – balanced diet
 Inform parents that jaundice may appear
worse before it resolves.
 Instruct the parents about the signs of the
child’s condition worsening, such as changes
in neurologic status, bleeding and fluid
retention.
 Immunoglobulin provides passive immunity
and may be effective for preexposure
prophylaxis to prevent HAV infection.
 Hepatitis B immunoglobin provides passive
immunity and may be effective in preventing
infection after a 1 –time exposure such as an
accidental needle puncture or other contact
of contaminated material with mucous
membranes; immunoglobulin should also be
given to newborns whose mothers are
positive for hepatitis B surface antigen.
 Fulminant hepatic failure is present when
acute, massive necrosis or sudden, severe
impairment of liver function occurs, leading to
liver failure and hepatic encephalopathy. It
can be due to infection or toxicity.
Acetaminophen (Tylenol) overdose is the
most likely etiology. Hepatic encephalopathy,
or invasion of brain cells by ammonia, occurs
because of the inability of the liver to detoxify
the ammonia being constantly produced by
the intestine in the process of digestion.
 Children may show mental aberrations such
as confusion, drowsiness, or disorientation.
Treatment involves reducing protein intake
and administering lactulose to prevent
absorption of ammonia in the colon or
administering nonabsorbable antibiotics such
as neomycin to decrease the production of
ammonia by the intestinal bacteria. Liver
transplantation (surgical replacement of a
malfunctioning liver by a donor liver) may be
necessary. If a cadaver liver is not available, a
lobe can be removed from a living donor such
as a parent and transplanted into a child. The
donor is then able to regenerate the lost lobe
of the liver without long-term effects.
OBSTRUCTION OF THE BILE DUCTS
 Obstruction of the bile ducts in children
generally occurs from congenital biliary
atresia, stenosis, or absence of the duct. It
also can occur from the plugging of biliary
secretions, although this is rare. When the
bile duct is obstructed, bile, unable to
 enter the intestinal tract, accumulates in
the liver. Bile pigments (direct bilirubin)
enter the bloodstream and jaundice
occurs, which increases in intensity daily.
Assessment:
 Although bile duct obstruction is a
congenital disorder, the chief sign
(jaundice) does not develop until between
2 and 6 weeks of age.
 This delay differentiates it clinically from
physiologic jaundice, which occurs in
almost all newborns on the third day of
life, or the jaundice of Rh or ABO
isoimmunization, which typically occurs
during the first 24 hours of life.
 The AST (SGOT) level is normal in the
early phase but later becomes abnormal,
when prolonged obstruction and back
pressure cause liver cell damage.
 In addition, because bile salts, which are
necessary for fat and fat-soluble vitamin
absorption, are not reaching the intestine,
absorption of fat and fat-soluble vitamins
(vitamins A, D, E, and K) becomes poor.
Calcium absorption, which depends on
vitamin D absorption, will fail as well.
Therapeutic Management:
 Before treatment is begun,
appropriate blood work and a liver
biopsy under local anesthesia may be
obtained to rule out hepatitis.
 Duodenal secretions may be collected
by endoscopy to assess for bile.
Radionuclide imaging to show that
bile ducts are not patent may confirm
the diagnosis.
 If atresia of the bile duct is the
problem, surgical correction is the
treatment (a Kasai procedure). With
this surgery, a Roux-en-Y loop of
bowel is sutured directly onto the
hilum of the liver so that the
remaining small bile ducts will drain
into the bowel.
NONALCOHOLIC FATTY LIVER DISEASE AND
CIRRHOSIS
 Nonalcoholic fatty liver disease (NAFLD) is the
accumulation of fatty deposits in the liver and
is usually associated with obesity.
 Cirrhosis is fibrotic scarring of the liver.
Cirrhosis means “yellow,” or the typical color
of hepatic scar tissue. It rarely occurs in
children, although it may be seen as a result
of congenital biliary atresia or as a
complication of chronic illnesses such as
protracted hepatitis, sickle-cell anemia, or
cystic fibrosis. When fibrotic infiltrates replace
normal liver cells, total liver function becomes
impaired, resulting in a decreased ability to
detoxify toxic substances, decreased protein
synthesis, inability to produce prothrombin,
decreased ability to produce bile, and,
possibly, hypoglycemia. Children will have
large, fatty stools resulting from the decrease
in bile production; avitaminosis of fat-soluble
vitamins; symptoms of hemorrhage from
decreased clotting ability; and anemia.
 Portal hypertension occurs from back
pressure of blood that cannot flow readily
through the scarred organ. This leads to
compromised heart action, ascites (an
exudate of fluid into the abdomen), possibly
esophageal varices (back pressure causes
them to dilate), and hypersplenism.
 Cholestyramine (Questran) may be prescribed
to reduce reabsorption of bile into the
circulation to minimize itching from
cholestasis. Once fatty or fibrotic infiltration
begins, however, there is no way to reverse
the changes. Nursing care focuses on
promoting comfort, providing adequate
nutrition by a high- carbohydrate, medium-
chain–triglyceride diet, and preventing further
involvement until liver transplantation can be
scheduled.
Esophageal Varices
Description:
1. Dilated and tortuous veins in the submucosa of the
esophagus.
2. Caused by portal hypertension, often associated
with liver cirrhosis; are at high risk for rupture if portal
circulation pressure rises.
3. Bleeding varices are an emergency.
4. The goal of treatment is to control bleeding,
prevent complications and prevents the recurrence of
bleeding.
Assessment:
 Hematemesis
 Melena
 Ascites
 Jaundice
 Hepatomegaly and splenomegaly
 Dilated abnormal veins
 Signs of shock
Management:
 Elevate the head of the bed
 Monitor vital signs
 Monitor hemoglobin and hematocrit values
and coagulation factors.
 Assist in inserting an NG tube or a balloon
tamponade as prescribed.
 Prepare to assist with administering
medications to induce vasoconstriction and
reduce bleeding,
 Instruct the client to avoid activities that will
initiate vasovagal responses.
 Prepare the client for endoscopic procedures
or surgical procedures or surgical procedures
as prescribed.
LIVER TRANSPLANTATION
 Liver transplantation is the surgical
replacement of a malfunctioning liver by a
donor liver. Child-size donor livers are not
readily available, so the waiting time for
surgery may be months. Adult livers can be
reduced in size for transplantation or a lobe of
a liver from a living donor can be used. Often,
the child is extremely ill with ascites, GI
bleeding, extreme pruritus, hepatic
encephalopathy, or renal dysfunction before
the surgery. This makes nursing care after
liver transplantation in a child complex
because it involves taking care of a child who
has had major surgery and who normally
would be categorized as too ill to undergo
surgery.
 Despite the severity of illness and the length
of surgery, however, children tend to recover
quickly after liver transplantation. Both
children and parents must have thorough
preoperative preparation, so they understand
the seriousness of the surgery and the
possibility that the graft will be rejected. It
helps to introduce the parents to others
whose children have successfully undergone
the procedure so they have support people
available for this critical time.
Preoperative Management
Preoperative management consists of keeping the
child in the best physiologic condition possible so that
when a liver is available, the transplantation can be
performed.
Surgical Procedure
Liver transplantation is a time-consuming procedure
and requires a wide subcostal incision. The vena cava
is temporarily clamped during the removal of the
natural liver to prevent bleeding, which means that all
IV lines must be placed in the upper extremities.
Postoperative Management
 Rejection of a liver transplant is most often
because of the function of T lymphocytes.
Careful tissue matching (human leukocyte
antigen [HLA] matching) is necessary to
reduce the possibility of stimulating T-cell
rejection. To further reduce the action of T
lymphocytes, children are given an
immunosuppressive drug such as
mycophenolate mofetil (CellCept),
cyclosporine (Sandimmune), or tacrolimus
(Prograf) before the transplantation. Children
may need assisted ventilation for
approximately 24 hours postoperatively to
prevent pulmonary complications such as
atelectasis and pneumonia because the large
abdominal incision makes coughing and deep
breathing difficult. In addition, ascites places
pressure against the diaphragm, interfering
with lung expansion, and preoperative
pulmonary edema may be present.
 After discontinuation of mechanical
ventilation and extubation, chest
physiotherapy may be started to mobilize
lung secretions. Advocate for adequate pain
control. Frequently assess blood pressure,
capillary refill, peripheral pulses, and skin
color to ensure adequate cardiovascular
 function, which is important for good tissue
perfusion of the transplanted liver. The child
may have a central venous pressure line or an
arterial line such as a Swan-Ganz catheter
inserted to assess hemodynamic status.
 Assess neurologic status hourly using a
modified Glasgow Coma Scale. Usually, a child
is positioned flat for the first 24 hours to
prevent cerebral air emboli, which may result
from any air remaining in the transplanted
liver. Typically, children have a nasogastric
tube inserted during surgery that is attached
to low intermittent suction postoperatively.
Irrigate the tube according to agency policy to
maintain patency.
 Assess the gastric pH by aspirating stomach
contents every 4 hours; based on this
assessment, administer antacids or H2 -
receptor antagonists such as cimetidine or
mucosal protectants as prescribed to help
prevent a stress ulcer. If preoperative
esophageal varices are present, assess
nasogastric drainage carefully for frank or
occult blood. A T-tube inserted into the bile
duct for drainage allows the amount of bile
being produced by the new liver to be
evaluated. Once bowel sounds become active,
nasogastric suction and the T-tube are usually
discontinued and liquids and then solid foods
are introduced gradually. If vomiting occurs
and is persistent, total parenteral nutrition
may be used for 3 or 4 days to rest the
intestinal tract before fluid is reintroduced.
Hypoglycemia is a major danger
postoperatively because glucose levels are
regulated by the liver, and the transplanted
organ may not function efficiently at first.
Assess serum glucose levels hourly by finger-
stick puncture.
INTUSSUSCEPTION
Description:
1. Telescoping of one portion of the bowel into
another portion.
2. The condition results in obstruction to the passage
of intestinal contents.
Assessment:
 Colicky abdominal pain that causes the child
to cream and draw the knees to the
abdomen, similar to the fecal position.
 Vomiting of gastric contents.
 Bile – stained fecal emesis.
 Currant jelly – like stools containing blood and
mucus.
 Hypoactive or hyperactive bowel sounds.
 Tender distended abdomen, possibly with a
palpable sausage – shaped mass in the upper
right quadrant.
Therapeutic Management:
1. Monitor for signs of perforation and shock as
evidence by fever, increased HR, changes in LOC or
blood pressure and respiratory distress.
2. Antibiotics, IV fluids and decompression via NGT
may be prescribed.
3. Monitor for the passage of normal, brown stool,
which indicates that the intussusception has reduced
itself.
4. If surgery is require, postoperative care is similar to
care after any abdominal surgery; procedure may be
done via lapascope.
VOLVULUS WITH MALROTATION
 A volvulus is a twisting of the intestine. The
twist leads to obstruction of the passage of
feces and to compromise of the blood supply
to the loop of intestine involved. Volvulus
occurs due to intestinal malrotation and may
be associated with other congenital
anomalies.
 Usually, the symptoms occur during the first 6
months of life and are those of intestinal
obstruction such as intense crying and pain,
pulling up the legs, abdominal distention, and
vomiting. A volvulus can be differentiated
from pyloric stenosis because vomiting with
pyloric stenosis occurs immediately after
feeding, whereas pain and vomiting from a
volvulus is unrelated to feeding.
 The diagnosis is made based on the history
and an abdominal examination, which reveals
an abdominal mass. It is confirmed by an
ultrasound or lower barium Xray. Surgery is an
emergency and should be performed before
necrosis of the intestine occurs from a lack of
blood supply to the involved loop of bowel.
 Preoperative and postoperative care will be
the same as for infants with intussusception.
NECROTIZING ENTEROCOLITIS
 Necrotizing enterocolitis (NEC) is a condition
that develops in approximately 5% of all
infants in neonatal intensive care nurseries,
with premature and low– birth-weight infants
at highest risk. Necrotic areas develop in the
bowel that interfere with digestion and can
lead to paralytic ileus, perforation, and
peritonitis.
 The cause of NEC is unknown and thought to
be due to a variety of factors. The necrosis
appears to result from ischemia or poor
perfusion of blood vessels in the entire bowel
or in isolated sections of the bowel.
Assessment:
 There is a lower incidence of the condition in
infants who are fed breast milk than in those
who are formula fed because intestinal
organisms grow more profusely with cow’s
milk than breast milk (cow’s milk lacks
antibodies). A response to the foreign protein
in cow’s milk may also be a mechanism that
starts the necrotic process. Therefore,
encouraging breastfeeding may help prevent
this disorder.
 Signs of NEC usually appear in the first week
of life. The infant’s abdomen becomes
distended and tense. If stomach contents are
aspirated before a feeding, a return of
undigested milk of more than 2 ml will be
obtained. Stool may test positive for occult
blood. Periods of apnea may begin or increase
in number. Signs of blood loss because of
intestinal bleeding, such as lowered blood
pressure and inability to stabilize
temperature, also may be present.
 Abdominal girth measurements made just
above the umbilicus every 4 to 8 hours will
show a gradual increase. Abdominal X-ray
films show a characteristic picture of air
invading the intestinal wall; if perforation has
occurred, there will be air in the abdominal
cavity.
Therapeutic Management:
 As soon as the condition is recognized,
breastfeedings or formula feedings are
discontinued, and the infant is maintained on
IV or total parenteral nutrition solutions to
rest the GI tract except for additional
supplements of enteral probiotics. An
antibiotic may be given to limit secondary
infection. Handle the infant’s abdomen gently
to lessen the possibility of a bowel
perforation.
 If the area of necrosis appears to be localized,
surgery to remove that portion of the bowel
may be successful. If a large portion of the
bowel is removed, the infant may be prone to
“short-bowel” syndrome or may have a
problem with digestion of nutrients in the
future. If the bowel perforates, peritoneal
drainage or a laparotomy will be necessary to
help remove fecal secretions from the
abdomen. An infant may need a temporary
colostomy performed to allow for bowel
function.
 NEC is a grave insult to an infant already
stressed by immaturity. The prognosis is
guarded until the infant can again take oral
feedings without bowel complications.
SHORT-BOWEL/SHORT-GUT SYNDROME
 Short-bowel or short-gut syndrome is an
absorptive disorder in which there is not
sufficient bowel surface area in the small
intestine for proper nutrient absorption. The
condition has several causes, including
surgery for NEC, volvulus, and GI tract trauma,
which resulted in a large portion of the
intestine being removed. The treatment
includes ensuring adequate hydration and
proper intake of essential vitamins and
minerals. Following bowel resection surgery,
total parenteral nutrition, including lipids,
may be used initially until the bowel can
tolerate enteral feedings. Oral or enteral
feedings are then given as tolerated. If
gastrostomy or nasogastric feedings are used,
nonnutritive sucking should be facilitated to
preserve the suck–swallow reflex. Because
long-term use of total parenteral nutrition
may cause liver damage, liver transplantation
may be needed in the future.
APPENDICITIS
Description:
Inflammation of the appendix. 4. Symptoms of the disorder occur mst often between
ages 1 – 5 years.

Assessment:
Assessment:
 Pain in periumbilical area that descends to the
right lower quadrant.  Acute or insidious diarrhea
 Abdominal pain that is most intense at  Steatorrhea
McBurney’s point.  Anorexia
 Referred pain indicating the presence of  Abdominal pain and distention
peritoneal irritation.  Muscle wasting, particularly in the buttocks
 Rebound tenderness and abdominal rigidity. and extremities
 Elevated white blood cell count.  Vomiting
 Low – grade fever  Anemia
 Anorexia, nausea and vomiting after pain  Irritability
develops.
Management:
 Diarrhea
 Maintain a gluten – free diet, substituting
Management: Appendectomy
corn, rice and millet as grain source.
 Instruct the parents and child about lifelong
elimination of gluten sources such as BROW.
MECKEL’S DIVERTICULUM
 Administer mineral and vitamin supplements,
 Is an outpouching or herniation of the including iron, folic acid, and fat soluble
mucosa. vitamin A, D, E, K
 The structure often contains some misplaced  Teach the child and parents about a gluten –
gastric mucosa, which secretes gastric acids free diet.
that flow into the intestine and irritate the
CONSTIPATION
bowel wall, leading to ulceration and
bleeding. Constipation is the infrequent and difficult passage of
 Children will have painless, tarry (black stools dry, hard stools.
or grossly bloody stools.
Assessment:
 Because the pouch is small, it does not fill,
and therefore, it may not be evident on X-ray  Abdominal pain and cramping without
or ultrasound. A nuclear medicine test called a distention.
Meckel’s scan is used to identify the area of  Palpable movable fecal masses.
gastric mucosa in the intestine.  Normal or decreased bowel sounds.
 Treatment is laparoscopy exploration and  Malaise and headache
removal of the vestigial structure.  Anorexia, nausea and vomiting

Management:
CELIAC DISEASE (MALABSORPTION SYNDROME,  Maintain a diet high in fiber and fluids to
GLUTEN-INDUCED ENTEROPATHY, CELIAC SPRUE) promote bowel elimination.
 Encourage child to sit on the toilet for 5-10
Description:
minutes approximately 20-30 minutes after
1. Intolerance to gluten, the protein component of breakfast and dinner to assist in defecation.
wheat, barley, rye and oats.
INGUINAL HERNIA
2. Celiac disease results in the accumulation of the
 A is a protrusion of a section of the bowel into
amino acid glutamine, which is toxic to intestinal
the inguinal ring.
mucosal cells.
 It usually occurs in boys (9:1) because, as the
3. Intestinal villous atrophy occurs, which affects testes descend from the abdominal cavity into
absorption of ingested nutrients. the scrotum late in fetal life, a fold of parietal
 peritoneum also descends, forming a tube
from the abdomen to the scrotum.
 In girls, the round ligament extends from the
uterus into the inguinal canal to its
attachment on the abdominal wall. In girls, an
inguinal hernia may occur because of a
weakness of the muscle surrounding the
round ligament.
Assessment:
 Hernia appears as a lump in the left or right
groin.
 Hernia is apparent only on crying (when
abdominal pressure increases).
 Inguinal hernias are painless.
Management:
 Treatment of inguinal hernia is laparoscopy
surgery.
 After surgery, keep the suture line dry and
free of urine or feces to prevent infection.
 Assess circulation in the leg on the side of the
surgical repair to be certain that edema of the
groin is not compressing blood vessels and
obstructing blood flow to the leg.
HIRSCHSPRUNG DISEASE (AGANGLIONIC
MEGACOLON)
 Hirschsprung disease, or aganglionic
megacolon, is an absence of ganglionic
innervation 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 intestine.
 This results in chronic constipation or
ribbonlike stools (stools passing through such
a small, narrow segment look like ribbons).
The portion of the bowel proximal to the
obstruction dilates, thus distending the
abdomen.
Assessment:
Newborns:
 Failure to pass meconium stool
 Refusal to suck
 Abdominal distention
 Bile – stained vomitus
Children:
 Failure to gain weight ad delayed growth
 Abdominal distention
 Vomiting
 Constipation alternating with diarrhea
 Ribbon – like and foul smelling stools
Therapeutic Management:
 Repair of aganglionic megacolon involves
dissection and removal of the affected
section, with anastomosis of the intestine
(termed a pull-through operation).
 Because this is a technically difficult operation
to perform in a small abdomen, the condition
is generally treated in infants by two-stage
surgery: First, a temporary colostomy is
established, followed by bowel repair at 12 to
18 months of age. After the final surgery,
children should have a functioning, normal
bowel. In the few instances in which the anus
is deprived of nerve endings, a permanent
colostomy will need to be established.
INFLAMMATORY BOWEL DISEASE: ULCERATIVE
COLITIS AND CROHN DISEASE
Ulcerative Colitis:
 Children with UC develop crampy abdominal
pain, urgency, tenesmus, and frequent bloody
stools.
 It is treated with oral and sometimes IV
medications such as infliximab (Remicade).
 If it does not respond to medical therapy,
surgery to remove the colon is performed,
which is curative for UC. There is an
association between UC and colon carcinoma
if the disease persists over 10 years. Yearly
colonoscopy should be performed once the
patient has reached 8 to 10 years from the
date of diagnosis.
Crohn Disease:
Description: an inflammation disease that can occur
anywhere in the gastrointestinal tract but most often
affects the terminal ileum to thickening and scarring, a
narrowed lumen, fistulas, ulcerations and abscess.
Assessment:
 Fever
 Cramplike and colicky pain after meals
 Diarrhea (semisolid) which may contain
mucus and pus
 Abdominal distention
 Anorexia, nausea, vomiting
 Anemia
COMPARISON OF CROHN DISEASE AND ULCERATIVE  Irritable bowel syndrome results from
COLITIS increased motility, which can lead to spasm
and pain.
Comparison Crohn Disease Ulcerative
Factor Colitis Assessment:
Part of bowel Ileum Colon and
affected rectum  Diffuse abdominal pain unrelated to meals or
Nature of Intermittent Continuous activity.
lesions  Alternating constipation and diarrhea with the
Diarrhea Moderate Severe and presence of undigested food and mucus in
bloody then stool.
Anorexia Severe Mild
Management:
Weight loss Severe Mild
Growth Marked Mild  Reassure the parents and child that the
retardation problem is self-limiting and intermittent and
Anal and Common None will resolve.
perianal lesions  Anticholinergics may be prescribed.
Association Rare Common  Encourage the maintenance of a healthy, well
with carcinoma
balanced, moderate – fiber and low fat diet.
 Encourage health promotion activities such as
Therapeutic Management; exercise and school activities.

 In mild to moderate cases, oral medications
are usually sufficient to control the symptoms.
Vitamin and mineral deficiencies should be
corrected.
 In more severe cases, bowel rest may be
indicated to allow the bowel to heal. Enteral
or total parenteral nutrition, therefore, is
usually provided for nutrition during the
resting period. A child can remain home
during this period as long as parents have
thorough education about the child’s
nutritional needs. When food is reintroduced
after the resting period, a high-protein,
highcarbohydrate, and high-vitamin diet is
prescribed to replace nutrients.
 In more severe cases, remission is usually
achieved with corticosteroids or infliximab
(Remicade), an antibody to the inflammatory
cytokine tumor necrosis factor alpha.
Maintenance therapy may be with infliximab
or mercaptopurine (immunomodulator) or
mesalamine alone or a combination of
medications. If surgery for UC becomes
necessary, the procedure is performed in two
stages. During the first stage, total colectomy
is performed and an ileostomy created.
Several months later, an ileoanal pouch is
created and the ileostomy is taken down. This
allows the child to be continent of stool.
IRRITABLE BOWEL SYNDROME
Description:
Disorders Caused by Food, Vitamin, and Mineral
Deficiencies
KWASHIORKOR:
 Kwashiorkor, a disease caused by protein
deficiency, occurs most frequently in children
ages 1 to 3 years because this age group
requires a high-protein intake.
 Growth failure is a major symptom. Because
edema is also a symptom, however, children
may not appear light in weight until the
edema is relieved. There is a severe wasting of
muscles, but, again, this is masked by the
edema. Edema results from hypoproteinemia,
which causes a shift of body fluid from the
intravascular compartments to the interstitial
space, causing ascites. The edema tends to be
dependent, so it is first noted in the lower
extremities.
 Children are generally irritable and
uninterested in their surroundings. They fall
behind other children of the same age in
motor development. If the child had a period
of good protein intake, then poor protein
intake, and then good intake again, hair shafts
develop a striped appearance of brown, then
white, and so on—a “zebra sign.” Children
also have diarrhea, iron-deficiency anemia,
and enlarged livers. Without treatment,
kwashiorkor is fatal.
 For therapy, a diet rich in protein is essential.
Even so, there is evidence to suggest that
 protein malnutrition early in life, even if eat polished numbness of
corrected later, may result in failure of rice as dietary extremities,
children to reach their full potential of staple because heart
intellectual and psychological development. B1 is contained palpitations,
in hull of rice exhaustion)
Diarrhea and
vomiting
NUTRITIONAL MARASMUS
Aphonia (crying
Children are most commonly younger than 1 year of without sound)
age. They have many of the same symptoms as Anesthesia of
children with kwashiorkor, including growth failure, feet
Niacin Common in Pellagra
muscle wasting, irritability, iron-deficiency anemia,
children who (dermatitis,
and diarrhea.
eat corn as resembles a
Whereas children with kwashiorkor are anorectic, dietary staple sunburn),
children with nutritional marasmus are invariably because corn is diarrhea,
hungry (starving) and will suck at any object offered to low in niacin mental
them, such as a finger or their clothing. Treatment is a confusion
(dementia)
diet rich in all nutrients. Like children with
Vitamin C Lack of fresh Scurvy (muscle
kwashiorkor, they may suffer cognitive challenges that
fruits in diet tenderness,
persist throughout life.
petechiae)
Vitamin D Lack of sunlight Poor muscle
tone, delayed
VITAMIN AND MINERAL DEFICIENCIES tooth formation
Rickets (poor
Both vitamin and mineral deficiencies occur at a low
bone
rate in children of the United States because so many formation)
foods are enriched (restoration of ingredients Craniotabes
removed by processing) or fortified (additional (softening of
vitamins and minerals not normally present have been the skull)
added). Milk, for example, is fortified with vitamins D Swelling at
and A. Orange juice is fortified with calcium. White joints,
bread is enriched with B vitamins. particularly of
wrists and
VITAMIN DEFICIENCY DISORDERS cartilage of ribs
Bowed legs,
Vitamin Cause of Signs and
tetany (muscle
Deficiency Symptoms
spasms)
Vitamin A Lack of yellow Tender tongue,
vegetables in cracks at
diet corners of
mouth, night
blindness NURSING CARE OF A FAMILY WHEN A CHLD HAS A
Xerophthalmia REPRODUCTIVE DISORDER
(dry and
Disorder caused by altered reproductive
lusterless
conjunctivae) development
Keratomalacia AMBIGUOUS GENITALIA
(necrosis of the
cornea with Characteristics:
perforation,
loss of ocular  An enlarged clitoris; resembles a penis
fluid, and  Closed labia resembles as a scrotum
blindness)  Lumps that feels like a testes
Vitamin B1 Most common Beriberi  Urethra does not fully extend up to the tip of
in children who (tingling and the penis
  Abnormally small penis with a urethral  Apply antibiotic ointment as prescribed
opening closer the scrotum  Circumcision is done if phimosis is seen
 Absence of one or both testicles
PHISMOSIS ND PARAPHIMOSIS
 Undescended testicles and empty scrotum
Signs and Symptoms:
Management:
 Tip of the penis is dark red or blue in color
 Reconstructive Surgery
 Pain when urinating
PRECOCIOUS PUBERTY  Decreased urinary stream

Signs and Symptoms: Management:

 Breast growth and first period in girls  Circumcision

 Enlarged testicles and penis, facial hair and
CRYPTORCHIDISM
deepening voice in boys
 Pubic or underarm hair Management:
 Acne
 Adult body odor  Chorionic gonadotropin hormone
 Orchiopexy
Management:
HYDROCELE
 Leuprolide acetate (Lupron) – drug of choice
 Medroxyprogesterone or cyproterone acetate Management:

DELAYED PUBERTY  Sclerotherapy

 Hypertonic
Signs: Male  Polidocanol
 The penis adnd testicles not starting to grow VARICOCELE
larger by age 14
 Genital growth that takes longer than 5 years. Signs and Symptoms:
 Short stature compared with their peers, who  Heavy feeling in the testicles
now are growing faster  One testicle that is smaller than the other
Females  Dull ache in the scrotum

 No breast development by age 14 Management:

 Not starting to menstruate within 5 years of  Varicolectomy
when breasts start to grow or by age 16
TESTICULAR TORSION
Management:
Signs and Symptoms:
 Administer estrogen
 Testosterone supplements  Sudden, severe pain and swelling in the
scrotum
 Abdominal pain
Reproductive disorder in males  A testicles that’s positioned higher than
normal or at an unusual angle
BALANITIS (BALANOPOSTHITIS)  Edema
 Fever
Signs and symptoms:
 Nausea and vomiting
 Tight, shiny skin on the glans
Management:
 Redness around the glans
 Painful urination  Laparoscopic surgery
Management: TESTICULAR CANCER
 Clean the penis every day Signs and Symptoms:
 Apply heat by warm soaks or warm baths
  Painless testicular enlargement METRORRHAGIA
 Feeling of heaviness in the scrotum
Signs and Symptoms:
 Pain or discomfort is a testicle or the scrotum
 Dull ache in the abdomen or groin  Light to heavy bleeding between regular
 Enlargement or tenderness of the breasts menstrual periods
(gynecomastia)  Abdominal pain with bleeding
 Miscarriage or ectopic pregnancy may cause
Management:
severe cramps with bleeding
 Orchiectomy and radiation or chemotherapy
Management:
is allowed
 Administer Oral contraceptive pills as
prescribed
Reproductive Disorders in Females  Administer NSAIDS as prescribed

Menstrual Disorders MENSTRUAL MIGRAINE

MITTELSCHMERZ Signs and Symptoms:

Signs and Symptoms:  Throbbing head pain, usually on one side of

the head
 Sharp cramps to several hours with vaginal
 Nausea
spotting
 Vomiting
Management:  Sensitivity to light and loud sounds

 Pain relievers Management:

DYSMENORRHEA  Take NSAIDS

 Take sumatriptan
Signs and Symptoms:
ENDOMETRIOSIS
 Bloated feeling
 Colichy (sharp) pain Signs and Symptoms:
 Acting pulling sensation of the vulva and inner
 Pelvic pain
thighs
 Mild diarrhea Management:
 Mild breast tenderness
 Estrogen and progesterone based oral
 Light cramping
contraceptive
 Dull, nagging pain across the lower abdomen
 Danazol (Danocrine)
 Abdominal distention
 Laparotomy with excision by laser surgery
Management:
AMENORRHEA
 Take NSAIDS (ibuprofen)
Signs and Symptoms:
 Massage lower back and abdomen
 Hormonal treatment is needed (combined  Absence of monthly period
estrogen and progesterone
Management:
MENORRHAGIA
 Lifestyle changes
Signs and Symptoms:  Birth control pills
 Hormone therapy
 Bleeding for longer than a week
 Pad or tampon is saturated within an hour PREMENSTRUAL DYSPHORIC DISORDER (PDD)
Management: Signs and Symptoms:
 Low dose of contraceptive or GnRH inhibitor  Abdominal bloating
 Iron supplementation  Fatigue
 Extreme moodiness
  Breast tenderness  A rash resembling a sunburn, particularly on
 Anxiety or tension the palms and soles
 Irritability or anger  Confusion
 Seizures
Treatment:
 Headaches
 Diet and lifestyle changes
Management:
 Birth control pills
 Administer Antidepressants as prescribed  Administer antibiotics as prescribed
(cephalosporins, oxacillins or clindamycins)
ADDITIONAL REPRODUCTIVE DISORDERS IN FEMALES
 Intravenous fluid therapy
Female circumcision  Osmotic therapy

 Incision and removal of the clitoris VULVOVAGINITIS

 Ritual in some cultures
Signs and Symptoms:
 Both a painful and mutilating procedure
 Major complication: may have difficulty with  Pain
conception or childbirth because volvor  Odor
scarring and perineal contraction  Pruritus
 Vaginal discharge
Imperforate Hymen
Management:
 The hymen is the membranous ring of tissue
that partly obstructs the vaginal opening  Application of local antibiotic ointment
 Totally occludes the vagina, preventing the  Warm baths
escape of vaginal secretion and menstrual  Removal of foreign object if any
blood.  For pinworms single dose of Mebendazole
 Daily washing of the perineum
POLYCYSTIC OVARY SYNDROME
 Wipe from front to back
Signs and Symptoms:
PELVIC INFLAMMATORY DISEASE
 Irregular periods
Signs and Symptoms:
 Excess androgen
 Polycystic ovaries  Pain in the lower abdomen
 Excessive hair growth  Heavy, purulent discharge
 Overweight  Fever
 Type 2 diabetes
Management:
 Acne
 Administer analgesics
Management:
 Administration of broad – spectrum
 Lifestyle changes (weight loss – low – calorie antibiotics (doxycycline or clindamycin)
diet and exercise)
BREAST DISORDERS
 Combination birth control pills
 Take metformin – to lower blood glucose GYNECOMASTIA
 Take clomid for fertility
Signs and Symptoms:
TOXIC SHOCK SYNDROME
 Swollen breast tissue
Signs and Symptoms:  Breast tenderness
 Sudden high fever Management:
 Hypotension
 Vomiting and diarrhea  Counselling
 Muscle aches  Liposuction
 Decreases platelet count  Mastectomy

ACCESSORY (SUPERNUMERARY) NIPPLES

Management:  Excisional biopsy

 Inform the parents of the child of the MASTITIS

condition
Signs and Symptoms:
 Surgical excision is done if needed or wanted
 Breast tenderness or warn to touch
BREAST HYPERTROPHY (MACROMASTIA)
 Breast swelling
Signs and Symptoms:  Fever
 Skin redness
 Bigger than normal size
Management:
Management:
 Administer antibiotics as prescribed
 Provide support
 Administer pain reliever
 Breast examination yearly
 Breast reduction is advised SEXUALLY TRANSMITTED INFECTIONS
 Lose weight
CANDIDIASIS
BREAST HYPOPLASIA
Signs and Symptoms:
Management:
 Itching and burning in the vagina and vulva
 Breast augmentation  Thick, cream cheese – line discharge
 White patches on the vagina
FAT NECROSIS
 Painful on coitus
Signs and Symptoms:
Management:
 Breast is tender
 Administer clotrimazole or miconazole vaginal
 Painful, inflamed r reddened
suppositories and cream
Management:  Administer fluconazole p.o.

 Needle aspiration TRICHOMONIASIS

 Surgical removal
Signs and Symptoms:
FIBROCYTIC BREAST DISEASE
 Vaginal itchi g
Signs and Symptoms:  Frothy white or grayish – green vaginal
discharge
 Round fluid – filled and freely movable cyst  Vagina is reddened and presence of petechiae
 It can change from firm to soft
Management:
Management:
 Metronidazole and Tinidazole are prescribed
 Decreases sodium intake or short term use of  Use of condom
mild diuretic \administer analgesic
(acetaminophen), NSAIDS BACTERIAL VAGINOSIS
 Warm compress
Signs and symptoms:
 Avoidance of trauma
 Use firm bra support  Vaginal discharge or milky-white to gray and
 Change of diet fishlike odor

FIBROADDENOMA Management:

Signs and Symptoms:  Administer Metronidazole for 7 days

 Metronidazole and Clindamycin for 7 days
 Round and well delineated
given also to pregnant women
 Painless and freely movable
 Partner should also be treated
Management:
CHLAMYDIA TRACHOMATIS INFECTION
Signs and Symptoms:  Generalized macular, cooper – colored rash
 Low – grade fever
 Heavy, grayish – white vaginal discharge
 Vulvar itching Management:

Management:  Administer Benzathine penicillin G IM as

prescribed
 Doxycyxline p.o. for 7 days or Azithromycin
 Erythromycin or Tetracycline are given for 10
one dose
– 15 days
HUMAN PAPILLOMAVIRUS
GROUP B STREPTOCOCCAL INFECTION
Signs and Symptoms:
Management:
 Flat lesions
 Ampicillin – drug of choice
 Small cauliflower-like bumps or tiny stemlike
protrusions

Management: NURSING CARE OF A FAMILY WHEN A CHILD HAS A

 Apply podophyllin (Podofin)
 Laser surgery
 Cryotherpy
 Immunization of Gardasil or Cervarix
 Trichloroacetic acid or bichloroacetic acid
applied to the lesions – for pregnant women
HERPE GENITALIS (HERPES SIMPLEX TYPE 2)
Signs and Symptoms:
NEUROLOGICAL DISORDER
Astereognosis – is a inability to identify an object by
active touch of the hands without other sensory input,
such as visual or sensory information.
Automatism – complex purposeless movement, such
as lip smacking
Autonomic Dysreflexia – is a syndrome in which there
is a sudden onsent of excessively high blood pressure.

 Pinpoint vesicles with erythematous base Choreoathetosis – rapid, purposeless movements.

 Moist, painful, open lesions
Choreoid – involuntary movement may become
 Flu – like symptoms
irregular and jerking.
 Pain during urination due to an acidic
Decerebrate Posturing – rigid extension snd adduction
Management:
of the arms and pronation of the wrists with fingers
 Administer Acyclovir and Valacyclovir as flexed.
prescribed
Decorticate Posturing – arms are adducted and flexed
 Apply ointment cream Aldare or Foscavir
on the chest with wrists flexed and hands fisted
HEPATITIS B AND C
Diplegia – spasticity primarily on the upper
GONORRHEA extremities.

Signs and Symptoms: Dyskinetic – disorder muscle tone

 Pain and frequency Graphesthesia – is the ability to recognize a shape

 Urethral discharge that has been traced on the skin.
 Slight yellowish vaginal discharge
Hemiplegia – spasticity involving both extremities on
Management: one side.

 Administer Ceftriaxone IM Infantile Spasms – a form of generalized seizure which

 Doxycycline and Azithromycin p.o. for 7 days is infantile myoclonic seizure.

SYPHILIS Kinesthesia – is the ability to distinguish movement.

Signs and Symptoms: Paraplegia – spasticity primarily on the lower

extremities
 Chancre on the genitalia, vagina, mouth, lips
and rectal
Pulse Pressure – the gap between the systolic and salivation, close eyes while
diastolic blood pressures. and taste you attempt to
open them.
Quadriplegia – spasticity involving all four extremities Note symmetry
Status Epilepticus – seizure that lasts continuously for of facial
expression
longer than 30 minutes.
(such as smile)
Stereognosis – refers to the ability of a child to and movement
recognize an object by touch; it is a test of sensory (such as
interpretation. wrinkling
forehead).
Assess taste by
asking child to
Cranial Nerve Function Assessment identify salt or
I (olfactory) Sense of Assess child’s sugar.
smell ability to VIII (acoustic) Equilibrium Assess hearing
recognize and by the response
common odors hearing to a whispered
such as peanut word or a
butter or an Weber or Rinne
orange while test.
eyes are closed. Equilibrium is
II (optic) Vision Assess vision not tested
fields and visual routinely.
acuity; examine IX Motor Assess gag
retinas. (glossopharyngeal impulses to reflex by
III (oculomotor) Motor Assess pupillary ) heart; pressing on
control and size, equality, sensation back of tongue
sensation reaction to from with tongue
for eye light, and ability pharynx, blade. Note
muscles to follow an thorax, and midline uvula
and upper object in all abdominal (tested together
eyelid directions. Note organs with nerve X).
any nystagmus X (vagus) Swallowing Assess ability to
(an abnormal and gag swallow; elicit
jerking motion). reflexes gag reflex by
IV (trochlear) Movement As for nerve III pressing a
of major tongue blade on
eye globe posterior
muscles tongue.
V (trigeminal) Mastication Assess ability to XI (accessory) Impulses to Ask child to turn
muscles discern light striated head to the
and some touch to test muscles of side; try to turn
facial sensory pharynx it to center. Ask
sensations component; and the child to
assess shoulders elevate
symmetry and shoulders while
strength of bite you press down
to test motor on them.
component. XII (hypoglossal) Motor Ask child to
VI (abducens) Movement As for nerves III impulses to protrude
and muscle and IV tongue and tongue. Assess
sense of skeletal for tremors.
eye globe muscles; Ask child to
VII (facial) Impulses Assess motor sensation press on side of
for facial strength by from skin cheek with
muscles, asking child to
 and viscera tongue; assess
tongue
strength.
Increased Intracranial Pressure
 Increased ICP is not a single disorder but a
group of signs and symptoms that occur with
many neurologic disorders
 Increased ICP occurs because of an increase in
the CSF volume, blood entering the CSF,
cerebral edema, head trauma or infection,
space-occupying lesions such as brain tumors,
or the development of hydrocephalus or
Guillain-Barré syndrome.
Sign or Symptom Indication of Increased
Intracranial Pressure
Increased head An increase >2 cm per month
circumference in first 3 months of life, >1 cm
per month in the second 3
months, and >0.5 cm per
month for the next 6 months
Fontanelle Anterior fontanelle tense and
changes bulging; closing late
Vomiting Occurring in the absence of
nausea, on awakening in
morning or after nap; possibly
projectile
Eye changes Diplopia (double vision) from
pressure on abducens nerves;
white of sclera evident over
pupil (setting sun sign); limited
visual fields, papilledema
Vital sign changes Elevated temperature and
blood pressure; decreased
pulse and respiration rates
Pain Headache, often present on
awakening and standing;
increasing with straining at
stool (Valsalva maneuver) or
holding breath
Mentation Irritability, altered
consciousness such as
sleepiness
Management:
 Monitor respiratory status
 Elevate head of the bed 30 – 40 degrees
 Decrease environmental stimuli
 Monitor electrolyte level and acid – base
imbalance
 Monitor intake and output
STURGE-WEBER SYNDROME
 A child with Sturge-Weber syndrome
(encephalofacial angiomatosis) has a
congenital port-wine birthmark on the skin of
the upper part of the face that follows the
distribution of the first division of the fifth
cranial nerve (trigeminal nerve).
Assessment:
 Hemiparesis (numbness)
 Seizure
 Blindness
Management:
 CT scan or MRI
 Lifelong seizure therapy
CEREBRAL PALSY
Description:
a. Disorder characterized by impaired movement and
posture resulting from abnormality in the
extrapyramidal motor system.
b. The most common type is spastic cerebral palsy,
which represents an upper motor neuron type of
muscle weakness.
c. Less common type are athetoid, ataxic, and mixed.
Assessment:
 Extreme irritability and crying
 Feeding difficulties
 Abnormal motor performance
 Alterations of muscle tone; stiff and regid
arms and legs
 Delayed developmental milestones
 Persistence of primitive infantile reflexes after
6 months
 Abnormal posturing, such as opisthotonos
(exaggerated arching of the back)
Management:
 The goal of management is early recognition
and interventions to maximize the child’s
abilities.
 An interprofessional team approach is
implemented to meet the many needs of the
child.
 Assess the child’s developmental level and
intelligence
 Provide a safe environment by removing
sharp objects.
  Provide safe, appropriate toys for the child’s
age and developmental level
 Position the child upright after meals
 Medications may be prescribed to relieve
muscle spasms, which cause intense pain,
antiseizure medications may also be
prescribed
 Provide the parents with information about
the disorder and treatment plan
 Encourage support for parents
BACTERIAL MENINGITIS
Description:
a. meningitis is an infectious process of the central
nervous system caused by bacteria or viruses that
may be acquired as a primary disease or as a
complications of neurosurgery, trauma, infection of
the sinuses or ears or systemic infections.
b. Diagnostic of bacterial meningitis is made by testing
CSF obtained by lumbar puncture; the fluid is cloudy
with increased pressure, increased white blood cell
count, elevated protein and decreased blood glucose.
c. Bacterial meningitis can be caused by various
organisms, most commonly Haemophilus influenza
type B, Streptococcus pneumonia or Nisseria
meningitides, meningococcal meningitis occurs in
epidemic form and can be transmitted by droplets
from nasopharyngeal secretions.
Assessment:
 Fever, chills, headache
 Vomiting diarrhea
 Poor feeding or anorexia
 Nuchal rigidity
 Poor or high, shrill cry
 Altered level of consciousness, such as
lethargy or irritability
 Bulging anterior fontanel in infant
 Positive Kernig’s sign (inability to extend the
leg when the thigh is flexed anteriorly at the
hip) and Brudzinski’s sign (neck flexion causes
adduction and flexion movements of the
lower extremities) in children and
adolescents.
 Muscle or joint pain (meningococcal infection
and H. influenza infection)
 Petechial or purpuric rashes (meningococcal
infection)
 Ear that chronically drains (pneumococcal
meningitis)
Management:
 Provide respiratory isolation precautions and
maintain it for at least 24 hours after
antibiotics are initiated
 Administer antibiotics and antipyretics as
prescribed (administer antibiotics as soon as
they are prescribed after lumbar puncture);
antiseizure medications may also be
prescribed.
 Perform neurological assessment and monitor
for the complication of inappropriate
antidiuretic hormone secretion, causing fluid
retention (cerebral edema) and dilutional
hyponatremia.
 Assess for changes in level of consciousness
and irritability
 Assess nutritional status; monitor intake and
output.
ENCEPHALITIS
Description:
a. Encephalitis is an inflammation of brain tissue and
possibly, the meninges as well.
b. It can arise from protozoan, bacterial, fungal, or
viral invasions.
Assessment:
 Headache, high temperature
 Ataxia (loss of usual muscle movements)
 Muscle weakness or paralysis
 Diplopia, confusion, and irritability
Management:
 Antipyretic is prescribed to control fever
 Mechanical ventilation may be required to
maintain the child’s respiration during the
acute phase.
 Medications such as acyclovir (Zovirax) and
carbamazepine (Tegretol)
 Steroid (Dexamethasone), mannitol
REYE SYNDROME
Description:
a. Reye syndrome is an acute encephalopathy that
follows a viral illness and is characterized
pathologically by cerebral edema and fatty changes in
the liver.
b. The exact cause is unclear; it most commonly Management:
follows a viral illness such as influenza or varicella
 Care is directed toward the treatment of
c. Administration of aspirin and aspirin – containing symptoms, including pain management
products is not recommended for children with a  Monitor respiratory status closely
febrile illness or children with varicella or influenza  Provide respiratory treatments
because its associated with Reye’s syndrome  Prepare to initiate respiratory support
 Monitor cardiac status
d. Acetaminophen or ibuprofen are considered the
 Assess for complications of immobility
medication of choice.
 Provide the client and family with support
Assessment:
CARPAL TUNNEL SYDROME
 History of systemic viral illness 4 to 7 days
 Carpal tunnel syndrome is nerve compression
before the onset of symptoms
of the median nerve that passes through the
 Fever
carpal tunnel at the wrist.
 Nausea, vomiting
 Compression of the nerve causes numbness
 Signs of altered hepatic function such as
and sharp pain and burning in the thumb and
lethargy
the second, third, and fourth fingers of the
 Progressive neurological deterioration
hand.
 Increased blood ammonia level
 Pain usually occurs at night and is enough to
Management: keep a child awake.

 Provide rest and decrease stimulation in the Management:

environment
 Application of a splint to the wrist, which
 Assess neurological status
holds the wrist holds the wrist in a neutral
 Monitor for altered level of consciousness and
position
signs of increased ICP
 Oran anti – inflammatory medication
 Monitor for signs of altered hapatic function
 Corticosteroid injection into the inflamed
and results of liver function studies.
wrist both help to relived pain
 Monitor intake and output
 Surgery
 Monitor for signs of bleeding and signs of
impaired coagulation, such as prolonged BELL PALSY (FACIAL PALSY)
bleeding time.
Description:
GULLAIN – BARRE SYNDROME
a. Caused by lower motor neuron lesion of cranial
Description: nerve VII that may result from infection, trauma,
hemorrhage, meningitis or tumor
a. An acute infectious neuronitis of the cranial and
peripheral nerve b. It results in paralysis of 1 side of the face

b. The immune system overreacts to the infection and c. Recovery usually occurs in a few weeks, without
destroys the myelin sheath residual effects

c. The syndrome usually is preceded by a mild upper Assessment:

respiratory infection or gastroenteritis
 Flaacid facial muscles
Assessment:  Inability to raise eyebrows, frown, smile, close
the eyelids or puff out the cheeks.
 Paresthesias
 Upward movement of the eye when
 Weakness of lower extremities
attempting to close the eyelid
 Gradual progressive weakness of the upper
 Loss of taste
extremities and facial muscles
 Possible progression to respiratory failure Management:
 Cardiac dysrhythmias
 Encourage facial exercises to prevent the loss
 CSF that reveals an elevated protein level
of muscle tone.
  Protect the eyes from dryness and prevent
injury
 Promote frequent oral care
 Instruct the client to chew on the unaffected
side
SEIZURE DISORDER
a. Excessive and unorganized neuronal discharge in
the brain that activate associated motor and sensory
organs.
b. Epilepsy is a disorder characterized by chronic
seizure activity and indicates brain or CNS irritation.
c. Causes includes genetic factors, trauma, tumors,
circulatory or metabolic disorders, toxicity and
infections.
d. Status epilepticus involves a rapid succession of
epileptic spasms without intervals of consciousness; it
is a potential complication that can occur with any
type of seizure and brain damage may result.
Assessment:
 Obtain information from the parents about
the time of onset, precipitating events, and
behavior before and after the seizure.
 Determine the child’s history related to
seizures.
 Ask the child about the presence of an aura (a
warning sign of impending seizures)/ monitor
for apnea and cyanosis.
 Postseizure: the child is disoriented and
sleepy
Management:
Seizure Precaution:
 Raise side rails when child is sleeping or
resting.
 Pad side rails and other hard objects.
 Place waterproof mattress or pad on bed or
crib.
 Instruct child to wear or carry medical
identification.
 Instruct child in precautions to take during
potentially hazardous activities.
 Instruct child to swim a companion.
 Instruct child to use a protective helmet and
padding when ungagged in bicycle riding,
skateboarding, and in – line skating
 Alert caregivers to need for any special
precautions.
Management:
Intervention for Seizure:
 Ensure airway patency.
 Have suction equipment and oxygen available
 Time the seizure episode.
 If the child is standing or sitting, ease the child
down to the floor and place the child in a side
- lying position.
 Place a pillow or folder blanket under tha
child’s head; if no bedding is available, place
your own hands under the child’s head ore
place the child’s head in your own lap.
 Loosen restrictive clothing.
 Remove eyeglasses from the child if present.
 Clear the area of any hazards or hard objects
 Allow the seizure to proceed and end without
interference.
 If vomiting occurs, turn the child to one side
as a unit.
 Do not restrain the child, place anything in the
child’s mouth, or give any food or liquids to
the child.
 Prepare to administer medications as
prescribed.
 Remain with the child until the child recovers
fully.
 Observe for incontinence, which may have
occurred during the seizure.
 Document the occurrence.
HEADACHE
Description:
a. Headache pain results because of meningeal or
vascular irritation.
o Tension Headache – a dull, steady pain across
the forehead, the temporal area, or the back
of the neck.
o Sinus Headache: accompanies sinusitis or is
associated with inflammation and possible
obstruction of the sinuses.
o Migraine Headache – a type of headache that
may or may not begin with an aura or visual
disturbances such as diplopia or a zigzag
pattern across the visual; field. The pain that
following is usually unilateral and extremely
intense with throbbing that is moderate to
severe.
Management:
 Sleep or lying down to relieve pain and
vomiting.
 Acetaminophen or NSAIDS
 neuron function because of a severed cord, the lower
motor neurons or reflex arcs cause the muscles to
Spinal Cord Injury
contract and remain that way. Parents and children
 Spinal injuries result when the spinal cord are quick to interpret the sudden spastic movement
becomes compressed or severed by the of a lower extremity as meaningful activity. This is
vertebrae; further cord damage can result particularly easy to believe with infants, who cannot
from hemorrhage, edema, or inflammation at tell you they have no control or cannot stop their legs
the injury site as the blood supply becomes from contracting. If the injury is very low in the spinal
impeded. tract, affecting mostly lower motor neurons, the
muscles will remain flaccid because the lower motor
First Recovery Phase neurons cannot send impulses for contraction.
Immediately after the injury, the child experiences a
spinal shock syndrome or loss of autonomic nervous
system function (loss of nerve fibers traveling through Third Recovery Phase
the anterior horn of the spinal canal), leading to loss
The third phase of recovery from spinal cord injury is
of motor function, sensation, reflex activity, and the
learning to live with the final outcome or permanent
presence of flaccid paralysis in body areas below the
limitation of motor and sensory function. If the
level of the injury. If a cervical or high thoracic injury is
compression of the spinal cord was only caused by
present, there will be loss of or decreased respiratory
edema that is then relieved, no permanent motor and
function because of flaccidity of the diaphragm or loss
sensory disability will occur.
of the accessory muscles of the chest. At all levels, the
child has no ability to sweat or shiver to change body Injury Site Highest Key Effects and
temperature below the level of the lesion because of Functions Still Possible
loss of autonomic nerve control; therefore, Present Interventions
hypothermia or hyperthermia always becomes a C1 – C3 Head and neck Respiratory
threat. Blood vessels below the level of the injury are muscles intact paralysis from
no longer able to constrict, so blood tends to pool in loss of phrenic
the lower body, leading to yet another concern— nerve
innervation;
upper body hypotension, especially if the upper body
will need
is elevated. Loss of bladder control occurs if the
ventilatory
bladder is left flaccid (it expands and continually assistance.
overflows). Loss of control in the bowel allows it to No voluntary
become equally distended; bowel sounds will be motion below
absent. This phase of spinal cord injury lasts from 1 to chin; possibly
6 weeks. As a rule, the shorter the phase of spinal able to learn to
shock, the better is the final outcome. Administration use mouth to
of a corticosteroid can help reduce edema and control pen for
possibly protect function of the spinal cord during this writing and
phase. A vasopressor agent such as dopamine may be mouth stick to
prescribed to maintain blood pressure and perfusion reach objects
to the cord. C4 Diaphragm Loss of motor
intact function of
Second Recovery Phase upper and
lower
During the second phase of recovery, the flaccid extremities and
paralysis of the shock phase is replaced by spastic trunk; able to
paralysis. The nerve pathways of the brain and the learn to use
descending tracts are termed upper motor neurons. abdominal
Those in the anterior horn cells and the spinal and muscles to
peripheral nerves are termed lower motor neurons. breathe
independently
Spasticity in the second phase is caused by the loss of C5 Shoulder Able to feed
upper level control or transmission of meaningful control; biceps, self and
innervation to the anterior horn. Lacking upper motor deltoid operate
 function wheelchair if o Ataxic disorders are often manifested by an
fitted with self- awkward gait or lack of coordination. Causes
care aids of ataxia differ, but degeneration of cerebellar
C6 Forearm Use of upper or vestibular function is always involved.
pronation; extremities for
wrist extension self-care; can ATAXIA-TELANGIECTASIA
transfer to
 Ataxia-telangiectasia, transmitted as an
wheelchair and
so have autosomal recessive trait attributable to a
increased defect of chromosome 11, is a primary
independence immunodeficiency disorder that results in
C7 Triceps Able to transfer progressive cerebellar degeneration.
function to wheelchair  . In addition, endocrine abnormalities may
readily; occur, and there is an increased risk of cancer,
increasing particularly brain tumor.
independence  Telangiectasias (red vascular markings)
C8 Thumb and Able to do fine appear on the conjunctiva and skin at the
finger function motor tasks; flexor creases. Both immunologic and
increases neurologic symptoms of this disorder vary in
selfcare ability severity and onset.
T1 – T7 Intercostal Full use of
 Children develop frequent infections
muscles (able upper
(primarily sinopulmonary) because of the
to breathe with extremities but
chest, not is still immunologic deficits. Tonsillar tissue in the
abdominal, dependent on pharynx appears scant. Neurologic symptoms
muscles) wheelchair caused by the degeneration process can
Possibly able to usually be detected in early infancy when
drive car with developmental milestones are not met.
hand controls  Choreoathetosis (rapid, purposeless
Possibly able to movements), nystagmus, an intention tremor,
have high leg or scoliosis may develop.
braces fitted for  Children may be unable to move their eyes or
standing follow movement through visual fields.
T10 – 12 Abdominal Use of long leg  Eye changes (conjunctival telangiectasia)
muscles braces and
develop by 5 years of age. Unfortunately,
four-point
there is no effective treatment. Children with
crutch to
this disorder often die in late adolescence of
ambulate
L2 – L4 Hip flexion Use of long or infection, respiratory failure, or a malignant
Leg extension short leg braces brain tumor.
to ambulate FRIEDREICH ATAXIA
L5 – S1 Gluteus Able to walk
maximus without aids  Friedreich ataxia, which is carried on the short
muscle arm of chromosome 9 as an autosomal
function recessive trait, involves a variety of
S4 Bladder and Able to control degenerative symptoms.
anal sphincter bladder and  Symptoms such as progressive cerebellar and
control bowel function spinal cord dysfunction occur in late
Penile erection
adolescence.
and ejaculation
 e. Teenagers develop a progressive gait
possible
disturbance, a lack of coordinated arm
movements, a high-arched foot (pes cavus),
ATAXIC DISORDERS hammer toes, and scoliosis.
 The combined symptoms of a positive
o Ataxia is failure of muscular coordination or
Babinski reflex, absence of deep tendon
irregularity of muscle action.
 reflexes in the ankle, and ataxia are strongly
diagnostic.
 Neurologic examination shows difficulty in
recognizing foot position (whether the foot is
moved up or down).
 . If the ataxia remains untreated, death occurs
in young adulthood from myocardial failure.
Antioxidant therapy may help to delay this
outcome by reducing ventricular hypertrophy.
NURSING CARE OF A FAMILY WHEN A CHILD HAS A
VISION AND HEARING DISORDER
 Laser in Situ Keratomileusis
 Photorefractive Keratectomy
ASTIGMATISM
Signs and symptoms:
 Headache
 Complaints eye strain
 Blurred vision or distorted vision
 Squinting or constantly closing eyes
 Closing one to read, watch TV or see better
 Shielding eyes or other signs of sensitivity to
light

Management:
Nystagmus – is rapid, irregular eye movement, either
vertically or horizontally  Corrective lenses
 Contact lenses
Amblyopia – is “lazy eye” or subnormal vision in one
 LASIK surgery
eye that causes a child to use only one eye for vision
while “resting” the other eye

Ptosis – is the inability to raise the upper eyelid the NYSTAGMUS

usual distance, so the eyelid always remains slightly
closed Signs and Symptoms:

Strabismus – is unequally aligned eye (cross-eyes)  Rapid, involuntary, shaking, ‘to and fro’
caused by an imbalance of the extraocular muscles movement of the eye
that control the movement of the eye globes. Similar  Dancing or jerking movements
to the handling of reins of a horse.

Orthoptics – the study or treatment of disorders f AMBLYOPIA

vision, especially eye movement or eye alignment.
Signs and Symptoms:
Enucleation – removal of an organ or tumor in such a
way that it comes out clean and whole  Misaligned eyes (strabismus)
 Frequent squinting
Photophobia – sensitivity to light  Turning head to see better
REFRACTIVE ERRORS  Closing or covering an eye to see

Light refration refers to the manner in which light is Management:

bent as it passes through the lens.  Eyeglasses
Hyperopia (farsightedness), I which vision is blurry at  Covering the good eye with a patch
a close range and clear at a far range.  LASIK surgery

Myopia (nearsightedness) occurs when light rays

focus anterior to the retina, causing objects that are PTOSIS
far away to be unfocused
Signs and Symptoms:

 Drooping of one or both eyelids

Management:  Blocked vision (from severe eyelid drooping)
 Contact lenses to be fitted for even young  Increased tearing
infants Management:
 Keep wearing glasses
 Surgery – eyelid lift
  There may be tearing, pain, and photophobia
(sensitivity to light)
STRABIMUS
 Eye pressure is measured by means of a
Signs and Symptoms: tonometer

 Eyes appear straight Management:

 Double vision
 Trabeculotomy
 Crossed eye
 Goniotomy
Therapeutic Management:  Administer acetazolamide (Diamox)

 Eye exercise (orthoptics) can strengthen the

weak muscle
EXTERNAL OTITIS
 Eyeglasses
 Contact lenses Signs and Symptoms:
 Surgery
 Ear pain
 Feeling full in the ear
 Painful to chew
TRAUMATIC INJURY TO THE EYE
 Outer ear look red or swollen
Signs and Symptoms:  Yellowish and pus – like discharge

 Acute pain Management:

 Eyes tear and are sensitive to light
 Antibiotics ear drops for 7-10 days
 Blink rapidly
 Hydrocortisone
 Vision may be blurred or lot in the affected
 Oral antibiotics if severe infection
eye
 Pain relievers

CONTUSION INJURIES
IMPACTED CERUMEN
Management:
 Commercial softeners are available if cerumen
 Ice pack applied to the eye accumulates to such an extent that hearing is
 Refer these children to an ophthalmologist affected a dilute solution of hydrogen
 Surgery peroxide.

ACUTE OTITIS MEDIA

CATARACTS Signs and Symptoms:

Signs and Symptoms:  Sharp and constant Ear pain

 Fever
 Cloudy patches in the lens  Tympanic membrane appears red, yellow or
 Poor vision cloudy
Management: Management:
 Surgical removal of the cloudy lens, followed  Antibiotic therapy
by insertion of an internal intraocular lens  Analgesic and antipyretic
 Decongestant nose drops

CONGENITAL GLAUCOMA

Signs and Symptoms: OTITIS MEDIA WITH EFFUSION

 Infants, the condition is bilateral Signs and Symptoms:

 Cornea appears enlarge, may also be  Muffled hearing
edematous and hazy  Feeling of pressure in the ear with otitis
  Glue – like discharge all increase
ADH release.
Management: Corticotro Secreted by ACTH
 Tympanocentesis pin (ACTH) the stimulates
 Tubal myringotomy adenohypoph the adrenal
ysis Target gland to
organ: produce
adrenal glucocorticoid
NURSING CARE OF A FAMILY WHEN A CHILD HAS AN glands and
ENDOCRINE OR METABOLIC DISOREDER mineralocorti
coid
hormones.
THE PITUITARY GLAND Increased
production of
 The work of the pituitary gland is directed by adrenal gland
the hypothalamus, an organ located in the secretions
center of the brain and which serves as the decreases
regulator of the autonomic nervous system. ACTH
About 1 cm long, 1.0 to 1.5 cm wide, and 0.5 production
cm thick, the pituitary gland rests in the sella and vice
turcica, a depression of the sphenoid bone. versa.
 The gland is divided into several distinct Somatotro Secreted by GH increases
regions: pin the bone and
(growth adenohypoph cartilage
The anterior lobe, or adenohypophysis;
hormone ysis Target growth by
The posterior lobe, or neurohypophysis; and
[GH]) organ: none; increasing the
The intermediate lobe, or pars intermedia, acts on all gastrointestin
which lies between the anterior and posterior body cells al absorption
lobe. of calcium. If
GH
production is
Pituitary Source and Actions and
inhibited,
Hormone Target Effects
undergrowth
Organs
will occur; if
Antidiureti Secreted by ADH helps GH
c hormone the regulate fluid production is
(ADH) neurohypoph volume by excessive,
ysis Target regulating overgrowth
organ: kidney urine output. will occur.
By decreasing
Thyrotropi Secreted by TSH
urine output,
n (TSH) the stimulates
it increases
adenohypoph the thyroid
the volume of
ysis Target gland to
extracellular
organ: produce
fluid volume;
thyroid gland thyroid
when
hormones
secretion of
(thyroxine
ADH is low,
and
urinary
triiodothyroni
output
ne). Too little
increases.
TSH leads to
Factors such
atrophy and
as trauma,
inactivity of
pain, anxiety,
the thyroid
and exposure
gland; too
to high
much TSH
temperatures
causes
 hypertrophy
(increase in
size) and
hyperplasia
(increase in
the number
of cells) of
the gland.
GROWTH HORMONE DEFICIENCY
 If production of human growth
hormone (GH, or somatotropin) is
deficient, children are not able to
grow to full size. As a result, children
may appear well proportioned but
measure well below the average on a
standard growth chart.
 Cause:
Deficient production of GH may result
from a nonmalignant cystic tumor of
embryonic origin that places pressure on
the pituitary gland.
From increased intracranial pressure as a
result of trauma.
In most children with hypopituitarism,
however, the cause of the defect is
unknown; it may have a genetic origin.
Assessment:
The face appears infantile because the mandible is
recessed and immature, and the nose is usually small.
The child’s teeth may be crowded in a small jaw (and
may erupt late).
The child’s voice may be high pitched, and the onset
of pubic, facial, and axillary hair and genital growth
will be delayed.
Nursing Responsibility:
1. Evaluate the family history for traits of shorts
stature or constitutional delay (familial late
development)
2. Obtain estimates of the parents; height and
siblings’ height and weight during their
periods of growth.
3. Assess the child’s prenatal and birth history
for any suggestion of intrauterine growth
restriction.
4. Assess also for any severe head trauma that
could have injured the pituitary gland or
chronic illness, such as a heart, kidney, or
intestinal disorder that could have
contributed to the decreased level of growth.
5. Take a 24 hours nutrition history to see if
“picky eating habits” are extensive enough to
halt growth.
6. Be certain to assess not only the child’s actual
height but also his r her feelings about being
short.
7. A physical assessment, including a
funduscopic examination, neurologic testing,
and blood analysis for hypothyroidism,
hypoarenalism, hypoaldosteronism and
growth factor binding proteins are also
helpful in ruling out a lesion or tumor.
8. Presume of any giagnostic procedures to be
conducted as follows:
Bone age is established by a wrist x-ray
(epiphyseal closure of long bones is delayed
with GH deficiency but is proportional to the
height (delay).
A skull series, computed tomography (CT)
scanning, magnetic resonance imaging (MRI),
or Ultrasound will be prescribed to detect
possible enlargement of the sella turcica,
which would suggest a pituitary tumor.
Medical Hormone Deficiency
 The administration of intramuscular
recombinant human growth hormone (rhGH)
usually given daily at bedtime, the time of day
at which GH normally peaks.
 Some children may need suppression of
luteinizing hormone–releasing hormone
(LHRH, or gonadotropin-releasing hormone
[GnRH]) to delay epiphyseal closure.
 Other children may need supplements of
gonadotropin or other pituitary hormones if
these are determined to be deficient as well.
SOMATROPIN (NUTROPIN, HUMATROPE)
Classification: Somatropin is an example of a
recombinant human growth hormone (rhGH).
Action: used for the long-term treatment of children
who have growth failure from inadequate production
of pituitary hormone, renal failure, or Turner
syndrome.
Pregnancy Risk Category: C
Dosage: Somatropin dosage is individualized. The
drug is administered by injection either SC or
intramuscularly.
Possible Adverse Effects: injection site pain, glucose
intolerance, hypothyroidism, bone problems
(particularly the hip), blood abnormalities, rare
intracranial hypertension in first 8 weeks of therapy.
Nursing Implications
• Advise parents that X-rays of the wrist or hip will be
performed before therapy begins. Thereafter, parents
should be alert for limping or knee or hip pain, which
should be reported to their primary healthcare
provider because slipped capital epiphysis is
associated with rhGH supplementation.
• Reinforce the need for periodic thyroid function
tests and funduscopic examination to detect rare
intracranial hypertension.
• Alert parents that rhGH may interact with
glucocorticoid therapy such as prednisone, causing a
decrease in the effectiveness of the rhGH. Urge
parents to inform all healthcare providers that the
child is receiving rhGH to avoid this type of
interaction.
GROWTH HORMONE EXCESS
 An overproduction of GH usually is caused by
a benign tumor of the anterior pituitary (an
adenoma). If the overproduction occurs
before the epiphyseal lines of the long bones
have closed, excessive or overgrowth will
result.
Assessment:
 Weight will become excessive also, but it
proportional to height
 The skull circumference typically exceeds
usual, and the fontanels may close late or not
at all.
 After epiphyseal lines close,
acromegaly(enlargement of the bones of the
head and soft parts of the hands and feet)
begins to be evident
 The tongue can become so enlarged and
thickened that protrudes from the mouth,
giving the child a dull, apathetic appearance
and making it difficult to articulate words. If
the condition remains untreated, a child may
reach a height of more than 8 ft.
Diagnostic and Management:
1. if x-rays or ultrasounds of the skull reveal that the
sella turcica is enlarged or that a tumor is present,
laser surgery to remove the tumor or cryosurgery
(freesing of tissue) is the primary treatment.
2. If no tumor is present, a GH antagonist such as
bromocriptine (Parlodel) taken orally or octrotide
(Sandostatin) taken by injection can slow the
production of GH.
3. When GH secretion is healted in this way, other
hormones may also be affected; therefore, the child
may need to receive supplemental thyroid extract,
cortisol, and gonadotropin hormones in later life.
4. A more permanent therapy is irradiation or
radioactive implants of the pituitary gland, again to
halt GH production.
GROWTH HORMONE DEFICIENCY AND GROWTH
HORMONE EXCESS
Nursing Diagnosis:
 Disturbed body image related to abnormal
height
 situational low self-esteem related to short
stature
Diabetes Insipidus
 Diabetes insipidus is a disease in which there
is decreased release of ADH by the pituitary
gland. This causes less reabsorption of fluid in
the kidney tubules. Urine becomes extremely
dilute, and a great deal of fluid is lost from the
body.
Cause:
1. Diabetes insipidus may reflect as X-linked dominant
trait, or it may be transmitted by an autosomal
recessive gene.
2. Result from a lesion, tumor, or injury to the
posterior pituitary
3. Unknown cause.
4. A kidney-related etiology
Assessment:
 Polydipsia with accompanying polyuria
 Specific gravity of the urine will be as low as
1.001 to 1.005 (normal values are more often
1.010 to 1.030)
 Urine output may reach 4 to 10L in a 24-hour
period (normal range, 1 to 2L), depending on
age.
  Sodium becomes concentrated or
hypernatremia
Diagnostic:
 MRI, CT scanning, or an ultrasound study of
the skull reveals whether a lesion or tumor is
present.
 A further test is the administration of
vasopressin (Pitressin) to rule out kidney
disease
Management:
 Surgery is the treatment of choice if a tumor
is present.
 If the cause is idiopathic, administration of
desmopressin (DDAVP), an arginine
vasopressin, in an emergency, this drug can
be given intravenously (IV).
 For long term use, it is given intranasally or
orally.
SYNDROME OF INAPPROPRIATE ANTIDIURETIC
HORMONE
 The syndrome of inappropriate antidiuretic
hormone (SIADH) is a rare condition in which
there is overproduction of ADH by the
posterior pituitary gland.
 This results in a decrease in urine production,
which leads to water intoxication. As sodium
levels fall in proportion to water, the child
develops hyponatremia or a lowered sodium
plasma level.
Cause:
1. Central nervous system infections such as bacterial
meningitis
2. Long – term positive ventilation
3. Pituitary compression such as could occur from
edema or a tumor.
Assessment:
 Weight gain
 Concentrated urine (increased specific
gravity)
 Nausea, and vomiting
 Hyponatremia grows severe, coma or seizures
occur from brain edema
Management:
 Restriction of fluid and supplementation of
sodium by IV fluid if needed.
 Demeclocycline (Declomycin), a tetracycline
antibiotic that has the side effect of blocking
the action of ADH in renal tubules and
reducing resorption of water, may be
prescribed.
CONGENITAL HYPOTHYROIDISM
 Congenital hypothyroidism – results from a
low level of T4 and high levels of TSH.
 Thyroid hypofunction causes reduced
production of both T4 and T3. Congenital
hypofunction (reduced or absent function)
occurs as a result of an absent or
nonfunctioning thyroid gland in a newborn.
Assessment:
“Early screening is Crucial”
 Child sleeps excessively
 Because the tongue is enlarged, they notice
respiratory difficulty, noisy respirations, or
obstruction and suck poorly
 The skin of the extremities usually feels cold,
dry, and perhaps scaly, and the child does not
perspire.
 Pulse, respiratory rate, and body temperature
all become subnormal.
 Prolonged jaundice may be present due to the
immature liver’s inability to conjugate
bilirubin
 Anemia may increase the child’s lethargy and
fatigue
 The hair is brittle and dry, and the child’s neck
appears short and thick
 The facial expression is dull and open
mouthed because of the infant’s attempts to
breather around the enlarged tongue
 The extremities appear short and fat; as
muscles become hypotonic, deep tendon
reflexes decrease and the infant develops a
floppy. Reg – doll appearance
 Generalized obesity usually occurs
 Dentition will be delayed, or teeth may be
defective when they do erupt.
 The hypotonia affects the intestinal tract as
well, so the infant develops chronic
constipation.
 The abdomen enlarges because of intestinal
distention and poor muscle tone. Many
infants have an umbilical hernia
  Infants have low radioactive iodine uptake
levels, low serum T4 and T3 levels, and
elevated thyroid – stimulating factor.
 Blood lipids are increased
 An x – ray reveal delayed bone growth.
 An ultrasound reveals a small or absent
thyroid gland. Untreated, the condition will
result in severe irreversible cognitive
deterioration or delay
Management:
 The oral administration of synthetic thyroid
hormone (sodium levothyroxine).
 Supplemental vitamin D may also be given to
prevent the development of rickets when,
with the administration of thyroid hormone,
rapid bone growth begins
 Periodic monitoring of T4 and T3 helps to
ensure an appropriate medication dosage.
ACQUIRED HYPOTHYROIDISM (HASHIMOTO
THYROIDITIS)
 Hashimoto disease is the most common form
of acquired hypothyroidism in childhood; the
age at onset is most often 10 to 11 years.
 There may be a family history of thyroid
disease and it occurs more often in girls than
in boys.
 The decrease in thyroid secretion is caused by
the development of an autoimmune
phenomenon that interferes with thyroid
production.
Assessment:
 Increased level of TSH
 Hypertropy of the thyroid gland (goiter)
 Body growth is impaired by a lack of T4, with
prominent symptoms of obesity, lethargy, and
delayed sexual development
 Antithyroid antibodies will be present in
serum if the illness was caused by an
autoimmune process.
 The thyroid enlarges, a nodular thyroid
Therapeutic Management:
 Administration of synthetic thyroid
hormone (sodium levothyroxine), the
same as for congenial hypothyroidism.
HYPERTHYROIDISM (GRAVES DISEASE)
 Hyperthyroidism is oversecretion of thyroid
hormones by the thyroid gland.
Caused:
1. Neonatal Graves disease develops in the newborns
of 1% to 2% of pregnant women who have the
disease. Like transient hypothyroidism, this usually
resolves between 3 to 12 weeks of age with no long-
term results as the maternal antibodies are cleared.
2. hyperthyroidism in children is caused by an
autoimmune reaction that results in overproduction
of immunoglobulin G (IgG), which stimulates the
thyroid gland to overproduce T4.
3. genetic predisposition
4. Graves disease often follows a viral illness or a
period of stress.
Assessment:
 children gradually experience nervousness,
tremors, loss of muscle strength, and easy
fatigue.
 basal metabolic rate, blood pressure, and
pulse all increase.
 skin feels moist, and they perspire freely.
 They always feel hungry and, although they
eat constantly, do not gain weight and may
even lose weight because of the increased
basal metabolic rate.
 On X-ray, bone age will appear advanced
beyond the chronologic age of the child.
Unless the condition is treated, the child is not
likely to reach usual adult height because
epiphyseal lines of long bones will close
before full height can be attained.
 a swelling on the anterior neck as goiter
develops.
 the eye globes become prominent
(exophthalmia), giving the child a wide-eyed,
staring appearance.
 Laboratory tests show elevated T4 and T3
levels and increased radioactive iodine
uptake. TSH is low or absent because the
thyroid is being stimulated by antibodies, not
by the pituitary gland.
 Ultrasound will reveal the enlarged thyroid.
Therapeutic Management:
 first course: β-adrenergic blocking agent,
such as propranolol, to decrease the
antibody response.
 Second course: the child is placed on an
antithyroid drug, such as propylthiouracil
 (PTU) or methimazole (Tapazole), to
suppress the formation of T4.
Nursing Responsibility:
A. While the child is taking these drugs, the blood is
monitored for leukopenia (decreased white blood cell
count) and thrombocytopenia (decreased platelet
count)—side effects of these drugs.
B. If either of these results, the drug is discontinued
until the white blood cell or platelet count returns to
normal, so the child does not develop an infection or
experience spontaneous bleeding.
Therapeutic Management:
 If the child has a toxic reaction to medical
management (severely lowered white blood
cell count or platelet count) or is
noncompliant about taking the medicine:
radioiodine ablative therapy with 131 I or
thyroid surgery - to reduce the size of the
thyroid gland can be accomplished.
The Adrenal Gland
The two adrenal glands are located retroperitoneally,
just above the kidneys. They are made up of two
distinct divisions; together, these divisions protect the
body against acute and chronic forms of stress.
Three hormones:
a. cortisol (a glucocorticoid responsible for glucose
and protein metabolism and preventing
inflammation).
b. androgen (a steroid hormone responsible for
muscle development).
c. aldosterone (a mineralocorticoid hormone
necessary for sodium and fluid balance) are important
in childhood illnesses.
Adrenal Gland Disorders
Disorders of the adrenal glands cause either
hypofunction, which can lead to acute or chronic
production of necessary hormones, or hyperfunction
(overactivity), which most often leads to
overproduction of androgen or cortisol.
ACUTE ADRENOCORTICAL INSUFFICIENCY
 Insufficiency (hypofunction) of the adrenal
gland can occur in either an acute or chronic
form. In either type, the function of the entire
gland suddenly becomes nonproductive.
 Usually, this occurs following a severe
overwhelming body infection such as
meningococcemia.
 It also can occur when corticosteroid therapy
such as prednisone, which has been
maintained at high levels for a long period, is
abruptly stopped and the gland does not
return to usual function.
Assessment:
 the child’s blood pressure drops to extremely
low levels, the child appears ashen gray, and
the pulse will be weak.
 Temperature gradually becomes elevated;
dehydration and hypoglycemia (an
abnormally low concentration of blood
glucose) become marked because cortisol is
no longer present to regulate this.
 As sodium and chloride blood levels fall from
a lack of aldosterone production, the
potassium level becomes elevated due to the
usual inverse relationship between sodium
and potassium values.
 The child appears prostrate, and seizures may
occur.
Therapeutic Management:
Acute adrenocortical insufficiency is a medical
emergency.
 immediate replacement of cortisol (with IV
hydrocortisone sodium succinate [Solu-
Cortef]).
 the administration of deoxycorticosterone
acetate (DOCA), the synthetic equivalent of
aldosterone;
 IV 5% glucose in normal saline solution to
restore blood pressure, sodium, and blood
glucose levels.
 A vasoconstrictor may be necessary to elevate
the blood pressure.
CONGENITAL ADRENAL HYPERPLASIA
 Congenital adrenal hyperplasia is a syndrome
that is inherited as an autosomal recessive
trait and which causes the adrenal glands to
not be able to synthesize cortisol.
 Because the adrenal gland is unable to
produce cortisol, the level of
adrenocorticotropic hormone (ACTH) secreted
by the pituitary increases in an attempt to
 stimulate the gland to increase function.
Although the adrenals enlarge (hyperplasia)
under the effect of ACTH, they still cannot
produce cortisol; instead, they overproduce
androgen.
Assessment:
 The excessive androgen production during
intrauterine life causes the genital organs in a
male fetus to “overgrow,” or increase in size;
 it masculinizes a female fetus (i.e., the clitoris
is so enlarged that it appears to be a penis; if
CUSHING SYNDROME
the labia are fused, she appears to be a boy
with undescended testes and hypospadias.
 If the condition is not recognized at birth and
the child remains untreated, bone age will
advance so the epiphyseal lines of the long
bones close early, preventing the child from
reaching a usual adult height; pubic and
axillary hair, acne, and a deep masculine voice
will appear precociously.
 At puberty, there will be no breast
development or menstruation.
 By 3 or 4 years of age, untreated boys develop
acne and a deep, mature voice; pubic hair and
still greater enlargement of the penis,
scrotum, and prostate occur. In contrast, the
testes do not enlarge and so appear small in
Assessment:
relation to the size of the penis.
Spermatogenesis does not occur with
puberty, leaving the child infertile.
Diagnosis:
 6 to 8 weeks of pregnancy by means of
maternal serum analysis and
 15 weeks by amniocentesis
 Usually condition is diagnosed in infancy by
serum analysis, which shows the increases
level of androgen.
Management:
“The ultimate goal of therapy is to replace the cortisol
that is missing, thereby suppressing ACTH
concentrations and normalizing adrenal size and
androgen production”.
 For therapy, both male and female infants are
given a corticosteroid agent, such as oral
hydrocortisone, to replace what they cannot
produce naturally.
Nursing Consideration:
 Because corticosteroid therapy needs to
continue indefinitely, the child needs periodic
analysis of serum cortisol levels and growth
measurements to estimate the effectiveness
of the therapy.
 Children may need to have a routine dose
increased when they are undergoing periods
of stress, such as during surgery or infection.
 They may need support throughout life if
their body image is distorted because of body
changes at birth.
 Cushing syndrome is caused by
overproduction of the adrenal hormone
cortisol; this usually results from increased
ACTH production due to either a pituitary or
adrenal cortex tumor.
 The peak age of occurrence is 6 or 7 years, but
the syndrome can occur as early as infancy.
 The inappropriate use of high-potency steroid
creams for diaper dermatitis may be a
possible cause.
 The overproduction of cortisol results in
increased glucose production; this causes fat
to accumulate on the cheeks, chin, and trunk,
causing a moon-faced, stocky appearance.
A. Elevated serum plasma cortisol and increased
urinary free-cortisol levels.
 A dexamethasone suppression test
may be administered for diagnosis.
For this test, a child is administered a
dose of dexamethasone (a
glucocorticoid); if the child has the
syndrome, the plasma level of adrenal
cortisol will fall. It will not fall in
children with adrenocortical tumors
because the tumor continues to
stimulate the adrenal glands to
oversecretion.
 If cosyntropin (Cortrosyn), a synthetic
corticotropin, or ACTH is
administered, plasma cortisol levels
will normally rise. In children with an
adrenal tumor, the gland is already
functioning at full capacity, so no
cortisol elevation occurs.
B. A CT scan or ultrasound reveals the enlarged
adrenal or pituitary gland, confirming the
diagnosis.
Therapeutic Management: Assessment Type 1 Type 2
Age at 5–7 years or 40–65 years (may
 Treatment of Cushing syndrome is the surgical onset at puberty occur in adolescents
removal of the causative tumor. as maturityonset
 If a major part of the adrenal glands are diabetes of youth
surgically removed, the child will need [MODY])
replacement cortisol therapy indefinitely. Type of Abrupt Gradual
 If a major portion of the pituitary gland is onset
removed because the problem was Weight Marked Associated with
overproduction of ACTH, the replacement of changes weight loss obesity
all pituitary hormones may be necessary. often initial
 After adrenal surgery, observe the child sign
carefully for signs of shock: Without Other Polydipsia and Polydipsia
epinephrine also produced by the gland, the symptoms polyphagia
Polyuria (often
body’s ability to maintain blood pressure is
begins as bed- Polyuria
severely compromised, and severe
wetting
hypotension can result.
Fatigue (marks
The Pancreas fall in school)
Blurred vision
 The pancreas is a unique organ in that it has (marks fall in Fatigue
both endocrine (ductless) and exocrine (with school)
duct) types of tissue. Mood changes
 The islets of Langerhans form the endocrine (may cause
portion, alpha islet cells have the behavior Blurred vision
responsibility to secrete glucagon, and beta problems in
islet cells secrete insulin. school)
 Insulin is essential for carbohydrate
Mood changes
metabolism and is also important in the
Therapy Hypoglycemia Diet, oral
metabolism of both fats and protein. agents never hypoglycemic
 It is formed from amino acids at a rate effective; agents, or insulin
between 35 and 50 units per day in adults and insulin
proportionately less in children. required
 When serum glucose that passes through the No dietary Nutrition
pancreas exceeds 100 mg/dl, beta cells foods used; concentrates on no
immediately begin insulin production. When should count excess weight gain
serum glucose levels are low, production carbohydrates and balanced intake
decreases. plus evaluate of carbohydrates,
 Insulin production is also stimulated by blood glucose protein, and fat
gastrin, a gastrointestinal hormone that rises levels to help
determine
when the stomach is full as well as the levels
insulin
of glucagon, cortisol, GH, progesterone, and
dosage.
estrogen. Commonsense Meticulous skin and
 Insulin production is also stimulated by foot care for foot care necessary
gastrin, a gastrointestinal hormone that rises growing
when the stomach is full as well as the levels children
of glucagon, cortisol, GH, progesterone, and Period of Period of Not demonstrable
estrogen. remission remission for
1–12 months
TYPE 1 DIABETES MELLITUS (“honeymoon
 Type 1 diabetes mellitus is a disorder that period”)
involves an absolute or relative deficiency of generally after
initial
insulin, which is in contrast to type 2, where
diagnosis
insulin production is only reduced.

Etiology
 The disease apparently results from
immunologic damage to islet cells in
susceptible individuals.
 children with the disorder have a high
frequency of certain human leukocyte
antigens (HLAs), particularly HLA-DR3 and
HLA-DR4, located on chromosome 6, that may
lead to susceptibility.
 If one child in a family has diabetes, the
chance that a sibling will also develop the
illness is higher than in other families because
siblings also tend to have one of the specific
HLA that are associated with the disease.
Disease Process
 Insulin can be thought of as a compound that
opens the doors to body cells, allowing them
to admit glucose, which is needed for
functioning.
 If glucose is unable to enter body cells
because of a lack of insulin, it builds up in the
bloodstream (hyperglycemia). As soon as the
kidneys detect hyperglycemia (greater than
the renal threshold of about 160 mg/dl), the
kidneys attempt to lower it to normal levels
by excreting excess glucose into the urine,
causing glycosuria, accompanied by a large
loss of body fluid (polyuria). Excess fluid loss,
in turn, triggers the thirst response
(polydipsia), producing the three cardinal
symptoms of diabetes: polyuria, polydipsia,
and hyperglycemia.
 Because body cells are unable to use glucose
but still need a source of energy, the body
begins to break down protein and fat. If large
amounts of fat are metabolized this way,
weight loss occurs and ketone bodies, the acid
end product of fat breakdown, begin to
accumulate in the bloodstream (creating high
serum cholesterol levels and ketoacidosis)
and spill into the urine as ketones.
 Potassium and phosphate, attempting to
serve as buffers, pass from body cells into the
bloodstream. From there, they are evacuated,
causing a loss of these important electrolytes.
Assessment:
 Parents notice increased thirst and increased
urination (which may be recognized first as
bed-wetting [enuresis] in a previously toilet-
trained child).
 The dehydration may cause constipation.
 Laboratory studies usually show a random
plasma glucose level greater than 200 mg/dl
(normal range, 70 to 110 mg/dl fasting; 90 to
180 mg/dl not fasting) and significant
glycosuria
Timing Value (mg/dl)
Before a meal 70 – 110
1 hr after a meal 90 – 180
2 hr after a meal 80 – 150
Between after a 70 – 120
meal
 Two diagnostic tests, the fasting blood
glucose test and the random blood glucose
test, are used to confirm diabetes. A diagnosis
of diabetes is established if one of the
following three criteria is present on two
separate occasions:
o Symptoms of diabetes plus a random
blood glucose level greater than 200
mg/dl
o A fasting blood glucose level greater
than 126 mg/dl
o A 2-hour plasma glucose level greater
than 200 mg/dl during a 75-g oral
glucose tolerance test (GTT)
Other Diagnostic Tests
 If diabetes is detected, the diagnostic workup
also usually includes an analysis of blood
samples for pH, partial pressure of carbon
dioxide (PCO2 ), sodium, and potassium
levels; a white blood cell count; and a
glycosylated hemoglobin (HbA1c) evaluation.
 Normally, the hemoglobin in red blood cells
carry only a trace of glucose. If serum glucose
is excessive, however, excess glucose attaches
itself to hemoglobin molecules, creating
HbA1c. In nondiabetic children, the usual
HbA1c value is 1.8 to 4.0. A value greater than
6.0 reflects an excessive level of serum
glucose.
Therapeutic Management:
 Therapy for children with type 1 diabetes
involves five measures: insulin administration,
regulation of nutrition and exercise, stress
management, and blood glucose and urine
ketone monitoring.
The Initial Regulation of Insulin

 To correct the metabolic imbalance, they are Therapeutic Management:

given insulin administered IV at a dose of 0.1
Insulin Administration
to 0.2 units per kilogram of body weight per
hour. Injection Technique:
 This initial IV infusion of insulin is then
gradually reduced once the blood glucose  Teach parents that when insulins are mixed in
level is lower than 200 mg/dl. Ideally, within one syringe, the regular or shortacting insulin
12 hours, the acidosis is considerably less than should be drawn into the syringe first.
when a child was admitted to the hospital,  Insulin is always injected SC except in
and the serum glucose level is near the emergencies, when half the required dose
normal range. may be given IV.
 The insulin given for emergency replacement  Subcutaneous tissue injection sites used most
this way is regular (short-acting) insulin such frequently in children include those of the
as Humulin-R because this is the form that upper outer arms and the outer aspects of the
takes effect most quickly. thighs. The abdominal subcutaneous tissue
injection sites commonly used in adults can be
Therapeutic Management: adequate sites, but most children dislike this
site because abdominal skin is tender.
Insulin Administration
Encourage children or parents to rotate sites
 Children can be regulated on a variety of in a pattern based on their planned activity.
insulin programs, but typically receive a  Absorption, for example, is increased if the
combined insulin dose of 0.4 to 0.7 units per muscles under the injection site are exercised,
kilogram of body weight daily in two divided so it is best to choose sites that will not be
doses (one before breakfast and one before exercised soon after the injection.
dinner)  Although parents should keep additional
 Adolescents may need as much as 1.2 units bottles of insulin in the refrigerator to
per kilogram daily divided into the two doses. increase the insulin’s shelf life, insulin should
The most common mixture of insulin used be administered at room temperature
with children is a combination of an because this diminishes subcutaneous
intermediate-acting insulin and a regular atrophy and ensures peak effectiveness.
insulin, usually in a 2:1 ratio or 0.75 units of  Because a short needle (less than 0.4 in.) is
the intermediate-acting insulin to 0.33 units used, insulin can be injected at a 90-degree
regular insulin, and given in the same syringe, angle. Although this is not a usual
although this prescription varies for individual subcutaneous injection technique, because
children. The morning dose is two thirds of the needle is so short, the insulin will be
the total daily dose; the evening dose is the deposited into the subcutaneous tissue.
remaining one third.
Therapeutic Management:
Preparation Onset Peak Duration
Insulin pumps
effect of Effect
(hr)  An insulin pump is an automatic device
Lispro Immediate 30 min–1 3–4 approximately the size of an iPhone. It
(Humalog) hr delivers insulin at a constant rate, so it
Aspart 15 min 30 – 40 3–5 regulates serum glucose levels better than
min
periodic injections.
Rregular 0.5 – 1.0 hr 2 – 4 hr 5 -7
 To use a pump, a syringe of regular insulin is
(Humulin –
placed in the pump chamber; a length of thin
R)
Lantus 1 hr 5 hr 24 polyethylene tubing leads to the child’s
Humulin – 1 – 2 hr 4 – 12 hr 24+ abdomen, where it is implanted into the
N subcutaneous tissue of the abdomen by a
Humulin – L 1 – 3 hr 6 – 14 hr 24+ small-gauge needle.
Humulin - U 6 hr 16 – 18 hr 36+
Therapeutic Management:
Inhalation Insulin:
 Inhalation insulin is not available as yet but
may be in the future; production of it is in
experimental trials. Difficulties with
development are constructing an accurate
delivery system and determining how the
development of a cold or allergies that cause
edema of the nasal membrane will affect drug
absorption.
Therapeutic Management:
Nutrition
 An insulin-to-carbohydrate ratio is then
calculated individually for each child
depending on age and activity to guide insulin
administration. For example, if a child is
prescribed an insulin-to-carbohydrate ratio of
1 unit of insulin to each 10 g of carbohydrates
and the meal the child will be served contains
50 g carbohydrates, the parent would
administer 5 units of regular insulin before
the meal.
 An overall meal pattern should include three
spaced meals that are high in fiber plus a
snack in the midmorning, midafternoon, and
evening to keep carbohydrate amounts as
level as possible during the day. Most parents
need to meet with a nutritionist to discuss
what a “meal high in fiber” means, how to
become adept at carbohydrate counting, and
what meals are best to serve to their age
child.
A. Here are some nutritional guidelines to help you:
• Be certain you understand your child’s insulin-to-
carbohydrate ratio and how to use this to plan meals.
As a rule, foods high in carbohydrates are fruit and
vegetables, “starchy foods” such as bread or pasta,
milk and yogurt, and “sugary” foods such as candy
bars or cake.
• Be aware of food portions. The total carbohydrate
on a package of pasta refers to what one serving of
pasta will contain, not the whole box of pasta.
• Provide three meals throughout the day, plus three
snacks. A total daily caloric intake divided to provide
20% as breakfast, 20% as lunch, 30% as dinner, and
10% as morning, afternoon, and evening snacks help
distribute carbohydrates throughout the day.
• Do not use dietetic food. This food is expensive and
not necessary.
• Urge your child not to omit meals. Getting him to
eat at every meal calls for creative planning so he likes
the foods served and eats readily.
• Maintain a positive outlook by stressing the foods
your child is allowed to eat, not those he should
avoid.
• Steer clear of concentrated carbohydrate sources,
such as candy bars, and be sure to include foods with
adequate fiber, such as broccoli, because fiber helps
prevent hyperglycemia.
• Keep complex carbohydrates available to be eaten
before exercise, such as swimming or a softball game,
to provide a sustained carbohydrate energy source to
prevent hypoglycemia.
• Teach children about carbohydrate counting as early
as possible so they can wisely select what to eat at
school or at a friend’s home and can begin
independent self-care.
Therapeutic Management:
Self-Monitoring of Blood Glucose
 Children as young as early school age can
learn the techniques of finger puncture and
reading a computerized monitor. Using a
spring-loaded injection pen helps minimize
pain; an automatic readout monitor simplifies
the procedure. Children are adolescents,
however, before they can be counted on to
independently monitor their serum glucose
levels on a daily basis.
Urinary testing
 Urine testing is not used routinely but is used
to test for ketonuria if the child develops a
gastrointestinal “flu” and is not able to eat.
Acetone revealed by a test strip is a sign fat is
being used for energy or that the child is
becoming acidotic.
The “Honeymoon” Period
 a honeymoon period may follow, during
which only a minimal amount of insulin, or
none at all, is needed for glucose regulation.
This apparently occurs because the
exogenous insulin stimulates the islet cells to
 produce a small amount of natural insulin, as
if they are being reminded of their function.
 After a month or even up to a year, however,
the islet cells will begin to fail once again, and
diabetic symptoms will recur. This can be
upsetting to parents if they began to believe
their child was wrongly diagnosed or that a
cure had taken place. Caution both the
parents and the child that symptoms will
inevitably recur.
Stress Adjustment
 Whenever children with diabetes undergo a
stressful situation, either emotionally or
physically, they may need increased insulin to
maintain glucose homeostasis. When children
are seen at healthcare facilities for periodic
checkups, ask them whether they are having
any difficulty with blood testing or insulin
injection and how things are at home and at
school to detect their stress level.
Pancreas Transplantation
 For children who develop severe kidney
disease or arteriosclerosis, pancreas
transplantation may be considered to prevent
further damage. In contrast to other organ
transplantation procedures, the child’s
pancreas is not removed entirely prior to
transplant. This is because the portion that
supplies digestive enzymes is still functioning
and so is left in place.
 The digestive enzymes of the new pancreas
are diverted into the intestine or bladder, or
the pancreatic ducts can be sclerosed, so the
digestive enzymes do not leave the
transplanted organ.
 Grafts may be taken from cadavers or from
live donors, who can donate up to 45% of
their pancreas and still maintain a functioning
organ for themselves.
 To reduce the child’s immune response and
protect against graft rejection, drugs such as
antilymphocyte globulin, cyclosporine,
prednisone, or azathioprine (Imuran) are
administered after surgery.
 If rejection does start to occur, the patient is
given monoclonal T-cell antibodies (OKT3) to
try to reverse this process.
 Pancreatic transplantation is a last resort
solution for children because it involves major
surgery, the outcome is guarded (about 50%
of transplanted organs are rejected), and the
result—continuous immunosuppressive
medication for life—may not be regarded as a
major improvement over the original illness,
which requires continuous daily insulin for
life. In addition, some pancreatic transplant
recipients have a recurrence of diabetes.
TYPE 2 DIABETES MELLITUS
T2D, characterized by diminished insulin secretion, is
a separate disease from type 1 diabetes because it is
not caused by autoimmune factors. Usually, children
with T2D do not need daily insulin because their
disease can be managed with diet alone or with diet
and an oral hypoglycemic agent. Once thought to
occur only in older adults, T2D is now seen as early as
in overweight school-aged children.
Cause:
o Strong family history of diabetes.
o Children from Africa, Hispanic, Asian, or
Native Indian descent.
o Those who eat a diet high in fats and
carbohydrates
o Those who do not exercise regularly
Assessment:
 Children’s urine will show glucose but few
ketones
 Children experience lessened amounts of
thirst or increased urination
 Abput 90% of children with T2D have dark
shiny patches on the skin (acanthhosis
nigricans), which are most often found
between the fingers and between the toes, on
the back of the neck (dirty neck), and in
axillary creases
Management:
 Therapy consists of nutrition and exercise, the
same as for type 1 diabetes, combined with
an oral antiglycemic agent such as a biguanide
(metformin), which decreases the amount of
glucose proced by the liver and increases
insulin sensitivity in both the liver and muscle
cells.
The Parathyroid Glands
 The four parathyroid glands, located posterior
and adjacent to the thyroid gland, regulate
serum levels of calcium in the body by
controlling the rate of bone metabolism
 through the secretion of parathyroid Assessment:
hormone.
 If the blood calcium level falls well below 7
 This hormone is unique in that it is not under
mg/dl, manifest tetany may result, which is
the control of the pituitary gland but rather is
commonly observed as muscular twitching
controlled by a negative feedback from the
and a carpopedal spasm (abduction of the
circulating serum levels of calcium and how
hand and flexion of the wrist with the thumb
much vitamin D is present to allow absorption
positioned across the palm). In pedal spasm
of calcium from the gastrointestinal tract into
(foot spasm), the foot is extended, the toes
the bloodstream.
flex, and the sole of the foot cups.
HYPOCALCEMIA  Without therapy at this point, generalized
seizures or spasm of the larynx, with the
 Hypocalcemia is a lowered blood calcium level
infant emitting a high-pitched, crowing sound
that occurs to some extent in all newborns
on inspiration, can occur. If the spasm is
before they begin sucking well.
prolonged, respirations may cease.
 It occurs because phosphorus and calcium
levels are always maintained in an inverse Therapeutic Management:
proportion to each other in the bloodstream
 Treatment is aimed at increasing the calcium
(if phosphorus levels rise, calcium levels
level in the blood above the point of latent
decrease, and vice versa).
tetany.
 Hypocalcemia may be caused, therefore, by a
 This can be administered orally as 10%
change in either calcium or phosphorus
calcium chloride if the infant can and will
metabolism.
suck. Otherwise, it will be given IV as a 10%
Assessment: solution of calcium gluconate.
 Newborns who are having generalized
 The chief sign of hypocalcemia is
seizures may require anticonvulsant therapy
neuromuscular irritability, referred to as
in addition to the calcium gluconate to halt
latent tetany. This occurs if the blood calcium
the seizures.
level falls below 7.5 mg/dl.
 Emergency equipment for intubation to
 The newborn will demonstrate jitteriness
relieve laryngospasm should be available.
when handled or if the infant has been crying
 After immediate therapy to increase the low
for an extended period.
blood calcium levels, infants are given oral
Sign Description calcium therapy until their calcium level
Chvostek When skin anterior to stabilizes at greater than 7.5 mg/dl. Because
external ear (just over vitamin D is necessary for the absorption of
sixth cranial nerve) is calcium from the gastrointestinal tract, the
tapped, facial muscles infant also may be given a vitamin D
surrounding eye, nose, supplement such as calcitriol.
and mouth contract
unilaterally. Metabolic Disorders (Inborn Errors of Metabolism)
Trousseau When upper arm is
 Many causes of hormonal deficiency or excess
constricted by
in children are not related to the endocrine
tourniquet for 2–3 min
and area becomes glands and the highly complex system of
blanched, carpal spasm feedback and communication between these
is elicited (hand abducts, glands and the pituitary but rather are due to
wrist flexes, thumb is inherited biochemical disorders that disrupt
positioned across the metabolism of amino acids, proteins,
cupped palm). carbohydrates, or lipids.
Peroneal When fibular side of leg  Many of these disorders are evident at or
over peroneal nerve is soon after birth and can cause irreversible
tapped, foot abducts cognitive challenge and early death, making
and dorsiflexes. early detection and treatment crucial. Gene
therapy is expected to be available in the
 future to reverse symptoms of these
disorders.
A. Phenylketunuria
B. Galactosemia
PHENYLKETONURIA
 PKU is a disease of metabolism, which is
inherited as an autosomal recessive trait. The
infant lacks the liver enzyme phenylalanine
hydroxylase, which is necessary to convert
phenylalanine, an essential amino acid, into
tyrosine (a precursor of epinephrine, T4 , and
melanin). As a result, excessive phenylalanine
levels build up in the bloodstream and tissues,
causing permanent damage to brain tissue
and leaving children severely cognitively
challenged.
 The metabolite phenylpyruvic acid (a
breakdown product of phenylalanine) spills
into the urine to give the disorder its name. It
causes urine to have a typical musty or
“mousy” odor that is so strong that it often
pervades not only the urine but the entire
child.
Assessment:
o A typical musty or “mousy” urine odor
o The child becomes blue – eyed with very fair
skin and light blonde hair
o The child fails to meet average growth
standards
o Children develop an accompanying seizure
disorder
o Skin is prone to eczema (atopic dermatitis)
Therapeutic Management:
Dietary restriction has been the main treatment of
PKU for over 50 years and still remains the main
therapy.
 large neutral amino acids have been
suggested as an alternative treatment to
improve outcomes.
 The drug sapropterin (Kuvan), which works by
increasing tolerance to phenylalanine,
 infants in whom this disease is detected
during the first few days of life are placed on a
formula that is extremely low in
phenylalanine, such as Lofenalac, to begin
dietary regulation.
 A dietitian may recommend a mother who
wants to breastfeed do so on a limited basis
so the child does receive some phenylalanine
(this essential amino acid is necessary for
growth and repair of body cells).
Unfortunately, a low amino acid formula can
cause stools to be loose and has a rather
disagreeable taste; therefore, some infants
may resist drinking the formula after tasting
breast milk.
GALACTOSEMIA
 Galactosemia is a disorder of carbohydrate
metabolism that is characterized by abnormal
amounts of galactose in the blood
(galactosemia) and in the urine (galactosuria).
 . It occurs in about 1 in every 60,000 births,
most often as an inborn error of metabolism,
which is transmitted as an autosomal
recessive trait. The child is deficient in the
liver enzyme galactose-1-phosphate
uridyltransferase.
 Lactose (the sugar found in milk) normally is
broken down into galactose and glucose;
galactose is then further broken down into
additional glucose. Without the galactose 1-
phosphate uridyltransferase enzyme, this
second step, the conversion of galactose into
glucose, cannot take place, and galactose
builds up in the bloodstream and spills out
into the urine. When it reaches toxic levels in
the bloodstream, it destroys body cells.
Assessment:
 Symptoms appear as soon as the child begins
formula or breastfeeding and include
lethargy, hypotonia, and perhaps diarrhea
and vomiting. The liver enlarges as cirrhosis
develops. Jaundice is often present and
persistent, and bilateral cataracts develop. If
the condition remains untreated, symptoms
can worsen so rapidly, a child may die by 3
days of age. Untreated children who survive
beyond this time may be cognitively
challenged and have bilateral cataracts.
Diagnosis is made by measuring the level of
the affected enzyme in the red blood cells. A
screening test (the Beutler test) can be used
to analyze cord blood if a child is known to be
at risk for the disorder.
Therapeutic Management:
  The treatment of galactosemia consists of Factor VII Stable factor or
placing the infant on a diet free of galactose proconvrtin
or giving the child formula made with milk Factor VIII Antihemophilic factor
substitutes such as casein hydrolysates Factor IX Christmas factor
(Nutramigen). Once the child’s condition is Factor X Stuart – power factor
regulated on this diet, symptoms of the Factor XI Plasma thromboplastin
disease do not progress; however, any antecedent
neurologic or cataract damage that is already Factor XII Hageman factor
present will persist. The duration of the Factor XIII Fibrin – stabilizing
restricted diet is controversial but probably
should be followed for life. BONE MARROW ASPIRATION AND BIOPSY
NURSING DIAGNOSIS  Provides samples of bone marrow so the type
Deficient fluid volume related to constant and quantity of cells being produced can be
excessive loss of fluid through urination determined.
Risk for imbalanced nutrition, less than body BLOOD TRANSFUSION
requirements, related to an inability to use
glucose because of diabetes mellitus  Transfusions of blood or its products are
Disturbed body image related to abnormal commonly used in the treatment of blood
height disorders.
Health – seeking behaviors related to the self
– administration in insulin
Deficient knowledge related to long – term Common Symptoms of Blood Transfusion Reactions
treatment needs
Symptoms Cause Time of Nursing
Fear related to the potential and unknown Occurrenc Interventi
illness outcome e on
Anticipatory grieving related to presumed Headaches, Anaphylac Immediate Discontinu
losses associated with diagnosis of long – chills, back tic ly after e
term illness pain, reaction start of transfusio
Interrupted family process related to the dyspnea to transfusio n
child’s chronic illness incompati n
Anxiety related to financial resources requires ble blood;
to maintain optimum family health agglutinati
on of red
Hypotensio Blood cells Saline
n, occurs; infusion
NURSING CARE OF A FAMILY WHEN A CHILD HAS A
hemoglobi kidney for
HEMATOLOGIC DISORDER nuria tubules accessible
HEMATOLOGIC DISORDERS may intravenou
become s line.
 Often called blood dyscrasias, occur when blocked, Administe
components of the blood are formed resulting r oxygen
incorrectly or either increase or decrease in in kidney as
amount beyond normal range. failure necessary.
Increased Possible Approxima Discontinu
temperatur contamina tely 1 hr e
e tion in after start transfusio
Factor I Fibrinogen
transfused of n. Obtain
Factor II Prothrombin
blood transfusio blood
Factor III Tissue thromboplastin n culture to
Factor IV Ionized calcium rule out or
Factor V Labile factor or identify
proaccelerin bacterial
Factor VI Unassigned invasion.
 Pruritus, Allergy to Within Discontinu  blood loss that is sufficient to cause anemia
urticaria, protein first hour e can occur from trauma such as automobile
wheezing componen after start transfusio accident with internal bleeding.
ts of of n
transfusio transfusio temporaril Manifestation/treatment:
n n y. Give
Children immediately Transfusing additional
oxygen as
appear pale RBCs
needed,
tachycardia Lay the child fat
anticipate
Children will also begin Keep the child warm
administra
to breathe rapidly with blankets
tion of
antihistam Gasping respirations Place the infant in an
ine to incubator or under a
reduce radiant heat warmer
symptoms cyanosis Blood expander such as
Fever, Hepatitis Weeks or Obtain plasma or intravenous
jaundice, from months transfusio fluid such as normal
lethargy, contamina after n history saline or lactated
tenderness ted transfusio of any rigner’s
over transfusio n child with
n hepatitis Anemia of acute infection- cause increased
symptoms destruction or decreased production of erythrocytes.
. Refer for
care of Anemia of renal disease- can cause loss of kidney
hepatitis cells.

Anemia of neoplastic disease- malignant growth such

HEMATOPOIETIC STEM CELL TRANSPLANTATION as leukemia or lymphoma result in normochromic,
ALLOGENEIC TRANSPLANTATION normocytic anemias.

 is the transfer of stem cells from an immune-
compatible donor.
GRAFT VERSUS HOST DISEASE (GVHD)
 is a potentially lethal immunologic response
of donor T cells to the bone marrow recipient.
SYNGENEIC TRANSPLANTATION
 involves a donor and recipient who are
genetically identical
NORMOCHROMIC, NORMOCYTIC ANEMIAS
Normochromic (normal color), normocytic (normal
cell size) anemias occur because of impaired
production of erythrocytes by the bone marrow or by
abnormal or uncompensated loss of circulating RBCs,
as with acute hemorrhage.
Hypersplenism- spleen becomes enlarged, however,
blood cells pass through more slowly, with more cells
being destroyed in the process. Overactive spleen.
Aplastic anemias - depression of hematopoietic
activity in the bone marrow.
Congenital aplastic anemia- is inherited as an
autosomal recessive trait.
Acquired aplastic anemia- is decrease in bone
marrow production, which occurs if a child is
excessively exposed to radiation, drugs, or chemicals
known to cause bone marrow damage.
Hypoplastic anemias - also result from depression of
hematopoietic activity in bone marrow and can also
be either congenital or acquired.
Congenital hypoplastic anemia- is a rare disorder
apparently caused by an inherent defect in RBC
formation that affects both sexes and shows
symptoms as early as the first 6 to 8 months of life.

ACUTE BLOOD-LOSS ANEMIA

HYPOCHRONIC ANEMIAS

Iron deficiency anemia

The infant
- newborn usually has enough iron in reserve to last
for the first 6 months of life.
-infants born preterm will have fewer iron stores than
those born at term.
Cause:
-Gastroesophageal reflux or chalasia
-pyloric stenosis
Assessment:
_poor muscle tone -enlarged heart
-pale mucous membrane -enlarged spleen
Koilonychia- spoon-shaped fingernails.
Chronic infection anemia- anemia of a hypochromic,
microcytic type occurs, which is probably caused by
impaired iron metabolism.
MACROCYTIC ANEMIAS
-cells are actual immature erythrocytes or
megaloblast (nucleated immature red cells.)
-so, these anemias are often also referred to as
megaloblastic anemias.
-are caused by nutritional deficiencies.
ANEMIA OF FOLIC ACID DEFICIENCY
- decrease folic acid from infant formula.
FA-help body maintain/produce new cells.
Tx: FA supplement
HEMOLYTIC ANEMIAS
-are those in which the number of erythrocytes is low
because there is increased erythrocyte destruction.
-the destruction may be caused by fundamental
abnormalities in erythrocyte structure or by
extracellular destruction forces.
-RBCs are small and have a short life span apparently
due to abnormalities of the protein of the cell
membrane.
Manifestation:
-chronic jaundice and splenomegaly also develop.
-cells are so small, the mean corpuscular hemoglobin
concentration will be increased.
GLUCOSE 6 PHOSPHATE DEHYDROGENASE
DEFICIENCY
-enzyme glucose 6 phosphate dehydrogenase (G6PD)
is necessary for maintenance of RBC life.
Dx: blood smear will show Heinz bodies
- avoid common drugs such as acetylsalicylic acid.
SICKLE-CELL ANEMIA
- erythrocytes become characteristically elongated
and crescent shaped when they are submitted to low
oxygen tension.
-a low blood pH or increased blood viscosity, such as
occurs with dehydration or hypoxia.
Sickle-cell crisis
- there is pooling of many new sickled cells in blood
vessels causing consequent tissue hypoxia beyond the
blockage.
Symptoms are sudden, severe, and painful.
3 primary needs to prevent sickle cell crisis.
1. Pain relief
2. Adequate hydration
3. Oxygenation
Acetaminophen (Tylenol) may be adequate pain relief
for some children.
THALASSEMIA’S
-autosomal recessive anemias
-a group of hereditary disorders associated with the
defective hemoglobin-chain synthesis.
-characterized by hypochromic, microcytosis,
hemolysis, and variable degree of anemia.
ALPHA-THALASSEMIA
- associated with defect or absence of alpha-chain
synthesis of hemoglobin.
-occurs mainly in people in Asia and Africa.
-it is a milder form and often without symptoms.
BETA-THALASSEMIA- with defect or absence of beta-
chain synthesis of hemoglobin.
THALASSEMIA INTERMEDIA- more severe with life
expectancy of only 3-4 decades
-suffer from chronic fatigue, debilitating bone pain,
cardiac disease and hypersplenism.
-may often have iron overload which is worsened by
transfusion.
THALASSEMIA MAJOR (COOLEY’S ANEMIA)-
characterized by severe anemia
-marked hemolysis
-ineffective erythropoiesis
-organ failure due to iron overload
Assessment:
-Pallor -icterus
-irritability -enlarged liver and spleen
-anorexia
-low grade fever
-a single blood transfusion may correct the
disturbance.
-corticosteroid therapy to reduce the immune
response is generally effective, increasing the RBC
count
POLYCYTHEMIA
-is an increase in the number of RBC’s.
-results from increased erythropoiesis
Plethora- occurs because of the increase in total RBC
volume.
PURPURA
-refers to a hemorrhagic rash or small hemorrhages in
the superficial layer of skin.
-two main types of purpuras occur in children;
idiopathic thrombocytopenic purpura and Henoch-
Schoenlein syndrome.
IDIOPATHIC THROMBOCYTOPENIC PURPURA
Clinical:
-Petechiae -menorrhagia
-gingival bleeding -GI bleeding
-epistaxis -intracranial hemorrhage
Management:
-supportive(children) -IVIG or anti-D
immunoglobulin
-platelets -splenectomy
-corticosteroids
NURSING CARE OF A FAMILY WHEN A CHILD HAS A
RENAL OR URINARY TRACT DISORDER
Alport syndrome - which also includes hearing loss
and ocular changes, is progressive chronic
glomerulonephritis inherited as an X-linked or
autosomal recessive disorder
Azotemia - accumulation of nitrogen waste from the
breakdown of protein in the bloodstream
Dialysis - is the separation and removal of solutes
from body fluid by diffusion through a semipermeable
membrane.
Dysfunctional elimination syndrome (DES) - is an
abnormal pattern of elimination of unknown cause,
characterized by both urine and stool and by bladder
and/or bowel incontinence.
Enuresis - is involuntary passage of urine past the age
when a child should be expected to have attained
bladder control
Epispadias - the opening of the urinary meatus on the
dorsal or superior surface of the penis
Exstrophy of the bladder - is a midline closure defect
that occurs during the 10th week of pregnancy.
Glomerular filtration rate - is the rate at which
substances are filtered from the blood to the urine
Glomerulonephritis - inflammation of the glomeruli of
the kidney, may occur as a separate entity but usually
occurs in children as an immune complex disease after
infection with nephritogenic streptococci
Hydronephrosis - is enlargement of the pelvis of the
kidney with urine as a result of back pressure in the
ureter.
Hypospadias - is a urethral defect in which the
urethral opening is not at the end of the penis but on
the ventral (lower) aspect of the penis
Nephrosis - is altered glomerular permeability
apparently due to an autoimmune process or a T-
lymphocyte dysfunction that results in fusion of the
glomeruli membrane surfaces, which, in turn, leads to
abnormal loss of protein in urine
Patent urachus - If this fails to close during
embryologic development, a fistula is left between
the bladder and umbilicus
Polycystic kidney - implies that large, fluid-filled cysts
have formed in place of normal kidney tissue
Postural proteinuria - also called postural albuminuria
 spill albumin into the urine when they stand
upright for an extended period
Prune belly syndrome - is a syndrome with a broad
spectrum of severity. The most common
abnormalities associated with PBS are cardiac,
pulmonary, orthopedic, and urologic
Vesicoureteral reflux - is the backflow of urine into
one or both ureters with voiding because the valve
that guards the entrance to the ureters is lax or the
ureters insert too low in the bladder.
 refers to retrograde flow of urine from the
bladder into the ureters.
KIDNEY FILTRATION
 The glomeruli in the kidney filter water and
solutes from the blood. The process is only
effective, however, if the blood pressure is
higher in the arteries going into the kidneys
than in the internal tubular arteries. Urine
production is also dependent on the blood
pressure being lower in the arteries leaving
the kidneys than in the internal tubular
arteries.
 For this reason, renal function must be
assessed carefully in children who present
with either decreased or increased blood
pressure. Whereas hypertension in adults is
most often associated with cardiac
dysfunction or disease, in pediatric patients,
hypertension is most often associated with
renal dysfunction.
URINE
 A significant decrease in urine production is
oliguria; absence of urine production is anuria
CHILD’S AVERAGE URINE OUTPUT IN 24 HOURS
Age Amount of Urine (ml)
6 months – 2 years 540 – 600
2 – 5 years 500 – 780
5 – 8 years 600 – 1,200
8 – 14 years 1,000 – 1,500
Over 14 years 1,500
Assessment of Renal and Urinary Tract Dysfunction:
 Assessment of urinary or renal tract disorders
is based on history, physical examination, and
laboratory/diagnostic tests.
 Remember when taking the history of a child
with a urinary or renal disorder that
discussing this area of the body may not be
comfortable for the child or parents
LABORATORY/DIAGNOSTIC TESTS
Urinalysis
 Urinalysis is not only one of the most
revealing tests of kidney function but also one
of the simplest.
 For best results, specimens collected should
be fresh because urine that stands at room
temperature for any length of time changes
composition.
 A chemical reagent strip can be used to detect
glucose, protein, and occult blood and to
measure pH. Specific gravity is best
determined by use of a refractometer.
Urine Culture
 A urinary tract infection (UTI), or the presence
of bacteria in urine, is diagnosed by urine
culture.
 Urine for culture can be obtained by several
techniques including midstream clean-catch,
catheterization, or sterile suprapubic
aspiration.
 The technique used should be determined by
the provider and will be influenced by the
patient’s age, medical history, toilet training
status, and cooperation.
 The test result interpretation varies
depending on the technique. For example, a
positive result from a clean-catch sample is
>50,000 CFU/ml, whereas the positive
 threshold for a sterile catheterized sample or
suprapubic aspirate is >10,000 CFU/ml.
Radioisotope Scanning
 The administration of radioisotopes (a
technetium scan) is another way to assess
glomeruli filtration ability. For this,
radioactively tagged substances are given
intravenously; the rate at which these
substances flow through the kidney and are
excreted in urine is then determined. The
level of radioisotopes used in these studies is
small, and urinating removes the substance
from the body immediately afterward. You
Intravenous Pyelogram
can assure parents that children do not
remain radioactive after the procedure so that
parents are not afraid to stay near their
children or to hold them.
Blood Studies
 A blood urea nitrogen (BUN) test measures
the level of urea in blood or how well the
kidneys can clear urea from the bloodstream.
A normal value is 5 to 20 mg/100 ml.
 Glomerular filtration rate is the rate at which
substances are filtered from the blood to the
urine. It is measured by the amount of
creatinine (the breakdown product of creatine
Voiding Cystourethrogram
from muscle contraction) in blood serum or
excreted in 24 hours as determined by a 24-
hour urine sample. A normal creatinine
clearance rate is 100 ml/min. A normal urine
creatinine level is 0.7 to 1.5 mg/100 ml;
creatinine in blood serum rarely exceeds 1
mg/dl.
Ultrasonography and Magnetic Resonance Imaging
 Either a sonogram or magnetic resonance
imaging (MRI) can show differing sizes of
kidneys or ureters and illustrate the difference
between solid or cystic kidney masses.
 Because they do not involve X-rays, both
ultrasound and MRI may be repeated at
frequent intervals for follow-up without
danger of radiation exposure.
 When explaining ultrasound and MRI tests,
compare the machines used to a camera so
it’s an object familiar to children and not as
frightening.
X-Ray Studies
 A flat-plate abdominal radiograph can provide
information about the size and contour of the
kidneys and may be referred to as a KUB
(kidney, ureters, and bladder). Computed
tomography (CT) scans of the kidneys reveal
both the size and density of kidney structures
and adequacy of urine flow.
 . If a contrast medium will be injected to
better outline urine flow, be certain to ask
about allergy to iodine before the study
because the injected medium is iodine based
and is therefore contraindicated in a person
with an iodine allergy.
 An intravenous pyelogram (IVP) is an X-ray
study of the upper urinary tract. For the
procedure, a radiopaque dye is injected into a
peripheral vein, circulates through the
bloodstream, and is almost immediately
identified as a foreign substance by the
kidneys and filtered out into the urine by the
glomeruli. Radiographs taken at frequent
intervals during the test show the outline of
collecting systems in the kidney and of the
ureters as the radiopaque dye passes through
them.
 A voiding cystourethrogram (VCUG), a study
of the lower urinary tract, reveals the
structure of the urethra and bladder and the
presence of reflux into the ureters.
 After bladder catheterization, a radiopaque
dye is injected into the bladder, and the
catheter is then removed. The child is asked
to void into a bedpan while serial X-ray films
are taken.
 Be sure children are told in advance that they
will be asked to do this and that it is all right if
a stranger watches them (something they
have been taught to avoid as well).
 The first void after catheterization may be
painful, but you can assure the child that this
is usually only a one-time occurrence and that
drinking plenty of water following the test
dilutes the urine and decreases dysuria.
 A VCUG should not be done if a child has an
active UTI because there is danger the
radiopaque material injected into the bladder
could spread bacteria from the bladder, up
the ureters to the kidneys, causing
 pyelonephritis. Therefore, report any
symptoms of a UTI, such as urinary frequency,
dysuria, or low-back pain, to the radiologic
service before the procedure so that the child
can be properly evaluated and the test
rescheduled if necessary.
Cystoscopy
PERITONEAL DIALYSIS
 or examination of the bladder and ureter
openings by direct examination with a
cystoscope introduced into the bladder
through the urethra, may be done to evaluate
for possible vesicoureteral reflux or urethral
stenosis.
 During the procedure, small catheters can be
threaded into the ureters for the introduction
of dye to outline them (retrograde
pyelography). Because the procedure is
painful and requires a child to lie still, it is
usually done under anesthesia.
 As with catheterization for VCUG, the first
void after cystoscopy may be uncomfortable,
and the child should be adequately prepared
for this.
Renal Biopsy
 Renal biopsy involves passing a thin biopsy
needle into the kidney through the skin over
the kidney.
 Renal biopsy may be done in an older child
under only local anesthesia, but conscious
sedation may be necessary for a younger child
who cannot cooperate easily. The kidney is
located first by ultrasound to accurately
locate the best place for the biopsy.
 Caution children they need to lie still while
the biopsy specimen is taken (if the child
Performing Peritoneal Dialysis
moves suddenly, the needle might puncture a
renal artery or vein or tear vital glomeruli). Be
certain children have support people to
remain with them for this procedure, so they
have someone to hold their hand or comfort
them when they feel the pressure of the
needle.
 After the biopsy, press a sterile square gauze
against the biopsy site for approximately 15
minutes to halt bleeding and then apply a
pressure dressing. Caution parents
beforehand that a large dressing will be used,
so they don’t think the size of the dressing
reflects the size of the specimen taken (the
amount of tissue removed is actually no more
than the lumen of the needle used, or about
the size of a pencil lead).
 Measure vital signs and observe the biopsy
site every 15 minutes for at least the first hour
afterward. Do not lift the dressing to assess
bleeding because doing so destroys the
protective function of the pressure dressing.
 Dialysis is the separation and removal of
solutes from body fluid by diffusion through a
semipermeable membrane.
 Peritoneal dialysis uses the membrane of the
peritoneal cavity to do this.
 Hemodialysis circulates blood through an
outside synthetic membrane to do this. Unlike
hemodialysis, peritoneal dialysis does not
require elaborate equipment or expense, but
it does take more time.
 Peritoneal dialysis may be used as a
temporary measure for children who
experience sudden renal failure caused by
trauma or shock. It is also used for fairly long
periods with children with chronic renal
disease to allow them to live until kidney
transplantation can be arranged.
 It is usually begun when the serum creatinine
level reaches 10 mg/100 ml. Other indications
are congestive heart failure, BUN of more
than 100 mg/100 ml, hyperkalemia
(potassium level of more than 6 mEq/L), and
uremic encephalopathy (confusion or coma).
Continuous peritoneal dialysis allows the
procedure to be done at home because less
rigorous monitoring of the procedure is
necessary.
 before peritoneal dialysis begins, a child’s
weight and vital signs need to be obtained to
provide baseline information. Ask the child to
void to reduce bladder size, so the bladder
occupies as little anterior space as possible; if
a child cannot void, catheterization may be
necessary.
 Following this, the child’s abdomen is cleaned
just below the umbilicus with an antiseptic
solution and covered with a sterile drape; a
local anesthetic is injected into the abdominal
wall, and a largebore needle is inserted into
the peritoneal cavity. If ascites fluid is present,
a quantity of this fluid is removed and then a
 warmed hypertonic glucose solution  e CCPD is continuous, electrolytes in the
(approximately 50 to 100 ml/kg of body bloodstream are maintained at more constant
weight) or a commercial dialysis solution is levels than when intermittent dialysis is used.
infused by gravity flow into the peritoneal A great deal of potassium is removed,
cavity. This distends the abdominal wall and however, so caution is needed or children
allows safe insertion of a peritoneal catheter, may become hypokalemic
which is sutured into place and covered with a  The main advantage is that CCPD allows
sterile dressing greater freedom for children to attend school.
 Peritoneal dialysis may be conducted
POSSIBLE COMPLICATIONS OF CONTINUOUS
continuously for periods of 12 to 72 hours,
CYCLING PERITONEAL DIALYSIS
depending on the effectiveness of the
procedure in restoring serum creatinine and Assessment Problem Interventions
BUN levels to normal. Redness, pain, Infection Report
 Monitor vital signs at least every hour, or per or swelling at findings; take
the provider’s order, while children are tube insertion culture of site;
undergoing peritoneal dialysis. site administer
 During each new infusion period and while antibiotics or
the solution is in the abdomen, carefully other site care
observe for shortness of breath because the as prescribed.
fluid exerts upward pressure on the Abdominal Peritonitis Report
pain, increased findings;
diaphragm. Elevating the head of the bed a
temperature, administer
little usually helps to increase breathing space
nausea and antibiotics as
and ease respirations. vomiting, prescribed;
Continuous Cycling Peritoneal Dialysis cloudy return auscultate for
in drainage bowel sounds
 Continuous cycling peritoneal dialysis (CCPD) solution with vital sign
allows a child to go to school or participate in assessment.
other activities while receiving dialysis. Cramps as fluid Irritation of Infuse
 a permanent dialysis catheter is inserted and is infused peritoneal solutions more
sutured into place at the abdomen. Although cavity slowly; warm
commercial devices may be used, for the temperature of
solution to
simplest method, the child or parent attaches
body
a bag of dialysis fluid and tubing to this and
temperature.
infuses a prescribed dialysis solution by
Difficulty with Kinked or Assess tubing
gravity drainage; the bag and tubing are then infusion or clotted tubing; for kinking;
rolled into a compact square under the child’s drainage of malpositioned change
clothes. The infused solution remains in the fluid catheter position of
child for 4 to 6 hours during the day (8 hours child; ask child
at night); the dialysate bag is then lowered, to cough to
and the solution drains from the peritoneal increase
cavity into it. The bag and fluid are then abdominal
discarded and a new bag of dialysate solution pressure; add
is attached and raised, and new solution is prescribed
infused. amount of
 CCPD requires careful monitoring and heparin to
dialysate bag
attention by the child or family, so there is a
(prevents
record of the amount of fluid infused.
clotting).
Children on CCPD can participate in gym
Weight Fluid overload Assess blood
programs but should not participate in increase; moist pressure and
contact sports or swimming. cough, weight;
 Teach parents to think ahead for holidays or shortness of decrease
family trips so they do not run short of breath sodium and
supplies. fluid oral
 intake as  To establish a site for initial blood removal,
prescribed; children may have a doublelumen central
possibly catheter inserted into a central vein, such as
decrease the subclavian or internal jugular vein.
strength of  A permanent technique is subcutaneous
dialysis fluid as anastomosis of a vein and artery, creating an
prescribed.
arteriovenous fistula (usually the brachial
Weight loss, Fluid loss Assess blood
artery and brachiocephalic vein; or internal
hypotension, pressure and
anastomosis of the artery and vein using a
poor skin weight;
turgor, increase fluid subcutaneous graft.
tachycardia and sodium  possibility of infection is reduced with internal
intake as anastomosis, although, unfortunately, two
prescribed. venipunctures, one from a low point in the
Blood-tinged Ruptured Report shunt to remove blood and one high in the
dialysis return capillary vessel findings; assess shunt to return it, are necessary for dialysis
pulse and (use an anesthetic cream beforehand to
blood pressure; reduce pain).
observe for  The risks of hemodialysis include infection
further introduced by venipuncture (severe because
bleeding in the infection immediately causes septicemia)
drainage; flush
and clotting of the access site, which can lead
catheter with
to emboli.
prescribed
amount of  During hemodialysis, if too much sodium is
heparin to removed, muscle cramping may occur.
keep clots from  A “first use” syndrome or symptoms such as
forming. dizziness or muscle cramping can occur from a
reaction to the fibers in the dialysis machine
coil. If urea is moved from the blood at too
HEMODIALYSIS rapid rate— faster than urea can be shifted
 Hemodialysis removes body wastes by using from the brain into the blood—children may
an external membrane as the diffusion begin to show signs of confusion, vomiting,
surface. For hemodialysis, a catheter is dizziness, visual blurring, or hallucinations
inserted into an artery and blood is removed from a dialysis disequilibrium syndrome.
from the child and circulated through a  This occurs because, as osmotic pressure is
dialysis coil. greater in the brain than the blood, fluid shifts
 Urea and electrolytes in the blood diffuse into into the brain, resulting in cerebral edema.
the surrounding fluid bath as the blood passes Hemodialysis must be temporarily halted if
through the coil. After diffusion is complete, these symptoms occur to allow equalization.
the blood is returned to the child’s venous  ptoms occur to allow equalization. Children
circulation. grow as bored during hemodialysis as they do
 can be done as a continuous process, but it is during peritoneal dialysis. Help parents
so effective that 3 hours of hemodialysis provide stimulating activities such as a playing
accomplish as much as 12 hours of peritoneal a board game or reading a favorite story,
dialysis. which are only used during that time period.
 Children who have renal failure or whose When children’s kidneys are removed prior to
kidneys have been removed while they await transplantation, they must remain on a
a kidney transplant can be maintained almost continuous program of hemodialysis. These
indefinitely by hemodialysis sessions two or children may come to resent a machine as
three times a week or by continuous “owning” or “controlling” them as they
ultrafiltration or continuous arteriovenous become aware they cannot exist apart from it.
hemofiltration. It can be used in infants as Allowing them to plan special activities to do
well as older children. during hemodialysis time can help not only to
 pass the time but also to give them a feeling
of control.
Management:
 The first intervention is to educate parents
and caregivers about wiping from front to
back when changing diapers of female infants.
 The second intervention is to prevent UTI in
girls by beginning education about perineal
hygiene measures from the time they are first
toilet trained.
 Remind parents of simple ways to prevent
UTI, such as not allowing children to bathe
with bubble bath. Teach parents to recognize
that abnormally colored urine (red, black, or
cloudy) should not be dismissed because this
could be the beginning of a UTI or kidney
disease.
 Educating parents about the importance of
giving the full course of antibiotics prescribed
for UTIs can help prevent return reinfection;
giving the full course of antibiotics after a
streptococcal infection can help prevent acute
glomerulonephritis.
PATENT URACHUS
 When the bladder first forms in utero, it is
joined to the umbilicus by a narrow tube, the
urachus. If this fails to close during
embryologic development, a fistula is left
between the bladder and umbilicus (patent
urachus). This occurs more commonly in
males than in females.
 Nurses are frequently the ones to discover
this condition as they notice clear fluid
draining from the base of the umbilical cord
while changing a newborn’s diaper. If you test
the fluid with Nitrazine paper for pH, its acid
content will identify it as urine. An ultrasound
will confirm the patent connection.
 A few patent urachus abnormalities heal
spontaneously, but most require surgical
correction to prevent pathogens from
entering the fistula site and causing persistent
bladder infection. This is done in the
immediate neonatal period using only a small
subumbilical incision.
EXSTROPHY OF THE BLADDER
 Exstrophy of the bladder is a midline closure
defect that occurs during the 10th week of
pregnancy. As a result, at birth, the bladder
lies exposed on the anterior abdominal wall.
Assessment:
 Exstrophy of the bladder is a midline closure
defect that occurs during the 10th week of
pregnancy. As a result, at birth, the bladder
lies exposed on the anterior abdominal wall.
 A skilled ultrasonographer may pick up on
possible exstrophy when they do not observe
a typical bladder-filling cycle during the
prenatal ultrasound. At birth, the bladder
appears bright red and continually drains
urine from the open surface.
 both sexes, pelvic bone defects, particularly a
wide pubic diastasis, are a hallmark of
exstrophy.
 . In females, the urethra may be abnormally
formed, and the vagina is approximately 50%
shorter and 30% wider than females without
exstrophy, frequently requiring vaginoplasty
after puberty in order to allow sexual
intercourse and tampon use without pain.
 Urethral defects in males, such as epispadias
—the opening of the urinary meatus on the
dorsal or superior surface of the penis—are
also common. The skin around the bladder
quickly becomes excoriated because of
constant exposure to acid urine.
 Kidney infection can occur from ascending
organisms from the open bladder. When
children with this disorder begin to walk, they
may demonstrate a “waddling” gait caused by
the wide pubic diastasis.
Management:
 The treatment of bladder exstrophy begins
with surgical closure of the bladder and the
anterior abdominal wall, and construction of a
urethra.
 the severe nature of the defect and the high
potential for initial closure failure, and the
lifelong negative sequelae of such a failure,
children born with bladder exstrophy should
immediately be referred to a pediatric
urologist at a major children’s center who has
undergone fellowship training in bladder
exstrophy treatment.
 If the bladder is of suitable size and quality, an
ideal timeline for closure is in the first 24 to
72 hours of life.
  If the bladder template is too small, however,
the bladder can be left to grow for 3 to 6
months before closure. In such instances, the
bladder mucosa should be kept moist and
covered with plastic wrap to prevent the
bladder surface both from drying out and
from adhering to bedclothes or diapers and
being injured.
 To prevent the skin of the abdomen from
excoriation, consult a wound, ostomy, and
continence nurse for the best approach,
which usually involves a protective topical
application such as A&D Ointment, Karaya
Gum, or Maalox. If this is done, do not
separate the infant’s legs to apply diapers;
just place them under the child instead. Be
certain to change diapers promptly after
defecation so feces are not brought forward
to the open bladder. Position the infant on
the back so urine drains freely. Sponge bathe
rather than tub bathe the infant to prevent
water from entering the ureters and
becoming a source of infection.
 important to help parents to view their child
as healthy in every aspect other than his or
her bladder defect.
 When a child with bladder exstrophy is
received into your care, remember to
congratulate the parents on the birth of their
baby. Bladder exstrophy affects only urinary
elimination, and in most cases, these children
are otherwise extremely healthy.
 With modern-day surgical approaches, these
children can lead normal, healthy lives, and it
is important for the emotional well-being of
the family to focus on these positive aspects.
In instances when the bladder closure is to be
delayed, teaching the parents to properly care
for the bladder at home is imperative.
Postoperative
Management:
 After bladder closure, a suprapubic tube is
placed for urine drainage and will typically
remain in place for 4 to 6 weeks to allow the
bladder to drain continuously and the surgical
anastomoses to heal.
 infant should be positioned on the back with
the legs raised in traction at 90 degrees. This
position is maintained for 4 to 6 weeks after
surgery and is essential to prevent failure of
the closure. Approximately 30% of patients
with bladder exstrophy at children’s medical
centers worldwide also undergo osteotomy at
the time of their bladder closure.
 Immediately after surgery, urine draining
from the catheter may be tinged with blood,
but this should clear after the first few days.
Children may experience sharp, painful
bladder spasms after surgery. Such spasms
are often the most painful and prominent
source of discomfort for the recovering child.
HYPOSPADIAS
 is a urethral defect in which the urethral
opening is not at the end of the penis but on
the ventral (lower) aspect of the penis.
 fairly common anomaly, occurring in
approximately 1 in 300 male newborns. It
tends to be familial or may occur from a
multifactorial genetic focus.
 Epispadias is a far more severe defect and
results from a defect in the dorsal wall of the
urethra, resulting in a dorsally located ectopic
meatus.
 The most extreme cases in males result in a
penopubic location of the meatus and
complete incontinence.
Assessment:
 Be certain to inspect all male newborns at
birth for hypospadias or epispadias as part of
a routine physical examination. The degree of
hypospadias may be minimal (on the glans but
inferior in site) or maximal (at the midshaft or
at the penal-scrotal junction).
 junction with hypospadias. If the penis defect
is so extensive that sex determination is
unclear, sex cell karyotyping or DNA analysis
should be done.
 Parents may have difficulty discussing this
condition with relatives or healthcare
personnel because it is a sensitive topic for
them. Help parents work through these
feelings by allowing them to talk about the
disorder, by answering honestly and openly
their questions about what the condition
includes, and by assisting the family in
receiving professional support when
necessary.
Management:
 In the newborn, the surgical procedure may
be a meatotomy—a procedure in which the
 urethra is extended to a usual position—to
establish better urinary function.
 When the child is older (age 12 to 18 months),
adherent chordee can be released. If the
repair will be extensive, all surgery may be
delayed until the child is 3 to 4 years of age.
 encourage penis growth and make the
procedure easier, the child may have
testosterone cream applied to the penis or
receive testosterone injections until surgery.
 important that hypospadias be corrected
before school age if at all possible so the child
looks and feels like other males.
 After surgical repair, a urethral urinary
drainage catheter will be inserted to allow
urine output without putting tension against
the urethral sutures.
 After hypospadias repair, children can be
expected to have usual urinary and
reproductive function unless accompanying
anomalies of the penis are present.
Infections of the Urinary System and Related
Disorders
 As the urinary system drains to the outside of
the body, infection can easily spread to the
bladder or kidneys.
URINARY TRACT INFECTION
 UTI occurs more often in females than in
males: about 8% in girls and 2% in boys.
 Urinary pathogens seem to enter the urinary
tract most often as an ascending infection
from the perineum and are gram-negative
rods such as Escherichia coli.
 UTIs also occur as a health care–acquired
infection in children who have urinary
catheters.
 UTIs occur more often in girls than boys
because the urethra is shorter in girls, and
because it is located close to the vagina and
anus, vulvovaginitis or rectal bacteria can
easily spread to the urethra.
Assessment:
 locate a UTI precisely as urethritis, cystitis,
ureteritis, or pyelonephritis, the signs and
symptoms in young children often are not
clear-cut, so all types are lumped together
and referred to as UTIs.
 typical symptoms that occur in older children
or in adults—pain on urination, frequency,
burning, and hematuria—may not be present
in young children, so UTI is suspected when a
child has a fever with no demonstrable cause
on physical examination.
 If the infection is confined to the bladder
(cystitis), the child may have a low-grade
fever, mild abdominal pain, and day- or
nighttime enuresis. If the infection progresses
to pyelonephritis, the symptoms are generally
more acute, with high fever, abdominal or
flank pain, vomiting, and malaise.
 Urine for culture can be collected using a
clean-catch technique, suprapubic aspiration,
or catheterization, so bacteria from the vulva
or foreskin do not contaminate the sample
and give a false result. Suprapubic aspiration
is generally limited to infants. Catheterization,
also frightening and a potential source of
infection, is limited in children of all ages.
Management:
 medical treatment for UTI is the oral
administration of a broad-spectrum antibiotic
such as sulfamethoxazole-trimethoprim
(Bactrim) or amoxicillin, or an antibiotic
specific to the causative organism that is
cultured.
 Nitrofurantoin is also a good choice for UTIs
because it is a broad-spectrum antibiotic that
concentrates in the urine and can be used for
both treatment and prophylaxis.
 In addition to the antibiotic, a child needs to
drink a large quantity of fluid to “flush” the
infection out of the urinary tract, particularly
if a sulfa drug is prescribed because these can
cause urinary crystals in concentrated urine.
 Cranberry juice is often recommended as
being highly effective in acidifying urine and
making it more resistant to bacterial growth.
 Remind parents that with a UTI, treatment
with antibiotics must be continued for the full
prescription or the infection will return.
 Help parents create a reminder system, such
as a sheet of paper for the refrigerator door
or a reminder on their smartphone, to help
ensure adherence.
 A repeat clean-catch urine sample obtained
after approximately 7 days of antibiotic dosing
is indicated for some children who have had
multiple recurrent UTIs.
“HONEYMOON” CYSTITIS
  Honeymoon cystitis refers to UTI seen in Assessment:
young women shortly after they initiate a first
 A child with reflux is usually first seen by
sexual relationship caused by the local
healthcare personnel because of a history of
irritation and inflammation that results from
repeated UTIs. A VCUG, CT scan, MRI,
coitus.
cystoscopy, or cystography with contrast
 Like most UTIs, these respond quickly to
material will show the ureteral reflux. Based
antibiotic therapy. Voiding as soon as possible
on diagnostic studies, reflux is graded from I
after coitus may help to flush pathogenic
to V by degree of reflux, with grade V being
organisms from the urethra and prevent such
the most serious.
infections. When cystitis first occurs in an
adolescent girl, it is an alert that she may be Management:
sexually active. In addition to the need for
counseling about personal hygiene measures  The majority of instances of vesicoureteral
to prevent UTI, the girl may need information reflux resolve with maturity without a need
about safer sex, reproductive planning, and for surgery. Until this normal growth occurs,
symptoms of sexually transmitted infections. however, the condition must be treated to
Recurrent UTIs in a school-age or preschool decrease the possibility of glomerular scarring
girl may suggest sexual maltreatment. from infection or back pressure.
 Teaching double voiding (having the child void
VESICOURETERAL REFLUX and then in a few minutes attempt to void
again) may help to empty the bladder more
 refers to retrograde flow of urine from the
fully and prevent recurrent infection from
bladder into the ureters
urinary stasis. Some girls need to remain on
 urine flows from the ureters into the bladder,
prophylactic antibiotics for a lengthy time to
with almost no flow reentering the ureters
prevent bladder infection from reoccurring.
from the bladder because the ureters enter
 After surgery, a suprapubic catheter will
the bladder obliquely and a bladder skin flap
remain in place to keep the bladder empty
or “valve” obscures the end of the ureter,
and prevent pressure against the surgical
preventing backflow.
area. Two ureteral catheters (stents),
 reflux of urine occurs with micturition
threaded into the ureters to drain urine
(voiding) when the bladder contracts because
directly from the kidney pelvis, also exit at the
the valve that guards the entrance from the
suprapubic tube site. All three tubes are
bladder to the ureter is defective either from
attached to a closed drainage system. Sterile
birth or because of scarring from repeated
gauze dressings and antibiotic cream are
UTIs; bladder pressure is stronger than usual;
placed around the tube insertion site to keep
or ureters are implanted at unusual angles or
it free of infection.
too low on the bladder wall.
 preparing children for this type of surgery, be
 Reflux has the potential to lead to bladder
certain to prepare them for the number of
infection because urine is retained in the
tubes they will have afterward. Explain that
ureters after voiding and then drains back into
even with the tubes in place, the child will be
the bladder after the child is finished voiding
allowed to walk and move about soon after
where it remains. Stasis of any fluid is subject
the operation (and should do so). Be sure that
to infection. The capacity for normal bladder
the child and parents understand the
tissue to lyse bacteria also becomes reduced
importance of not raising the collection
because of the large residual urine volume
system above the child’s bladder level when
that is always present. If the reflex is enough
helping the child out of bed. This helps
that it leads to back pressure on the kidneys,
prevent potentially contaminated urine from
it has the potential to lead to nephron
flowing from the tubes back into the bladder
destruction and, subsequently,
or ureters.
hydronephrosis or dilatation of the renal
 To help keep the ends of stents or the
pelvis. As the condition tends to appear in
suprapubic tube from becoming
families, it is most likely caused by a
contaminated, care should be taken to
heterogeneous gene disorder.
maintain aseptic technique when emptying
 drainage bags. Once drainage occurs primarily
from the suprapubic tube, and renal status
and good drainage are ensured, the stents are
removed.
HYDRONEPHROSIS
 is enlargement of the pelvis of the kidney with
urine as a result of back pressure in the
ureter. The back-pressure is generally caused
by obstruction, either of the ureter or of the
point where the ureter joins the bladder, as
with vesicoureteral reflux. Although this may
occur at any age, it occurs most often in the
first 6 months of life and is often diagnosed by
ultrasound during intrauterine life.
Disorders Affecting Normal Urinary Elimination
 Common disorders can interfere with urine
elimination, such as dysfunctional elimination
syndrome (DES), including enuresis, and rarer
disorders such as kidney agenesis. DES is an
abnormal pattern of elimination of unknown
cause, characterized by both urine and stool
and by bladder and/or bowel incontinence. It
occurs in a previously toilet trained child
without anatomic or neurologic
abnormalities.
ENURESIS
 Enuresis is involuntary passage of urine past
the age when a child should be expected to
have attained bladder control.
 Enuresis may be nocturnal (occurs only at
night), diurnal (occurs during the day), or
both. It is primary if bladder training was
never achieved and is considered acquired or
secondary if control was established but has
now been lost.
Assessment:
 older than 5 years of age need an evaluation
to determine whether there is an organic
cause for the disorder.
 During history taking, ask how parents have
tried to correct the problem; identify whether
it is primarily a problem for the child or the
parents (treatment will be most effective if
the child wants the situation corrected).
 Assess whether there are stresses in the
family, such as parents who expect more
mature behavior of a child than the child can
manage, the introduction of a new brother or
sister, an uncomfortable school situation such
as bullying, or marital discord.
 If children wet only on nights when they are
exceptionally tired or troubled, a functional
rather than an organic cause is suggested.
 If children wet only when they are engrossed
in an interesting activity, they may simply
need more reminders to empty their bladder.
 If children have symptoms other than
bedwetting, such as abdominal pain, burning,
or frequency, UTI is suggested.
 It is a common practice for many parents to
lift children out of bed every night and take
them to the bathroom so they don’t wet the
bed.
 the child should be brought to full awareness
when they are woken up at night. They should
walk to the bathroom under their own power
(a parent can assist to avoid any accidents
given their fatigued state) and should be told
that they are going to sit on the toilet because
their bladder is full and the toilet is the proper
place to empty.
 abnormal electroencephalographic patterns.
Management:
 If stress factors have been identified, not all of
these can be eliminated because certain
circumstances, such as the birth of a new
sibling, cannot be changed, but frank
discussion with children regarding what
causes the stress and attempts to help them
cope better with their daytime activities may
lessen incidents.
 In many children, it helps to limit fluids during
the 2 hours before bed.
 Alarm bells that ring when children wet at
night can be effective in some children.
 Bladder-stretching exercises—drinking a large
quantity of water and then refraining from
voiding as long as possible—to increase the
functional size of the bladder are
contraindicated and can cause both
dysfunctional voiding and renal damage.
POSTURAL (ORTHOSTATIC) PROTEINURIA
 postural albuminuria
 The amount of spilling decreases when they
rest in a supine position.
 To identify a possible cause for the condition,
an MRI of kidneys and ureters may be
prescribed. To document that the proteinuria
 is related to posture, collect urine after the
child has been recumbent during the night (a
first-voided specimen) and then again after
the child has been up and active for several
hours. Make certain when collecting these
urine specimens to record the child’s activity
accurately.
 If the child stood by the crib rail crying for a
parent or was held in a nurse’s lap for most of
the night, the urine may show protein in the
morning specimen because it is not truly a
“resting specimen.” Likewise, the “active”
specimen should be collected after the child
was truly active, not lying in a supine position
reading a book for most of the time. Play a
game if necessary, such as follow the leader,
so the child is active.
KIDNEY AGENESIS
 Agenesis means lack of growth (literally, lack
of a beginning) or that no organ formed in
utero. Absence of kidneys in a newborn is
suggested when the volume of amniotic fluid
on ultrasound or at birth is severely less than
usual (oligohydramnios), indicating that fetal
urine was not added to the volume of
amniotic fluid.
 The infant often has Potter syndrome or
accompanying misshapen, low-set ears and
hypoplastic (stiff, inflexible) lungs from
compression caused by the lack of amniotic
fluid in utero.
 Bilateral absence of kidneys is obviously
incompatible with life unless a renal
transplantation can be accomplished; the
associated condition of nonfunctioning lungs,
however, lessens the infant’s eligibility for a
successful transplantation.
POLYCYSTIC KIDNEY
 implies that large, fluid-filled cysts have
formed in place of normal kidney tissue.
 The most frequent type of polycystic kidney
seen in children is inherited as an autosomal
recessive trait. A more rare form is inherited
as an autosomal dominant trait. With either
type, there is abnormal development of the
collecting tubules.
 The kidneys grow large and feel soft and
spongy. If the disorder is bilateral, an infant
will not be able to pass urine so the mother
will develop oligohydramnios during
pregnancy. The newborn can have a flattened
nose or micrognathia (small jaw), findings of
Potter syndrome. A sonogram during
pregnancy or at birth will reveal the fluidfilled
cysts.
 If the condition is unilateral, urine production
will be decreased (oliguria), not absent. For
this reason and because kidneys are difficult
to locate in newborns, a unilateral polycystic
kidney may be missed until later in life, when,
with increased kidney growth, an abdominal
mass can be palpated. The cystic growth
offers such resistance to blood circulation that
systemic hypertension often results by school
age.
Assessment:
 In many children, the condition is
associated with a cerebral aneurysm, and
the liver is filled with identical cysts. This
is most evident later in life when
increased difficulty with portal circulation
occurs (blood cannot perfuse the cystic
liver structures either).
Management:
 The treatment for polycystic formation is
surgical removal of the diseased kidney if only
one is cystic. If both kidneys are cystic,
treatment is renal transplantation (difficult in
the young child because few infant kidneys
are available for transplantation and because
of the technical challenge presented by such
small blood vessels). Because this kidney
disease is inherited, parents and children at
adolescence need genetic counseling to
inform them that future children may have
this problem.
RENAL HYPOPLASIA
 Hypoplasia means reduced growth, so
hypoplastic kidneys are small and
underdeveloped and contain fewer lobes
than usual. In addition to having poor
kidney function, hypertension from
stenosis of the renal arteries may
develop. If hypoplasia is bilateral, the
child may need a kidney transplant in
later life to maintain kidney function and
prevent extreme hypertension.
PRUNE BELLY SYNDROME
  is a syndrome with a broad spectrum of
severity.
 Occurring mainly in boys, the severe
dilation of ureters and the bladder causes
back pressure and destruction of kidneys.
 The condition is typically marked by the
presence of three main urologic
symptoms: bilateral undescended testes,
the dilated faulty development of the
bladder and upper urinary tract, and renal
dysplasia.
 The infant’s abdomen appears wrinkled
(like a prune) because of the poorly
developed abdominal muscles.
 Some children need kidney transplants as
they reach school age because of
destruction of glomeruli from continual
Management:
back pressure of urine on nephrons.
ACUTE POSTSTREPTOCOCCAL
GLOMERULONEPHRITIS
 Glomerulonephritis, inflammation of the
glomeruli of the kidney, may occur as a
separate entity but usually occurs in children
as an immune complex disease after infection
with nephritogenic streptococci (most
commonly subtypes of group A beta-
hemolytic streptococci) where complement, a
cascade of proteins activated by antigen–
antibody reactions, plugs or obstructs
glomeruli. Immunoglobulin G (IgG) antibodies
against streptococci can be detected in the
bloodstream of children with acute
glomerulonephritis, proof the illness follows a
streptococcal infection.
 Intravascular coagulation occurs in the minute
renal vessels; ischemic damage from this
leads to scarring and decreased glomerular
function. The glomerular filtration rate
decreases, leading to an accumulation of
sodium and water in the bloodstream. The
inflammation of the glomeruli allows protein
molecules to escape into the urine.
Assessment:
CHRONIC GLOMERULONEPHRITIS
 Acute glomerulonephritis is most common in
children between the ages of 5 and 10 years,
the age group most susceptible to
streptococcal infections.
 Boys appear to develop the disease more
often than girls; it occurs more often during
the winter and spring, as do pharyngeal
streptococcal infections.
 The child typically has a history of a recent
respiratory infection (within 7 to 14 days) or
impetigo (within 3 weeks).
 The disorder is announced by a sudden onset
of hematuria and proteinuria.
 Urinary sediment will contain white blood
cells, epithelial cells, and hyaline, granular,
and red blood cell casts.
 The hematuria is usually so extreme that the
child’s urine appears tea-colored, reddish –
brown, or smoky.
 Blood analysis will indicate a lowered blood
protein level (hypoalbuminemia) caused by
the massive proteinuria.
 A course of antibiotics may be prescribed to
be certain all streptococci are removed from
the child’s system.
 If heart failure occurs, keeping the child in a
semi-Fowler’s position, digitalization, and
oxygen administration are helpful.
 If diastolic blood pressure rises to more than
90 mmHg, antihypertensive therapy with an
antihypertensive such as labetalol will be
prescribed.
 Phosphate binders, such as aluminum
hydroxide to reduce phosphate absorption in
the gastrointestinal tract, or a potassium-
removing resin agent, such as sodium
polystyrene sulfonate (Kayexalate), may be
necessary in children who have rising
phosphate and potassium levels because the
kidneys are unable to clear these from the
circulation.
 Caution parents that the results of a urine
protein test may remain abnormal for up to a
year, so if their child has this test done as a
routine screening procedure at a health
checkup, they don’t worry that the finding
means reinfection or the beginning of further
disease.
 The child is found to have proteinuria at a
routine health assessment. Further
investigation indicates hypertension and the
presence of red cell or white cell casts and
occult blood in urine with low specific gravity
(below 1.003). Blood studies may indicate an
 increased BUN or creatinine levels. An MRI or Assessment:
a renal biopsy will reveal permanent
 Children develop swelling around the eyes
destruction of glomerular membranes.
(periorbital edema) upon waking in the
 The disorder may result in either diffuse or
morning after sleeping with their head flat on
local nephron damage. In both instances, the
a bed. Parents may notice that clothing no
undamaged nephrons increase their
longer fits a child around the waist because
glomerular filtration rate to compensate for
edematous fluid is beginning to collect in the
the damaged nephrons.
abdominal cavity (ascites).
 Alport syndrome, which also includes hearing
 Ascites may become so extensive that the
loss and ocular changes, is progressive chronic
resultant pressure on the stomach and
glomerulonephritis inherited as an X-linked or
intestine leads to anorexia, vomiting, or
autosomal recessive disorder.
diarrhea.
 With chronic glomerulonephritis, if the child
 protein loss with nephrotic syndrome is
has acute symptoms of edema, hematuria,
almost entirely albumin, differentiating it
hypertension, or oliguria, bed rest may be
from the proteinuria of glomerulonephritis, in
necessary. If children have only a chronic
which protein loss tends to be nonspecific.
manifestation, such as proteinuria, and
continue to feel well, they can maintain COMPARISON OF FEATURES OF ACUTE
normal activity, including school attendance. GLOMERULONEPHRITIS AND NEPHROTIC SYNDROME
Children should not engage in competitive
activities such as contact sports, however, Factor Acute Nephrotic
Glomerulonephr Syndrome
because of the risk of kidney injury.
itis
NEPHROTIC SYNDROME (NEPHROSIS) Cause Immune reaction Idiopathic or an
to group A beta- autoimmune
 Nephrosis is altered glomerular permeability hemolytic process or a
apparently due to an autoimmune process or streptococcal congenital
a T-lymphocyte dysfunction that results in infection inherited type
fusion of the glomeruli membrane surfaces, Onset Abrupt Insidious
which, in turn, leads to abnormal loss of Hematuria Profuse Rare
protein in urine. The highest incidence is at 3 Edema Mild Extreme
years of age, and it occurs more often in boys Hypertensio Marked Mild
than in girls. n
 Nephrotic syndrome occurs in three forms: Hyperlipide Rare or mild Marked
(a) congenital, as an autosomal recessive mia
disorder; Peak age 5–10 years 2–3 years
(b) secondary, as a progression of frequency
glomerulonephritis or in connection with Intervention Limited activity; Corticosteroid
antihypertensive and
systemic diseases such as sickle-cell anemia or
s as needed; cyclophosphami
systemic lupus erythematosus (SLE);
symptomatic de
(c) idiopathic (primary). therapy for administration;
 Nephrosis can be further classified according congestive heart possibly diuretic
to the amount of membrane destruction: failure and potassium
minimal change nephrotic syndrome (MCNS), supplements
focal glomerulosclerosis (FGS), and Diet Normal for age Normal for age
membranoproliferative glomerulonephritis with some salt
(MPGN). restriction
 The four characteristic symptoms of nephrotic Prevention Prevention or None known
syndrome: thorough
proteinuria, treatment of
edema, group A
betahemolytic
hypoalbuminemia (low serum albumin level),
streptococcal
and hyperlipidemia (increased blood lipid
infections
level)

Management:
 Therapy for nephrotic syndrome is directed
toward reducing the proteinuria and
subsequent edema. This is typically achieved
through a course of corticosteroids, such as IV
methylprednisolone or oral prednisone, and
keeping the child free of infection while the
immune system is suppressed by these drugs.
An initial dose of prednisone is given until
diuresis without protein loss is accomplished;
the dosage is then reduced for maintenance
and continued for as long as 1 to 2 months.
 Instruct parents to test the first urine
specimen of the day for protein with a
chemical reagent strip and keep an accurate
chart showing the pattern of protein loss.
Approximately once a week, parents are
usually asked to collect a 24-hour urine
specimen so total protein loss can be
measured.
 Parents may need to be assured that
alternate-day therapy is best to keep them
from changing the schedule to every day or
giving twice the calculated dose by adding
extra tablets on alternate days as an attempt
to make their child well sooner. Prednisone
tastes bitter, so parents may welcome
suggestions regarding how to disguise the
taste, such as by mixing it with applesauce or
flavored syrup.
 Be certain that both the parents and the child
are aware long-term administration of
prednisone will cause a cushingoid
appearance or a “moon face,” extra fat at the
base of the neck, and increased body hair. Be
certain also that parents know to plan ahead
for pharmacy refills so prednisone therapy is
not stopped abruptly because an abrupt stop
can lead to adrenal insufficiency.
 need supplemental potassium and should eat
foods high in potassium such as bananas and
milk.
 important that the diuretic be administered
after the albumin infusion or the child could
develop a fluid overload and, subsequently,
heart failure.
 course of a cytotoxic agent, such as
cyclophosphamide (Cytoxan) or cyclosporine
(Sandimmune), or a stronger
immunosuppressant agent, such as
mycophenolate mofetil, may be effective in
reducing symptoms or preventing further
relapses of the disease
FOODS HIGH IN POTASSIUM
Food Group Examples
Fruits Bananas, peaches,
prunes, raisins, oranges,
orange juice
Vegetables Carrots, celery, lima
beans, potatoes,
collards, dandelion
greens, spinach
Protein Nuts, peanuts, red meat
Dairy products Milk, whole or skim;
low-sodium milk
Miscellaneous Salt substitutes,
chocolate and cocoa,
bran
HENOCH–SCHÖNLEIN SYNDROME NEPHRITIS
 Approximately one quarter of the children
who develop this type of purpura develop
renal disease as a secondary complication.
The renal involvement becomes apparent
within a few days after the manifestations of
purpuric symptoms. Children will show either
urinary abnormalities such as proteinuria or a
rapidly progressing glomerulonephritis. Most
children recover completely. A few will
develop chronic symptoms and long-term
kidney disease.
SYSTEMIC LUPUS ERYTHEMATOSUS
 SLE is an autoimmune disease in which, when
autoantibodies and antigens meet, they cause
deposits of complement in the kidney
glomerulus. As a result, some children with
SLE develop symptoms of acute or chronic
glomerulonephritis; glomerulonephritis or
heart disease is the ultimate cause of death in
many adults with SLE. Therapy with
corticosteroids or cytotoxic agents may be
effective to stop the renal destruction. If
kidney transplantation is required, the
transplant should be successful because the
same damage rarely occurs in the
transplanted kidney.
HEMOLYTIC-UREMIC SYNDROME
 With hemolytic-uremic syndrome, the lining
of glomerular arterioles becomes inflamed,
swollen, and occluded with particles of
 platelets and fibrin. The child’s red blood cells
and platelets become damaged as they flow
through the partially occluded blood vessels.
As the damaged cells reach the spleen, they
are destroyed by the spleen and removed
from circulation, leading to a hemolytic
anemia.
 Ninety percent of children who develop this
ACUTE RENAL FAILURE
syndrome have recently experienced an E. coli
gastrointestinal infection from a source such
as undercooked hamburger (E. coli is found in
the intestine of beef cattle). Whether to treat
E. coli infections with antibiotics is
controversial because some children who
have their initial E. coli infection treated with
an antibiotic appear to have a more serious
form of anemia than those not treated.
Assessment:
 The syndrome occurs most often during the
summer months and in children 6 months to 4
years of age. Children usually develop only a
transient diarrhea from the E. coli infection,
although this can progress to severe fluid loss
and bowel wall necrosis. Fever may become
so elevated that the child experiences stupor
and hallucinations. Oliguria accompanied by
proteinuria, hematuria, and urinary casts in
urine follows. The oliguria will lead to
increased serum creatinine and BUN and
Assessment:
extensive edema. Children appear pale from
anemia; easy bruising or petechiae may be
present from thrombocytopenia (reduced
platelet level). Laboratory studies will show
fibrin split products in the serum as the fibrin
deposits in glomerular vessels are degraded.
Thrombocytopenia will be present because
platelets are damaged by the irregular blood
vessels.
Management:
 The child needs renal replacement therapy
(supportive therapy) to maintain kidney and
heart function. The extreme oliguria can be
treated with peritoneal dialysis; anemia can
be corrected by careful transfusion of packed
red cells.
 Ensure that parents understand the
importance of follow-up care and have an
appointment for this. Help them begin to view
the child as well again so they do not continue
to shelter the child unnecessarily but allow for
normal growth and development.
 Despite the extent of the illness, most infants
with hemolytic-uremic syndrome recover
completely. Some children, however, die of
the acute illness or continue to have chronic
renal involvement.
 Renal failure occurs in either an acute or
chronic form. The acute form most often
occurs because of a sudden body insult, such
as severe dehydration. The chronic form
results from extensive kidney disease, such as
hemolytic-uremic syndrome or
glomerulonephritis,
 Other causes of acute renal failure include
prolonged anesthesia, hemorrhage, shock,
severe diarrhea, or sudden traumatic injury. It
also can occur in children who are placed on
cardiopulmonary bypass while undergoing
heart surgery, who receive common
antibiotics (aminoglycosides, penicillin,
cephalosporins, and sulfonamides), who
swallow a poison such as arsenic (found in rat
poison), or who are exposed to industrial
wastes such as mercury. All of these
conditions appear to lead to renal ischemia,
which ultimately leads to acute renal failure.
 oliguria, a urine output of less than 1 ml/kg of
the child’s body weight per hour.
 indwelling urinary catheter may be inserted to
rule out the possibility that urinary retention
in the bladder, rather than kidney
dysfunction, is causing the severe oliguria.
 azotemia (accumulation of nitrogen waste
from the breakdown of protein in the
bloodstream) and
 uremia (extra accumulation of nitrogen
wastes in the blood, with additional toxic
symptoms such as cerebral irritation)
 Hyperkalemia (elevated potassium level),
 manifested by a weak,
 irregular pulse,
 abdominal cramps,
 lowered blood pressure,
 and muscle weakness, begins to occur as
potassium can no longer be excreted.
 muscle twitching
  seizures (tetany); chronic hypocalcemia leads
to withdrawal of calcium from bones
(osteodystrophy)
Management:
 IV fluid is needed to replace plasma volume.
 Administer such fluid slowly, however, to
avoid heart failure because extra fluid cannot
be removed by the nonfunctioning kidneys.
 Be certain the fluid prescribed does not
contain potassium until it is established that
kidney function is adequate; otherwise, the
buildup of potassium could cause heart block.
 Administering sodium bicarbonate is another
method for causing a shift of potassium from
the bloodstream into cells, temporarily
reducing the circulating potassium level.
CHRONIC KIDNEY DISEASE (END-STAGE KIDNEY
DISEASE)
 Chronic renal failure results from
developmental abnormalities, when acute
failure becomes long term, or when chronic
kidney disease has caused extensive nephron
destruction. The nephrons that are not
destroyed appear to function as usual; they
simply are inadequate in number to sustain
kidney function. Beginning approximately
when 50% of nephrons are destroyed, kidney
function diminishes by degree until the child
develops endstage kidney disease (the point
when kidneys can no longer effectively
evacuate waste products from the body).
Assessment:
 polyuria,
 manifested as enuresis
 reabsorb enough sodium
 nephrons are lost
 polyuria decreases
 Hypocalcemia and hyperphosphatemia occur
from the kidney’s inability to excrete
phosphate.
 Osteodystrophy occurs as calcium is
withdrawn from bones to compensate for the
low level of calcium.
 Erythropoietin, formed by the kidneys,
stimulates red cell production. With
decreased erythropoietin production, anemia
develops.
 Pruritus may be present from skin irritation
due to excretion of nitrogenous wastes.
Management:
 Children with chronic renal failure are
generally placed on a low-protein,
lowphosphorus, low-potassium diet to
prevent rapid urea and phosphate buildup.
Children may be prescribed aluminum
hydroxide gel to take with meals to bind
phosphorus in the intestines and prevent
absorption.
 . Milk usually is not given because it is high in
sodium, potassium, and phosphate—
electrolytes children may have difficulty
clearing.
 Meat is restricted, and even beans are high
enough in protein to be eliminated, making
this a difficult diet for children to follow over
an extended period.
 children may actually need additional salt
because, due to poor tubular reabsorption,
they dump sodium in urine. Low-sodium
formulas such as Lonalac are recommended
for children with heart failure who need a
low-sodium intake.
Kidney Transplantation
 The ultimate possibility for prolonging the life
of children with renal failure is kidney
transplantation. With complete renal failure,
children who have extensive hypertension
may have their damaged kidneys removed
and be placed on hemodialysis or CCPD to
await kidney transplantation. Kidney removal
this way is an important step for both the
parents and the child because although
parents realize their child’s kidneys are no
longer functioning, this step removes all hope
that a miracle might make them function once
more. Parents may ask whether it is possible
to leave one of the child’s kidneys because
only one kidney will be transplanted (not
recommended because the hypertension
would continue). Be certain that parents have
a thorough explanation of why hypertension
is destructive and that it could lead to a
cerebrovascular accident or coronary artery
disease. Help them understand that their
child’s renal biopsy shows that, short of a
miracle, their child’s kidneys will not function
again, and so their removal is not a loss but
only recognition of a loss.
PREOPERATIVE CARE
  Kidney transplantation is most effective (the
kidney is less likely to be rejected) if the
kidney is taken from a living twin, parent, or
sibling.
 Rejection occurs at a higher incidence if a
kidney comes from a cadaver or recently
deceased child. Most people consider that
children should be of legal age to give consent
to supply a kidney for transplantation, so few
children have a sibling who is eligible to
donate a kidney.
Human Leukocyte Antigen Typing
 HLAs are a group of antigens found on the
surfaces of all cells with a nucleus, including
blood components such as leukocytes and
platelets. The name is derived from the fact
they were first identified on white blood cells.
Such antigens are inherited from both parents
and are specific for each individual. They are
carried on the short arm of chromosome 6 in
each cell and denote tissue type or determine
which tissue the immune system will identify
as foreign tissue. They also serve as the basis
for paternity typing and may cause reactions
to blood product transfusions and bone
marrow and organ transplants.
 When two people have the same, or mostly
Transplant Rejection
the same, HLA antigens, they are said to be
histocompatible. Identical twins have
complete histocompatibility; family members
have partial histocompatibility; any two
people can have histocompatibility on at least
one antigen site.
 Children who are awaiting kidney
transplantation are HLA typed, and this
information is circulated to major medical
centers. When a kidney is available for
transplantation, the child’s tissue type is
compared with the donor kidney, and factors
such as “best match,” general condition, size
of the child, and length of time the child has
been on the waiting list are considered. The
chance of receiving a kidney is increased
today because, with new immunosuppressive
drugs, even donor kidneys that are not fully
matched have a chance to successfully graft.
POSTOPERATIVE CARE
 After renal transplantation, children are cared
for in an environment that is as sterile as
possible as they are placed on
immunosuppressive therapy such as
cyclosporine, azathioprine (Imuran), and
methylprednisolone (Solu-Medrol), and
possibly antilymphocyte globulin and
antithymocyte globulin to reduce the
possibility of kidney rejection. Although some
transplanted kidneys begin to function
immediately, hemodialysis may be continued
until the implanted kidney can fully function
after recovering from the initial insult of
transplantation.
 Children may pass through a “honeymoon”
period after the transplantation or a period
during which a child models perfect behavior
on the belief the success of the transplant
depends on good behavior rather than the
condition of renal veins and arteries, the
transplanted kidney, or antigen–antibody
formation.
 Children with end-stage renal disease are
usually behind in growth at the time of a
transplant. Although the rate of growth will
be improved after kidney transplantation,
they may never reach full height, related to
the already lost growth plus need for
corticosteroid maintenance therapy to
continue immunosuppression long term.
 Acute transplant rejection, if it occurs, usually
develops within the first 3 months after
transplantation. Children begin to develop
fever, proteinuria, oliguria, weight gain,
hypertension, and tenderness over the
kidney. Serum creatinine and BUN levels will
rise. Increasing the dose of
immunosuppressants may be effective in
stopping this type of rejection.
 Rejection may also be chronic, in which the
transplanted kidney gradually loses function
after the first 6 months. Hypertension and
anemia result. An MRI or a biopsy will show
vascular changes such as narrowing of arterial
lumens and interstitial changes such as
fibrosis and tubular atrophy. This type of
rejection is difficult to halt, although it may be
such a slow, steady process that it will be 2 or
3 years before the kidney actually fails. If a
kidney is rejected, it is removed, and a child is
returned to a program of hemodialysis.
Because one kidney was rejected does not
mean a second transplant will also be
rejected. Unfortunately, because the number
 of kidneys available for transplantation is
limited, kidney rejection of this type becomes
an ominous sign for the child’s long-term
survival.
 Malignant disease is more common in
transplantation recipients than in the normal
population probably because of the long-term
immunosuppression. The original disease for
which the child underwent transplantation,
such as glomerulonephritis, may also recur in
the transplanted kidney. During adolescence,
typically an age of poor adherence to
medication regimens, monitor kidney
recipients closely to be certain they are taking
their immunosuppressive therapy. Parents
cannot help but overprotect the child after a
kidney transplant; they worry a roughhousing
session with a sibling or playing a game such
as baseball may injure the transplanted
kidney. The child may be afraid to engage in
any activity for the same reason. Ask at
healthcare visits if the family needs help to
return to a healthy lifestyle after this major
life change.
NURSING CARE OF A FAMILY WHEN A CHILD HAS
A CARDIOVASCULAR DISORDER
Congestive Heart Failure (CHF)
 Is defined as the inability of the heart to
supply adequate oxygenated blood to
meet the metabolic demands of the body.
 Is the inability of the heart to pump a
sufficient amount of blood to meet the
metabolic and oxygen needs of the body.
 Heart failure is a cluster of symptoms and
physical examination findings that are
secondary to an underlying process. The
primary processes can be systemic or
directly related to the heart.
 The most common causes of CHF in children
are congenital heart defects that produce an
excessive workload on the myocardium,
cardiomyopathies due to metabolic disorders,
infectious diseases, drugs, Kawasaki disease,
and myocardial dysfunction after heart
surgery.
 In infants and children, a combination of
leftside and right – sided HF is usually present.
 The goals of treatment are to improve cardiac
function, remove accumulated fluid and
sodium, decrease cardiac demands, improve
tissue oxygenation, and decrease oxygen
consumption.
Assessment:
o Tachycardia, especially during rest and slight
exertion.
o Tachypnea
o Profuse scalp diaphoresis, especially in infants
o Fatigue and irritability
o Sudden weight gain
o Respiratory distress
Management:
(a) symptomatically manage the patient and
(b) treat the underlying cause of the heart failure
The goal is decrease any fluid overload, enhance
myocardial contractility, and decrease afterload in
order to ensure adequate perfusion and decrease the
work of the heart.
(M-A-M-L-A)
1. monitor for sigh of HF
a. monitor for respiratory distree (count respiration
for 1 minute).
b. monitor apical pulse (count apical pulse for 1
minutes), and monitor for dysrthythmias.
c. monitor temperature for hyperthermia and for
other signs of infection, particularly respiratory
infection.
d. monitor strict intake and output; weigh diapers as
appropriate for most accurate output.
e. monitor daily weight to asses for fluid retention; a
weight gain of 0.5 kg (1lb) in 1 day is caused by the
accumulation of fluid.
f. monitor for facial r peripheral dependent edema,
auscultate lung sounds, and report abnormal findings
indicating excessive fluid in the body.
2. Adequate oxygen and rest.
a. Elevate the head of the bed in a semi-Fowler's
position.
b. Maintain a neutral thermal environment to prevent
cold stress in infants.
c. Provide rest and decrease environmental stimuli. d.
Administer cool humidified oxygen as prescribed,
using an oxygen hood for young infants and a nasal
cannula or face mask for older infants and children.
d. Organize nursing activities to allow for
uninterrupted sleep.
3. Maintain adequate nutritional status.
a. Feed when hungry and soon after awakening,
conserving energy and oxygen supply.
b. Provide small, frequent feedings, conserving energy
and oxygen supply.
4. Limit fluid intake as prescribed.
a. Monitor for signs and symptoms of dehydration,
including sunken fontanel (infant), nonelastic skin
turgor, dry mucous membranes, decreased tear
production, decreased urine output, and
concentrated urine. b. Monitor sodium levels as
prescribed. Normal level is 135 to 145 mEq/L (135-145
mmol/L).
b. Many infant formulas have slightly more sodium
than breast milk
5. Administer Medications, as prescribed.
5.1. DIGOXIN
a. Assess apical heart rate for 1 minute before
administration.
b. Withhold digoxin if the apical pulse is less than 90
to 110 beats/minute in infants and young children and
less than 70 beats/ minute in older children, as
prescribed.
c. Be aware that infants rarely receive more than 1 ml
(50 mcg or 0.05 mg) of digoxin in 1 dose.
d. Monitor digox?a levels and for signs of digoxin
toxicity, including anorexia, poor feeding, nausea,
vomiting, bradycardia, and dysrhythmias.
e. The optimal therapeutic digoxin level range is 0.5 to
0.8 ng/ml (0.64-1.02 nmol/L).
f. Digoxin toxicity is present when level is greater than
0.8 ng/ml (1.02 nmol/L).
g. Instruct the parents regarding administration of
digoxin.
MANAGEMENT:
5.2. ACE Inhibitors
a. Monitor for hypotension, renal dysfunction, and
cough when angiotensin-converting enzyme inhibitors
are administered.
b. Assess blood pressure; serum protein, albumin,
blood urea nitrogen, and creatinine levels; white
blood cell count; urine output; urinary specific gravity;
and urinary protein level.
5.3. DIURETICS; such as furosemide
a. monitor for signs and symptoms of hypokalemia
(serum potassium level <3.5 mEq/L[3.5 mmol/L),
including muscle weakness and cramping , confusion,
irritability, restlessness, and inverted T waves or
prominent U waves on the electrocardiogram.
b. if signs and symptoms of hypokalemia are present
and the child is also being administered digoxin,
monitor closely for digoxin toxicity because
hypokalemia potentiates digoxin toxicity.
5.4. POTASSIUM (K) SUPPLEMENT AND PROVIDE
DIETARY SOURCES OF POTASSIUM
a. supplemental potassium should be given only if
indicated serum potassium levels and if adequate
renal function is evident and is usually necessary
when administering a potassium wasting diuretic such
as furosemide.
b. encourage foods that thechid will wat that are high
otassium, as appropriate, such as bananas, baked
potato skins, and peanut butter.
c. monitor serum electrolyte levels, particularly the
potassium evel (normal level is 3.5 to 5.0 mEq/L[3.5-
5.0 mmol/L]).
Congenital heart defects can be classified in many
ways based on embryologic formation, structure, or
physiology.
a.”increasing pulmonary blood flow”.
b. “decreasing pulmonary blood flow”
c. “obstruction to systemic blood flow”
d. single – ventricle defects such as hypoplastic left
heart syndrome.
Administer sedation as prescribed during the acute
stage to promote rest.
Types of Heart Defects based on Blood Flow
Cyanotic heart disease - when venous blood from the
right side of the heart mixes with blood on the left
side, this is a "right-to-left" shunt that delivers
deoxygenated blood to the body.
Acyanotic heart disease - if the blood shunts left to
right, then oxygenated blood from the left side mixes
with blood in the right side of the heart and goes back
to the lungs again.
Cyanotic Congenital Heart Disease (R -> L)
[5T's with 1-5 mnemonic]
Truncus arteriosus – vessels join to make 1
Transposition of great vessels – 2 major vessels
switched
Tricuspid atresia – 3 (tricuspid)
Tetralogy of fallot – 4 defects
Total anomalous pulmonary vascular return – 5 letters
(TAPVR)
Acyanotic Congenital Heart Disease (L-> R)
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Patent ductus arteriosus (PDA)
Coarctation of aorta (CoA)
DEFECTS THAT INCREASE PULMONARY BLOOD FLOW
Patent Ductus Arteriosus
Patent ductus arteriosus is failure of the fetal ductus
arteriosus (shunt connectir the aorta and the
pulmonary artery) to close within the first weeks of
life.
Occurs when this fetal shunt fails to close after several
days of life. This remnant fetal circulation remaining
patent occurs more frequently in children born
prematurely, with an incidence ranging from 20% to
60%.
If a ductus arteriosus does not close after birth, it
allows blood to flow from the aorta (area of high
pressure) through the PDA and into the main
pulmonary artery (area of low pressure" The shunted
blood then returns to the left atrium of the heart and
repeats the cycle. This extra blood flow increases
pulmonary circulation.
This is an acyanotic defect, as the blood flowing from
the aorta is fully
Assessment:
A characteristic machinery-like murmur is present.
An infant may be asymptomatic or may show signs of
HF.
A widened pulse pressure and bounding pulses are
present.
Signs and symptoms of decreased cardiac output may
be present.
Signs and Symptoms of Decreased Cardiac Output
o Decreased peripheral pulses
o Exercise intolerance
o Feeding difficulties
o Hypotension
o Irritability, restlessness, lethargy
o Oliguria
o Pale, cool extremities
o Tachycardia
Management:
a. Indomethacin, a prostaglandin inhibitor,
may be administered to close a patent ductus
in premature infants and some newborns.
b. The defect may be closed during cardiac
catheterization, or the defect may require
surgical management.
C. Surgical closure of a PDA is done via a left-
sided thoracotomy incision
Patent Ductus Arteriosus
A patent ductus arteriosus (PDA) occurs when this
fetal shunt fails to close after several days of life.
Patent ductus arteriosus is failure of the fetal ductus
arteriosus (shunt connecting the aorta and the
pulmonary artery) to close within the first weeks of
life.
This remnant of fetal circulation remaining patent
occurs more frequently in children born prematurely,
with an incidence ranging from 20% to 60%.
If a ductus arteriosus does not close after birth, it
allows blood to flow from the aorta (area of high
pressure) through the PDA and into the main
pulmonary artery (area of low pressure" The shunted
blood then returns to the left atrium of the heart and
repeats the cycle. This extra blood flow increases
pulmonary circulation.
This is an acyanotic defect, as the blood flowing from
the aorta is fully
Atrial Septal Defect
An ASD is created when a portion of the atrial septal
tissue does not completely form.
ASD is an abnormal opening between the atria that
causes an increased flow of oxygenated blood into the
right side of the heart.
Right atrial and ventricular enlargement occurs.
Infant may be asymptomatic or may develop HF.
Types of ASD:
ASD 1 (ostium primum): Opening is at the lower end
of the septum.
ASD 2 (ostium secundum): Opening is near the center
of the septum.
ASD 3 (sinus venosus defect): Opening is near the
junction of the superior vena cava and the right
atrium
Assessment:
If the defect is small, it may go undetected or, if
noted, may cause no clinical concern and require no
intervention. If the defect is large enough, a child may
show symptoms of the ASD.
The child will present with symptoms of pulmonary
overcirculation, such as rales, congestion, tiring with
activity, or poor weight gain. Over time, the right
heart may also dilate as a result of the increased
volume.
Systolic Murmur due to increase blood volume
traveling to the pulmonary valve. An ASD is confirmed
with an echocardiogram.
Management:
Defect may be closed during a cardiac catheterization.
Open repair with cardiopulmonary bypass may be
performed and usually is performed before school
age.
Ventricular Septal Defect
Ventricular septal defects (VSDs) are the most
common defect found in children, either in isolation
or combined with other defects.
A VSD occurs when a portion of the ventricular
septum does not completely close.
VSD is an abnormal opening between the right and
left ventricles.
Many VSDs close spontaneously during the first year
of life in children having small or moderate defects.
VSDs may be single or multiple and are defined based
on their anatomical location within the septum.
Assessment:
A characteristic murmur is present.
Signs and symptoms of HF are commonly present.
Signs and symptoms of decreased cardiac output may
be present
Management:
a. Medically managed to allow for spontaneous
closure of the defect
B. If the child does exhibit signs of pulmonary
overload, such as tachypnea, retractions, or rales,
management will include use of a diuretic such as
furosemide and possibly an increase in the caloric
density of the child's formula or breast milk if there
are concerns for poor weight gain
Closure during cardiac catheterization may be
possible.
b. Open repair may be done with cardiopulmonary
bypass.
Atrioventricular Septal Defect
The defect results from incomplete fusion of the
endocardial cushions.
This defect comprises several congenital heart
defects: a primum ASD, a high VSD and failure of the
tricuspid and mitral valves to develop and attach
correctly.
Varying degrees of abnormality occur with this lesion,
from mild septal defects to a complete lack of central
septa with incompetent valves on both sides.
In a complete AVSD, blood freely mixes between the
right and left sides. As with other septal defects,
pulmonary blood flow can be significantly increased,
but a complete AVSD also allows for right-to-left
shunting, which may lead to desaturation.
The defect is the most common cardiac defect in
Down syndrome
Assessment:
A characteristic murmur is present.
The infant usually has mild to moderate HF, with
cyanosis increasing with crying.
Signs and symptoms of decreased cardiac output may
be present.
Management:
Management typically includes medications such as
furosemide, digoxin, and an ACE inhibitor like
captopril or enalapril. These children may also require
concentrated feeds to help maintain weight.

Management can include pulmonary artery banding
for infants with severe symptoms (palliative)- if
surgical intervention needs to be delayed
Surgical management- Surgical repair of an AVSD
consists of closing atrial and VSDs and repairing the
mitral and tricuspid valves to make them functional
Children with Down syndrome may need for surgical
correction by 3 months of age or earlier if the
transthoracic echocardiogram demonstrates signs of
increased pulmonary pressures. Children without
Down syndrome are referred for repair by 5 or 6
months of age.
Transposition of the Great Arteries
The pulmonary artery leaves the left ventricle, and the
aorta exits from the right ventricle.
This is the second most common congenital defect
and is described as reversal of the great arteries. The
exact etiology is not completely understood.
No communication exists between the systemic and
pulmonary circulation.
Infants with minimal communication are severely
cyanotic and depressed at birth.
Infants with large septal defects or a patent ductus
arteriosus may be less severely cyanotic, but may
have symptoms of HF
All other intracardiac structures are normal, with VSDs
noted in 50% of these infants.
Transposition of the Great Arteries
The resultant anatomy has the aorta coming off of the
right ventricle and the pulmonary artery arising from
the left ventricle. This results in essentially Superior
Pulmonarartery two separate circulations whereby
the oxygenated vena cava blood returns from the
lungs to the left atrium, to Aorta the left ventricle, and
then proceeds back through Rightatrium the
pulmonary artery and to the lungs again, whereas the
deoxygenated blood returns from the Right body to
the right atrium, the right ventricle, and
ventricleInterior proceeds back out the aorta,
supplying venacava deoxygenated blood to the
systemic circulation
Assessment:
The infant is typically tachypneic, and a murmur may
not be noted. Blood must mix to provide oxygenated
blood to the systemic circulation.
Infants with large septal defects or a patent ductus
arteriosus may be less severely cyanotic, but may
have symptoms of HF.
Cardiomegaly is evident a few weeks after birth.
Management:
Nonsurgical management:
a. Prostaglandin E1 (PGE1) may be initiated to keep
the ductus arteriosus open and to improve blood
mixing temporarily. Side effects of a PGE1 infusion can
include apnea and hypotension.
b. Balloon atrial septostomy during cardiac
catheterization may be performed to increase mixing
and to maintain cardiac output over a longer period.
Surgical management:
The arterial switch procedure reestablishes normal
circulation with the left ventricle acting as the
systemic pump and creation of a new aorta.
Anomalous Pulmonary Venous Return
The defect is a failure of the pulmonary veins to join
the left atrium.
The defect results in mixed blood being returned to
the right atrium and shunted from the right to the left
through an ASD.
The right side of the heart hypertrophies, whereas the
left side of the heart may remain small.
APVR is a result of failure of the pulmonary venous
connections to unite with the left atrium in utero.
Instead, they return to another vessel (left
innominate, portal, or coronary sinus vein) or directly
to the right atrium, and the oxygenated pulmonary
blood return drains back into the right side of the
heart. This can be seen with one, two, or three of the
veins (partial APVR), or all four veins (total APVR),
draining to the venous side. Total APVR requires
urgent surgical intervention. Partial PVR, if only one
vessel, can be missed because it may cause no
significant clinical effects.
Assessment:
The right side of the heart hypertrophies, whereas the
left side of the heart may remain small.

Signs and symptoms of HF develop.
Cyanosis worsens with pulmonary vein obstruction;
when obstruction occurs, the infant's condition
deteriorates rapidly.
Management:
a. Surgical management
b. Corrective repair is performed in early infancy.
c. The pulmonary vein is anastomosed to the left
atrium, the ASD is closed, and the anomalous
pulmonary venous connection is ligated.
Truncus Arteriosus
TA is characterized by a single arterial vessel that
originates from the heart, overrides the ventricular
septum, and supplies all of the systemic, coronary,
and pulmonary blood flow.
Truncus arteriosus is failure of normal septation and
division of the embryonic bulbar trunk into the
pulmonary artery and the aorta, resulting in a single
vessel that overrides both ventricles. 2. Blood from
both ventricles mixes in the common great artery,
causing desaturation and hypoxemia.
The branch pulmonary arteries arise at some point
along this large vessel. Truncus has four
classifications, depending on where the pulmonary
arteries arise from the truncal vessel. It occurs as a
result of the great artery failing to divide in utero into
two vessels, the pulmonary artery and the aorta. After
birth, the truncus vessel arises from the ventricles;
blood ejects and follows the path of least resistance
to the pulmonary bed. This is a cyanotic lesion that
also requires urgent surgery.
Assessment:
A characteristic murmur is present.
The infant exhibits moderate to severe HF and
yariable cyanosis, poor growth, and activity
intolerance.
Management:
Surgical management: Corrective surgical repair is
performed in the first few months of life.
Tetralogy of Fallot
Tetralogy of Fallot includes 4 defects- VSD, pulmonary
stenosis, overriding aorta, and right ventricular
hypertrophy.
If pulmonary vascular resistance is higher than
systemic resistance, the shunt is from right to left; if
systemic resistance is higher than pulmonary
resistance, the shunt is from left to right.
This defect accounts for about 7% to 10% of cases of
congenital heart disease and is one of the most
common congenital heart lesions requiring
intervention in the first year of life.
TOF occurs equally among males and females. The
right ventricular hypertrophy is not an isolated
problem but occurs secondary to the pulmonary
stenosis.
Assessment:
Infants
An infant may be acutely cyanotic at birth or may
have mild cyanosis that progressesover the first year
of life as the pulmonic stenosis worsens.
A characteristic murmur is present.
Acute episodes of cyanosis and hypoxia
(hypercyanotic spells), called blue spells or tet spells,
occur when the infant's oxygen requirements exceed
the blood supply, such as during periods of crying,
feeding, or defecating.
Assessment:
Children:
With increasing cyanosis, squatting, clubbing of the
fingers, and poor growth may occur.
Squatting is a compensatory mechanism to facilitate
increased return of blood flow to the heart for
oxygenation.
Clubbing is an abnormal enlargement in the distal
phalanges; seen in the fingers.
Surgical management: Palliative shunt
a. The shunt increases pulmonary blood flow and
increases oxygen saturation in infants who cannot
undergo primary repair.
b. The shunt provides blood flow to the pulmonary
arteries from the left or right subclavian artery.
Surgical management: Complete repair
a. Complete repair usually is performed in the first
year of life.

b. The repair requires a median sternotomy and
cardiopulmonary bypass.
Tricuspid Atresia
Tricuspid atresia is failure of the tricuspid valve to
develop.
No communication exists from the right atrium to the
right ventricle.
Blood flows through an ASD or a patent foramen
ovale to the left side of the heart and through a VSD
to the right ventricle and out to the lungs.
The defect often is associated with pulmonic stenosis
and transposition of the great arteries. The defect
results in complete mixing of unoxygenated and
oxygenated blood in the left side of the heart,
resulting in systemic desaturation, pulmonary
obstruction, and decreased pulmonary blood flow.
Assessment:
Cyanosis, tachycardia, and dyspnea are seen in the
newborn.
Older children exhibit signs of chronic hypoxemia and
clubbing.
Management:
If the ASD is small, the defect may be closed during
cardiac catheterization; otherwise, surgery is needed.
Coarctation of the Aorta
This defect is typically located at the level of the
ductus arteriosus insertion; the mechanism is
thought to be migration or extension of ductal
tissue into the wall of the fetal thoracic aorta,
causing the tissue to constrict.
Coarctation of the aorta is localized narrowing
near the insertion of the ductus arteriosus.
Blood pressure is higher in the upper extremities
than in the lower extremities; bounding pulses in
the arms, weak or absent femoral pulses, and
cool lower extremities may be present.
Assessment:
o Signs of HF may occur in infants.
o Signs and symptoms of decreased cardiac
output may be present.
o Children may experience headaches,
dizziness, fainting, and epistaxis resulting from
hypertension.
Management:
o Management of the defect may be done via
balloon angioplasty in children; restenosis can
occur.
Surgical management:
a. Mechanical ventilation and medications to improve
cardiac output are often necessary before surgery.
b. Resection of the coarcted portion with endto-end
anastomosis of the aorta or enlargement of the
constricted section, using a graft, may be required.
c. Because the defect is outside the heart,
cardiopulmonary bypass is not required, and a
thoracotomy incision is used.
Aortic Stenosis
Aortic stenosis is a narrowing or stricture of the aortic
valve, causing resistance to blood flow from the left
ventricle into the aorta, resulting in decreased cardiac
output, left ventricular hypertrophy, and pulmonary
vascular congestion.
Obstruction out the left ventricle can occur below the
aortic valve (subvalvar), at the valve (valvar), or above
the valve (supravalvar). These can be isolated
abnormalities or occur with other defects. Regardless
of the location of the restriction, the resultant
physiology is the same. The narrowing prevents blood
from passing freely from the left ventricle of the heart
into the aorta. Because the heart must work harder to
pass blood through the narrowed area, increased
pressure and hypertrophy occur in the left ventricle. If
this pressure becomes severe, pressure in the left
atrium will increase as well, resulting in back pressure
through the pulmonary veins to the lungs, possibly
causing pulmonary edema. Aortic stenosis accounts
for about 10% of congenital cardiac abnormalities
Valvular stenosis is the most common type and
usually is caused by malformed cusps, resulting in a
bicuspid rather than a tricuspid valve, or fusion of the
cusps.
Management:
a. Stabilization with a beta-blocker or a calcium
channel blocker may be necessary to reduce or
prevent further ventricular hypertrophy
b. Dilation of the narrowed valve may be done during
cardiac catheterization.
c. Surgical aortic valvotomy (palliative) may be done; a
valve replacement may be required at a second
procedure.
SINGLE-VENTRICLEDEFECTS
Hypoplastic Left Heart Syndrome
Underdevelopment of the left side of the heart
occurs, resulting in a hypoplastic left ventricle and
aortic atresia
HLHS is a rare disorder, accounting for only 1% to 3%
of congenital heart disease, and is detectable on
prenatal ultrasound.
SINGLE-VENTRICLEDEFECTS
HLHS results when there is poor or no flow to the left
ventricle, typically secondary to mitral or aortic
stenosis or atresia. Because of the limited amount of
blood in the left ventricle, it does not develop
appropriately. The ascending aorta is also hypoplastic,
and the coronary arteries are perfused through
retrograde flow down the ascending aorta. A PFO will
occur, although the atrial septum is thickened. In
utero, the circulation is adequate to meet the needs
of the developing fetus. But at birth, survival is
dependent on a PDA. Infants are typically male, rarely
premature, and have no other associated cardiac
anomalies.
ASD = Atrial Septal Defect
PDA = Patent Ductus Arteriosus
IVC = InferiorVenaCava
PV = Pulmonary Vein
LA = Left Atrium
RA = RightAtrium
LV = LeftVentricle
PA = Pulmonary Artery
RV = Right Ventricle
SVC = Superior Vena Cava
Assessment:
Mild cyanosis and signs of HF occur until the ductus
arteriosus closes; then progressive deterioration with
cyanosis and decreased cardiac output are seen,
leading to cardiovascular collapse.
The defect is fatal in the first few months of life
without intervention.
Management:
Surgical treatment
a. Surgical treatment is necessary; transplantation in
the newborn period may be considered.
b. In the preoperative period, the newborn requires
mechanical ventilation and a continuous infusion of
prostaglandin E1 to maintain ductal patency, ensuring
adequate systemic blood flow.
RHEUMATIC FEVER
Rheumatic fever is an inflammatory autoimmune
disease that affects the connective tissues of the
heart, joints, skin (subcutaneous tissues), blood
vessels, and central nervous system.
The most serious complication is rheumatic heart
disease, which affects the cardiac valves, particularly
the mitral valve.
Rheumatic fever manifests 2 to 6 weeks after an
untreated or partially treated group A b-hemolytic
streptococcol infection of the upper respiratory tract.
Jones criteria are used to help determine the
diagnosis
Assessment:
1. Fever: Low-grade fever that spikes in the late
afternoon
2. Elevated anti-streptolysin O titer
3. Elevated erythrocyte sedimentation rate
4. Elevated C-reactive protein level
5. Aschoff bodies (lesions): Found in the heart, blood
vessels, brain, and serous surfaces of the joints and
pleura
"Assessment of a child with suspected rheumatic
fever includes inquiring about a recent sore throat
because rheumatic fever manifests 2 to 6 weeks after
an untreated or partially treated group A 6-hemolytic
streptococcol infection of the upper respiratory tract"
Management:
1. Assess vital signs.
2. Control joint pain and inflammation with massage
and alternating hot and cold applications as
prescribed.
3. Provide bed rest during the acute febrile phase.
4. Limit physical exercise in a child with carditis.
5. Administer antibiotics as prescribed.
6. Administer salicylates and anti-inflammatory agents
as prescribed; these medications should not be
administered before the diagnosis is confirmed
because the medications mask the polyarthritis.
7. Initiate seizure precautions if the child is
experiencing chorea.
8. Instruct the parents about the importance of
follow-up and the need for antibiotic prophylaxis for
dental work, infection, and invasive procedures.
9. Advise the child to inform the parents if anyone in
school develops a streptococcol throat infection.
KAWASAKI DISEASE
Kawasaki disease, also known as mucocutaneous
lymph node syndrome, is an acute systemic
inflammatory illness.
7. Administer soft foods and liquids that are neither
too hot nor too cold.
8. Weigh child daily.
9. Provide passive range-of-motion exercises to
facilitate joint movement.
10. Administer acetylsalicylic acid as prescribed for its
antipyretic and antiplatelet effects (additional
anticoagulation may be necessary if aneurysms are
present).
11. Administer immunoglobulinintravenously as
prescribed to reduce the duration of the fever and the
incidence of coronary artery lesions and aneurysms;
intravenous immunoglobulinis a blood product, so
blood precautions when administering it are
warranted.
12. Parent education.

The cause is unknown, but may be associated with an

infection from an organism or toxin.

Cardiac involvement is the most serious complication;

aneurysms can develop. Signs & Symptoms of
Kawasaki Disease

Assessment:
1. Acute stage
a. fever
b. conjunctival hyperemia
c. red throat
d. swollen hands, rash, and enlargement of cervical
lymph nodes

2. Subacute stage
a. Cracking lips and fissures
b. Desquamation of the skin on the tips of the fingers
and toes
c. Joint pain
d. Cardiac manifestations
e. Thrombocytosis

3. Convalescent stage:
Child appears normal, but signs of inflammation may
be present.

Management:

1. Monitor temperature frequently.

2. Assess heart sounds and heart rate and rhythm.
3. Assess extremities for edema, redness, and
desquamation.
4. Examine eyes for conjunctivitis.
5. Monitor mucous membranes for inflammation.
6. Monitor strict intake and output.