BACHELOR OF SCIENCE IN NURSING

CARE OF MOTHER AND CHILD AT RISK OR

WITH PROBLEMS (ACUTE AND CHRONIC):
COURSE MODULE COURSE UNIT WEEK
3 11 13
Alterations with Infectious, Inflammatory and Immunologic
Responses/ Cellular Aberrations

✓ Read course and unit objectives

✓ Read study guide prior to class attendance
✓ Read required learning resources; refer to unit terminologies for jargons
✓ Proactively participate in classroom discussions
✓ Answer and submit course unit tasks

At the end of the course unit (CU), learners will be able to:

Cognitive:
1. Identify and understand the different alterations with infectious, inflammatory and immunologic responses
/ cellular aberrations in children.
2. Verbalize the importance and relevance of these topics to nursing practice

Affective:
1. Listen attentively during class discussions
2. Demonstrate tact and respect when challenging other people’s opinions and ideas
3. Accept comments and reactions of classmates on one’s opinions openly and graciously.

Psychomotor:
1. Participate actively during class discussions and group activities
2. Express opinion and thoughts in front of the class
 OVERVIEW:

I. ALTERATIONS WITH INFECTIOUS, INFLAMMATORY AND IMMUNOLOGIC RESPONSES

1. Juvenile Rheumatoid Arthritis

2. Allergic Rhinitis
3. Eczema
4. Asthma

II. CELLULAR ABERRATIONS

1. Basic Concepts on Oncology

A. Leukemia
B. Lymphomas
C. Wilms’ tumor
D. Brain tumors

2. Basic Concepts on Cancer management and Nursing care

I. ALTERATIONS WITH INFECTIOUS, INFLAMMATORY AND IMMUNOLOGIC RESPONSES

JUVENILE RHEUMATOID ARTHRITIS ( JUVENILE IDIOPATHIC ARTHRITIS)

Juvenile idiopathic arthritis (JIA) is the name replacing juvenile rheumatoid arthritis (JRA) in the research
literature and now in clinical practice. The JRA nomenclature revision to JIA was partly attributable to the minimally
applicable reference to “rheumatoid” in JRA. Only a small percentage of children have a positive rheumatoid factor,
yet the name burdens the family with images of adult disfiguring rheumatoid arthritis, a distinctly different disease.

JIA is a chronic autoimmune inflammatory disease causing inflammation of joints and other tissue with
an unknown cause. JIA starts before age 16 years with a peak onset between 1 and 3 years of age. Twice as
many girls as boys are affected. The reported incidence of chronic childhood arthritis varies from 1 to 20 cases per
100,000 children with a prevalence of 10 to 400 per 100,000 (Cassidy and Petty, 2011). The cause is unknown, but
two factors are hypothesized: immunogenic susceptibility and an environmental or external trigger such as a virus
(e.g., rubella, Epstein-Barr virus, parvovirus B19).

PATHOPHYSIOLOGY: The disease process is characterized by chronic inflammation of the synovium with joint
effusion and eventual erosion, destruction, and fibrosis of the articular cartilage. Adhesions between joint surfaces
and ankylosis of joints occur if the inflammatory process persists.

CLINICAL MANIFESTATIONS: The outcome of JIA is variable and unpredictable. The disease, even in severe
forms, is rarely life threatening but can cause significant disability. The arthritis tends to wax and wane; however,
patterns of clinical remission indicate approximately 25% will obtain clinical remission off medication for a follow-up
duration of at least 4 years. Children with arthritis in four or fewer joints had the greatest likelihood for a sustained
remission. Children with extensive arthritis and a positive rheumatoid factor were less likely to have a sustained
remission (Wallace, Huang, and Bandeira, 2005). Their arthritis can cause significant joint deformity and functional
disability, requiring medication, physical therapy, and perhaps future joint replacement. Chronic and acute uveitis
can cause permanent vision loss if undiagnosed and not aggressively treated.

Classification of Juvenile Idiopathic Arthritis:

1. Systemic arthritis is arthritis in one or more joints associated with at least 2 weeks of quotidian fever,
rash, lymphadenopathy, hepatosplenomegaly, and serositis.

2. Oligoarthritis is arthritis in one to four joints for the first 6 months of disease. It is subdivided to
persistent oligoarthritis if it remains in four joints or fewer or becomes extended oligoarthritis if it involves
more than four joints after 6 months.

3. Polyarthritis rheumatoid factor negative affects five or more joints in the first 6 months with a
negative rheumatoid factor.

4. Polyarthritis rheumatoid factor positive also affects five or more joints in first 6 months, but these
children have a positive rheumatoid factor.

5. Psoriatic arthritis is arthritis with psoriasis or an associated dactylitis, nail pitting, or onycholysis or
psoriasis in a first-degree relative.

6. Enthesitis-related arthritis is arthritis or enthesitis associated with at least two of the following:
sacroiliac or lumbosacral pain, HLA-B27 antigen, arthritis in a boy older than 6 years, acute anterior
uveitis, inflammatory bowel disease, Reiter syndrome, or acute anterior uveitis in a first-degree relative.

7. Undifferentiated arthritis fits no other category above or fits more than one category.

DIAGNOSTIC EVALUATION: Juvenile idiopathic arthritis is a diagnosis of exclusion; there are no definitive tests.
Classifications are based on the clinical criteria of age of onset before age 16 years, arthritis in one or more joints
for 6 weeks or longer, and exclusion of other causes. Laboratory tests may provide supporting evidence of disease.
The ESR may or may not be elevated. Leukocytosis is frequently present during exacerbations of systemic JIA.
Antinuclear antibodies are common in JIA but are not specific for arthritis; however, they help identify children who
are at greater risk for uveitis. Plain radiographs are the best initial imaging studies and may show soft-tissue swelling
and joint space widening from increased synovial fluid in the joint. Later films can reveal osteoporosis, narrow joint
space, erosions, subluxation, and ankylosis.

THERAPEUTIC MANAGEMENT: There is no cure for JIA. The major goals of therapy are to control pain,
preserve joint range of motion and function, minimize effects of inflammation such as joint deformity, and
promote normal growth and development. Outpatient care is the mainstay of therapy; lengthy hospitalizations are
infrequent in this era of managed care. The treatment plan can be exhaustive and intrusive for the child and family,
including medications, physical and occupational therapy, ophthalmologic slit lamp examinations, splints, comfort
measures, dietary management, school modifications, and psychosocial support.

MEDICATIONS: Many arthritis medications are available, and most are effective in suppressing the inflammatory
process and relieving pain. These drugs may be given alone or in combination and are prescribed in a stepwise
manner dependent on arthritis severity.

NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS) are the first drugs used. Naproxen, ibuprofen,
tolmetin, indomethacin, celecoxib, meloxicam, and aspirin are approved for use in children. They are effective with
few common side effects other than gastrointestinal irritation and bruising; with naproxen, skin fragility is a possible
side effect. NSAIDs must be taken with food. Aspirin, once the drug of choice, has been replaced by other NSAIDs
because they have fewer side effects and easier administration schedules.

METHOTREXATE is the second-line medication used in children who have failed with NSAIDs alone. It is started
in combination with an NSAID. It is effective, with acceptable toxicity, which requires monitoring of complete blood
cell counts and liver functions. Patient education about possible side effects, including discussions with teens about
birth defects and avoiding alcohol, is essential. Corticosteroids are potent immuno-suppressives used for life-
threatening complications, incapacitating arthritis, and uveitis. They are administered at the lowest effective dosage
for the briefest period and discontinued on a tapering schedule. Prolonged use of systemic steroids is associated
with significant side effects, including Cushing syndrome, osteoporosis, increased infection risk, glucose
intolerance, cataracts, and growth suppression.

BIOLOGIC AGENTS that work by several mechanisms to interrupt and minimize the inflammatory process are
used in children with severe or progressive arthritis. Biologic agents may be used in combination with
methotrexate. The Food and Drug Administration (FDA) has approved etanercept, adalimumab and abatacept
use in children with JIA.

NURSING CARE:

Relieve Pain. The pain of JIA is related to several aspects of the disease, including disease severity, functional
status, individual pain threshold, family variables, and psychological adjustment. The aim is to provide as much
relief as possible with medication and other therapies to help children tolerate the pain and cope as effectively as
possible. Non-pharmacologic modalities such as behavioral therapy and relaxation techniques have proved
effective in modifying pain perception and activities that aggravate pain. Opioid analgesics are typically avoided in
juvenile arthritis; however, for children immobilized with refractory pain, short-term opioid analgesics can be part of
a comprehensive plan that uses multiple pain relief techniques (Connelly and Schanberg, 2006).

Promote General Health. The child’s general health must be considered. A well-balanced diet with sufficient
calories to maintain growth is essential. If the child is relatively inactive, caloric intake needs to match energy needs
to avoid excessive weight gain, which places additional stress on affected joints.

Encourage Heat and Exercise. Heat has been shown to be beneficial to children with arthritis. Moist heat is best
for relieving pain and stiffness, and the most efficient and practical method is in the bathtub with warm water.

ALLERGIC RHINITIS

Allergic rhinitis is inflammation of the inside of the nose caused by an allergen, such as pollen, dust, mold or
flakes of skin from certain animals. Allergic rhinitis is caused by the immune system reacting to an allergen as if it
were harmful. This results in cells releasing a number of chemicals that cause the inside layer of your nose (the
mucous membrane) to become swollen and too much mucus to be produced.

Common allergens that cause allergic rhinitis include pollen (this type of allergic rhinitis is known as hay fever), as
well as mold spores, house dust mites, and flakes of skin or droplets of urine or saliva from certain animals.

Symptoms of allergic rhinitis

Allergic rhinitis typically causes cold-like symptoms, such as sneezing, itchiness and a blocked or runny nose.
These symptoms usually start soon after being exposed to an allergen. Some people only get allergic rhinitis for a
few months at a time because they're sensitive to seasonal allergens, such as tree or grass pollen. Other people
get allergic rhinitis all year round. Most people with allergic rhinitis have mild symptoms that can be easily and
effectively treated. But for some people symptoms can be severe and persistent, causing sleep problems and
interfering with everyday life. The symptoms of allergic rhinitis occasionally improve with time, but this can take
many years and it's unlikely that the condition will disappear completely.

Treatment / Management. It's difficult to completely avoid potential allergens, but you can take steps to reduce
exposure to a particular allergen you know or suspect is triggering your allergic rhinitis. This will help improve the
symptoms. If the condition is mild, it can also help reduce the symptoms by taking over-the-counter medications,
such as non-sedating antihistamines, and by regularly rinsing the nasal passages with a salt water solution to keep
the nose free of irritants. A stronger medication, such as a nasal spray containing corticosteroids may be prescribed.

ATOPIC DERMATITIS (ECZEMA)

Eczema or eczematous inflammation of the skin refers to a descriptive category of dermatologic diseases and
not to a specific etiology. AD is a type of pruritic eczema that usually begins during infancy and is associated
with an allergic contact dermatitis with a hereditary tendency (atopy) (Jacob, Yang, Herro, and others, 2010).
AD manifests in three forms based on the child’s age and the distribution of lesions:

1. Infantile (infantile eczema)—Usually begins at 2 to 6 months of age; generally undergoes spontaneous

remission by 3 years of age
2. Childhood—May follow the infantile form; occurs at 2 to 3 years of age; 90% of children have manifestations
by age 5 years
3. Preadolescent and adolescent—Begins at about 12 years of age; may continue into the early adult years
or indefinitely

CLINICAL MANIFESTATIONS OF ATOPIC DERMATITIS

Distribution of Lesions
• Infantile form—Generalized, especially cheeks, scalp, trunk, and extensor surfaces of extremities
• Childhood form—Flexural areas (antecubital and popliteal fossae, neck), wrists, ankles, and feet
• Preadolescent and adolescent form—Face, sides of neck, hands, feet, face, and antecubital and
popliteal fossae (to a lesser extent)

APPEARANCE OF LESIONS

Infantile Form
• Erythema
• Vesicles
• Papules
• Weeping
• Oozing
• Crusting
• Scaling
• Often symmetric

Childhood Form
• Symmetric involvement
• Clusters of small erythematous or flesh-colored papules or minimally scaling patches
• Dry and may be hyperpigmented
• Lichenification (thickened skin with accentuation of creases)
• Keratosis pilaris (follicular hyperkeratosis) common

Adolescent or Adult Form

• Same as childhood manifestations
 • Dry, thick lesions (lichenified plaques) common Confluent papules
• Other Physical Manifestations
• Intense itching
• Unaffected skin dry and rough
• African-American children likely to exhibit more papular or follicular lesions than are white children
May exhibit one or more of the following:
• Lymphadenopathy, especially near affected sites
• Increased palmar creases (many cases)
• Atopic pleats (extra line or groove of lower eyelid)
• Prone to cold hands
• Pityriasis alba (small, poorly defined areas of hypopigmentation)
• Facial pallor (especially around nose, mouth, and ears)
• Bluish discoloration beneath eyes (“allergic shiners”)
• Increased susceptibility to unusual cutaneous infections (especially viral)

Therapeutic Management The major goals of management are to (1) hydrate the skin, (2) relieve pruritus, (3)
reduce flare-ups or inflammation, and (4) prevent and control secondary infection. The general measures for
managing AD focus on reducing pruritus and other aspects of the disease. Management strategies include
avoiding exposure to skin irritants or allergens; avoiding overheating; and administrating medications such as
antihistamines, topical immunomodulators, topical steroids, and (sometimes) mild sedatives as indicated.
Enhancing skin hydration and preventing dry, flaky skin are accomplished in a number of ways, depending on
the child’s skin characteristics and individual needs.

NURSING CARE:

• Assessment of the child with AD includes a family history for evidence of atopy, a history of previous
involvement, and any environmental or dietary factors associated with the present and previous
exacerbations.

• The skin lesions are examined for type, distribution, and evidence of secondary infection.

• Controlling the intense pruritus is imperative if the disorder is to be successfully managed because
scratching leads to new lesions and may cause secondary infection.

• Fingernails and toenails are cut short, kept clean, and filed frequently to prevent sharp edges. Gloves
or cotton stockings can be placed over the hands and pinned to shirtsleeves.

• One-piece outfits with long sleeves and long pants also decrease direct contact with the skin. If gloves
or socks are used, the child needs time to be free from such restrictions. An excellent time to remove
gloves, socks, or other protective devices is during the bath or after receiving sedative or antipruritic
medication.

ASTHMA

Asthma is a chronic inflammatory disorder of the airways characterized by recurring symptoms, airway
obstruction, and bronchial hyperresponsiveness (National Asthma Education and Prevention Program
[NAEPP], 2007). In susceptible children, inflammation causes recurrent episodes of wheezing, breathlessness,
chest tightness, and cough, especially at night or in the early morning. The airflow limitation or obstruction is
reversible either spontaneously or with treatment. Inflammation causes an increase in bronchial
hyperresponsiveness to a variety of stimuli (NAEPP, 2007). Recognition of the key role of inflammation has made
the use of antiinflammatory agents, especially inhaled steroids, a major component in the treatment of asthma.
The classic manifestations of asthma are dyspnea, wheezing, and coughing. An attack may develop gradually or
appear abruptly and may be preceded by An upper respiratory tract infection.

ASTHMA SEVERITY CLASSIFICATION IN CHILDREN

TRIGGERS TENDING TO PRECIPITATE OR AGGRAVATE

ASTHMA EXACERBATIONS

• Allergens
• Outdoor—Trees, shrubs, weeds, grasses, molds, pollens, air
pollution, spores
• Indoor—Dust or dust mites, mold, cockroach antigen
• Irritants—Tobacco smoke, wood smoke, odors, sprays
• Exposure to occupational chemicals
• Exercise
• Cold air
• Changes in weather or temperature
• Environmental change—Moving to new home, starting new
school, and so on
• Colds and infections
• Animals—Cats, dogs, rodents, horses
• Medications—Aspirin, NSAIDs, antibiotics, beta-blockers
• Strong emotions—Fear, anger, laughing, crying
• Conditions—Gastroesophageal reflux, tracheoesophageal fistula
• Food additives—Sulfite preservatives
• Foods—Nuts, milk or other dairy products
• Endocrine factors—Menses, pregnancy, thyroid disease

Therapeutic Management. The overall goals of asthma

management are to maintain normal activity levels, maintain
normal pulmonary function, prevent chronic symptoms and
recurrent exacerbations, provide optimum drug therapy with minimum or no adverse effects, and assist the child in
living as normal and happy a life as possible.

Drug Therapy. Asthma medications are categorized into two general classes: longterm control medications
(preventive medications) to achieve and maintain control of inflammation, and quick-relief medications (rescue
medications) to treat symptoms and exacerbations (NAEPP, 2007)

• Corticosteroids are anti-inflammatory drugs used to treat reversible airflow obstruction, control
symptoms, and reduce bronchial hyperresponsiveness in chronic asthma.

• β-Adrenergic agonists (short acting) (primarily albuterol, levalbuterol [Xopenex], and terbutaline) are
used for treatment of acute exacerbations and for the prevention of exercise-induced bronchospasm
 • Salmeterol (Serevent) is a long-acting β2-agonist (bronchodilator) that is used twice a day (no more
frequently than every 12 hours). This drug is added to antiinflammatory therapy and used for long-term
prevention of symptoms, especially nighttime symptoms, and exercise induced bronchospasm.

• Theophylline is a methylxanthine drug used for decades to relieve symptoms and prevent asthma
attacks; however, it is now used primarily in the ED when the child is not responding to maximal therapy.

• Cromolyn sodium is a medication used in maintenance therapy for asthma. It stabilizes mast cell
membranes; inhibits activation and release of mediators from eosinophil and epithelial cells; and inhibits
the acute airway narrowing after exposure to exercise, cold dry air, and sulfur dioxide.

• Anticholinergics (atropine and ipratropium [Atrovent]) may also be used for relief of acute
bronchospasm. However, these drugs have adverse side effects that include drying of respiratory
secretions, blurred vision, and cardiac and CNS stimulation.

II. CELLULAR ABERRATIONS

1. BASIC CONCEPTS OF ONCOLOGY

CANCER is a complex of diseases which occurs when normal cells mutate into abnormal cells that take over
normal tissue, eventually harming and destroying the host

A large group of diseases characterized by:

• Uncontrolled growth and spread of abnormal cells

• Proliferation (rapid reproduction by cell division)
• Metastasis (spread or transfer of cancer cells from one organ or part to another not directly connected)

ONCOLOGY

• Branch of medicine that deals with the study, detection, treatment and management of cancer and
neoplasia.

Characters of Neoplasia:

Uncontrolled growth of abnormal cells

1. Benign
➢ Well-differentiated
➢ Slow growth
➢ Encapsulated
➢ Non-invasive
➢ Does NOT metastasize

2. Malignant
➢ Undifferentiated
➢ Erratic and Uncontrolled Growth
➢ Expansive and Invasive
➢ Secretes abnormal proteins
➢ METASTASIZES
 3. Borderline

ETIOLOGY

1. PHYSICAL AGENTS
 Radiation
 Exposure to irritants
 Exposure to sunlight
 Altitude, humidity

2.CHEMICAL AGENTS
 Smoking
 Dietary ingredients
 Drugs

3. Genetics and Family History

 Colon Cancer
 Premenopausal breast cancer

A. LEUKEMIA

Leukemia is cancer that starts in the tissue that forms blood. Most blood cells develop from cells in the bone
marrow called stem cells. In a person with leukemia, the bone marrow makes ABNORMAL WHITE BLOOD
CELLS. The abnormal cells are leukemia cells. Unlike normal blood cells, leukemia cells don't die when they
should. They may crowd out normal white blood cells, red blood cells, and platelets. This makes it hard for
normal blood cells to do their work. The four main types of leukemia are:

• Acute lymphoblastic leukemia (ALL)

• Acute myelogenous leukemia (AML)
• Chronic lymphocytic leukemia (CLL)
• Chronic myelogenous leukemia (CML)

ETIOLOGY: THE RISK FACTORS OF LEUKEMIA

Genetic disorders
 Down syndrome
 Klinefelter syndrome
 Patau syndrome
 Ataxia telangiectasia
 Shwachman syndrome
 Kostman syndrome
 Neurofibromatosis
 Fanconi anemia
 Li-Fraumeni syndrome
Radiation exposure
 Nontherapeutic, therapeutic radiation

Physical and chemical exposures

 BenzeneDrugs such as pipobroman
 PesticidesCigarette smoking
 Embalming fluids
 Herbicides

Chemotherapy
 Alkylating agents
 Topoisomerase-II inhibitors
 Anthracyclines
 Taxanes

MANIFESTATIONS:

The symptoms of Acute Leukemia develop very quickly (within a few days or weeks ) whereas, Chronic Leukemia
can go unnoticed for years and is usually found in a routine blood test.
The following conditions can develop in Leukemia patients
• Anemia (a deficiency of red blood cells and hemoglobin)
• Thrombocytopenia (a low blood platelet count)
• Enlarged liver or Spleen (leukemia cells build up in the liver or spleen )
• Leukopenia (A low white blood cell count
• Other Symptoms
o Leukemia can also cause vomiting, confusion, loss of muscle control and seizures.
o Swollen Lymph nodes
o Fever or Chills
o Night Sweating
o Joint and bone pain

CHRONIC MYELOID LEUKEMIA

• This type affects the lymphoid cells created in the bone marrow. It is classified as chronic leukemia, because
the affected cells carry out some of their normal functions initially, making it difficult to detect.

ACUTE MYELOID LEUKEMIA

• The more severe form of the disease is acute myeloid leukemia, which is characterized by faster
progression of the disease. This is the most commonly incident type among adults. If detected early,
statistics show that 20% to 40% of patients survive for at least 60 months.

CHRONIC LYMPHOCYTIC LEUKEMIA

• This type almost never occurs among children and has a very high incidence rate among people aged more
than 60.
• Men are more likely to be affected by it, than women.
• Progression of this disease is slow.
 • If the disease has affected the B-cells, then life expectancy can be anywhere between 10 to 20 years, if
treatment begins early. However, those with T cell chronic lymphocytic leukemia have a very low life
expectancy.

ACUTE LYMPHOCYTIC LEUKEMIA

• The most common form of cancer in children is acute lymphocytic leukemia. One-fourth of all cancers
in children belong to this type.
• It has a high incidence rate among adults, older than 45 years of age. Chemotherapy is the established
treatment method for this disease.
• Before chemotherapy and other cancer cure methods were invented, a patient with acute lymphocytic
leukemia could survive for 4 months at the most.
• However, thanks to modern treatment methods, about 80% of the affected children are completely cured.
Adults have been seen to have a 40% chance of complete cure.
• The prognosis for this type will vary, depending on the stage of disease progression, but children in the age
group of 3 to 7 seem to have the highest chance of complete recovery.

DIAGNOSTICS:

• Physical exam. Your doctor will look for physical signs of leukemia, such as pale skin from anemia and
swelling of your lymph nodes, liver and spleen.
• Blood tests. By looking at a sample of your blood, your doctor can determine if you have abnormal levels
of white blood cells or platelets, which may suggest leukemia.
• Bone marrow test. Your doctor may recommend a procedure to remove a sample of bone marrow from
your hipbone. The sample is sent to a laboratory to look for leukemia cells.

TREATMENT:

Most treatment plans for acute lymphoblastic leukemia have 3 steps. These are induction, consolidation, and
maintenance.
• Induction Therapy: Killing of leukemia cells in the blood and bone marrow. Treatments include
chemotherapy. Induction usually lasts for 4 weeks.
• Consolidation Therapy: Killing of leukemia cells that may be present even though they don’t show up in
tests. If these cells are not killed, they could regrow and could cause a relapse. Treatment include
chemotherapy and may include stem cell transplant (replacement of damaged bone marrow cells with
healthy ones).
• Maintenance Therapy: Preventing any remaining leukemia cells from growing by using low doses of
chemotherapy and intravenous treatment (the infusion of liquid substances directly into a vein).

B. LYMPHOMAS

Pediatric lymphomas are the third most common group of malignancies in children and adolescents. The
lymphomas, a group of neoplastic diseases that arise from the lymphoid and hematopoietic systems, are divided
into Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL). These diseases are further subdivided
according to tissue type and extent of disease. Whereas NHL is more prevalent in children younger than 14
years of age, HL is prevalent in adolescence and the young adult period, with a striking increase between ages
15 and 19 years.
Hodgkin Lymphoma

Hodgkin lymphoma is a neoplastic disease that originates in the lymphoid system and primarily involves
the lymph nodes. It predictably metastasizes to non-nodal or extralymphatic sites, especially the spleen, liver,
bone marrow, and lungs, although no tissue is exempt from involvement. It is classified according to four
histologic types: (1) lymphocytic predominance, (2) nodular sclerosis, (3) mixed cellularity, and (4) lymphocytic
depletion. Accurate staging of the extent of disease is the basis for treatment protocols and expected
prognoses.

Asymptomatic enlarged cervical or supraclavicular lymphadenopathy is the most common presentation of HL.
Other systemic symptoms may be manifested, including cough, abdominal discomfort, and anorexia. Because
multiple organs may be involved, diagnosis is based on several tests and the extent of metastatic disease.
Tests include a CBC, erythrocyte sedimentation rate, serum copper, ferritin level, fibrinogen, immunoglobulins,
uric acid level, liver function tests, T-cell function studies, and urinalysis. Radiographic tests include chest
radiography and computed tomography (CT) of the neck and chest; CT and magnetic resonance imaging of
the abdomen and pelvis; and positron emission tomography (PET), which is replacing the gallium scan and
bone scan to identify metastatic disease. A lymph node biopsy is essential to establish histologic diagnosis and
staging. The presence of Reed-Sternberg cells is characteristic of HL. These large cells, which are
multilobed and nucleated with abundant cytoplasm and a typically halolike clear zone around the nucleolus, are
often described as having an “owl’s eyes” appearance (Metzger, Krasin, Hudson, and others, 2011). A bone
marrow aspiration and biopsy is usually performed in patients with advanced disease, B symptoms, or disease
recurrence (Metzger, Krasin, Hudson, and others, 2011). With the advent of CT and PET scans to identify
metastatic disease and multiagent therapy to eradicate metastatic disease, surgical staging involving a
laparotomy with splenectomy is no longer performed.

The primary modalities of therapy are radiation and chemotherapy. Each may be used alone or in combination
based on the clinical staging. Radiation may involve only the involved field (IF), an extended field (EF) (involved
areas plus adjacent nodes), or total nodal irradiation (TNI), depending on the extent of involvement.

Prognosis. Long-term survival for all stages of HL is excellent. The goal for pediatric HL’s curative treatment
is to provide minimal morbidity with the highest quality of life (Metzger, Krasin, Hudson, and others, 2011).

Nursing Care Management. Nursing care involves the same objectives as for patients with other types of
cancer, specifically: (1) preparation for diagnostic and operative procedures, (2) explanation of treatment side
effects, and (3) child and family support. Because this is most often a disease of adolescents and young adults,
the nurse must have an appreciation of their psychologic needs and reactions during the diagnostic and
treatment phases.

Non-Hodgkin Lymphoma

Non-Hodgkin lymphoma occurs more frequently in children than HL. Histologic classification of childhood NHL
is strikingly different from that of HL, as demonstrated in the following statements:

• The disease is usually diffuse rather than nodular.

• The cell type is either undifferentiated or poorly differentiated.
• Dissemination occurs early, more often, and rapidly.
• Mediastinal involvement and invasion of meninges are common.
NHL exhibits a variety of morphologic, cytochemical, and immunologic features, similar to the diversity seen in
leukemia. Classification is based on the histologic pattern: (1) lymphoblastic, (2) Burkitt or non-Burkitt, or (3)
large cell. Immunologically, these cells are also classified as T cells; B cells; or non-T, non-B cells (lacking
immunologic properties). The clinical staging system used in HL is of little value in NHL, although it has been
modified, and other systems have been developed.

Diagnostic Evaluation. Because the clinical presentation of most children with NHL is widespread
disseminated disease, thorough pathologic staging is unnecessary. Clinical manifestations depend on the
anatomic site and extent of involvement. These manifestations include many of those seen in Hodgkin disease
and leukemia, as well as organ symptoms related to pressure from enlargement of adjacent lymph nodes, such
as intestinal or airway obstruction, cranial nerve palsies, and spinal paralysis. Recommendations for staging
include a surgical biopsy of an enlarged node, histopathologic confirmation of disease with cytochemical and
immunologic evaluation, bone marrow examination, radiographic studies (especially tomograms of the lungs
and GI organs), and lumbar puncture.

Therapeutic Management. The treatment protocols for NHL include aggressive use of irradiation and
chemotherapy. Similar to leukemic therapy, the protocols include induction, consolidation, and maintenance
phases, some with intrathecal chemotherapy. Several antineoplastic agents used in the treatment of NHL
include vincristine, prednisone, L-asparaginase, methotrexate, 6-mercaptopurine, cytarabine,
cyclophosphamide, anthracyclines, and teniposide or etoposide. Chemotherapy is the main component of
treatment for NHL in children (Gross and Perkins, 2011). Prognosis. The prognosis is excellent for children
with NHL. In developed countries, more than 80% of children with NHL are now cured with modern therapy,
even patients with widely disseminated disease (Gross and Perkins, 2011).

C. WILMS TUMOR

Wilms tumor, or nephroblastoma, is the most common malignant renal and intra-abdominal tumor of
childhood. The incidence is estimated to be 8.0 cases per million children. Approximately 500 new cases are
diagnosed each year in the United States, with 6% involving both kidneys (Cendren and Gomez, 2010).Wilms
tumor occurs about three times more often in African Americans than in East Asians in the United States. The
peak age at diagnosis is approximately 3 years, and occurrence is slightly more frequent in boys than in girls.
The majority of patients with Wilms tumor are diagnosed at younger than 5 years of age, with 1% to 2.5% having
a familial origin. Unfortunately, there is no method of identifying gene carriers at this time.

CLINICAL MANEFESTATIONS:

Abdominal swelling or mass:

• Firm
• Nontender
• Confined to one side

Hematuria (less than one fourth of cases)

Fatigue and malaise Hypertension (occasionally)
Weight loss
Fever

Manifestations resulting from compression of tumor mass Secondary metabolic alterations from tumor or
metastasis If metastasis, symptoms of lung involvement:
• Dyspnea
• Cough
• Shortness of breath
• Chest pain (sometimes)

Diagnostic Evaluation. In a child suspected of having Wilms tumor, special emphasis is placed on the history
and physical examination for the presence of congenital anomalies, a family history of cancer, and signs of
malignancy (e.g., weight loss, size of liver and spleen, indications of anemia, lymphadenopathy). Most children
with Wilms tumor are brought to the practitioner because of abdominal swelling or an abdominal mass. Specific
tests include radiographic studies, including abdominal ultrasonography and abdominal and chest computed
tomography scan; hematologic studies; biochemical studies; and urinalysis. Studies to demonstrate the
relationship of the tumor to the ipsilateral kidney and the presence of a normal, functioning kidney on the
contralateral side are essential. If a large tumor is present, an inferior venacavogram is necessary to
demonstrate possible tumor involvement adjacent to the vena cava. A bone marrow aspiration may be
performed to rule out metastasis, which is rare in children with Wilms tumor.

STAGING OF WILMS TUMOR

• Stage I—Tumor is limited to kidney and completely resected.
• Stage II—Tumor extends beyond kidney but is completely resected.
• Stage III—Residual nonhematogenous tumor is confined to abdomen.
• Stage IV—Hematogenous metastases; deposits are beyond stage III, namely, to lung, liver, bone, and
brain.
• Stage V—Bilateral renal involvement is present at diagnosis

Therapeutic Management. Combined treatment with surgery and chemotherapy with or without radiation is
based on the histologic pattern and clinical stage

Nursing Care Management. Nursing care of the child with Wilms tumor is similar to that of children with other
cancers treated with surgery, irradiation, and chemotherapy. However, there are some significant differences;
these are discussed for each phase of nursing intervention

D. BRAIN TUMORS

Brain tumors are the most common solid tumor in children and are the second most common childhood cancer.
In children, the use of reference terms benign or malignant is generally avoided because any tumor, despite its
nature, can be fatal or associated with significant morbidities in the developing brain of a child.

Diagnostic Evaluation. The signs and symptoms of brain tumors are directly related to their anatomic location
and size and, to some extent, the child’s age.
Diagnosis of a brain tumor is based subjectively on presenting clinical signs, objectively on neurologic tests,
along with surgical confirmation of the histologic diagnosis. A number of tests may be used in the neurologic
evaluation, but the most common diagnostic procedure is MRI, which determines the location and extent of the
tumor. Other tests that may be used include CT, angiography, EEG, and lumbar puncture. CT or MRI is routinely
performed before a lumbar puncture procedure to identify intracranial abnormalities that may cause a
contraindication to the procedure (Lin and Safdieh, 2010). Lumbar puncture is dangerous in the presence of
increased ICP because of the possibility of brainstem herniation after a sudden release of pressure. The
definitive diagnosis of a brain tumor is based on brain tissue specimens obtained during surgery.
Therapeutic Management. Treatment may involve the use of surgery, radiotherapy, and chemotherapy or a
combination of these treatment modalities. The optimum treatment is complete surgical resection of the primary
tumor with preservation of adequate neurologic function. Radiation therapy is an integral part of treatment for
many brain tumors but can cause significant neurocognitive side effects as well as endocrinopathies. Because
rapid brain development occurs during the first 3 years of life, radiation therapy, particularly craniospinal
radiation, is avoided in children younger than 3 years of age. Chemotherapy may be used as primary treatment
or in an effort to delay radiation therapy until patients are older and may experience fewer neurocognitive side
effects

Nursing Care Management. If a brain tumor is suspected in a child admitted to the hospital for cerebral
dysfunction, establishing baseline data with which to compare preoperative and postoperative changes is an
essential step. It also allows the nurse to assess the degree of physical incapacity and the family’s emotional
reaction to the diagnosis. Vital signs, including blood pressure and pulse pressure (the difference between
systolic and diastolic pressures), are taken routinely and more often when any change is noted. Any sudden
variations are reported immediately. Observation for symptoms of Cushing triad—a hallmark sign of increased
ICP, which includes bradycardia, hypertension, and irregular respirations—is a crucial role of the nurse. It is
also important to note a change in vital signs during or after diagnostic procedures. A routine neurologic
assessment is performed at the same time as vital signs, and head circumference should be measured for
infants and very young children. The child is observed for evidence of headache, vomiting, and any seizure
activity. The location, severity, and duration of the headache are noted, as well as its relationship to activity,
time of day, and any associated factors. Behaviors such as lying flat and facing away from light or refusing to
engage in play are clues to discomfort in nonverbal children. The child’s gait is observed at least once daily.
Head tilt while talking or performing an activity as well as other changes in posturing should always be
documented.

TREATMENT MODALITIES

• Aimed towards:
– CURE - free of disease after treatment → normal life
– Control - Goal for chronic cancers
– Palliative Care: Quality of life maintained at highest level for the longest possible time
• Surgery – surgical removal of tumors; most commonly used treatment
• Preventive or prophylactic
• Diagnostic surgery
• Curative surgery
• Reconstructive surgery
• Palliative surgery
• Chemotherapy – use of antineoplastic drugs to
promote tumor cell death, by interfering with
cellular functions and reproduction
• Radiotherapy – directing high-energy ionizing radiation to destroy malignant tumor cells without harming
surrounding tissues

Types:
– Teletherapy (external): radiation delivered in uniform dose to tumor; Teletherapy is external beam irradiation
and uses a device located at a distance from the patient. It produces X-rays of varying energies and is
administered by machines a distance from the body 31½ to 39 inches (80 to 100 cm).
– Brachytherapy: delivers high dose to tumor and less to other tissues; radiation source is placed in tumor or
next to it; In brachytherapy, the radiation device is placed within or close to the target tissue. Radiation is
delivered in a high dose to a small tissue volume with less radiation to adjacent normal tissue, but requires
direct tumor access.
• Immunotherapy – use of chemical or microbial agents to induce mobilization of immune defenses.
• Biologic response modifiers (BRMs) – use of agents that alters immunologic relationship between tumor
and host in a beneficial way
• Bone marrow peripheral stem cell transplantation – aspirating bone marrow cells from compatible donor
and infusing them into the recipient
• Gene therapy – transfer of genetic materials into the client’s DNA

NURSING MANAGEMENT

1. Promote measures that relieve pain and discomfort.

• Pharmacologic and non-pharmacologic interventions
2. Promote measures to maintain intact skin integrity
3. Promote measures that maintain oral mucosa
4. Promote measures to prevent injury from abnormal bleeding
• Monitor platelet count; avoid aspiring products, etc

NURSING MANAGEMENT

1. Promote measures that identify and prevent infection

• Monitor WBC count; encourage frequent handwashing and overall cleanliness
2. Help decrease the client’s fatigue and increase his activity level
3. Promote measures that ensure adequate nutritional intake
• High protein, high calorie diet
4. Ensure adequate fluid and electrolyte balance

NURSING MANAGEMENT

1. Promote measures to enhance body image.

• Take an honest gentle, caring approach; encourage client to express and verbalize feelings
2. Promote measures that address preventing complications of cancer therapy
3. Instruct client and family about the disease process and treatments; provide necessary information for self-
care.
4. Help client and family cope effectively
5. Promote measures to reduce social isolation.

Care of Clients Receiving Chemotherapy

• Classes of Chemotherapy Drugs:

• Alkylating agents:
– Action: create defects in tumor DNA
– Ex: Nitrogen Mustard, Cisplatin
– Toxic Effects: reversible renal tubular necrosis
Classes of Chemotherapy Drugs
• Antimetabolites:
– Action: phase specific
– Ex: Methotrexate; 5 fluorouracil
– Toxic Effects: nausea, vomiting, stomatitis, diarrhea, alopecia, leukopenia

Classes of Chemotherapy Drugs

• Antitumor Antibiotics:
– Action: non- phase specific; interfere with DNA
– Ex: Actinomycin D, Bleomycin, adriamycin (doxorubicin)
– Toxic Effect: damage to cardiac muscle

• Miotic inhibitors:
– Action: Prevent cell division during M phase of cell division
– Ex: Vincristine, Vinblastine
– Toxic Effects: affects neurotransmission, alopecia, bone marrow depression

• Hormones:
– Action: stage specific G1
– Ex: Corticosteroids

• Hormone Antagonist:
– Action: block hormones on hormone- binding tumors ie: breast, prostate, endometrium; cause tumor
regression
– Ex: Tamoxifen (breast); Flutamide (prostate)
– Toxic Effects: altered secondary sex characteristics

Effects of Chemotherapy
• Tissues: (fast growing) frequently affected
• Examples: mucous membranes, hair cells, bone marrow, specific organs with specific agents, reproductive
organs (all are fetal toxic; impair ability to reproduce)

Chemotherapy Administration

• Routes of administration:
– Oral
– Body cavity (intraperitoneal or intrapleural)
– Intravenous
• Use of vascular access devices because of threat
of extravasation (leakage into tissues) & long term
therapy
• Types of vascular access devices:
– PICC lines: (peripherally inserted central catheters)
– Tunneled catheters: (Hickman, Groshong)
– Surgically implanted ports: (accessed with 90o angle needle- Huber needles)

NURSING CARE OF CLIENTS RECEIVING CHEMOTHERAPY

• Assess and manage:
– Toxic effects of drugs (report to physician)
–Side effects of drugs: manage nausea and vomiting, inflammation and ulceration of mucous membranes, hair
loss, anorexia, nausea and vomiting with specific nursing and medical interventions
• Monitor lab results (drugs withheld if blood counts seriously low); blood and blood product administration
• Assess for dehydration, oncologic emergencies
• Teach regarding fatigue, immunosuppression precautions
• Provide emotional and spiritual support to clients and families

• M. Hockenberry, D. Wilson (2013). Wong’s Essentials of Pediatric Nursing 9th Edition

• Devakumar (2019). Oxford Textbook of Global Health of Women, Newborns, Children, and Adolescents.
PB Publishing.
• Hockenberry (2019). Wong’s Nursing Care of Infants and Children, 11th edition. Elsevier. Leifer (2019).
• Introduction to Maternity and Pediatric Nursing, 8 th edition. Elsevier. Murray (2019).
• Foundations of Maternal-Newborn and Women’s Health Nursing, 7th edition. Elsevier. Flagg (2018).
• Maternal and Child Health Nursing: Care of the Childbearing and Chilrearing Family. Wolters Kluwer

1. Create a summary table consisting of definition, etiology, manifestations, diagnosis, treatment and
management for the following: (100pts)

a. ALTERATIONS WITH INFECTIOUS, INFLAMMATORY AND IMMUNOLOGIC RESPONSES

• Juvenile Rheumatoid Arthritis

• Allergic Rhinitis
• Eczema
• Asthma

b. CELLULAR ABERRATIONS

• Leukemia
• Lymphomas
• Wilms’ tumor
• Brain tumors
BACHELOR OF SCIENCE IN NURSING:
CARE OF MOTHER AND CHILD AT RISK OR
WITH PROBLEMS (ACUTE AND CHRONIC)
COURSE MODULE COURSE UNIT WEEK
3 12 14

Alterations in Nutrition and Gastrointestinal,

Metabolism & Endocrine

Read course and unit objectives

Read study guide prior to class attendance
Read required learning resources; refer to unit
terminologies for jargons
Proactively participate in classroom discussions
Participate in weekly discussion board (Canvas)
Answer and submit course unit tasks

At the end of this unit, the students are expected to:

Cognitive:
1. Identify the different signs and symptoms associated with GIT problems
2. Discuss the different GIT problem seen in pediatric clients
3. Describe the characteristics of infants that affect their ability to adapt to fluid loss or gain
 4. Discuss the pathophysiologic processes associated with specific gastrointestinal disorders
5. Identify the nursing interventions necessary to provide education needed to care for a child
with gastrointestinal disorders.
6. Describe the common diagnostic tests used in the diagnosis and treatment of gastrointestinal
disorders.
7. Identify and describe the different Metabolic and Endocrine Disorders.
8. Summarize signs and symptoms that may indicate a disorder of the endocrine system.
9. Differentiate among the various categories of diabetes mellitus.
10. Discuss the management and nursing care of the child with diabetes mellitus in the acute care
setting
Affective:
• Listen attentively during class discussions
• Demonstrate tact and respect when challenging other people’s opinions and ideas
• Accept comments and reactions of classmates on one’s opinions openly and graciously.
• Develop heightened interest in studying Nursing Informatics
Psychomotor:
1. Participate actively during class discussions and group activities
2. Express opinion and thoughts in front of the class

Hockenberry, M. and Wilson, D. (2015). Wong’s Nursing Care of Infants and Children 1st Philippine
Edition, The Child with Gastrointestinal Dysfunction (Volume 2, pp. 1051-1121). Mosby.

PROBLEMS IN NUTRITION AND GASTROINTESTINAL

The gastrointestinal (GI) system involves a long body tract and numerous organs. Because it is so long
and diverse, a multitude of possible disorders can occur along it, including both congenital disorders and
acquired illnesses. Because the GI system is responsible for taking in and processing nutrients for all
parts of the body, any problem with the system can quickly affect other body systems and, if not
adequately treated, can affect overall health, growth, and development.

CLEFT LIP/ PALATE

Cleft lip and cleft palate are two distinct facial defects that can occur singly or in combination. Cleft lip
with or without cleft palate occurs in 1 out of every 750 to 1000 live births. The incidence is higher in
Asian (1 in 500) than in White children (1 in 750). The defect is less common in African Americans, with
an incidence of 1 of every 2000 live births. Cleft lip and palate occur together in approximately 45% of
cases, while cleft palate occurs alone approximately 35% of the time, and cleft lip occurs alone
approximately 20% of the time.
Cleft lip with or without cleft palate results when the maxillary processes fail to fuse with the elevations
on the frontal prominence during the sixth week of
gestation. Normally, union of the upper lip is complete
by the seventh week. Fusion of the secondary palate
occurs between 5 and 12 weeks of gestation. Failure of
the tongue to move downward at the correct time
prevents the palatine processes from fusing. The
intrauterine development of the hard and soft palates is
completed in the first trimester. It is during this time that
other major organ systems develop. Approximately
30% of children with cleft and/or palate will have
another congenital anomaly. There is an increased
incidence in families with a prior history of cleft lip or
palate. The cause is believed to be multifactorial,
involving a combination of environmental and genetic influences. Etiologic factors include smoking during
pregnancy, maternal use of alcohol, and use of medications such as anticonvulsants and steroids during
pregnancy.
A cleft that involves the lip is readily apparent at birth. It may be a simple dimple in the vermilion
border of the lip or a complete separation extending to the floor of the nose. The defect may be unilateral
or bilateral and may occur alone or in combination with a cleft palate defect. Varying degrees of nasal
deformity may also be present. Cleft palate defects are less obvious when they occur without a cleft lip
and may not be detected at birth. Clefts of the hard palate form a continuous opening between the mouth
and nasal cavity and may be unilateral or bilateral, involving just the soft palate or both the soft and hard
palates.
Cleft lip and palate are usually diagnosed at birth or during the newborn assessment, but may be
diagnosed in utero. Successful imaging of the face via transabdominal ultrasound can be performed as
early as 13 to 14 weeks’ gestation. Use of three-dimensional ultrasound or magnetic resonance imaging,
if available, allows for a clearer picture of the defect and enhances the ability to detect isolated cleft palate
prenatally. After the child is born, cleft lip and cleft palate are diagnosed by characteristic physical
findings. The upper lip, alveolar arches, nostrils, and primary and secondary palates should be inspected
and palpated.
Management is directed toward closure of the cleft(s), prevention of complications, and facilitation of
normal growth and development in the child. Cleft lip repair typically occurs at most centers between 2
and 3 months of age. Most physicians adhere to the “rule of tens”: the infant must be 10 weeks old, weigh
10 pounds, and have a hemoglobin of 10. The two most common procedures for repair of CL are the
Tennison-Randall triangular flap (Z-plasty) and the Millard rotational advancement technique. The
difference between these two is that the Tennison-Randall procedure crosses the philtral line and the
Millard procedure advances a triangle of tissue in the upper third of the lip and does not cross the midline.
Surgeons often use a combination of these two techniques to address individual differences. Cleft palate
repair typically occurs between 6 and 12 months. There is concern that early CP repair interferes with
skeletal growth of the midface, but postponing palate closure beyond the child’s first words may result in
increased speech disorders. The most common techniques to repair CP include the Veau-Wardill-Kilner
V-Y pushback procedure and the Furlow double-opposing Z-plasty. Approximately 20% to 30% of
children with repaired CP will need a secondary surgery to improve velopharyngeal closure for speech.
Secondary procedures may include palatal lengthening, pharyngeal flap, sphincter pharyngoplasty, or
posterior pharyngeal wall augmentation.
 Children with CL may require multiple surgeries to achieve optimal aesthetic outcomes but are not at
risk for increased speech problems. Although some children with CP and CL/P do not require speech
therapy, many have some degree of speech impairment that requires speech therapy at some point
throughout childhood. Articulation errors result from a history of velopharyngeal dysfunction, incorrect
articulatory placement, improper tooth alignment, and varying degrees of hearing loss. Improper drainage
of the middle ear as a result of inefficient function of the Eustachian tube relating to the history of CP
contributes to recurrent otitis media, which leads to conductive hearing loss in many children with CP;
many children with clefts will have pressure-equalization tubes placed. Extensive orthodontics and
prosthodontics may be needed to correct malposition of the teeth and maxillary arches. Academic
achievement, social adjustment, and behavior should be monitored, particularly in children with
syndromic cleft conditions.
Feeding the infant with a cleft presents a challenge to nurses and parents. Growth failure in infants
with CL/P or CP has been attributed to preoperative feeding difficulties. After surgical repair, most infants
who have isolated CL, CP, or CL/P with no associated syndromes gain weight or achieve adequate
weight and height for age. Post-operative care for infants include:
• Assess vital signs frequently and maintain the infant’s airway.
• Measure intake and output.
• Prevent aspiration through proper positioning during and after feeding.
• Prevent the infant from rubbing the suture line on the bedding by positioning the infant in a supine
position.
• Maintain soft elbow immobilizers.
• Maintain the suture line or Steri-Strips placed over the incision. Place antibiotic body ointment on
the incision site as ordered.
• Medicate the infant as prescribed to control pain and to minimize crying and stress on the suture
line.
• After cleft palate surgery, avoid the use of metal utensils or straws, which may disrupt the surgical
site.
Throughout the child’s development, an important goal is the development of a healthy personality
and self-esteem. Many communities have CP parents’ groups that offer help and support to families.
Agencies that provide services and information for children with CL/P and their families.

HIRSCHSPRUNG DISEASE
Hirschsprung disease, also known as congenital aganglionic
megacolon, is a congenital anomaly in which inadequate motility
causes mechanical obstruction of the intestine. The disease
occurs in approximately 1 in 5000 live births, and is more
common in males than females. Hirschsprung disease can occur
as a single anomaly or in combination with other anomalies such
as congenital heart defects, Down syndrome, and urinary tract
anomalies.
Hirschsprung disease is the congenital absence of ganglion
cells (nerve cells) in the wall of a variable segment of rectum and
colon. The absence of autonomic parasympathetic ganglion
cells in the colon prevents peristalsis at that portion of the
intestine, resulting in the accumulation of intestinal contents and abdominal distention. In most cases, the
area lacking ganglion cells is limited to the rectosigmoid region of the colon.
Clinical manifestations of Hirschsprung disease vary depending on the child’s age at onset.
Symptoms in newborns generally include abdominal distention, feeding intolerance, bilious vomiting, and
failure to pass meconium within the first 24 to 48 hours after birth. Enterocolitis (inflammation of the
intestines) is a complication of Hirschsprung disease that can be fatal if not recognized and treated early.
Symptoms of enterocolitis include fever, foul smelling and/or bloody diarrhea (frequent, watery stools),
abdominal pain, and vomiting. The older infant or child may have a history of failure to gain weight,
malnutrition, and chronic severe constipation (difficult and infrequent defecation with passage of hard,
dry stool).
Diagnosis is made on the basis of the history, bowel patterns, radiographic contrast studies, and
rectal biopsy for presence or absence of ganglion cells. The rectum is small in size on palpation and does
not contain stool. Abdominal radiographs generally show a distended bowel with dilated bowel loops
throughout the abdomen. Water-soluble contrast studies reveal a transition zone between the normal
and aganglionic bowel.
The primary repair of Hirschsprung disease is to remove the aganglionic portion of the bowel using a
pull-through procedure. A primary repair may not be possible in the presence of extensive dilated
proximal bowel, enterocolitis, or bowel perforation. In that case, a temporary colostomy is created and is
closed when the definitive surgery takes place. nger, 2013). The return of normal bowel function depends
on the amount of bowel involved. Some fecal incontinence and constipation may persist following surgery.
Enterocolitis is a serious complication that can occur before or after surgery, resulting in ischemia and
ulceration of the bowel wall. Treatment for enterocolitis associated with Hirschsprung disease includes
rectal irrigations and antibiotics.
Nursing care includes monitoring for infection, managing pain, maintaining hydration, measuring
abdominal circumference to detect any distention, and providing support to the child and family.

INTUSSUSCEPTION
Intussusception is the most common cause of intestinal
obstruction in children between the ages of 3 months and 3 years.
Intussusception is more common in boys than in girls and is more
common in children with cystic fibrosis. Although specific intestinal
lesions occur in a small percentage of the children, generally the
cause is not known. More than 90% of intussusceptions do not have
a pathologic lead point, such as a polyp, lymphoma, or Meckel
diverticulum. The idiopathic cases may be caused by hypertrophy of
intestinal lymphoid tissue secondary to viral infection.
Intussusception occurs when one segment of the bowel
telescopes into another segment, pulling the mesentery with it. The
mesentery is compressed and angled, resulting in lymphatic and
venous obstruction. As the edema from the obstruction increases,
pressure within the area of intussusception increases. When the
pressure equals the arterial pressure, arterial blood flow stops,
resulting in ischemia and the pouring of mucus into the intestine.
Venous engorgement also leads to leaking of blood and mucus into
the intestinal lumen, forming the classic currant jelly–like stools. The
most common site is the ileocecal valve (ileocolic), where the ileum invaginates into the cecum and then
further into the colon. Other forms include ileoileal (one part of the ileum invaginates into another section
of the ileum) and colocolic (one part of the colon invaginates into another area of the colon)
intussusceptions, usually in the area of the hepatic or splenic flexure or at some point along the transverse
colon.
Frequently, subjective findings lead to the diagnosis (abdominal pain, abdominal mass, bloody
stools), which can be confirmed by ultrasonography. Spontaneous reduction occurs in up to 10% of
patients.
Conservative treatment consists of radiologist-guided pneumo-enema (air enema) with or without
water-soluble contrast or ultrasound guided hydrostatic (saline) enema, the advantage of the latter being
that no ionizing radiation is needed. Intravenous fluids, NG decompression, and antibiotic therapy may
be used before hydrostatic reduction is attempted. If these procedures are not successful, the child may
require surgical intervention. Surgery involves manually reducing the invagination and, when indicated,
resecting any nonviable intestine. Laparoscopic surgical repair is commonly performed.

ACUTE APPENDICITIS
Appendicitis is an inflammation of the vermiform appendix, the small sac near the end of the cecum,
and is the most common cause of emergency surgery in children. The condition occurs most often in
children and adolescents ages 10 to 19 years. While the overall rate of perforated appendix is 20% to
35%, the rate in children less than 3 years of age is 80% to 100% as compared to 10% to 20% in children
10 to 17 years of age (Minkes & Alder, 2014).
Appendicitis almost always results from an obstruction in the appendiceal lumen. It can be caused by
a fecalith (hard fecal mass), parasitic infestations, stenosis, hyperplasia of lymphoid tissue, or a tumor.
Continued secretion of mucus following acute obstruction of the lumen increases pressure, causing
ischemia, cellular death, and ulceration. The appendix may perforate or rupture, resulting in fecal and
bacterial contamination of the peritoneum. Peritonitis spreads quickly and if untreated can result in small
bowel obstruction, electrolyte imbalances, septicemia, and hypovolemic shock.
At onset, symptoms include periumbilical cramps, abdominal tenderness, anorexia, nausea, and
fever. As the inflammation progresses, pain in the right lower abdomen becomes constant. Pain is often
most intense at the McBurney point, halfway between the anterior superior iliac crest and the umbilicus.
Symptoms progress to include guarding, rigidity, nausea, vomiting, onset of pain before vomiting,
anorexia, and rebound tenderness following palpation over the right lower quadrant. As appendicitis
progresses, the child remains motionless, usually in a side-lying position with knees flexed. Sudden relief
of pain usually means that the appendix has perforated.
Diagnosis of appendicitis in young children can be difficult because their pain may be less localized
and their symptoms more diffuse than in the older child. Continuing evaluations over several hours are
often needed to establish the diagnosis. The presence of an elevated white blood cell count (above
10,000/mm3 ), increased neutrophil ratio, and an elevated C-reactive protein combined with the
symptoms supports a diagnosis of appendicitis. A white blood cell count greater than 15,000/mm3 in a
patient with appendicitis is a strong indicator that the appendix has perforated. Abdominal ultrasound is
preferred as the initial screening tool in the diagnosis of appendicitis; however, CT scans are more
sensitive and may be used, especially when the appendix cannot be seen well on ultrasound or the
results are inconclusive.
Treatment of uncomplicated appendicitis involves immediate surgical removal (appendectomy),
generally through a laparoscopic appendectomy. Preoperatively, the child is kept NPO. Intravenous fluids
and electrolytes, and antibiotics are administered. Postoperatively, the child has an abdominal incision
with a dressing covering the incision. Antibiotics may be administered. The child is generally discharged
within 24 to 36 hours as long as they have adequate oral intake, are afebrile, and receive effective pain
relief with oral pain medication. With perforated appendix, laparoscopic appendectomy is generally
performed. Postoperatively, the child with a perforated appendix may have a nasogastric tube to
decompress the abdomen and will remain NPO until signs of bowel function return. Bowel function is best
indicated by the passage of flatus or stool. The child will also have a peripheral or temporary central line
for administration of intravenous fluids and medications. After surgery for a perforated appendix, the child
will receive antibiotics for several days. Morphine is generally given for pain.

ESOPHAGEAL ATRESIA (EA)/ TRACHEOESOPHAGEAL FISTULA (TEF)

Congenital esophageal atresia and
tracheoesophageal fistula are rare malformations that
represent a failure of the esophagus to develop as a
continuous passage and a failure of the trachea and
esophagus to separate into distinct structures. These
defects may occur as separate entities or in combination,
and without early diagnosis and treatment, they pose a
serious threat to the infant’s well-being. The defect affects
occurs in approximately 1 in 4500 neonates. At least 90%
of those affected also have a tracheoesophageal fistula.
The cause of EA/ TEF is unknown. In esophageal
atresia, the foregut fails to lengthen, separate, and fuse
into two parallel tubes (the esophagus and trachea) during
fetal development. Instead the esophagus may end in a
blind pouch or develop as a pouch connected to the
trachea by a fistula. Esophageal atresia is often
associated with a maternal history of polyhydramnios.
Symptoms in the newborn include excessive salivation
and drooling, often accompanied by three classic signs for
this defect: cyanosis, choking, and coughing. Sneezing may also be noted. During feeding, fluid returns
through the infant’s nose and mouth. Aspiration places the infant at risk for pneumonia. Depending on
the type of defect, the infant’s abdomen may be distended because of air trapping.
Esophageal atresia is suspected based on the presence of polyhydramnios and a small or absent
fetal gastric bubble noted on prenatal ultrasound. After the child is born, a radiopaque catheter is inserted
into the hypopharynx and advanced until it encounters an obstruction. Chest radiographs are taken to
ascertain esophageal patency or the presence and level of a blind pouch. Sometimes fistulas are not
patent, which makes them more difficult to diagnose. The presence of gas in the stomach or small bowel
is indicative of a coexisting TEF.
Primary repair is preferred when possible and involves connecting the two ends of the esophagus
and ligating the fistula if present. If primary repair of the esophageal atresia is not possible in the neonatal
period, a gastrostomy tube is placed for feedings and the fistula is ligated.
Esophageal atresia is a surgical emergency. Preoperatively the infant requires close observation and
intervention to maintain a patent airway. Specific interventions include:
• Have suction readily available to remove any secretions that accumulate in the nasopharyngeal
 airway.
• Place the infant with the head of the bed slightly elevated to minimize aspiration of secretions into
the trachea.
• Use continuous or low intermittent suction to remove secretions from the blind pouch.
• Withhold oral fluids, and provide maintenance intravenous fluids.
• Constantly monitor the infant’s vital signs and overall condition.
After surgery administer intravenous fluids and antibiotics. Monitor strict intake and output. Total
parenteral nutrition may be needed until gastrostomy or oral feedings are tolerated. Monitoring and
assessment of feeding tolerance are ongoing. Feedings are introduced slowly and in small amounts.

PYLORIC STENOSIS
Hypertrophic pyloric stenosis (HPS) occurs when the
circumferential muscle of the pyloric sphincter becomes
thickened, resulting in elongation and narrowing of the pyloric
channel. This produces an outlet obstruction and
compensatory dilation, hypertrophy, and hyperperistalsis of
the stomach. This condition usually develops in the first 2 to 5
weeks of life, causing projectile nonbilious vomiting,
dehydration, metabolic alkalosis, and growth failure. The
precise etiology is unknown. The reported incidence is 1 to 3
per 1000 live births with a male-to-female ratio of 4 to 6 :1.
There is a genetic predisposition, and siblings and offspring of
affected persons are at increased risk of developing HPS. It is
more common in full-term than in preterm infants and is seen
less frequently in African-American and Asian infants than in
white infants.
The circular muscle of the pylorus thickens as a result of hypertrophy (increased size) and hyperplasia
(increased mass). This produces severe narrowing of the pyloric canal between the stomach and the
duodenum, causing partial obstruction of the lumen. Over time, inflammation and edema further reduce
the size of the opening, resulting in complete obstruction. The hypertrophied pylorus may be palpable as
an olivelike mass in the upper abdomen. Pyloric stenosis is not a congenital disorder. Substantial
evidence supports decreased expression of neuronal nitric oxide synthase in the nerve fibers of the
pyloric circular muscle in infants with HPS.
Symptoms usually become evident 2 to 8 weeks after birth, although onset may vary (Taylor et al.,
2013). Initially, the infant appears well or regurgitates slightly after feedings. The parents may describe
the infant as a “good eater” who vomits occasionally. As the obstruction progresses, the vomiting
becomes projectile. In projectile vomiting, the contents of the stomach may be ejected up to 3 feet from
the infant. The vomitus is nonbilious and may become blood tinged because of repeated irritation to the
esophagus. The infant generally appears hungry, especially after emesis; irritable; fails to gain weight;
and has fewer and smaller stools. The child may present with dehydration and metabolic alkalosis
depending on how long the child has been vomiting. On physical examination, peristaltic waves may be
observed across the abdomen as the stomach attempts to move contents past the narrowed pyloric
canal. An olive-sized mass in the right upper quadrant may be evident.
An abdominal ultrasound to determine the diameter and length of the pyloric muscle is the preferred
method performed to confirm the diagnosis. Blood tests will determine if the child is dehydrated or has
an electrolyte or acid–base imbalance. Infants with pyloric stenosis are at risk for hypochloremia,
hypokalemia, and metabolic alkalosis; however, recent studies show that normal laboratory values are
found most often. This could be attributed to earlier diagnosis and the increased use of ultrasound to
confirm the diagnosis.
Surgery is performed as soon as possible after the infant’s fluid and electrolyte balance is restored.
Laparoscopic pyloromyotomy is the preferred surgical method to correct pyloric stenosis. The prognosis
is good. The infant is usually taking fluids within a few hours following surgery and discharged on full-
strength formula within 24 hours after surgery.
Nursing care management includes meeting the infant’s fluid and electrolyte needs, minimizing weight
loss, promoting rest and comfort, preventing infection, and providing supportive care for parents.

IMPERFORATED ANUS
Imperforate anus includes several forms of malformation without an obvious opening. Frequently a
fistula leads from the distal rectum to the perineum or genitourinary system. The fistula may be evidenced
when mecomium is evacuated through the vaginal opening, the perineum below the vagina, the male
urethra, or the perineum under the scrotum. The presence of meconium on the perineum does not
indicate anal patency. A fistula may not be apparent at birth, but as peristalsis increases, meconium is
forced through the fistula into the urethra or onto the newborn’s perineum.
The anus and rectum originate from an embryologic structure called the cloaca. Lateral growth of the
cloaca forms the urorectal septum that separates the rectum dorsally from the urinary tract ventrally. The
rectum and urinary tract separate completely by the seventh week of gestation. Anomalies that occur
reflect the stage of development of these processes. Rectal atresia and stenosis occur when the anal
opening appears normal, there is a midline intergluteal
groove, and usually no fistula exists between the rectum
and urinary tract. Rectal atresia is a complete obstruction
(inability to pass stool) and requires immediate surgical
intervention. Rectal stenosis may not become apparent
until later in infancy when the infant has a history of
difficult stooling, abdominal distention, and ribbonlike
stools.
The diagnosis of an anorectal malformation is based
on the physical finding of an absent anal opening. Other
symptoms may include abdominal distention, vomiting,
absence of meconium passage, or presence of
meconium in the urine. Additional physical findings with
an anorectal malformation are a flat perineum and the
absence of a midline intergluteal groove. The appearance
of the perineum alone does not accurately predict the extent of the defect and associated anomalies.
The primary management of anorectal malformations is surgical. After the defect has been identified,
take steps to rule out associated life-threatening defects, which need immediate surgical intervention.
Provided no immediate life-threatening problems exist, the newborn is stabilized and kept NPO for further
evaluation. IV fluids are provided to maintain glucose and fluid and electrolyte balance. The current
recommendation is that surgery be delayed at least 24 hours to properly evaluate for the presence of a
fistula and possibly other anomalies.
The surgical treatment of anorectal malformations varies according to the defect but usually involves
one or possibly a combination of several of the following procedures: anoplasty, colostomy, posterior
sagittal anorectoplasty (PSARP) or other pull-through with colostomy, and colostomy (take-down)
closure. The first nursing responsibility is assisting in identification of anorectal malformations. A newborn
who does not pass stool within 24 hours after birth or has meconium that appears at a location other than
the anal opening requires further assessment. Preoperative care includes diagnostic evaluation, GI
decompression, bowel preparation, and IV fluids. For the newborn with a perineal fistula, an anoplasty is
performed, which involves moving the fistula opening to the center of the sphincter and enlarging the
rectal opening. Postoperative nursing care after anoplasty is primarily directed toward healing the surgical
site without other complications. A program of anal dilations is usually initiated when the child returns for
the 2-week check-up. Feedings are started soon after surgical repair, and breastfeeding is encouraged
because it causes less constipation.

CELIAC DISEASE (Malabsorption Syndrome)

Celiac disease is a sensitivity or abnormal immunologic response to
protein, particularly the gluten factor of protein found in grains—wheat, rye,
oats, and barley. When children with the disorder ingest gluten, changes
occur in their intestinal mucosa or villi that prevent the absorption of foods,
especially fat, across the intestinal villi into the bloodstream. Celiac
disease, also known as gluten-induced enteropathy, gluten sensitive
enteropathy, and celiac sprue, is a permanent intestinal intolerance to
dietary wheat gliadin and related proteins that produces mucosal lesions
in genetically susceptible individuals. As a result, children develop
steatorrhea (bulky, foul-smelling, fatty stools); deficiency of fat-soluble
vitamins A, D, K, and E (the vitamins are not absorbed because the fat is
not absorbed); malnutrition; and a distended abdomen from the fat, bulky
stools. Because vitamin D is one of the fat-soluble vitamins, rickets or loss
of calcium from bones may occur. Hypoprothrombinemia may occur from loss of vitamin K. In addition,
children may have hypochromic anemia (iron-deficiency anemia) and hypoalbuminemia from poor protein
absorption.
Celiac disease is characterized by villous atrophy in the small bowel in response to the protein
gluten. Gluten is found in wheat, barley, rye, and oat grains. When individuals are unable to digest the
gliadin component of gluten, an accumulation of a toxic substance that is damaging to the mucosal cells
occurs. Damage to the mucosa of the small intestine leads to villous atrophy, hyperplasia of the crypts,
and infiltration of the epithelial cells with lymphocytes. Villous atrophy leads to malabsorption caused by
the reduced absorptive surface area.
Genetic predisposition is an essential factor in the development of celiac disease. Membrane
receptors involved in preferential antigen presentation to CD4+ T cells play a crucial role in the immune
response characteristic of celiac disease. Genes located on the HLA region of chromosome 6, namely
HLA-DQ2 or HLA-DQ8, are found in almost 100% of those affected with celiac disease (Murdock and
Johnston, 2005). When the inflammatory reaction is activated by gluten, CD4+ T cells produce cytokines,
which are likely to contribute to the intestinal damage. The damage consists of infiltration of the lamina
propria, crypt hyperplasia, and villous atrophy and flattening. With sufficient villous atrophy,
malabsorption occurs.
Typically, children are seen with impaired growth, chronic diarrhea, abdominal distention, muscle
wasting with hypotonia, poor appetite, and lack of energy. The clinical manifestations are usually insidious
and chronic. The first evidence may be growth failure and diarrhea.
Less typical presentation has been observed in children ages 5 to 7
years who have abdominal pain; nausea; vomiting; bloating;
constipation; or extraintestinal manifestations, including iron
deficiency anemia, short stature, pubertal delay, dental enamel
defects, alopecia, and abnormal LFT results. Older children have
been found to have osteoporosis. Untreated celiac disease can
evolve into celiac crisis, characterized by abdominal distention,
explosive watery diarrhea, and dehydration with electrolyte
imbalance, leading to hypotensive shock and lethargy.
The diagnosis of celiac disease is based on a biopsy of the
small intestine demonstrating the characteristic changes of villous
atrophy with hyperplasia of the crypts and abnormal surface
epithelium while the patient is eating adequate amounts of gluten and
a full clinical remission after gluten is withdrawn. Within 1 or 2 days of instituting the diet, most children
with celiac disease demonstrate a favorable response, including weight gain and improved appetite.
Within a few weeks, there is resolution of the diarrhea and steatorrhea.
Commercially available serologic tests for celiac disease include antigliadin antibodies of both the
immunoglobulin A and G classes (IgA and IgG); antiendomysium IgA; and antitissue transglutaminase
IgA (anti-TG2) and IgG antibodies for screening first-degree relatives of known celiac disease patients
and those with known celiac disease– associated disorders such as type 1 diabetes, thyroiditis, arthritis,
primary biliary cirrhosis, Down syndrome, Turner syndrome, Williams syndrome, and osteopenia or
osteoporosis. False-positive results are likely when only one serologic test is used because patients with
these disorders can also test positive for these antibodies. Use of more than one test increases diagnostic
accuracy. Ruling out total IgA deficiency is necessary to minimize false-negative results
Treatment is to continue the gluten-free diet for life because there is some suggestion that these
children are more prone to GI carcinoma later in life if they do not continue the diet into adulthood. In
addition to this, children need to have water-soluble forms of vitamins A and D administered. Both iron
and folate may be necessary as well to correct any anemia present.
The main nursing consideration is helping the child adhere to the dietary regimen. This requires
a wheat-, barley-, and rye-free diet; oats may be safe for most patients but contamination with other
gluten products may occur in harvesting; therefore, caution should be exercised with oats. Children who
have silent celiac disease, without clinical manifestations, should also adhere to a strict gluten-free diet.
Considerable time is involved in explaining the disease process to the child and parents, the specific role
of gluten in aggravating the disorder, and the foods that must be restricted. It is difficult to maintain a diet
indefinitely when the child has no symptoms and temporary transgressions result in no difficulties.
However, most individuals who relax their diet will experience a relapse of their disease and possibly
exhibit growth restriction, anemia, or osteomalacia. There is also the risk of developing malignant
lymphoma of the small intestine or other GI malignancies. Although the chief source of gluten is cereal
and baked goods, grains are frequently added to processed foods as thickeners or fillers. To compound
the difficulty, gluten is added to many foods as hydrolyzed vegetable protein, which is derived from cereal
grains. The nurse must advise parents of the necessity of reading all label ingredients carefully to avoid
hidden sources of gluten.
Many of children’s favorite foods contain gluten, including bread, cake, cookies, crackers, donuts,
pies, spaghetti, pizza, prepared soups, some processed ice cream, many types of chocolate candy, milk
preparations such as malts, hot dogs, luncheon meats, meat gravy, and some prepared hamburgers.
Many of these products can be eliminated from an infant’s or young child’s diet easily but monitoring the
diet of a school-age child or adolescent is more difficult. Luncheon preparation away from home is
particularly difficult because bread, luncheon meats, and instant soups are not allowed. For families on
restricted food budgets, the diet adds an additional financial burden because many inexpensive and
convenient foods cannot be used.
In addition to restricting gluten, other dietary alterations may be necessary. For example, in some
children who have more severe mucosal damage, the digestion of disaccharides is impaired, especially
in relation to lactose. Therefore, these children often need a temporarily lactose-free diet, which
necessitates eliminating all milk products. In general, dietary management includes a diet high in calories
and proteins with simple carbohydrates such as fruits and vegetables but low in fats. Because the bowel
is inflamed because of the pathologic processes in absorption, the child must avoid high-fiber foods, such
as nuts, raisins, raw vegetables, and raw fruits with skin, until inflammation has subsided.
It is important to stress long-range complications and to remind parents of the child’s physical
status before dietary treatment and the dramatic improvement after treatment. The nurse can be
instrumental in allowing the child to express concerns and frustration while focusing on ways in which the
child can still feel normal. Encourage the child and parents to find new recipes using suitable ingredients,
such as Mexican or Chinese dishes that use corn or rice. Consult a registered dietitian to provide children
and their families with detailed dietary instructions and education.

PROBLEMS IN METABOLISM AND ENDOCRINE

GROWTH HORMONE DEFICIENCY
If production of human growth hormone (GH, or somatotropin) is deficient, children cannot grow to full
size. As a result, children remain in proportion but well below the average on a standard growth chart.
Deficient production of GH may result from a nonmalignant cystic tumor of embryonic origin that places
pressure on the pituitary gland or from increased intracranial pressure because of trauma. In most
children with hypopituitarism, the cause of the defect is unknown. It may have a genetic origin.
HYPOPITUITARISM (DWARFISM)
Hypopituitarism is diminished or deficient secretion of pituitary hormones. The consequences
of the condition depend on the degree of dysfunction and can lead to gonadotropin deficiency with
absence or regression of secondary sex characteristics; growth hormone (GH) deficiency, in which
children display retarded somatic growth; thyroid-stimulating hormone (TSH) deficiency, which
produces hypothyroidism; and corticotropin deficiency, which results in manifestations of adrenal
hypofunction.
• Congenital Hypopituitarism can be seen in newborn infants, often because of birth trauma.
Symptoms of hypoglycemia and seizure activity often manifest within the first 24 hours
after birth.
• Idiopathic Hypopituitarism, or idiopathic pituitary growth failure, is usually related to GH
deficiency, which inhibits somatic growth in all cells of the body.
Growth failure is defined as an absolute height of less than −2 standard deviation (SD) for age
or a linear growth velocity consistently less than −1 SD for age. When this occurs without the presence
of hypothyroidism, systemic disease, or malnutrition, then an abnormality of the GH–insulin-like
growth factor (IGF-I) axis should be considered. Not all children with short stature have GH deficiency.
In most instances, the cause is either familial short stature or constitutional growth delay. Familial
short stature refers to otherwise healthy children who have ancestors with adult height in the lower
percentiles. Constitutional growth delay refers to individuals (usually boys) with delayed linear growth,
generally beginning as a toddler, and skeletal and sexual maturation that is behind that of age mates.
Typically, these children will reach normal adult height. Often there is a history of a similar pattern of
growth in one of the child’s parents or other family members. The untreated child will proceed through
normal changes as expected based on bone age. Although treatment with GH is not usually indicated,
its use has become controversial, especially in relation to parental and child requests for treatment to
accelerate growth.
Children with hypopituitarism generally grow
normally during the first year and then follow a slowed
growth curve that is below the third percentile. Skeletal
proportions and weight are normal for the age, but these
children may appear younger than their chronologic age.
Dentition is delayed, and teeth may be overcrowded and
malposition because of the undeveloped jaw. Sexual
development is usually delayed but is otherwise normal
unless the gonadotropin hormones are deficient. Growth
may extend into the third or fourth decade of life, but
permanent height is usually diminished if the disorder is
left untreated. Symptoms such as headache and vision changes may indicate the presence of a
tumor.
Only a small number of children with delayed growth or short stature have hypopituitary
dwarfism. Usually, the cause is constitutional delay. Diagnostic evaluation is aimed at isolating
organic causes, which, in addition to GH deficiency, may include hypothyroidism, over-secretion of
cortisol, gonadal aplasia, chronic illness, nutritional inadequacy, Russell-Silver dwarfism, or
hypochondroplasia. A complete diagnostic evaluation should include a family history, a history of the
child’s growth patterns and previous health status, physical examination, psychosocial evaluation,
radiographic surveys, and endocrine studies. Accurate measurement of height (using a calibrated
stadiometer) and weight and comparison with standard growth charts are essential. Multiple height
measures reflect a more accurate assessment of abnormal growth patterns. Parental height and
familial patterns of growth are important clues to diagnosis.
A skeletal survey in children younger than 3 years of age and radiographic examination of the
hand–wrist for centers of ossification (bone age) in older children are important in evaluating growth.
Definitive diagnosis is based on absent or subnormal reserves of pituitary GH. Because GH
levels are variable in children, GH stimulation testing is usually required for diagnosis. Initial
assessment of the serum IGF-I and IGF binding protein 3 (IGFBP3) indicates a need for further
evaluation of GH dysfunction if levels are less than −1 SD below the mean for age. It is recommended
that GH stimulation tests be reserved for children with low serum IGF-I and IGFBP3 levels and poor
growth who do not have other causes for short stature. GH stimulation testing involves the use of
pharmacologic agents such as levodopa, clonidine, arginine, insulin, propranolol, or glucagon to
provoke the release of GH. Children with poor linear growth, delayed bone age, and abnormal GH
stimulation tests are considered GH deficient.
Treatment of GH deficiency caused by organic lesions is directed toward correction of the
underlying disease process (e.g., surgical removal or irradiation of a tumor). The definitive treatment
of GH deficiency is replacement of GH, which is successful in 80% of affected children. Biosynthetic
GH is administered subcutaneously on a daily basis. Growth velocity increases in the first year and
then declines in subsequent years. Final height is likely to remain less than normal (Bryant, Baxter,
Cave, and others, 2007), and early diagnosis and intervention are essential.
The principal nursing consideration is identifying children with growth problems. Even though
most growth problems are not a result of organic causes, any delay in normal growth and sexual
development poses special emotional adjustments for these children. The nurse may be a key person
in helping to establish a diagnosis. Preparation of the child and family for diagnostic testing is
especially important if a number of tests are being performed, and the child requires particular
attention during provocative testing. Blood samples are usually taken every 30 minutes for a 3-hour
period. Children also have difficulty overcoming hypoglycemia generated by tests with insulin, so they
must be observed carefully for signs of hypoglycemia, but those receiving glucagon are at risk of
nausea and vomiting. Clonidine may cause hypotension, requiring administration of intravenous (IV)
fluids.
Children undergoing hormone replacement require additional support. The nurse should
provide education for patient self-management during the school-age years. Nursing functions
include family education concerning medication preparation and storage, injection sites, injection
technique, and syringe disposal.
PITUITARY HYPERFUNCTION (GIGANTISM)
Excess GH before closure of the epiphyseal shafts
results in proportional overgrowth of the long bones until the
individual reaches a height of 2.4 m (8 ft) or more. Vertical
growth is accompanied by rapid and increased
development of muscles and viscera. Weight is increased
but is usually in proportion to height. Proportional
enlargement of head circumference also occurs and may
result in delayed closure of the fontanels in young children.
Children with a pituitary-secreting tumor may also
demonstrate signs of increasing intracranial pressure,
especially headache.
If over-secretion of GH occurs after epiphyseal
closure, growth is in the transverse direction, producing a condition known as acromegaly. Typical
facial features include overgrowth of the head, lips, nose, tongue, jaw, and paranasal and mastoid
sinuses; separation and malocclusion of the teeth in the enlarged jaw; disproportion of the face to the
cerebral division of the skull; increased facial hair; thickened, deeply creased skin; and an increased
tendency toward hyperglycemia and diabetes mellitus (DM). Acromegaly can develop slowly, leading
to delays in diagnosis and treatment.
Diagnosis is based on a history of excessive growth during childhood and evidence of
increased levels of GH. Radiographic studies may reveal a tumor in an enlarged sella turcica, normal
bone age, enlargement of bones (e.g., the paranasal sinuses), and evidence of joint changes.
Endocrine studies to confirm excess of other hormones, specifically thyroid, cortisol, and sex
hormones, should also be included in the differential diagnosis.
If a lesion is present, surgery is performed to remove the tumor when feasible. Other therapies
aimed at destroying pituitary tissue include external irradiation and radioactive implants. New
pharmacologic agents have evolved and may be used in combination with other therapies. Depending
on the extent of surgical extirpation and degree of pituitary insufficiency, hormone replacement with
thyroid extract, cortisone, and sex hormones may be necessary.
 The primary nursing consideration is early identification of children with excessive growth
rates. Although medical management is unable to reduce growth already attained, further growth can
be retarded. The earlier the treatment, the more control there is in predetermining a normal adult
height. Nurses should also observe for signs of a tumor, especially headache, and evidence of
concurrent hormonal excesses, particularly the gonadotropins, which cause sexual precocity.
Children with excessive growth rates require as much emotional support as those with short stature.

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)

Syndrome of inappropriate antidiuretic hormone (SIADH)
results from an excessive amount of serum ADH. It is seen in
children with central nervous system infections, brain tumors,
and brain trauma; in children with pulmonary disorders such as
pneumonia, asthma, or cystic fibrosis; and in children receiving
positive-pressure ventilation. Some medications, including
diuretics and chemotherapy, have been associated with SIADH.
Failure of normal feedback mechanisms from the
hypothalamus, pituitary gland, and kidney results in excessive
secretion of ADH, leading to water reabsorption despite the
presence of low serum osmolality. ADH secretion causes
increased permeability of the distal renal tubules and collecting ducts and resulting in water reabsorption.
Elevated ADH also causes suppression of the renin-angiotensin mechanism and sodium excretion. The
outcome is water intoxication (an abnormal proportion of water to sodium in the extracellular fluid) and
hyponatremia.
Signs of SIADH are related to water intoxication and hyponatremia, and include elevated blood
pressure, distended jugular veins, crackles in lung fields, weight gain without edema, fluid and electrolyte
imbalance, and concentrated urine with decreased urine output. As serum sodium levels continue to fall,
lethargy, confusion, headache, altered level of consciousness, seizures, and coma occur because of
cerebral edema.
Laboratory findings include a high urine osmolality, low serum osmolality, low serum sodium, high
urine sodium, and decreased blood urea nitrogen. Fluids are restricted to prevent further dilution of the
blood. Medications include diuretics, demeclocycline to block action of ADH at the renal collecting
tubules, and hypertonic saline IV fluids.
Nursing care focuses on preventing injury, monitoring fluid balance, administering medications, and
managing nutritional intake. Monitor intake and output, serum sodium, urine osmolality, and specific
gravity. Educate the parents about the child’s fluid restrictions and the hidden sources of water and fluids
in foods to help avoid excessive fluid intake.

HYPOTHYROIDISM (CRETINISM)
Hypothyroidism is a disorder in which levels of active thyroid hormones
are decreased. It may be congenital or acquired. Congenital
hypothyroidism occurs in approximately 1 in 3000 to 1 in 4000 live
births worldwide. It is twice as common in females as it is in males.
Thyroid hormones are important for growth and development and
for metabolizing nutrients and energy. When these hormones are not
available to stimulate other hormones or specific target cells, growth is
delayed, and intellectual disability develops. Congenital hypothyroidism is usually caused by a
spontaneous gene mutation, an autosomal recessive genetic transmission of an enzyme deficiency,
hypoplasia or aplasia of the thyroid gland, failure of the CNS–thyroid feedback mechanism to develop,
or iodine deficiency. Intellectual disability is irreversible if the disorder is not treated. Acquired
hypothyroidism can be idiopathic or result from autoimmune thyroiditis (Hashimoto thyroiditis), late-onset
thyroid dysfunction, isolated thyroid-stimulating hormone (TSH) deficiency caused by pituitary or
hypothalamic dysfunction, or exposure to drugs or substances such as lithium that interfere with thyroid
hormone synthesis. In the case of Hashimoto thyroiditis, the thyroid is infiltrated by lymphocytes that
cause an autoimmune reaction and an enlarged thyroid. A genetic predisposition to autoimmune
thyroiditis and an autosomal dominant inheritance of thyroid antibodies has been identified.
Infants with congenital hypothyroidism have few clinical signs of the disorder in the first weeks of life.
Symptoms may include jaundice, thick tongue, hypotonia, umbilical hernia, hoarse cry, dry skin,
constipation, and large fontanelles. Children with acquired hypothyroidism have many of the same signs
as adults: decreased appetite; dry, cool skin; thinning hair or hair loss; depressed deep tendon reflexes;
bradycardia; constipation; sensitivity to cold temperatures; abnormal menses; and a goiter (a nontender
enlarged thyroid gland). Manifestations unique to children include change in past normal growth patterns
with a weight increase, decreased height velocity, delayed bone and dental age, hypotonia with poor
muscle tone, and delayed or precocious puberty.
Congenital hypothyroidism is usually detected during newborn screening. A decreased T4, normal
T3, and elevated thyroid-stimulating hormone level indicate hypothyroidism. An elevated TSH level
indicates that the disease originated in the thyroid, not the pituitary.
Levothyroxine is the drug of choice for newborns with congenital hypothyroidism. The recommended
starting dose is 10 to 15 mcg/kg per day. The dose is increased gradually as the child grows to ensure a
euthyroid (thyroid hormones in appropriate balance) state. A pediatric endocrinologist monitors treatment.
To ensure an adequate growth rate and prevent intellectual disability, the hormone must be taken
throughout life. Periodic evaluation of T4 and TSH serum levels, bone age, and growth parameters is
necessary to assess for signs of excess or inadequate thyroid hormone.
Antithyroid antibodies are measured in children with a goiter and suspected Hashimoto thyroiditis
because increased titers of antithyroglobulin and anti-microsomal antibodies are often found. Children
with congenital hypothyroidism that are diagnosed before 3 months of age have the best prognosis for
optimal mental development. Children with acquired hypothyroidism usually have normal growth following
a period of catch-up growth. Many adolescents with Hashimoto thyroiditis have a spontaneous remission.
Nursing care focuses on teaching the parents and child about the disorder and its treatment and
monitoring the child’s growth rate. Explain how to administer thyroid hormone (e.g., tablets can be
crushed and mixed in a small amount of formula or applesauce if the child gets all of the medication).
Advise parents that the child may experience temporary sleep disturbances or behavioral changes in
response to therapy. Teach the parents how to assess for an increased pulse rate, which could indicate
the presence of too much thyroid hormone, and advise them to report problems such as fatigue, which
could indicate an improper drug dose that needs to be adjusted.

HYPERTHYROIDISM
Hyperthyroidism occurs when thyroid hormone levels are increased, resulting in excessive levels of
circulating thyroid hormones. Graves disease is the most common cause of hyperthyroidism in children,
occurring more often in females and in children ages 11 to 15 years.
Graves disease is an autoimmune disorder. Immunoglobulins produced by the B lymphocytes
stimulate over secretion of thyroid hormones, resulting in the clinical symptoms. It has a high familial
incidence. Other less common causes of hyperthyroidism result from thyroiditis and thyroid hormone–
producing tumors, including thyroid adenomas and carcinomas, and pituitary adenomas. Congenital
hyperthyroidism can occur in infants of mothers with Graves disease as a result of transplacental transfer
of immunoglobulins. This condition generally resolves by 6 to 12 weeks of age but can last longer.
Signs and symptoms are caused by hyperactivity of
the sympathetic nervous system and may include an
enlarged, nontender thyroid gland (goiter), prominent or
bulging eyes (exophthalmos), eyelid lag, tachycardia,
nervousness, increased appetite with weight loss,
emotional lability, moodiness, heat intolerance,
hypertension, hyperactivity, irregular menses, insomnia,
tremor, and muscle weakness. The thyroid gland may be
slightly enlarged or grow to 3 to 4 times its normal size;
feel warm, soft, and fleshy; and have an auditory bruit on
auscultation. Onset is subtle, and the condition often
goes unrecognized for 1 to 2 years. Children with Graves
disease usually have difficulty concentrating, behavioral
problems, and declining performance in school. They
become easily frustrated in the classroom and overheated and fatigued during physical education class.
Children with this disorder find it difficult to relax or sleep. These symptoms usually prompt parents to
seek medical treatment for the child. The most serious complication of hyperthyroidism is severe
thyrotoxicosis, also called thyroid crisis or thyroid storm. It is a life-threatening emergency resulting from
extreme hyperthyroidism, in which elevated circulating levels of TH result in a hypermetabolic state.
Symptoms include muscle weakness, diaphoresis, tachycardia, tremor, palpitations, diarrhea, irritability,
nervousness, and anxiety.
Diagnostic studies include laboratory evaluation of serum TSH, T3, and T4 levels and a thyroid scan.
T3 and T4 levels are markedly elevated, whereas the TSH level is decreased. Serum studies are also
performed to detect thyroid autoantibodies anti-TG (antithyroglobulin) and anti-TPO (antiperoxidase),
usually present in Graves disease and Hashimoto thyroiditis. A thyroid scan is performed to identify
nodules or to confirm the high uptake of radioactive iodine associated with Graves disease.
The goal of clinical therapy is to inhibit excessive secretion of thyroid hormones. Treatment may
include medication therapy, radiation therapy, or surgery. Medication therapy is most often the initial
treatment, but compliance is often a problem because of side effects. Methimazole (Tapazole) and
propylthiouracil (PTU) are antithyroid drugs that are used in children with hyperthyroidism. Because of
the concern for severe liver disease with the administration of PTU, current recommendations are that
children with hyperthyroidism receive methimazole instead.
Symptoms usually improve within weeks of starting treatment. Adjunct therapy with beta-adrenergic
blocking agents such as propranolol or atenolol may be administered to relieve symptoms of tremors,
tachycardia, lid lag, and excessive sweating.
Less than 30% of children achieve remission after a 2-year course of treatment with medication.
Radiation therapy or thyroidectomy are other options if medication therapy is not effective. Thyroidectomy
(removal of most of the thyroid) provides an immediate cure and avoids radiation and possible long-term
complications of radioactive iodine. Removal of the thyroid gland results in hypothyroidism. Complications
of thyroidectomy include hemorrhage, hypocalcemia, and damage to the laryngeal nerve paresis.
 Nursing care focuses on teaching the child and parents about the disorder and its treatment,
promoting rest, providing emotional support, and, if the child needs surgery, providing preoperative and
postoperative teaching and care. Promote increased caloric intake by providing five or six moderate
meals per day. Encourage the child and family to express their feelings and concerns about the disorder.
Pointing out even slight improvements in the child’s condition increases adherence with therapy.

CUSHING SYNDROME
Cushing syndrome, also called adrenocortical
hyperfunction, is characterized by a group of
symptoms resulting from excess blood levels of
glucocorticoids (especially cortisol). The most
common cause of Cushing syndrome is the
prolonged administration of glucocorticoid hormones.
Cushing disease is a type of Cushing syndrome and
is caused by a pituitary tumor. During infancy most
cases of endogenous Cushing disease are caused
by a functioning adrenocortical tumor. The most
common cause of endogenous Cushing syndrome in
children older than 7 years of age is Cushing disease in which a pituitary tumor (adenoma) secretes
excessive ACTH. This leads to bilateral adrenal hyperplasia. The remainder of this discussion will focus
on the child with Cushing syndrome caused by a pituitary tumor (Cushing disease).
Obesity is common in children with Cushing syndrome. Excessive weight gain is followed by slowed
linear growth. The child develops the characteristic cushingoid features, which include a rounded (moon)
face with prominent cheeks. Additional manifestations include hirsutism, acne, deepening of the voice,
and hypertension. Older children may also experience delayed puberty, irregular menstrual periods,
headaches, weakness, pathologic fractures, emotional problems, and hyperglycemia.
Diagnosis is based on characteristic physical findings and laboratory values, including increased 24-
hour urinary levels of free cortisol and elevated nighttime salivary cortisol level. The child will also have
an abnormal glucose tolerance test.
The adrenal-suppression test using an 11 p.m. dose of dexamethasone reveals that adrenal cortisol
output is not suppressed overnight as would occur normally in children. Computed tomography (CT) and
magnetic resonance imaging (MRI) are used to detect the specific location of tumors in the adrenal and
pituitary glands.
Surgical removal of the pituitary adenoma is the current treatment of choice when this is the cause of
Cushing syndrome. Irradiation of the pituitary is performed when surgical removal of the adenoma does
not substantially reduce cortisol levels. Bilateral removal of the adrenal glands may be necessary in some
cases to stop the excessive secretion of cortisol. Lifelong hormone replacement is required when both
adrenal glands are removed.
Nursing assessment includes monitoring the child’s vital signs, fluid status, nutritional status, and
weight. Additional assessment includes monitoring muscle strength and endurance. Teach the child and
family about the disorder and its treatment. For children undergoing surgery, provide preoperative and
postoperative teaching and care.
DIABETES MELLITUS
Diabetes mellitus, the most common metabolic disease in children, is a disorder of hyperglycemia
resulting from defects in insulin secretion, insulin action, or both, leading to abnormalities in carbohydrate,
protein, and fat metabolism. There are two main types of diabetes. Most children have immune-mediated
type 1 diabetes, formerly called insulin-dependent diabetes mellitus or juvenile diabetes.
Type 1 Diabetes
Type 1 diabetes results from destruction of pancreatic islet beta cells, which fail to secrete
insulin. The body becomes dependent on exogenous sources of insulin. Type 1 diabetes is a
multifactorial disease caused by autoimmune destruction of insulin-producing pancreatic beta cells in
individuals who are genetically predisposed. Type 1 diabetes has familial tendencies but does not
show any specific pattern of inheritance. The number of autoantibodies helps predict the risk of
developing type 1 diabetes. For children with one antibody, the risk is only 10% to 15%, while those
with three or more antibodies have a risk of 55% to 90%. The child inherits a susceptibility to the
disease rather than the disease itself. It is believed that an event such as a virus or other
environmental factors trigger the inflammatory process, resulting in development of islet cell serum
antibodies. These antibodies can be detected in the blood months to years before the onset of beta
cell destruction.

Insulin helps transport glucose into the cells so that the body can use it as an energy source.
It also prevents the outflow of glucose from the liver to the general circulation. Environmental factors
such as enteroviruses or toxins are believed to lead to an autoimmune destruction of the beta cells
in the islets of Langerhans. Antigens are generated, leading to production of antibodies that indicate
ongoing destruction of the islet cells. Chronic immune-mediated destruction of the beta cells
continues over a period of time. Symptoms of type 1 diabetes are evident when approximately 90%
of the beta cells have been destroyed. As the secretion of insulin decreases, the blood glucose level
rises and the glucose level inside the cells decreases. When the renal threshold for glucose (180
mg/dL) is exceeded, glycosuria (abnormal amount of glucose in the urine) occurs as a result of
osmotic diuresis. Fluids follow the highly osmotic glucose and water is excreted in large volumes of
urine (polyuria). When glucose is unavailable to the cells for metabolism, free fatty acids provide an
alternate source of energy. The liver metabolizes fatty acids at an increased rate, producing acetyl
coenzyme A (CoA). The by-products of acetyl CoA metabolism (ketone bodies) accumulate in the
body, resulting in a state of metabolic acidosis, or ketoacidosis.
 Type 2 Diabetes
Type 2 diabetes usually arises because of insulin resistance in which the body fails to use
insulin properly combined with relative (rather than absolute) insulin deficiency. People with type 2
can range from predominantly insulin resistant with relative insulin deficiency to predominantly
deficient in insulin secretion with some insulin resistance. It typically occurs in those who are older
than 45 years of age, are overweight and sedentary, and have a family history of diabetes. The
symptomatology of diabetes is more readily recognizable in children than in adults, so it is surprising
that the diagnosis may sometimes be missed or delayed. Diabetes is a great imitator; influenza,
gastroenteritis, and appendicitis are the conditions most often diagnosed when it turns out that the
disease is really diabetes.

CAUSE CLINICAL MANIFESTATIONS CLINICAL THERAPY

TYPE 1 DM Polyuria, polydipsia Blood glucose monitoring
Immune mediated, insulin May have polyphagia Insulin
deficiency due to pancreatic Weight loss Dietary management, balancing
beta-cell destruction Ketoacidosis may be present at carbohydrate intake to insulin
diagnosis, at continued risk for Exercise
ketoacidosis
Short duration of symptoms
Initial period of decreased insulin
requirement, then need insulin for
survival.
TYPE 2 DM Obese, little or no weight loss, or may Diet with decreased calories and low-
Insulin resistance with have significant weight loss fat foods
relative insulin secretory Acanthosis nigricans Decrease sedentary activity time or
defect Long duration of symptoms increase routine physical activity
Polyuria, polydipsia, may be mild or Blood glucose monitoring
absent Oral medication (metformin) to
Glycosuria with or without ketonuria improve insulin sensitivity
Ketoacidosis may be present May need insulin
Lipid disorders
Hypertension
Androgen-mediated problems such as
acne, hirsutism, menstrual
disturbances, polycystic ovary disease
Excessive weight gain and fatigue due
to insulin resistance

Insulin is needed to support the metabolism of carbohydrates, fats, and proteins, primarily by
facilitating the entry of these substances into the cells. Insulin is needed for the entry of glucose into the
muscle and fat cells, prevention of mobilization of fats from fat cells, and storage of glucose as glycogen
in the cells of liver and muscle. Insulin is not needed for the entry of glucose into nerve cells or vascular
tissue. The chemical composition and molecular structure of insulin are such that it fits into receptor sites
on the cell membrane. Here it initiates a sequence of poorly defined chemical reactions that alter the cell
membrane to facilitate the entry of glucose into the cell and stimulate enzymatic systems outside the cell
that metabolize the glucose for energy production.
With a deficiency of insulin, glucose is unable to enter the cells, and its concentration in the
bloodstream increases. The increased concentration of glucose (hyperglycemia) produces an osmotic
gradient that causes the movement of body fluid from the intracellular space to the interstitial space and
then to the extracellular space and into the glomerular filtrate to “dilute” the hyperosmolar filtrate.
Normally, the renal tubular capacity to transport glucose is adequate to reabsorb all the glucose in the
glomerular filtrate. When the glucose concentration in the glomerular filtrate exceeds the renal threshold
(6180 mg/dl), glucose spills into the urine (glycosuria) along with an osmotic diversion of water (polyuria),
a cardinal sign of diabetes. The urinary fluid losses cause the excessive thirst (polydipsia) observed in
diabetes. This water “washout” results in a depletion of other essential chemicals, especially potassium.
Protein is also wasted during insulin deficiency. Because glucose is unable to enter the cells, protein is
broken down and converted to glucose by the liver (glucogenesis); this glucose then contributes to the
hyperglycemia. These mechanisms are similar to those seen in starvation when substrate (glucose) is
absent. The body is actually in a state of starvation during insulin deficiency. Without the use of
carbohydrates for energy, fat and protein stores are depleted as the body attempts to meet its energy
needs. The hunger mechanism is triggered, but increased food intake (polyphagia) enhances the problem
by further elevating blood glucose.
Long-term complications of diabetes involve both the microvasculature and the macrovasculature.
The principal microvascular complications are nephropathy, retinopathy, and neuropathy. Microvascular
disease develops during the first 30 years of diabetes, beginning in the first 10 to 15 years after puberty,
with renal involvement evidenced by proteinuria and clinically apparent retinopathy. Macrovascular
disease develops after 25 years of diabetes and creates the predominant problems in patients with type
2 DM. The process appears to be one of glycosylation, wherein proteins from the blood become deposited
in the walls of small vessels (e.g., glomeruli), where they become trapped by “sticky” glucose compounds
(glycosyl radicals). The buildup of these substances over time causes narrowing of the vessels, with
subsequent interference with microcirculation to the affected areas.
With poor diabetic control, vascular changes can appear as early as 2 1 2 to 3 years after diagnosis;
however, with good to excellent control, changes can be postponed for 20 or more years. Intensive insulin
therapy appears to delay the onset and slow the progression of retinopathy, nephropathy, and
neuropathy. Hypertension and atherosclerotic cardiovascular disease are also major causes of morbidity
and mortality in patients with DM.
Other complications have been observed in children with type 1 DM. Hyperglycemia appears to influence
thyroid function, and altered function is frequently observed at the time of diagnosis and in poorly
controlled diabetes. Limited mobility of small joints of the hand occurs in 30% of 7- to 18-year-old children
with type 1 DM and appears to be related to changes in the skin and soft tissues surrounding the joint
because of glycosylation.
Three groups of children who should be considered as candidates for diabetes are (1) children who
have glycosuria, polyuria, and a history of weight loss or failure to gain despite a voracious appetite; (2)
those with transient or persistent glycosuria; and (3) those who display manifestations of metabolic
acidosis, with or without stupor or coma. In every case, diabetes must be considered if there is glycosuria,
with or without ketonuria, and unexplained hyperglycemia. Glycosuria by itself is not diagnostic of
diabetes. Other sugars, such as galactose, can produce a positive result with certain test strips, and a
mild degree of glycosuria can be caused by other conditions, such as infection, trauma, emotional or
physical stress, hyperalimentation, and some renal or endocrine diseases. An 8-hour fasting blood
glucose level of 126 mg/dl or more, a random blood glucose value of 200 mg/dl or more accompanied by
classic signs of diabetes, or an oral glucose tolerance test (OGTT) finding of 200 mg/dl or more in the 2-
hour sample is almost certain to indicate diabetes. Postprandial blood glucose determinations and the
traditional OGTTs have yielded low detection rates in children and are not usually necessary for
establishing a diagnosis. Serum insulin levels may be normal or moderately elevated at the onset of
diabetes; delayed insulin response to glucose indicates impaired glucose tolerance.
The management of the child with type 1 DM consists of a multidisciplinary approach involving the
family; the child (when appropriate); and professionals, including a pediatric endocrinologist, diabetes
nurse educator, nutritionist, and exercise physiologist. The definitive treatment is replacement of insulin
that the child is unable to produce. However, insulin needs are also affected by emotions, nutritional
intake, activity, and other life events such as illnesses and puberty. The complexity of the disease and its
management requires that the child and family incorporate diabetes needs into their lifestyle. Medical
and nutritional guidance are primary, but management also includes continuing diabetes education,
family guidance, and emotional support.

CAUSE CLINICAL MANIFESTATIONS CLINICAL THERAPY

HYPOGLYCEMIA
• Insulin dose too high for food Rapid onset If conscious, give 15g of
eaten Irritability, nervousness, tremors, shaky carbohydrate. Wait 15 minutes and
• Insulin injection into muscle feeling, difficulty concentrating or recheck blood glucose level. Give
• Too much exercise for insulin speaking, behavior change, confusion, another 15g of carbohydrate if 70
dose repeating something over and over mg/dL or below. Recheck the blood
• Too long between meals/ Unconsciousness, seizure, shallow glucose level in 15 minutes.
snacks breathing, tachycardia
• Too few carbohydrates eaten Pallor, sweating If unconscious, give
• Illness, stress Moist mucous membranes, hunger glucagon by injection.
Headache, dizziness, blurred vision,
double vision, photophobia
Numb lips or mouth
HYPERGLYCEMIA
• Insulin dose too low for food Gradual onset Give additional insulin at usual
eaten Lethargy, sleepiness, slowed injection time.
• Illness or injury, stress responses, or confusion
• Too many carbohydrates Deep, rapid breathing Give correction scale insulin doses
eaten Flushed skin, dry skin for specific blood glucose levels
• Meals/ snacks too close Dry mucous membranes, thirst, hunger, when ill or injured.
together dehydration
• Insulin injected just under skin Weakness, fatigue Give extra injections if
or injected into hypertrophied Headache, abdominal pain, nausea, hyperglycemia and moderate to
areas vomiting large ketones.
• Decreased activity Blurred vision
Shock Increase fluids.

Nursing care focuses on teaching the child and parents about the disease and its management,
planning dietary intake, providing emotional support, and planning strategies for daily management in the
community.

DIABETIC KETOACIDOSIS (DKA)

When insulin is absent or insulin sensitivity is altered, glucose is unavailable for cellular metabolism,
and the body chooses alternate sources of energy, principally fat. Consequently, fats break down into
fatty acids, and glycerol in the fat cells is converted by the liver to ketone bodies (β-hydroxybutyric acid,
acetoacetic acid, acetone). Any excess is eliminated in the urine (ketonuria) or the lungs (acetone breath).
The ketone bodies in the blood (ketonemia) are strong acids that lower serum pH, producing ketoacidosis.
Ketones are organic acids that readily produce excessive quantities of free hydrogen ions, causing a
fall in plasma pH. Then chemical buffers in the plasma, principally bicarbonate, combine with the
hydrogen ions to form carbonic acid, which readily dissociates into water and carbon dioxide. The
respiratory system attempts to eliminate the excess carbon dioxide by increased depth and rate
(Kussmaul respirations, or the hyperventilation characteristic of metabolic acidosis). The ketones are
buffered by sodium and potassium in the plasma. The kidneys attempt to compensate for the increased
pH by increasing tubular secretion of hydrogen and ammonium ions in exchange for fixed base, thus
depleting the base buffer concentration.
With cellular death, potassium is released from the cells (intracellular fluid) into the bloodstream
(extracellular fluid) and excreted by the kidneys, where the loss is accelerated by osmotic diuresis. The
total body potassium is then decreased even though the serum potassium level may be elevated as a
result of the decreased fluid volume in which it circulates. Alteration in serum and tissue potassium can
lead to cardiac arrest.
If these conditions are not reversed by insulin therapy in combination with correction of the fluid
deficiency and electrolyte imbalance, progressive deterioration occurs, with dehydration, electrolyte
imbalance, acidosis, coma, and death. Diabetic ketoacidosis (DKA) should be diagnosed promptly in a
seriously ill patient and therapy instituted in an intensive care unit.
Ketoacidosis must be differentiated from other causes of acidosis or coma, including hypoglycemia,
uremia, gastroenteritis with metabolic acidosis, salicylate intoxication encephalitis, and other intracranial
lesions. DKA is a state of relative insulin insufficiency and may include the presence of hyperglycemia
(blood glucose level ≥200 mg/ dl), ketonemia (strongly positive), acidosis (pH <7.30 and bicarbonate <
15 mmol/L), glycosuria, and ketonuria. Tests used to determine glycosuria and ketonuria are the glucose
oxidase tapes (Keto-Diastix).
Diabetic ketoacidosis, the most complete state of insulin deficiency, is a life-threatening situation.
Management consists of rapid assessment, adequate insulin to reduce the elevated blood glucose level,
fluids to overcome dehydration, and electrolyte replacement (especially potassium). Because DKA
constitutes an emergency situation, the child should be admitted to an intensive care facility for
management. The priority is to obtain a venous access for administration of fluids, electrolytes, and
insulin. The child should be weighed, measured, and placed on a cardiac monitor. Blood glucose and
ketone levels are determined at the bedside, and samples are obtained for laboratory measurement of
glucose, electrolytes, BUN, arterial pH, PO2, PCO2, hemoglobin, hematocrit, white blood cell count and
differential, calcium, and phosphorus. Oxygen may be administered to patients who are cyanotic and in
whom arterial oxygen is less than 80%. Gastric suction is applied to unconscious children to avoid the
possibility of pulmonary aspiration. Antibiotics may be administered to febrile children after appropriate
specimens are obtained for culture. A Foley catheter may or may not be inserted for urine samples and
measurement. Unless the child is unconscious, a collection bag is usually sufficient for accurate
assessments.

Cushing syndrome - is characterized by a group of symptoms resulting from excess blood levels of
glucocorticoids (especially cortisol).
Diabetes mellitus - is a disorder of hyperglycemia resulting from defects in insulin secretion, insulin
action, or both, leading to abnormalities in carbohydrate, protein, and fat metabolism.

Gastroenteritis - is an inflammation of the stomach and intestines that may be accompanied by

vomiting and diarrhea.

Ball, J.W., Bindler, R. C., Cowen, K. J., Shaw, M. R., (2017). Principles of Pediatric Nursing: Caring
for Children, 7th Edition, (pp. 655-697). Pearson Education, Inc.

Rudd, K., Kocisko, D.M. (2014). Pediatric Nursing: The Critical Components of Nursing Care, 1st
edition, (pp. 313-349). F.A. Davis Company, Philadelphia.

Study Questions

• Formulate a nursing care plan for a 14-year-old adolescent client with Diabetes Mellitus Type
1. The client is very active in school and loves playing basketball.
1. What nursing diagnosis and goal of care will the nurse come up with this client?
2. What nursing interventions will be identified to meet the nurse’s goal for this client?
3. What is the expected outcome for this goal?

Baker S, Barlow S, Cochran W, and others: Overweight children and adolescents: a clinical report of
the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, J Pediatr
Gastroenterol Nutr 40:533–543, 2005

Ball, J.W., Bindler, R. C., Cowen, K. J., Shaw, M. R., (2017). Principles of Pediatric Nursing: Caring
for Children, 7th Edition, (pp. 655-697). Pearson Education, Inc.

Beaty TH: Invited commentary: two studies of genetic control of birth weight where large data sets
were available, Am J Epidemiol 165:753–755, 2007
Cavataio F, Guandalini S: Gastroesophageal reflux. In Guandalini S, editor: Essential pediatric
gastroenterology and nutrition, New York, 2005, McGraw-Hill.

Hannon TS, Gungor N, Arslanian SA: Type 2 diabetes in children and adolescents: a review for the
primary care provider, Pediatr Ann 35(12):880–887, 2006

Hockenberry, M. and Wilson, D. (2015). Wong’s Nursing Care of Infants and Children 1st Philippine
Edition, The Child with Gastrointestinal Dysfunction (Volume 2, pp. 1251-1317). Mosby.

Hockenberry, M. and Wilson, D. (2013). Wong’s Essentials of Pediatrics, 9th Edition, The Child with
Gastrointestinal Dysfunction. (pp. 762-816). Mosby

Khan S, Orenstein SR: Esophageal atresia and tracheoesophageal fistula. In Kliegman RM, Stanton
BF, St. Geme JW, and others, editors: Nelson textbook of pediatrics, ed 19, Philadelphia, 2011,
Saunders.

Loening-Baucke V, Pashankar DS: A randomized, prospective, comparison study of polyethylene

glycole 3350 without electrolytes and milk of magnesia for children with constipation and fecal
incontinence, Pediatrics 118(2):528–535, 2006

Minkes, R. K., & Alder, A. C. (2014). Pediatric appendicitis. Retrieved from

http://emedicine.medscape.com/ article/926795-overview

Muscari, M. E. (2005). Pediatric Nursing, 4th edition, (pp. 220-252). Lippincott Williams & Wilkins.
Wolters Kluwer.

Rudd, K., Kocisko, D.M. (2014). Pediatric Nursing: The Critical Components of Nursing Care, 1st
edition, (pp. 313-349). F.A. Davis Company, Philadelphia.
Waseem M, Rosenberg HK: Intussusception, Pediatric Emergency Care 24(11):793–800, 2008.
BACHELOR OF SCIENCE IN NURSING:
CARE OF MOTHER AND CHILD AT RISK OR
WITH PROBLEMS (ACUTE AND CHRONIC):
COURSE MODULE COURSE UNIT WEEK
3 13 15

Alterations in Perception and Coordination

Read course and unit objectives

Read study guide prior to class attendance
Read required learning resources; refer to unit
terminologies for jargons
Proactively participate in classroom discussions
Participate in weekly discussion board (Canvas)
Answer and submit course unit tasks

At the end of this unit, the students are expected to:

Cognitive:
1. Identify and describe the different neurologic, cognitive, musculoskeletal and neuromuscular disorders.
2. Differentiate between the signs of a seizure and status epilepticus in infants and children
3. Formulate a plan of care for pediatric clients with seizure disorders
4. Demonstrate an understanding of manifestations and management of child with neurologic,
 cognitive, musculoskeletal and neuromuscular disorders
5. Discuss the nursing role in helping parents care for the child who has cerebral palsy.
Affective:
• Listen attentively during class discussions
• Demonstrate tact and respect when challenging other people’s opinions and ideas
• Accept comments and reactions of classmates on one’s opinions openly and graciously.
• Develop heightened interest in studying Maternal and Child Nursing
Psychomotor:
1. Participate actively during class discussions and group activities
2. Express opinion and thoughts in front of the class

Hockenberry, M. and Wilson, D. (2015). Wong’s Nursing Care of Infants and Children 1st Philippine
Edition, The Child with Cerebral Dysfunction (Volume 2, pp. 1425-1490). Mosby.

NEUROLOGIC AND COGNITIVE DYSFUNCTION

SEIZURE DISORDERS
Seizures are the most common pediatric neurologic disorder. About 4% of children will have at least
one seizure by the age of 15 years with half of those episodes being febrile seizures. Seizures are caused
by excessive and disorderly neuronal discharges in the brain. The manifestation of seizures depends on
the region of the brain in which they originate and may include unconsciousness or altered
consciousness; involuntary movements; and changes in perception, behaviors, sensations, and posture.
Seizures are a symptom of an underlying disease process. Causes of seizures may be infectious,
neurologic, metabolic, traumatic, or related to ingestion of toxins. Some seizures may result from an acute
medical or neurologic illness and cease after the illness is treated. In other cases, children may have a
single seizure without the cause ever being known.
Seizures in children have many different causes. Seizures are classified not only according to type
but also according to etiology. Acute symptomatic seizures are associated with an acute insult such as
head trauma or meningitis. Remote symptomatic seizures are those without an immediate cause but with
an identifiable prior brain injury such as major head trauma, meningitis or encephalitis, hypoxia, stroke,
or a static encephalopathy such as cognitive impairment or cerebral palsy. Cryptogenic seizures are
those occurring with no clear cause. Idiopathic seizures are genetic in origin.
Regardless of the etiologic factor or type of seizure, the basic mechanism is the same. Abnormal
electrical discharges (1) may arise from central areas in the brain that affect consciousness; (2) may be
restricted to one area of the cerebral cortex, producing manifestations characteristic of that particular
anatomic focus; or (3) may begin in a localized area of the cortex and spread to other portions of the
brain and, if sufficiently extensive, produce generalized seizure activity. Seizure activity begins with a
group of neurons in the CNS that because of excessive excitation and loss of inhibition amplify their
discharge simultaneously. In response to physiologic stimuli, such as cellular dehydration, severe
hypoglycemia, electrolyte imbalance, sleep deprivation, emotional stress, and endocrine changes, these
hyperexcitable cells activate normal cells in surrounding areas and in distant, synaptically related cells.
A generalized seizure develops when the neuronal excitation from the epileptogenic focus spreads to the
brainstem, particularly the midbrain and reticular formation. These centers within the brainstem, known
as the centrencephalic system, are responsible for the spread of the epileptic potentials. The discharges
can originate spontaneously in the centrencephalic system or be triggered by a focal area in the cortex.
Based on these characteristic neuronal discharges (as recorded by the EEG), seizures are designated
as partial, generalized, and unclassified epileptic seizures.
Hallmark early systemic clinical changes during a generalized seizure include tachycardia,
hypertension, hyperglycemia, and hypoxemia. Brief seizures rarely produce significant durable side
effects. In contrast, prolonged seizures can lead to lactic acidosis rhabdomyolysis, hyperkalemia,
hyperthermia, and hypoglycemia. All of these changes can cause long-term neurologic damage.
There are many different types of seizures, and each has unique clinical manifestations. Seizures are
classified into categories:
1. Partial seizures, which have a local onset and involve a relatively small location in the brain.
o Simple Partial Seizures with Motor Signs
▪ Characterized by:
• Localized motor symptoms
• Somatosensory, psychic, autonomic symptoms
• Combination of these
• Abnormal discharges remaining unilateral
▪ Manifestations:
• Aversive seizure (most common motor seizure in children)—Eye or eyes
and head turn away from the side of the focus, awareness of movement or
loss of consciousness
• Rolandic (Sylvan) seizure—Tonic-clonic movements involving the face,
salivation, arrested speech; most common during sleep
• Jacksonian march (rare in children)—Orderly, sequential progression of
clonic movements beginning in a foot, hand, or face and moving, or
“marching,” to adjacent body parts
o Simple Partial Seizures with Sensory Signs
▪ Uncommon in children younger than 8 years of age
▪ Characterized by various sensations, including:
• Numbness, tingling, prickling, paresthesia, or pain originating in one area
(e.g., face or extremities) and spreading to other parts of the body
• Visual sensations or formed images
• Motor phenomena such as posturing or hypertonia
o Complex Partial Seizures (Psychomotor Seizures)
▪ Observed more often in children from 3 years through adolescence
▪ Characterized by:
• Period of altered behavior
• Amnesia for event (no recollection of behavior)
• Inability to respond to environment
• Impaired consciousness during event
 • Drowsiness or sleep usually following seizure
• Confusion and amnesia possibly prolonged
• Complex sensory phenomena (aura)—Most frequent sensation is strange
feeling in the pit of the stomach that rises toward the throat and is often
accompanied by odd or unpleasant odors or tastes; complex auditory or
visual hallucinations; ill-defined feelings of elation or strangeness (e.g.,
déjà vu, a feeling of familiarity in a strange environment); strong feelings of
fear and anxiety; a distorted sense of time and self; and in small children,
emission of a cry or attempt to run for help
▪ Patterns of motor behavior:
• Stereotypic
• Similar with each subsequent seizure
• May suddenly cease activity, appear dazed, stare into space, become
confused and apathetic, and become limp or stiff or display some form of
posturing
• May be confused
• May perform purposeless, complicated activities in a repetitive manner
(automatisms), such as walking, running, kicking, laughing, or speaking
incoherently, most often followed by postictal confusion or sleep; may
exhibit oropharyngeal activities, such as smacking, chewing, drooling,
swallowing, and nausea or abdominal pain followed by stiffness, a fall, and
postictal sleep; rarely manifests actions such as rage or temper tantrums;
aggressive acts uncommon during seizure
2. Generalized seizures, which involve both hemispheres of the brain and are without local onset.
o Tonic-Clonic Seizures (Formerly Known as Grand Mal)
▪ Most common and most dramatic of all seizure manifestations
▪ Occur without warning
▪ Tonic phase lasts approximately 10 to 20 seconds
• Manifestations:
o Eyes roll upward
o Immediate loss of
consciousness
o If standing, falls to
floor or ground
o Stiffens in
generalized,
symmetric tonic
contraction of entire
body musculature
o Arms usually flexed
o Legs, head, and
neck extended
o May utter a peculiar
piercing cry
 o Apneic, may become cyanotic
o Increased salivation and loss of swallowing reflex
▪ Clonic phase lasts about 30 seconds but can vary from only a few seconds to a
half hour or longer
• Manifestations:
o Violent jerking movements as the trunk and extremities undergo
rhythmic contraction and relaxation
o May foam at the mouth
o May be incontinent of urine and feces
o As event ends, movements less intense, occurring at longer
intervals and then ceasing entirely
▪ Status epilepticus—Series of seizures at intervals too brief to allow the child to
regain consciousness between the time one event ends and the next begins
• Requires emergency intervention
• Can lead to exhaustion, respiratory failure, and death
▪ Postictal state:
• Appears to relax
• May remain semiconscious and difficult to arouse
• May awaken in a few minutes
• Remains confused for several hours
• Poor coordination
• Mild impairment of fine motor movements
• May have visual and speech difficulties
• May vomit or complain of severe headache
• When left alone, usually sleeps for several hours
• On awakening, is fully conscious
• Usually feels tired and complains of sore muscles and headache
• No recollection of entire event
o Absence Seizures (Formerly Called Petit Mal or Lapses)
▪ Characterized by:
• Onset usually between 4 and 12 years of age
• More common in girls than boys
• Usually cease at puberty
• Brief loss of consciousness
• Minimum or no alteration in
muscle tone
• May go unrecognized because
of little change in child’s
behavior
• Abrupt onset; suddenly
develops 20 or more attacks
daily
• Event often mistaken for
inattentiveness or daydreaming
 • Events possibly precipitated by hyperventilation, hypoglycemia, stresses
(emotional and physiologic), fatigue, or sleeplessness
▪ Manifestations:
• Brief loss of consciousness
• Appear without warning or aura
• Usually last about 5 to 10 seconds
• Slight loss of muscle tone may cause child to drop objects
• Ability to maintain postural control; seldom falls
• Minor movements such as lip smacking, twitching of eyelids or face, or
slight hand movements
• Not accompanied by incontinence
• Amnesia for episode
• May need to reorient self to previous activity
o Atonic and Akinetic Seizures (Also Known as Drop Attacks)
▪ Characterized by:
• Onset usually between 2 and 5 years of age
• Sudden, momentary loss of muscle tone and postural control
• Events recurring frequently during the day, particularly in the morning hours
and shortly after awakening
▪ Manifestations:
• Loss of tone causing child to fall to the floor violently
• Unable to break fall by putting out hand
• May incur a serious injury to the face, head, or shoulder
• Loss of consciousness only momentary
o Myoclonic Seizures
▪ A variety of seizure episodes
▪ May be isolated as benign essential myoclonus
▪ May occur in association with other seizure forms
▪ Characterized by:
• Sudden, brief contractures of a muscle or group of muscles
• Occur singly or repetitively
• No postictal state
• May or may not be symmetric
• May or may not include loss of consciousness
3. Unclassified Epileptic Seizures are seizures that lack sufficient information to classify
o Infantile Spasms
▪ Also called infantile myoclonus, massive spasms, hypsarrhythmia, salaam
episodes, or infantile myoclonic spasms
▪ Most commonly occur during the first 6 to 8 months of life
▪ Twice as common in boys as girls
▪ Numerous seizures during the day without postictal drowsiness or sleep
▪ Poor outlook for normal intelligence
▪ Manifestations:
• Possible series of sudden, brief, symmetric, muscular contractions
 • Head flexed, arms extended, and legs drawn up
• Eyes sometimes rolling upward or inward
• May be preceded or followed by a cry or giggling
• May or may not include loss of consciousness
• Sometimes flushing, pallor, or cyanosis
▪ Infants who are able to sit but not stand:
• Sudden dropping forward of the head and neck with trunk flexed forward
and knees drawn up—the salaam or jackknife seizure Less often: alternate
clinical forms
• Extensor spasms rather than flexion of arms, legs, and trunk, and head
nodding
• Lightning events involving a single, momentary, shock-like contraction of
the entire body

Febrile Seizure
Febrile seizures are one of the most common neurologic conditions of childhood, affecting
approximately 2% to 5% of children between the ages of 6 and 60 months. Febrile seizures are classified
as simple or complex. Simple febrile seizures occur in children between the ages of 6 months and 5 years
with no preexisting neurologic abnormality and consist of a general tonic-clonic seizure that occurs with
a fever (>38.0° C) and resolves within 15 minutes with a return to alert mental status after the seizure
and no further seizure occurring within a 24-hour period. On the other hand, complex febrile seizures can
occur in children of any age usually with a previous neurologic impairment and consist of a prolonged
seizure lasting more than 15 minutes that can reoccur within 24 hours and can result in neurologic deficits
after the seizure. Most febrile seizures occur between 6 months and 5 years of age, with the peak
incidence occurring at 18 months of age.
The cause of febrile seizures is still uncertain. Risk factors for simple febrile seizures include viral
infections and a family history of febrile seizures. Associations with chromosomal mutations, premature
birth, and developmental delay have been evaluated but have not demonstrated any conclusive
evidence. Most febrile seizures have stopped by the time the child is taken to a medical facility and require
no treatment. However, if the seizure continues, treatment consists of controlling the seizure with IV or
rectal diazepam and reducing the temperature with acetaminophen or ibuprofen. Antiepileptic prophylaxis
is usually not indicated. Antipyretic therapy may lower the child’s temperature and provide symptomatic
relief but will not prevent a seizure. Tepid sponge baths are not recommended for several reasons: they
are ineffective in significantly lowering the temperature, the shivering effect further increases metabolic
output, and cooling causes discomfort to the child. Parental education and emotional support are
important interventions, and information may need to be repeated depending on the parents’ anxiety and
education level. Parents need reassurance regarding the benign nature of simple febrile seizures.
Several large studies show no difference in neurologic deficits, cognitive functioning, or memory
impairments in children with simple or complex febrile seizures compared with population control
participants.
Long-term antiepileptic therapy is usually not required for children with simple febrile seizures.
Whereas children with a simple febrile seizure have only a 1% risk of developing epilepsy, children with
a complex febrile seizure along with a preexisting neurologic abnormality and a family history of afebrile
seizure have a 10% risk of developing epilepsy.
Epilepsy
Epilepsy is a condition characterized by two or more unprovoked seizures and can be caused by a
variety of pathologic processes in the brain. A single seizure event should not be classified as epilepsy
and is generally not treated with long-term antiepileptic drugs.
The process of diagnosis in a child suspected of having epilepsy includes (1) determining whether
epilepsy or seizures exist and not an alternative diagnosis and (2) defining the underlying cause, if
possible. The assessment and diagnosis rely heavily on a thorough history, skilled observation, and
several diagnostic tests. It is especially important to differentiate epilepsy from other brief alterations in
consciousness or behavior. Clinical entities that mimic seizures include migraine headaches, toxic effects
of drugs, syncope (fainting), breath-holding spells in infants and young children, movement disorders
(tics, tremor, chorea), prolonged QT syndrome, sleep disturbances (night terrors), psychogenic seizures,
rage attacks, and transient ischemic attacks (rare in children).
After the child’s first seizure, a thorough history is taken from the parent, primary caretaker, or
witnesses to the event. The description and length of the seizure, presence or absence of an aura, and
whether the child lost consciousness are noted. This information helps to identify the type of seizure
according to the International Classification of Epileptic Seizures. Based on the physical findings and
history, diagnostic tests ordered may include a complete blood cell count, blood chemistry, and urine
toxicology. A urine culture, blood culture, and lumbar puncture are performed if meningitis is suspected.
A lead level and tests for inborn errors of metabolism may be considered. Radiologic tests such as CT
scanning or MRI and angiography may be performed to identify a cerebral lesion or metabolic disorder
in the brain. An EEG is often performed at a follow-up visit between seizures. If the child is taking any
anticonvulsants, a serum drug level is obtained. Many seizures are self-limiting and require no emergency
intervention. When the seizure is prolonged, emergency therapy includes airway management,
supplemental oxygen, intravenous benzodiazepines, and careful monitoring of vital signs. Serum
electrolytes, glucose, and blood gases may be monitored. The postictal period ranges from 30 minutes
to 2 hours. When the child’s seizure does not stop as expected with emergency intervention, treatment
for status epilepticus is initiated.
Care of the child with epilepsy involves physical care and instruction regarding the importance of the
drug therapy and, probably more significant, the problems related to the emotional aspects of the
disorder. Nursing care is directed toward educating the child and family about epilepsy and helping them
develop strategies to cope with the psychologic and sociologic problems related to epilepsy.
Most seizure disorders are treated with antiepileptic drugs (AEDs). A single (monotherapy) AED is
preferred for seizure control to minimize the side effects such as sleepiness, decreased attention and
memory, difficulty with speech, ataxia, and diplopia. A low dose is used initially and gradually increased
until seizures are controlled. An alternate AED may be tried if seizure control is not achieved with a high
therapeutic dose of the first medication or when unacceptable side effects occur. Some children have
refractory or intractable seizures, requiring two or more AEDs. Medication dosage adjustments are often
needed as the child grows. Blood tests to monitor for liver and hematologic problems and therapeutic
drug levels are often performed.

Status Epilepticus
Status epilepticus refers to a seizure that lasts continuously for longer than 30 minutes or a series of
seizures from which the child does not return to the previous level of consciousness. This is an
emergency requiring immediate treatment. Otherwise, exhaustion, respiratory failure, permanent brain
injury, or death may occur. Oxygen may be necessary to relieve cyanosis. An IV benzodiazepine such
as diazepam (Valium) or lorazepam (Ativan) halts seizures dramatically. This may be followed by IV
phenobarbital or phenytoin (Dilantin). Diazepam must be administered with extreme caution because the
drug is incompatible with many other medications, and any accidental infiltration into subcutaneous tissue
causes extensive tissue sloughing. When a benzodiazepine (diazepam or lorazepam) is ineffective,
fosphenytoin followed by phenobarbital is given as the next line of treatment. This combination of therapy
places the child at high risk for apnea; therefore, respiratory support is generally necessary. Children may
also receive an antiepileptic medication, intravenous valproate, which does not cause respiratory
compromise. Children who continue to have seizures despite this drug treatment may require general
anesthesia with a continuous infusion of midazolam, propofol, or pentobarbital. In this situation, the
patient may need to be intubated and continuous EEG monitoring is typically done to monitor for and
treat electrographic seizures.
Nursing care of a child with status epilepticus includes, in addition to the ABCs of life support,
monitoring blood pressure and body temperature. During the first 30 to 45 minutes of the seizure, the
blood pressure may be elevated. Thereafter, the blood pressure typically returns to normal but may be
decreased depending on the medications being administered for seizure control. Hyperthermia requiring
treatment may occur because of increased motor activity.

SPINA BIFIDA (SB)

Spina bifida refers to a defect in one or more vertebrae that allows spinal cord contents to protrude.
The malformation can occur anywhere along the vertebral column but is most common at the lumbar or
sacral portion of the spine. Spina Bifida is categorized into two types, SB occulta and SB cystica.
• Spina bifida occulta refers to a defect that is not visible externally. It occurs most frequently in the
lumbosacral area (L5 and S1). SB occulta may not be apparent unless there are associated
cutaneous manifestations or neuromuscular disturbances.
• Spina bifida cystica refers to a visible defect with an external saclike protrusion. The two major
forms of SB cystica are meningocele, which encases meninges and spinal fluid but no neural
elements, and myelomeningocele (or meningomyelocele), which contains meninges, spinal fluid,
and nerves. Meningocele is not associated with neurologic deficit, which occurs in varying, often
serious, degrees in myelomeningocele. Clinically, the term spina bifida is used to refer to
myelomeningocele.

The cause of spina bifida is unknown, although environmental factors have been implicated, such as
chemicals (excessive use of alcohol), medications (e.g., valproic acid and carbamazepine used for
seizures, isotretinoin for acne), genetic factors, and maternal health conditions (diabetes mellitus,
gestational diabetes, folic acid deficiency, and maternal obesity). The increased incidence of the condition
in families points to a possible genetic influence.
The pathophysiology of SB is best understood when related to the normal formative stages of the
nervous system. At approximately 20 days of gestation, a decided depression, the neural groove,
appears in the dorsal ectoderm of the embryo. During the fourth week of gestation, the groove deepens
rapidly, and its elevated margins develop laterally and fuse dorsally to form the neural tube. Neural tube
formation begins in the cervical region near the center of the embryo and advances in both directions—
caudally and cephalically—until by the end of the fourth week of gestation, the ends of the neural tube,
the anterior and posterior neuropores, close.
A saclike protrusion on the infant’s back indicates meningocele or myelodysplasia
(meningomyelocele). The clinical manifestations (paralysis, weakness, and sensory loss) depend on the
location of the defect. The higher the defect on the spinal cord, the greater the neurologic dysfunction:
• Thoracic level—paralysis of the legs, weakness and sensory loss in the trunk and lower body
region
• Lumbar 1–2 level—some hip flexion and adduction, cannot extend knees
• Lumbar 3 level—can flex hips and extend the knees: paralyzed ankles and toes
• Lumbar 4–5 level—can flex hips and extend the knees, weak or absent ankle extension, toe
flexion, and hip extension
• Sacral level—mild weakness in ankles and toes
Sensory loss is more pronounced on the back of the legs, and the loss of lower extremity motor and
sensory functioning may not be symmetric. Bowel and bladder incontinence occurs with all but the sacral
level lesions, but bowel and bladder function may still be affected at the sacral level. Renal damage may
result from neurologic impairment and urinary retention (neurogenic bladder). Hydrocephalus is usually
present in children with a myelomeningocele defect above the sacral level, along with the Arnold Chiari
type II malformation.
Children with myelodysplasia have mobility problems, intellectual disability, and visual impairment.
Additional complications include spinal curvatures, musculoskeletal and joint abnormalities, skin sores,
precocious puberty, and sexual dysfunction.
The diagnosis of Spina Bifida is made on the basis of clinical manifestations and examination of the
meningeal sac. Diagnostic measures used to evaluate the brain and spinal cord include MRI,
ultrasonography, and CT. A neurologic evaluation will determine the extent of involvement of bowel and
bladder function as well as lower extremity neuromuscular involvement. Flaccid paralysis of the lower
extremities is a common finding with absent deep tendon reflexes.
Ultrasonographic scanning of the uterus and elevated maternal concentrations of α-fetoprotein (AFP,
or MS-AFP), a fetal specific γ-1-globulin, in amniotic fluid may indicate anencephaly or
myelomeningocele. The optimum time for performing these diagnostic tests is between 16 and 18 weeks
of gestation before AFP concentrations normally diminish and in sufficient time to permit a therapeutic
abortion. It is recommended that such diagnostic procedures and genetic counseling be considered for
all mothers who have borne an affected child, and testing is offered to all pregnant women.
Management of the child who has a myelomeningocele requires a multidisciplinary team approach
involving the specialties of neurology, neurosurgery, pediatrics, urology, orthopedics, rehabilitation,
physical therapy, occupational therapy, and social services, as well as intensive nursing care in a variety
of specialty areas. The collaborative efforts of these specialists focus on (1) the myelomeningocele and
the problems associated with the defect—hydrocephalus, paralysis, orthopedic deformities (e.g.,
developmental dysplasia of the hip, clubfoot; scoliosis), and genitourinary abnormalities; (2) possible
acquired problems that may or may not be associated, such as Chiari II malformation, meningitis,
seizures, hypoxia, and hemorrhage; and (3) other abnormalities, such as cardiac or gastrointestinal (GI)
malformations. Many hospitals have routine outpatient care by multidisciplinary teams to provide the
complex follow-up care needed for children with myelodysplasia. Many authorities believe that early
closure, within the first 24 to 72 hours, offers the most favorable outcome. Surgical closure within the first
24 hours is recommended if the sac is leaking CSF.
A variety of neurosurgical and plastic surgical procedures are used for skin closure without disturbing
the neural elements or removing any portion of the sac. The objective is satisfactory skin coverage of the
lesion and meticulous closure. Wide excision of the large membranous covering may damage functioning
neural tissue. Associated problems are assessed and managed by appropriate surgical and supportive
measures. Shunt procedures provide relief from imminent or progressive hydrocephalus. When
diagnosed, ventriculitis, meningitis, urinary tract infection, and pneumonia are treated with vigorous
antibiotic therapy and supportive measures. Surgical intervention for Chiari II malformation is indicated
only when the child is symptomatic (i.e., high-pitched crowing cry, stridor, respiratory difficulties, oral-
motor difficulties, upper extremity spasticity).
Initial care of the newborn involves preventing infection; performing a neurologic assessment,
including observing for associated anomalies; and dealing with the impact of the anomaly on the family.
Surgery to close and repair the lesion usually occurs within 24 to 48 hours of the infant’s birth to reduce
infection risk. As the child grows, braces are used to support joint position and mobility. Assistive devices
such as walkers, crutches, and wheelchairs are used to enhance mobility. To minimize the risk for
osteoporosis, the diet should ensure adequate calcium and vitamin D, and weight-bearing activities
should be encouraged. Surgery to release a tethered spinal cord may be needed. An orthotic jacket may
be prescribed to correct spinal deformities that affect lung capacity and interfere with mobility and sitting.
Interventions for a neurogenic bladder are initiated early to prevent kidney damage, to maintain bladder
function, and to promote urinary continence. Clean intermittent catheterization is performed on a regular
schedule (every 3 to 4 hours). A Mitrofanoff procedure that creates a reservoir for urine and a stoma for
catheterization in the umbilicus may be performed. Dietary fiber, stool softeners, and glycerin or bisacodyl
suppositories are prescribed for bowel evacuation and to promote bowel continence. Surgery to create a
channel between the skin and bowel using the appendix (Malone antegrade continence enema) is often
performed in children with fecal incontinence or severe constipation at the same time as the Mitranoff
procedure. This procedure enables a child or adolescent to infuse an enema into the ascending and
transverse colon to promote bowel evacuation to eliminate fecal soiling and incontinence. Prognosis
depends on the type of defect, the level of the lesion, and other complicating factors, such as renal
dysfunction.

HYDROCEPHALUS
Hydrocephalus is a condition caused by an imbalance in the production and absorption of CSF in the
ventricular system. When production is greater than absorption, CSF accumulates within the ventricular
system, usually under increased pressure, producing passive dilation of the ventricles. The condition may
be congenital or acquired as a result of intraventricular hemorrhage, meningitis, traumatic brain injury, or
brain tumor. An estimated 1 to 2 infants per 1000 are born with hydrocephalus
Hydrocephalus may be either communicating or noncommunicating. In communicating
hydrocephalus, the CSF flows freely among normal channels and pathways, but CSF absorption in the
subarachnoid space and the arachnoid villi is impaired. It may be acquired or caused by a congenital
malformation in the subarachnoid spaces. Noncommunicating hydrocephalus accounts for most cases
in children. It results from a blockage in the ventricular system that prevents CSF from entering the
subarachnoid space, resulting in enlargement of one or more ventricles. This obstruction can be caused
by infection, hemorrhage, tumor, surgery, or structural deformity. Congenital structural defects include
the Chiari type II malformation (found in children with myelomeningocele), aqueduct of Sylvius stenosis,
and the Dandy-Walker syndrome (includes hydrocephalus, a posterior fossa cyst, and hypoplasia of the
cerebellum).
The Arnold-Chiari malformation (Chiari type II) involves a downward placement of the medulla and
lower cerebellum through the foramen magnum of the skull into the cervical vertebrae. This displacement
can cause sudden death, respiratory difficulty, swallowing difficulties, and the need for assisted
ventilation. Symptoms during infancy may include stridor, a weak cry, and apnea. An older child may
have an extremity weakness, difficulty swallowing, choking, hoarseness, vocal cord paralysis, and breath-
holding episodes. This defect is also associated with intellectual disability and epilepsy.
The factors that influence the clinical picture in hydrocephalus are the time of onset, acuity of onset,
and associated structural malformations. In infancy, before closure of the cranial sutures, head
enlargement is the predominant sign, but in older infants and children, the lesions responsible for
hydrocephalus produce other neurologic signs through pressure on adjacent structures before causing
CSF obstruction. In infants with hydrocephalus, the head grows at an abnormal rate; fontanels are bulging
and nonpulsatile; scalp veins are dilated, especially when the infant cries; and skull bones are thin with
separated sutures, causing a cracked-pot sound (Macewen sign) when palpated. In severe cases, infants
display frontal protrusion (frontal bossing), eyes depressed and rotated downward (setting-sun sign), and
sluggish pupils. The signs and symptoms in early to late childhood are caused by increased ICP, and
specific manifestations are related to the focal lesion. Most commonly resulting from posterior fossa
neoplasms and aqueduct stenosis, the clinical manifestations are primarily those associated with space-
occupying lesions (e.g., headaches on awakening with improvement after emesis or being in an upright
position, strabismus, ataxia).
Hydrocephalus in infants is based on head circumference that crosses at least one percentile line on
the head measurement chart within 2 to 4 weeks.
In evaluation of a preterm infant, specially adapted
head circumference charts are consulted to
distinguish abnormal head growth from normal
rapid head growth. The primary diagnostic tools to
detect hydrocephalus in older infants and children
are CT and MRI. Diagnostic evaluation of children
who have symptoms of hydrocephalus after
infancy is similar to that used in those with
suspected intracranial tumor. In neonates,
echoencephalography is useful in comparing the
ratio of lateral ventricle to cortex.

The treatment of hydrocephalus is directed

toward relief of the hydrocephalus, treatment of the
cause, treatment of associated complications, and management of problems related to the effect of the
disorder on psychomotor development. The treatment is, with few exceptions, surgical. This is
accomplished by direct removal of an obstruction (e.g., a tumor) or placement of a shunt that provides
primary drainage of the CSF from the ventricles to an extracranial compartment, usually the peritoneum
(ventriculoperitoneal [VP] shunt). Most shunt systems consist of a ventricular catheter, a flush pump, a
unidirectional flow valve, and a distal catheter. In all models, the valves are designed to open at a
predetermined intraventricular pressure and close when the pressure falls below that level, thus
preventing backflow of secretions. The major complications of VP shunts are malfunction and infection.
All shunts are subject to mechanical difficulties, such as kinking, plugging, or separation or migration of
the tubing. Malfunction is most often caused by mechanical obstruction either within the ventricles from
particulate matter (tissue or exudate) or at the distal end from thrombosis or displacement as a result of
growth. Revisions are needed when signs of malfunction appear. The child with a shunt obstruction is
often first seen in an emergency department with clinical manifestations of increased ICP, frequently
accompanied by worsening neurologic status. The most serious complication, shunt infection, can occur
at any time, but the period of greatest risk is 1 to 2 months after placement. The infection is generally a
result of intercurrent infections at the time of shunt placement. Infections include septicemia, bacterial
endocarditis, wound infection, shunt nephritis, meningitis, and ventriculitis. Meningitis and ventriculitis are
of greatest concern because any complicating CNS infection is a significant predictor of poor intellectual
outcome. Infection is treated with antibiotics administered intravenously or intrathecally for a minimum of
7 to 10 days. A persistent infection requires removal of the shunt until the infection is controlled. External
ventricular drainage (EVD) is used until CSF is sterile. The EVD allows for removal of CSF through a
tube that is placed in the child’s ventricle and flows by gravity into a collection device. An alternative to
shunt placement is the endoscopic third ventriculostomy in children with noncommunicating
hydrocephalus. In this procedure, a small opening is made in the floor of the third ventricle that allows
the CSF to flow freely through the previously blocked ventricle. Complications include CSF leak,
intraventricular hemorrhage, meningitis, cranial nerve injury, obstruction, and hypothalamic injury.
The prognosis for children with treated hydrocephalus depends largely on the rate at which
hydrocephalus develops, the duration of increased ICP, the frequency of complications, and the cause
of the hydrocephalus. For example, children with malignant tumors may have a high mortality rate
regardless of other complicating factors. Surgically treated hydrocephalus with continued neurosurgical
and medical management has a survival rate of about 80%, with the highest incidence of mortality
occurring within the first year of treatment. Approximately 60% were reported to have normal intellectual
ability, but only 30% had an intelligence quotient (IQ) above 90.
An infant with diagnosed or suspected hydrocephalus is observed carefully for signs of increasing
ventricular size and increasing ICP. In infants, the head is measured daily at the largest point, the
occipitofrontal circumference. Fontanels and suture lines are palpated for size, signs of bulging,
tenseness, and separation. Irritability, lethargy, or seizure activity, as well as altered vital signs and
feeding behavior, may indicate an advancing pathologic condition. In older children, the most valuable
indicators of increasing ICP are alterations in the child’s LOC, headaches, and changes with
environmental interactions. Changes are identified by observation and by comparison of present behavior
with customary behavior, sleep patterns, developmental capabilities, and habits, obtained through a
detailed history and a baseline assessment. This baseline information serves as a guide for postoperative
assessment and evaluation of shunt function. The nurse is responsible for preparing the child for
diagnostic tests such as MRI or CT scan and for assisting with procedures such as a ventricular tap,
which is often performed to relieve excessive pressure during the preoperative period and for CSF
examination. Sedation is required because the child must remain still during diagnostic testing.

In addition to routine postoperative care and observation, the infant or child is positioned carefully on
the unoperated side to prevent pressure on the shunt valve. The child is kept flat to avoid complications
resulting from too-rapid reduction of intracranial fluid. The surgeon indicates the position to be maintained
and the extent of activity allowed. Pain management can be achieved with acetaminophen with or without
codeine for mild to moderate pain and opioids for severe pain. Observation is continued for signs of
increased ICP, which indicates obstruction of the shunt. Neurologic assessment includes evaluation of
pupillary dilation (pressure causes compression or stretching of the oculomotor nerve, producing dilation
on the same side as the pressure) and blood pressure (hypoxia to the brainstem causes variability in
these vital signs). If there is increased ICP, the surgeon will prescribe elevation of the head of the bed
and allow the child to sit up to enhance gravity flow through the shunt.
Because infection is the greatest hazard of the postoperative period, nurses are continually on the
alert for the usual manifestations of CSF infection, such as elevated temperature, poor feeding, vomiting,
decreased responsiveness, and seizure activity. There may be signs of local inflammation at the
operative sites and along the shunt tract. The child is also observed for abdominal distention because
CSF may cause peritonitis or a postoperative ileus as a complication of distal catheter placement.
Antibiotics are administered by the IV route as ordered, and the nurse may also need to assist with
intraventricular instillation. The incision site is inspected for leakage, and any suspected drainage is
tested for glucose, an indication of CSF. The management of hydrocephalus in a child is a demanding
task for both family and health professionals and helping a family cope with the child’s difficulties is an
important nursing responsibility. Children with hydrocephalus have lifelong special health care needs and
require evaluation on a regular basis. The overall aim is to establish realistic goals and an appropriate
educational program that will help the child to achieve his or her optimal potential.

MUSCULOSKELETAL AND NEUROMUSCULAR DYSFUNCTION

SOFT TISSUE INJURY
Injuries to the muscles, ligaments, and tendons are common in children. In young children, soft-tissue
injury usually results from mishaps during play. In older children and adolescents, participation in sports
is a common cause of such injuries.
1. Contusions
A contusion (bruise) is damage to the soft tissue, subcutaneous structures, and muscle. The
tearing of these tissues and small blood vessels and the inflammatory response led to
hemorrhage, edema, and associated pain when the child attempts to move the injured part. The
escape of blood into the tissues is observed as ecchymosis, a black and blue discoloration.
Large contusions cause gross swelling, pain, and disability and usually receive immediate
attention from health personnel. Smaller injuries may go unnoticed, allowing continued
participation. However, they can become disabling after rest because of pain and muscle spasm.
Immediate treatment consists of cold application, as in the treatment of sprains described below.
Return to participation is allowed when the strength and range of motion of the affected extremity
are equal to those of the opposite extremity or are demonstrated under conditions such as sport-
specific tests. Myositis ossificans may occur from deep contusions to the biceps or quadriceps
muscles; this condition may result in a restriction of flexibility of the affected limb.
Crush injuries occur when children’s extremities or digits are crushed (e.g., fingers slammed
in doors, folding chairs, or equipment) or hit (as when hammering a nail). A severe crush injury
involves the bone, with swelling and bleeding beneath the nail (subungual) and sometimes
laceration of the pulp of the nail. The subungual hematoma can be released by creating a hole at
the proximal end of the nail with a special cautery device or a heated sterile 18-gauge needle.
2. Dislocations
Long bones are held in approximation to one another at the joint by ligaments. A dislocation
occurs when the force of stress on the ligament is so great as to displace the normal position of
the opposing bone ends or the bone end to its socket. The predominant symptom is pain that
increases with attempted passive or active movement of the extremity. In dislocations, there may
be an obvious deformity and inability to move the joint. Children with naturally lax joints are more
prone to dislocation of joints. Dislocation of the phalanges is the most common type seen in
children, followed by elbow dislocation. In the adolescent population, shoulder dislocations are
more common and dislocation unaccompanied by fracture is rare.
A common injury in young children is subluxation, or partial dislocation, of the radial head,
also called pulled elbow or nursemaid’s elbow. In the majority of cases, the injury occurs in a child
younger than 5 years of age who receives a sudden longitudinal pull or traction at the wrist while
the arm is fully extended, and the forearm pronated. It usually occurs when an individual who is
holding the child by the hand or wrist gives a sudden pull or jerk to prevent a fall or attempts to lift
the child by pulling the wrist or when the child pulls away by dropping to the floor or ground. The
child often cries, appears anxious, complains of pain in the elbow or wrist, and refuses to use the
affected limb. The practitioner manipulates the arm by applying firm finger pressure to the head
of the radius and then supinates and flexes the forearm to return the bone structure to normal
alignment. A click may be heard or felt, and functional use of the arm returns within minutes.
Immobilization is not required. However, the longer the subluxation is present, the longer it takes
for the child to recover mobility after treatment. No anesthetic is usually required, but a mild pain
reliever such as acetaminophen or ibuprofen may be administered. In an older child, severe elbow
injury or dislocation should be immediately evaluated by a practitioner. If a traumatic elbow injury
in a younger child is not a subluxation or if attempts at reduction are unsuccessful, the child should
be carefully evaluated, with the consideration of radiographs.
In children younger than 5 years of age, the hip can be dislocated by a fall. The greatest risk
after this injury is the potential loss of blood supply to the head of the femur. Relocation of the hip
within 60 minutes after the injury provides the best chance for prevention of damage to the femoral
head.
Shoulder dislocations and separations occur most often in older adolescents and are often
sports related. Temporary restriction of the joint, with a sling or bandage that secures the arm to
the chest in a shoulder dislocation, can provide sufficient comfort and immobilization until medical
attention is received. Simple dislocations should be reduced as soon as possible with the child
under procedural sedation combined with local anesthesia. An unreduced dislocation may be
complicated by increased swelling, making reduction difficult and increasing the risk of
neurovascular problems. Treatment is determined by the severity of the injury.
3. Sprains
A sprain occurs when trauma to a joint is so severe that a ligament is partially or completely
torn or stretched by the force created as a joint is twisted or wrenched, often accompanied by
damage to associated blood vessels, muscles, tendons, and nerves. Common sprain sites include
ankles and knees.
The presence of joint laxity is the most valid indicator of the severity of a sprain. In a severe
injury, the child complains of the joint “feeling loose” or as if “something is coming apart” and may
describe hearing a “snap,” “pop,” or “tearing.” Pain may or may not be the principal subjective
symptom, and in some children, it may prevent optimal examination of ligamentous instability.
 There is a rapid onset of swelling, often diffuse, accompanied by immediate disability and
appreciable reluctance to use the injured joint.
4. Strains
A strain is a microscopic tear to the musculotendinous unit and has features in common with
sprains. The area is painful to touch and swollen. Most strains are incurred over time rather than
suddenly, and the rapidity of the appearance provides clues regarding severity. In general, the
more rapidly the strain occurs, the more severe the injury. When the strain involves the muscular
portion, there is more bleeding, often palpable soon after injury and before edema obscures the
hematoma.
The first 12 to 24 hours are the most critical period for virtually all soft-tissue injuries. Basic principles
of managing sprains and other soft-tissue injuries are summarized in the acronyms RICE and ICES.
Rest Ice
Ice Compression
Compression Elevation
Elevation Support

Soft-tissue injuries should be iced immediately. This is best accomplished with crushed ice wrapped
in a towel, a screw-top ice bag, or a resealable plastic storage bag. Chemical-activated ice packs are
also effective for immediate treatment but are not reusable and must be closely monitored for leakage. A
wet elastic wrap, which transfers cold better than dry wrap, is applied to provide compression and to keep
the ice pack in place. A cloth barrier should be used between the ice container and the skin to prevent
trauma to the tissues. Ice has a rapid cooling effect on tissues that reduces edema and pain. Ice should
never be applied for more than 30 minutes at a time.
Elevating the extremity uses gravity to facilitate venous return and reduce edema formation in the
damaged area. The point of injury should be kept several inches above the level of the heart for therapy
to be effective. Several pillows can be used for elevation. Allowing the extremity to be dependent causes
excessive fluid accumulation in injury, delaying healing and causing painful swelling.
Torn ligaments, especially those in the knee, are usually treated by immobilization with a knee
immobilizer or a knee brace that allows flexion and extension until the child is able to walk without a limp.
Crutches are used for mobility to rest the affected extremity. Passive leg exercises, gradually increased
to active ones, are begun as soon as sufficient healing has taken place. Parents and children are
cautioned against using any form of liniment or other heat-producing preparation before examination. If
the injury requires casting or splinting, the heat generated in the enclosed space can cause extreme
discomfort and even tissue damage. In some cases, torn knee ligaments are managed with arthroscopy
and ligament repair or reconstruction as necessary depending on the extent of the tear, ligaments
involved, and child’s age. Surgical reconstruction of the anterior cruciate ligament may be performed in
young athletes who wish to continue in active sports.

FRACTURES
Bone fractures occur when the resistance of bone against the stress being exerted yields to the stress
force. Fractures are a common injury at any age but are more likely to occur in children and older adults.
Because childhood is a time of rapid bone growth, the pattern of fractures, problems of diagnosis, and
methods of treatment differ in children compared with adults. In children, fractures heal much faster than
in adults. Consequently, children may not require as long a period of immobilization of the affected
extremity as an adult with a fracture.
 Fracture injuries in children are most often a result of traumatic incidents at home, at school, in a
motor vehicle, or in association with recreational activities. Children’s everyday activities include vigorous
play that predisposes them to injury, including climbing, falling, running into immovable objects,
skateboarding, trampolines, skiing, playground activities, and receiving blows to any part of their bodies
by a solid, immovable object.
Aside from automobile accidents or falls from heights, true injuries that cause fractures rarely occur
in infancy. Bone injury in children of this age group warrants further investigation. In any small child,
radiographic evidence of fractures at various stages of healing is, with few exceptions, a result of
nonaccidental trauma (child abuse). Any investigation of fractures in infants, particularly multiple
fractures, should include consideration of osteogenesis imperfecta (OI) after nonaccidental trauma has
been ruled out.
Fractures in school-age children are often a result of playground falls or bicycle–automobile or
skateboard injuries. Adolescents are vulnerable to multiple and severe trauma because they are mobile
on bicycles, all-terrain vehicles, skateboards, skis, snowboards, trampolines, and motorcycles and are
active in sports.
A distal forearm (radius, ulna, or both) fracture is the most common fracture in children. The clavicle
is also a common fracture sustained in childhood, with approximately half of clavicle fractures occurring
in children younger than 10 years of age. Common mechanisms of injury include a fall with an
outstretched hand or direct trauma to the bone. In neonates, a fractured clavicle may occur with a large
newborn and a small maternal pelvis. This may be noted in the first few days after birth by a unilateral
Moro reflex or at the 2-week well-child check, when a fracture callus is palpated on the infant’s healing
clavicle.
A fractured bone consists of fragments—the fragment closer to the midline, or the proximal fragment,
and the fragment farther from the midline, or the distal fragment. When fracture fragments are separated,
the fracture is complete; when fragments remain attached, the fracture is incomplete. The fracture line
can be any of the following:
• Transverse—Crosswise at right angles to the long axis of the bone
• Oblique—Slanting but straight between a horizontal and a perpendicular direction
• Spiral—Slanting and circular, twisting around the bone shaft
The twisting of an extremity while the bone is breaking results in a spiral break. If the fracture does
not produce a break in the skin, it is a simple, or closed, fracture. Open, or compound, fractures are those
with an open wound through which the bone protrudes. If the bone fragments cause damage to other
organs or tissues (e.g., lung, liver), the injury is said to be a complicated fracture. When small fragments
of bone are broken from the fractured shaft and lie in the surrounding tissue, the injury is a comminuted
fracture. This type of fracture is rare in children. The types of fractures that are seen most often in children
are:
1. Plastic deformation—Occurs when the bone is bent but not broken. A child’s flexible bone can be
bent 45 degrees or more before breaking. However, if bent, the bone will straighten slowly but not
completely, producing some deformity but without the angulation seen when the bone breaks.
Bends occur most commonly in the ulna and fibula, often in association with fractures of the radius
and tibia.
2. Buckle, or torus, fracture—Produced by compression of the porous bone; appears as a raised or
bulging projection at the fracture site. These fractures occur in the most porous portion of the
bone near the metaphysis (the portion of the bone shaft adjacent to the epiphysis) and are more
common in young children.
 3. Greenstick fracture—Occurs when a bone is angulated beyond the limits of bending. The
compressed side bends, and the tension side fails, causing an incomplete fracture similar to the
break observed when a green stick is broken.
4. Complete fracture—Divides the bone fragments. These fragments often remain attached by a
periosteal hinge, which can aid or hinder reduction.

The weakest point of long bones is the cartilage growth plate, or the physis. Consequently, this is a
frequent site of damage of childhood trauma. Growth plate fractures are classified with the Salter-Harris
classification system. Detection of physeal injuries is sometimes difficult but critical. Close monitoring and
early treatment, if indicated, is essential to prevent longitudinal or angular growth deformities (or both).
Treatment of these fractures may include surgical open reduction and internal fixation to prevent or
reduce growth disturbances. Immediately after a fracture occurs, the muscles contract and physiologically
splint the injured area. This phenomenon accounts for the muscle tightness observed over a fracture site
and the deformity that is produced as the muscles pull the bone ends out of alignment. This muscle
response must be overcome by traction or complete muscle relaxation (e.g., anesthesia) to realign the
distal bone fragment to the proximal bone fragment.
Bone healing is rapid in growing children because of the thickened periosteum and generous blood
supply. When there is a break in the continuity of bone, the osteoblasts are stimulated to maximal activity.
New bone cells are formed in immense numbers almost immediately after the injury and, in time, are
evidenced by a bulging growth of new bone tissue between the fractured bone fragments. This is followed

by deposition of calcium salts to form a callus. Remodeling is a process that occurs in the healing of long
bone fractures in growing children. The irregularities produced by the fracture become indistinct as the
angles and bone overgrowth are smoothed out, giving the bone a straighter appearance. A general rule
of thumb is that an angulated fracture in a growing child will remodel by one degree per month.
Fractures heal in less time in children than in adults. The approximate healing times for a femoral
shaft are as follows: Neonatal period—2 to 3 weeks, Early childhood—4 weeks, Later childhood—6 to 8
weeks, and Adolescence—8 to 12 weeks.
A history of the injury may be lacking in childhood injuries. Infants and toddlers are unable to
communicate, and older children may not volunteer information (even under direct questioning) when the
injury occurred during questionable activities. Whenever possible, it is helpful to obtain information from
someone who witnessed the injury. In cases of nonaccidental trauma, providers may give false
information to protect themselves or family members. The child may exhibit generalized swelling, pain or
tenderness, deformity, and diminished functional use of affected limb or digit. They may also demonstrate
bruising, severe muscular rigidity, and crepitus (grating sensation at fracture site). However, often a
fracture is remarkably stable because of intact periosteum. The child may even be able to use an affected
arm or walk on a fractured leg. Because bones are highly vascular, a soft, pliable hematoma may be felt
around the fracture site.
Radiographic examination is the most useful diagnostic tool for assessing skeletal trauma. The
calcium deposits in bone make the entire structure radiopaque. Radiographic films are taken after fracture
reduction and, in some cases, may be taken during the healing process to determine satisfactory
progress.
The goals of fracture management are:
• To regain alignment and length of the bony fragments (reduction)
• To retain alignment and length (immobilization)
• To restore function to the injured parts
• To prevent further injury and deformity.
Fractures are splinted or casted to immobilize and protect the injured extremity. Children with
displaced fractures may have immediate surgical reduction and fixation (internal or external) rather than
being immobilized by traction. Some conditions require immediate medical attention, including open
fractures, compartment syndrome, fractures associated with vascular or nerve injury, and joint
dislocations that are unresponsive to reduction maneuvers.
In children, immobilization is used until adequate callus is formed. The position of the bone fragments
in relation to one another influences the rapidity of healing and residual deformity. Weight bearing and
active movement for the purpose of regaining function may begin after the fracture site is determined to
be stable by the medical provider. The child’s natural tendency to be active is usually sufficient to restore
normal mobility, and physical or occupational therapy is rarely indicated.
Nursing care focuses on care of the child before and after fracture reduction, encouraging mobility as
ordered, maintaining skin integrity, preventing infection, and teaching the parents and child how to care
for the fracture. If sedation or pain blocks are used, nursing care for these procedures is needed.

DEVELOPMENTAL DYSPLASIA OF THE HIP

Developmental dysplasia of the hip (DDH) describes a spectrum of disorders related to abnormal
development of the hip that may occur at any time during fetal life, infancy, or childhood. A change in
terminology from congenital hip dysplasia and congenital dislocation of the hip to DDH more properly
reflects a variety of hip abnormalities in which there is a shallow acetabulum, subluxation, or dislocation.
The incidence of hip instability is approximately 1.5 per 1000 live births, and approximately 15% to 50%
of infants with DDH are born breech. Girls are affected more commonly (80%) and there is a positive
family history in approximately 12% to 33% of affected individuals.
The cause of DDH is unknown, but certain factors such as gender, birth order, family history,
intrauterine position, delivery type, joint laxity, and postnatal positioning are believed to affect the risk of
DDH. Predisposing factors associated with DDH may be divided into three broad categories:
1. physiologic factors, which include maternal hormone secretion and intrauterine positioning;
2. Mechanical factors, which involve breech presentation, multiple fetus, oligohydramnios, and large
infant size (other mechanical factors may include continued maintenance of the hips in adduction
and extension that will in time cause a dislocation);
3. Genetic factors, which entail a higher incidence of DDH in siblings of affected infants and an even
greater incidence of recurrence if a sibling and one parent were affected.
 Three degrees of DDH are:
1. Acetabular dysplasia—This is the mildest form of DDH, in which there is neither
subluxation nor dislocation. There is a delay in acetabular development evidenced by
osseous hypoplasia of the acetabular roof that is oblique and shallow, although the
cartilaginous roof is comparatively intact. The femoral head remains in the acetabulum.
2. Subluxation—The largest percentage of DDH, subluxation, implies incomplete dislocation
of the hip and is sometimes regarded as an intermediate state in the development from
primary dysplasia to complete dislocation. The femoral head remains in contact with the
acetabulum, but a stretched capsule, and ligamentum teres cause the head of the femur
to be partially displaced. Pressure on the cartilaginous roof inhibits ossification and
produces a flattening of the socket.
3. Dislocation—The femoral head loses contact with the acetabulum and is displaced
posteriorly and superiorly over the fibrocartilaginous rim. The ligamentum teres is
elongated and taut.
Developmental dysplasia of the hip is often not detected at the initial examination after birth; thus, all
infants should be carefully monitored for hip dysplasia at follow-up visits throughout the first year of life
at routine well-child checks. In the newborn period, hip dysplasia usually appears as hip joint laxity rather
than as outright dislocation. Subluxation and the tendency to dislocate can be demonstrated by the
Ortolani or Barlow tests. The Ortolani and Barlow tests are most reliable from birth to 4 weeks of age.
With the Barlow test, the thighs are adducted; the Ortolani test involves abducting the thighs to test for
hip subluxation or dislocation. Other signs of DDH are shortening of the limb on the affected side,
asymmetric thigh and gluteal folds, broadening of the perineum (in bilateral dislocation), and decreased
hip abduction on the affected side.
Radiographic examination in early infancy is not reliable because ossification of the femoral head
does not normally take place until the fourth to sixth month of life. However, the cartilaginous head can
be visualized directly by ultrasonography. Universal newborn screening with ultrasonography has been
proposed; however, numerous studies reveal that this approach has a high rate of false-positive results
and subsequent overtreatment. Therefore, ultrasonography is recommended as an adjunct to other
diagnostic procedures. In infants older than age 4 months and in children, radiographic examination is
useful in confirming the diagnosis. An upward slope in the roof of the acetabulum (the acetabular angle)
greater than 30 degrees with upward and outward displacement of the femoral head is a frequent finding
in older children. Computed tomography (CT) may be useful to assess the position of the femoral head
relative to the acetabulum after closed reduction and casting.
Treatment should begin as soon as the condition is recognized because early intervention is more
favorable to the restoration of normal bony architecture and function. The longer treatment is delayed,
the more severe the deformity, the more difficult the treatment, and the less favorable the prognosis. The
treatment varies with the child’s age and the extent of the dysplasia. The goal of treatment is to obtain
and maintain a safe, congruent position of the hip joint to promote normal hip joint development. The hip
joint is maintained by dynamic splinting in a safe position with the proximal femur centered in the
acetabulum in an attitude of flexion. Of the numerous devices available, the Pavlik harness is the most
widely used, and with time, motion, and gravity, the hip works into a more abducted, reduced position.
 The harness is worn continuously until the hip
is proved stable on clinical and ultrasound
examination, usually in 6 to 12 weeks. When
adduction contracture is present, other devices
(Bryant traction) are used to stretch the hip slowly
and gently to full abduction, after which wide
abduction is maintained until stability is attained.
When there is difficulty in maintaining stable
reduction, a hip spica cast is applied and changed
periodically to accommodate the child’s growth.
After 3 to 6 months, sufficient stability is acquired
to allow transfer to a removable protective
abduction brace. The duration of treatment depends on development of the acetabulum but is usually
accomplished within the first year. For ages 6 to 24 months, the dislocation is often not recognized until
the child begins to stand and walk, when attendant shortening of the limb and contractures of hip adductor
and flexor muscles become apparent (DDH hip radiograph). A surgical closed reduction is performed,
and the child is placed in a spica cast for approximately 12 weeks. An abduction orthosis may be used
instead of a hip spica cast. In the event that the hip remains unstable, an open reduction is performed.
Correction of the hip deformity in older children is inherently more difficult than in the preceding age
groups because secondary adaptive changes and other etiologic factors (juvenile arthritis or non-
ambulatory cerebral palsy) complicate the condition. Operative reduction, which may involve preoperative
traction, tenotomy of contracted muscles, and any one of several innominate osteotomy procedures
designed to construct an acetabular roof, often combined with proximal femoral osteotomy, are usually
required. After cast removal, range-of-motion exercises help restore movement. Successful reduction
and reconstruction become increasingly difficult after the age of 4 years and are usually impossible or
inadvisable in children older than 6 years of age because of severe shortening and contracture of muscles
and deformity of the femoral and acetabular structures.
Nursing care varies according to the medical treatment and the child’s age. Management includes
maintaining traction, if ordered; providing cast care; preventing complications resulting from immobility;
promoting normal growth and development; and teaching parents about the condition and care
(management of a cast or a Pavlik harness). Because treatment may interfere with the child’s normal
movement, the treatment plan should take into consideration the age and developmental stage of the
child to substitute activities to stimulate development.

SCOLIOSIS
Scoliosis is a lateral S- or C-shaped curvature of the spine that is often associated with a rotational
deformity of the spine and ribs. Many people exhibit some degree of spinal curvature; curvatures of more
than 10 degrees are considered abnormal. Curves are either idiopathic or compensatory, the latter
occurring as the spine curves to compensate for a structural deformity such as leg length discrepancy.
Idiopathic scoliosis occurs most often in girls, especially during the growth spurt between the ages of 10
and 13 years. From 1% to 3% of adolescents manifest with idiopathic scoliosis of greater than 10 degrees.
A smaller number of children manifest infantile scoliosis before 3 years of age or juvenile scoliosis from
3 to 10 years.
The cause of scoliosis is complex. Structural scoliosis may be congenital, idiopathic, or acquired
(associated with neuromuscular disorders such as muscular dystrophy or myelodysplasia, or secondary
to spinal cord injuries). In idiopathic structural scoliosis (the most common type), the spine for unknown
reasons begins to curve laterally, with vertebral rotation. The most common curve is a right thoracic and
left lumbar deformity. As the curve progresses, structural changes occur. The ribs on the concave side
(inside of the curve) are forced closer together, while the ribs on the convex side separate widely, causing
narrowing of the thoracic cage and formation of the rib hump. The lateral curvature affects the vertebral
structure. Disc spaces are narrowed on the concave side and spread wider on the convex side, resulting
in an asymmetric vertebral canal.
Scoliosis can also occur in congenital diseases involving the spinal structure and in the
musculoskeletal changes seen in conditions such as myelomeningocele, cerebral palsy, or muscular
dystrophy. Disturbances in platelet function, melatonin levels, and bone-related trace substances are
sometimes evident. Scoliosis can also be acquired after
injury to the spinal cord.
The classic signs of scoliosis include truncal
asymmetry, uneven shoulder and hip height, a one-
sided rib hump, and a prominent scapula. The child
does not usually complain of pain or discomfort.
Generally, observation and radiographic examination
are used to diagnose scoliosis. Additional diagnostic
studies include MRI, CT, and bone scanning, which are
used occasionally to assess the degree of curvature.
The goal of medical management is to limit or stop
progression of the curvature.
Early detection is essential to successful treatment.
Adequate treatment and follow-up maximize the child’s chances for proper spinal alignment. The
treatment regimen chosen depends on the degree and progression of the curvature and the reaction of
the child and family to medical management. Treatment of children with mild scoliosis (curvatures of 10
to 20 degrees) consists of exercises to improve posture and muscle tone and to maintain, or possibly
increase, flexibility of the spine. Emphasis is placed on building strength toward the outside of the curve
while stretching the inside of the curve. However, these exercises are not a cure, and the child should be
evaluated by a physician at 3-month intervals, with radiographic evaluation every 6 months. Medical
management of moderate scoliosis (curvatures of 20 to 40 degrees) includes bracing with a Boston brace.
The goal of wearing a brace is to maintain the existing spinal curvature with no increase. Brace wear
begins immediately after diagnosis. To achieve maximum effectiveness, the brace should be worn 23
hours per day. Brace treatment is lengthy, favorite sports may not be allowed, it can affect body image,
and it requires a high degree of compliance, all of which can be difficult for adolescents. Children with
severe scoliosis (curvatures of 40 to 50 degrees or more) generally require surgery, which involves spinal
fusion. Majority of spinal fusions are performed using segmental instrumentation of the spinal cord with
hooks, wires, rods, and screws. Examples of surgical approaches include Luque wires, Cotrel-Dubousset
(CD) instrumentation, Texas Scottish Rite Hospital system, and Moss-Miami system. These treatments
stabilize the spine well during surgery, may be accompanied by bone grafting to the spine, and require
no long-term therapy or postoperative casting; instrumentation remains permanently in the back.
Following surgery with wires or instrumentation, the child is on bed rest during a recovery period and then
is generally fitted with anteroposterior plastic shells (also called thoracolumbar sacral orthotics) that are
worn for several months to provide stability for the spine.
An important aspect of nursing care is client education. Client adherence to prescribed measures is
critical to the success of treatment. Children and their families need to understand the condition and the
stages of treatment; this is particularly true for adolescents undergoing treatment for scoliosis. Children
or adolescents facing surgery require education, reassurance, and support. Teach about pain control and
the patient-controlled analgesia (PCA) pump. Often children donate some of their own blood prior to
surgery, and the family may also donate so blood transfused in surgery is the children’s or a family
member’s. Teach the child the safety that this ensures. The adolescent will benefit from learning about
deep breathing, positioning, surgical incision, and all other aspects of postoperative care.

CEREBRAL PALSY (CP)

Cerebral palsy a common syndrome of movement and posture development disorders, is caused by
a nonprogressive lesion abnormality in the fetal or infant brain that results in activity limitations. The
condition may also have associated hearing, vision, communication, perceptual, cognitive, and
behavioral problems. An estimated prevalence of CP is 3.9 children per 1000. Four types of motor
dysfunction seen— spastic, dyskinetic, ataxic, and mixed—are related to the location of brain insult.
Dystonia and athetosis are sometimes categorized together as dyskinesia.
• Spastic
o Cerebral cortex or pyramidal tract injury
o 75% of cases
o Manifestations:
▪ Increased muscle tone through a joint’s range of motion
▪ Leads to contractures and abnormal curvature of the spine
▪ Exaggerated deep tendon reflexes, clonus
▪ Persistent common newborn reflexes, positive Babinski sign
• Dyskinetic-Athetosis
o Extrapyramidal, basal ganglia injury
o 10-15% of cases
o Manifestations:
▪ Muscle tone abnormalities affecting the entire body
▪ Difficulty with fine and purposeful movements or coordinating the timing of
movement; tremors
▪ Slow involuntary writhing motions that interfere with ability to maintain a stable
posture
• Dyskinetic-Dystonia
o Basal ganglia, extrapyramidal injury
o Manifestations:
▪ Involuntary sustained muscle contractions that lead to sustained or intermittent
exaggerated and distorted posturing, twisting, or repetitive movements
▪ Rigid muscles when awake; normal or decreased muscle tone when asleep
• Ataxic
o Cerebellar (extrapyramidal) injury
o 5-10% of cases
o Manifestations:
▪ Abnormalities of voluntary movement (muscle instability) involving balance and
position of the trunk and limbs, difficulty maintaining posture, wide-based unsteady
gait
 ▪ Difficulty controlling hand and arm movements during reaching
▪ Increased or decreased muscle tone, hypotonia in first couple of years
• Mixed
o Multiple areas of brain are injured
o Manifestations:
▪ No dominant motor pattern; may have mild spasticity, dystonia, and/ or athetoid
movement

Most cases occur during the prenatal and perinatal periods. Risk factors include low birth weight,
placental abnormalities, birth defects, meconium aspiration, birth asphyxia, neonatal seizures, respiratory
distress syndrome, hypoglycemia, and neonatal infections. Postnatal cases are related to meningitis,
encephalitis, and traumatic brain injury.
Muscle growth is usually coordinated with bone growth, but muscle spasticity interferes. Contractures
can develop that limit joint movement or cause deformities such as scoliosis. Because of more limited
weight-bearing activity and potential nutritional problems with swallowing and independent feeding,
children with CP are at greater risk for osteoporosis and fractures.
Cerebral palsy is characterized by abnormal muscle tone and lack of coordination. Children have a
variety of symptoms depending on their ages, and the pattern or extremities involved may vary:
• Diplegia—both legs are affected
• Hemiplegia—one side of the body is involved the arm is usually more severely affected than the
leg
• Quadriplegia—all four extremities are affected
All children with CP have motor impairment, with spasticity present more commonly than ataxia or
athetosis and dystonia. Even if both sides of the body are affected, the impairment is usually more severe
on one side. Spasticity is also associated with muscle weakness that interferes with gross motor activities.
Children with CP usually have delayed developmental milestones. The functional consequences of
motor deficits become more obvious as the child grows even though the brain injury is nonprogressive.
Other complications include intellectual disabilities, vision impairments, hearing loss, speech and
language impairments, and seizures. Feeding may be difficult because of oral motor involvement,
including hypotonia, with poor sucking and swallowing coordination that may result in aspiration or poor
nutrition.
 Diagnosis is usually based on clinical findings of delayed development and increased or decreased
muscle tone. CP is difficult to diagnose in the early months of life because it must be distinguished from
other neurologic conditions and signs may be subtle. Ultrasonography can be used to detect fetal and
neonatal abnormalities of the brain, such as intraventricular hemorrhage. Neuromotor tests are used to
evaluate the presence of normal movement patterns, absence of common newborn reflexes, and
abnormal tone. Once CP is suspected, CT and MRI imaging provide information about anatomic
structures and help identify the cause of CP. Genetic and metabolic tests are performed if congenital
anomalies are present. Hearing and vision should be evaluated. Standardized tools, such as the
Functional Mobility Scale and Manual Ability Classification System, are used to describe the child’s
capabilities.
Clinical therapy focuses on helping the child develop to a maximum level of independence and to
perform activities of daily living. This involves promoting mobility, an optimal range of motion, muscle
control, balance, and communication with braces and splints, serial casting, and positioning devices
(prone wedges, standers, and side-lyers). Referrals are made for physical, occupational, and speech
therapy, as well as special education to improve motor function and ability. Orthopedic surgery may be
required to improve function by balancing muscle power and stabilizing uncontrollable joints. Surgical
interventions may include Achilles tendon lengthening to increase the ankle range of motion, hamstring
release to correct knee flexion contractures, procedures to improve hip adduction or correct spinal
deformities, or dorsal rhizotomy (cutting the afferent fibers that contribute to spasticity).
Medications are given to control seizures, to control spasms (skeletal muscle relaxants, baclofen, and
benzodiazepines), and to minimize gastrointestinal side effects (cimetidine or ranitidine).
Benzodiazepines affect brain control of muscle tone to help control spasticity. Dantrolene is a calcium
channel blocker that is a muscle relaxant. Baclofen is administered orally or by intrathecal pump to
decrease spasticity. Botulinum toxin injection into specific muscles is a therapy that helps to temporarily
control spasticity.
Nursing care focuses on providing adequate nutrition, maintaining skin integrity, promoting physical
mobility, promoting safety, promoting growth and development, teaching parents how to care for the child,
and providing emotional support.

CONGENITAL CLUBFOOT
Clubfoot is a congenital abnormality in which the foot is twisted out of its normal position. It occurs in
approximately 1 to 2 in 1000 births, affects boys nearly twice as often as girls, and is bilateral in about
half of affected infants. Clubfoot is a complex deformity of the ankle and foot that includes forefoot
adduction, midfoot supination, hindfoot varus, and ankle equinus. Deformities of the foot and ankle are
described according to the position of the ankle and foot. The more common positions involve the
following variations:
• Talipes varus—An inversion, or bending inward
• Talipes valgus—An eversion, or bending outward
• Talipes equinus—Plantar flexion, in which the
toes are lower than the heel
• Talipes calcaneus—Dorsiflexion, in which the
toes are higher than the heel
• Talipes equinovarus—Toes lower than the heel
and facing inward
 The exact cause of clubfoot is unknown; however, several possible etiologies have been proposed.
Some authorities believe abnormal intrauterine positioning causes the deformity. Others suspect
neuromuscular or vascular problems as causes. There is a genetic component in some cases because
the risk of having a second child with clubfoot when an earlier child is affected is 25%.
Diagnosis is made at birth on the basis of visual inspection. Radiographs are used to confirm the
severity of the condition. Early treatment is essential to achieve successful correction and reduce the
chance of complications. Serial casting is the treatment of choice. Casting should begin as soon as
possible after birth. Timing is critical because the short bones of the foot, which are primarily cartilaginous
at birth, begin to ossify shortly thereafter. The foot is manipulated to achieve maximum correction first of
the varus deformity and then of the equinus deformity. A long leg cast holds the foot in the desired
position. The cast is changed every 1 to 2 weeks. This regimen of manipulation and casting continues
for approximately 8 to 12 weeks until maximum correction is achieved. If the deformity has been
corrected, the child may begin wearing a splint or reverse cast (shaped so that the foot turns outward
away from the body instead of the normal inward turn) or corrective shoes to maintain the correction. If
the deformity has not been corrected, surgery is required. Casting holds the foot in position until surgery
is performed. The age at which a child undergoes clubfoot surgery varies among surgeons. However,
most children have surgery between 3 and 12 months of age. The one-stage posteromedial release
procedure, which involves realignment of the bones of the foot and release of the constricting soft tissue,
is most common. The foot is held in the proper position by one or more stainless steel pins. A cast is then
applied with the knee flexed to prevent damage to the pin and to discourage weight bearing. Casting
continues for 6 to 12 weeks. The child may then need to wear a brace or corrective shoes, depending on
the severity of the deformity and the surgeon’s preference.
The goal of treatment for clubfoot is to achieve a painless, plantigrade, and stable foot. Treatment of
clubfoot involves three stages: (1) correction of the deformity, (2) maintenance of the correction until
normal muscle balance is regained, and (3) follow-up observation to avert possible recurrence of the
deformity. Some feet respond to treatment readily; some respond only to prolonged, vigorous, and
sustained efforts; and the improvement in others remains disappointing even with maximal effort on the
part of all concerned. A common approach to clubfoot management is the Ponseti method. Serial casting
is begun shortly after birth. Weekly gentle manipulation and serial long-leg casts allow for gradual
repositioning of the foot. The extremity or extremities are casted until maximum correction is achieved,
usually within 6 to 10 weeks. Majority of the time, a percutaneous heel cord tenotomy is performed at the
end of the serial casting to correct the equinus. After the tenotomy, a long-leg cast is applied and left in
place for 3 weeks. A Denis Browne bar with Ponseti sandals or straightlaced shoes placed in abduction
are then fitted to prevent recurrence. Inability to achieve normal foot alignment after casting and tenotomy
indicates the need for surgical intervention.
Nursing management involves providing emotional support, educating the family about home care of
the child in a cast and the importance of keeping appointments at the outpatient facility for cast changes,
preparing the family for the child’s hospitalization if surgery is to occur, and providing postsurgical care.

Cerebral palsy - a group of permanent disorders of the development of movement and posture,
causing activity limitation, that are attributed to nonprogressive disturbances that occurred in the
developing fetal or infant brain.

Developmental dysplasia of the hip (DDH) - describes a spectrum of disorders related to abnormal
development of the hip that may occur at any time during fetal life, infancy, or childhood.

Epilepsy - is a condition characterized by two or more unprovoked seizures and can be caused by
a variety of pathologic processes in the brain.

Scoliosis - is a lateral S- or C-shaped curvature of the spine that is often associated with a rotational
deformity of the spine and ribs.

Spina bifida - refers to a defect in one or more vertebrae that allows spinal cord contents to
protrude.

Ball, J.W., Bindler, R. C., Cowen, K. J., Shaw, M. R., (2017). Principles of Pediatric Nursing: Caring
for Children, 7th Edition, (pp. 739-788). Pearson Education, Inc.

Study Questions

• Jack, age 6 years, was admitted to the pediatric unit for diagnosis and treatment of a possible
seizure.
1. What are the two major foci of the process of diagnosis in a child with a seizure
disorder?
2. While the nurse is assisting with breakfast, Jack has a brief loss of consciousness. The
nurse noted that his eyelids twitched, and his hands moved slightly. He then needed to
reorient himself to previous activity. How would the nurse keep Jack safe?
Ball, J.W., Bindler, R. C., Cowen, K. J., Shaw, M. R., (2017).
Principles of Pediatric Nursing: Caring for Children, 7th
Edition, (pp. 739-788). Pearson Education, Inc.

Fetveit A: Assessment of febrile seizures in children, Eur J

Pediatr 167:17–27, 2008.

Hampers LC, Spina LA: Evaluation and management of

pediatric febrile seizures in the emergency department,
Emerg Med Clin North Am 29(1):83–93, 2011.

Hockenberry, M. and Wilson, D. (2015). Wong’s Nursing Care

of Infants and Children 1st Philippine Edition, The Child
with Cerebral Dysfunction (Volume 2, pp. 1425-1490).
Mosby.

Hockenberry, M. and Wilson, D. (2013). Wong’s Essentials of

Pediatrics, 9th Edition, The Child with Cerebral
Dysfunction. (pp. 927-971, 1090-1103). Mosby

Ostergaard JR: Febrile seizures, Acta Paediatr 98:771–773,

2009

Rosenbaum P, Paneth N, Leviton A, and others: A report: the definition and classification of
cerebral palsy April 2006, Dev Med Child Neurol 49(S109):1–44, 2007.

Steering Committee on Quality Improvement and Management, Subcommittee on Febrile

Seizures American Academy of Pediatrics: Febrile seizures: clinical practice guideline for
the long-term management of the child with simple febrile seizures, Pediatrics 121(6):1281–
1286, 2008
BACHELOR OF SCIENCE IN NURSING
CARE OF MOTHER AND CHILD AND ADOLESCENT
COURSE MODULE COURSE UNIT WEEK
3 14 16
Life-threatening Conditions/ Acutely Ill/ Multi-organ Problems/ High Acuity and Emergency Situations
(Acute and Chronic)

✓ Read course and unit objectives

✓ Comprehend study guide prior to class attendance
✓ Read required learning resources; refer to unit
terminologies for jargons
✓ Proactively participate in online discussions Participate
in weekly discussion board (Canvas)
✓ Answer and submit course unit tasks

At the end of the course unit (CM), learners will be able to:

Cognitive
• Differentiate and understand the Care of a Child with Life
Threatening Conditions/ Acutely Ill/ Multi-organ Problems/
High Acuity and Emergency Situations
• Can easily assess patient Child with Life Threatening
Conditions.

Affective
 • Listen attentively during discussion
• Develop interest in studying Nursing Care of a Child with Life
Threatening Conditions/ Acutely Ill/ Multi-organ Problems/
High Acuity and Emergency Situations (Acute and Chronic)

Psychomotor
• Used the knowledge acquired into their OJT/ RLE
• Express opinions and thoughts during the discussions.

[Computer device, Laptop with internet access]

BASIC NURSING ASSESSMENT

Each nurse develops her own routine for completing a basic nursing assessment. There is no right or wrong
way, although it should be consistent and complete. The following outline for basic assessment is a simple
approach to the assessment and one you may wish to adopt until you have established a good system for
yourself.
The basic assessment is completed at the beginning and end of each shift. The assessment should take no
longer than five to ten minutes to complete. You should concentrate on the specific system that correlates
with the patient’s diagnosis.

Moreover, Guidelines 2021 are based on the International Liaison Committee on

Resuscitation 2020 Consensus on Science and Treatment Recommendations for
Basic Life Support and Automated External Defibrillation and the European Resuscitation Council
Guidelines for Resuscitation (2021) Adult Basic Life Support. Refer to the ERC guidelines publications for
supporting reference material.
Guidelines 2021 prioritizes supporting members of our communities to have the confidence, knowledge and
skills to act when someone sustains an out of hospital cardiac arrest. Few major changes have been
introduced as the principles of CPR remain unchanged. The guidelines emphasize that it is more important
that people feel able to do something to help than they become focused on small details or concerned about
causing harm. No greater harm can occur than failing to act when someone requires CPR and defibrillation.

The following outline will assist you in completing a basic physical assessment
1. Vital Signs
a. Temperature
b. Radial Pulse: rate, volume, rhythm
c. Respirations: rate, depth, rhythm
d. Blood Pressure: Korotkoff’s sounds

2.State of comfort: location and intensity of pain, response to medications given.

3.Emotional responses: patient behavior, reactions and demeanor, and general mood (crying/ depressed)

4.Skin: presence/ absence of abrasions, contusions, erythema, decubitus ulcers, incision line, color, turgor,
temperature.

5.Musculoskeletal: activity level, general mobility, gait, range of motion

6.Neurological: pupil (size, response, equality), hand grip strength and sensation of all extremities; ability
to follow commands; level of consciousness.

7.Respiratory: breath sounds; sputum color and consistency; cough (productive/ non-productive)

8.Cardiovascular: heart sounds; presence of pulses; edema

9.Gastrointestinal: bowel pattern and sounds; presence of nausea/ vomiting; abdominal distention;
consumption of diet

10.Genitourinary: voiding, color, odor, and consistency of urine, dysuria; vaginal drainage discomfort;
penile discharge

TRIAGE is a method of prioritizing patient care according to the type of illness or injury and the urgency of
the patient’s condition. It is used to ensure that each patient receives care appropriate to his need and in a
timely manner.

Level Acuity Treatment & Sample Condition

Reassessment Time
1 Resuscitation Immediate nursing & Cardiopulmonary
medical attention arrest, major trauma,
severe respiratory
distress, seizures
2 Emergent Immediate nursing Head injuries, chest
assessment & rapid pain, stroke asthma,
treatment
 sexual assault injuries,
poisoning
3 Urgent Quick attention but can Signs of infection, non-
wait as long as 30 mins cardiac chest pain, mild
for assessment & respiratory distress,
treatment moderate abdominal
pain
4 Less Urgent Patient can wait up to 1 Strains & sprains, ear
hour for assessment & ache, upper respiratory
treatment symptoms, mild
headache
5 Non-Urgent Patient can wait up to 2 Menstrual cramps &
hours (possibly longer) other minor symptoms

GLASSGOW COMA SCALE

In this test of baseline mental status, a score of 15 indicates that the patient is alert, can the follow simple
commands, and is oriented to person, place and time. A decreased score in one or more categories may
signal an impending neurologic crisis. A score of 7 or less indicates severe neurologic damage.

Test Score Patient Response Patient Response

(Adult) (Infant)

Eye opening response

Spontaneously 4 • Opens eyes • Opens eyes
To speech 3 spontaneously spontaneously
• Opens eyes in • Opens eyes in
To pain 2
response to verbal response to verbal
None 1 stimulus stimulus
• Opens eyes in • Opens eyes in
response to painful response to verbal
stimulus stimulus
• Doesn’t opens eyes • Doesn’t opens eyes
in response to in response to
stimuli stimuli

Test Score Patient Response Patient Response

(Adult) (Infant)
Verbal response
Oriented 5 • Oriented, converse • Smiles, orients to
normally sounds, follows
Confused 4 objects, interacts
Inappropriate words 3 • Cries but
consolable,
 Incomprehensible 2 • Confused, inappropriate
No response 1 disoriented interactions
• Inconsistently
inconsolable,
• Utters inappropriate
moaning
words
• Inconsolable,
agitated
• Moans or screams • No response
• No response

Test Score Patient Response Patient Response

(Adult) (Infant)
Motor response
Obeys 6 • Responds to simple • Moves
commands spontaneously/
Localizes 5 • Localizes painful purposefully
Withdraws 4
stimuli • Withdraws from
Abnormal flexion 3 • Withdraws from touch
painful stimuli • Withdraws from
Abnormal extension 2 • Abnormal flexion to painful stimuli
pain (decorticate) • Abnormal flexion to
None 1
• Extension to painful pain (decorticate)
stimuli (decerebrate) • Extension to painful
• Makes no stimuli (decerebrate)
movement • No motor response

Total score

MENTAL STATUS
Mental status assessment begins when you talk to the patients. Responses to your questions reveal clues
about the patient’s orientation and memory. Use such clues as a guide during the physical assessment.

LOC ASSESMENT
Level of consciousness (LOC) is a measurement of arousability and responsiveness to stimuli from the
environment. An altered level of consciousness can result from a variety of factors, including alterations in
the chemical environment of the brain (e.g., exposure to poisons), insufficient oxygen or blood flow in the
brain, and excessive pressure within the skull. Prolonged unconsciousness is understood to be a sign of a
medical emergency. A decreased level of consciousness correlates to increased morbidity (disability) and
mortality (death). Thus it is a valuable measure of the patient’s and neurological status. In fact, some sources
consider level of consciousness to be one of the vital signs.

Classification Description
Alert • Follows commands &responds completely &appropriately to
GCS Score: stimuli
 14-15 • Oriented to time, place, & person

Lethargic • Limited spontaneous movement or speech

GCS Score: • Easy to arouse by normal speech or touch
12-13
• Possible disorientation to time, place, or time

Obtunded • Mild to moderate reduction in arousal

GCS Score: • Limited responsiveness to environment
10-11
• Able to fall asleep easily
• Answers questions with minimum response

Stuporous • State of deep sleep or unresponsiveness

GCS Score: • Arousable only to vigorous & repeated stimulation
8-9
• Withdrawal or grabbing response to stimulation

Light coma • (+) to all forms of painful stimulation

GCS Score:
4-7
Deep coma • (-) to all forms of painful stimulation
GCS Score:
3

CARDIOPULMONARY RESUSCITION: FIRST AID

The NEW chain of Survival
Early Access: immediate recognition and activation
Early CPR
Early Defibrillation
Early advanced Care
Integrated Post- Cardiac Arrest Care

Cardiopulmonary resuscitation (CPR) is a lifesaving technique useful in many emergencies, including heart
attack or near drowning, in which someone’s breathing or heartbeat has stopped. Ideally, CPR involves two
elements: chest compressions combined with mouth-to-mouth rescue breathing.
It is a combination of artificial respiration which supplies oxygen to the lungs and chest compressions which
causes blood to move through the heart and circulatory system that will contribute oxygen to the lungs and
vital organs.

CPRS is administered to prolong ventricular fibrillation which is the abnormal rhythm that causes cardiac
arrest. Effective chest compressions provide 16% oxygen content--, enough to sustain life.

Most people suffering a fatal heart attack die within 2 hours of the first sign and symptoms of the attack.
Activate the EMS (emergency medical services) system and start CPR as soon as possible. Victims have
a good chance of surviving if:

CPR is started as soon as possible after the heart stops beating or if breathing either stops or is ineffective.
They receive advanced cardiac life support within the next 4 minutes.
Any delay in starting CPR reduces the chances of survival. In addition, the brain cells begin to die after 4-6
minutes without oxygen that could lead to irreversible brain damage.

0-4 minutes: brain damage unlikely if CPR started

4-6 minutes: brain damage possible
6-10 minutes: brain damage probable
>10 minutes: severe brain damage or brain death is certain

Signs of Major Emergencies:

• Stroke
• Cardiac Arrest
• Respiratory Arrest
• FBAO (foreign body airway obstruction)
• Electric Shock
• Drowning
• Excessive bleeding
• Drug overdose

ADULT AND CHILD RESUSCITATION

Check Responsiveness if you see a motionless person.

• If head or neck injury is suspected, move only if absolutely necessary.

• Tap or gently shake victim’s shoulder
• Speak in a loud voice near the victim, “are you ok?”

Activate EMS system for help.

• Ask a bystander to call the local emergency telephone number and ask for him/ her to come back
to you.
• If alone, shout for help. If no one quickly, call the local emergency phone no.

Roll person onto back.

• Gently roll victim’s head, body and legs over at the same time. Do this without furthering injuring
the victim.
Quick check for pulse
• Feel for carotid pulse (within 5-10 seconds). Carotid artery is used because it lies close to the heart
and is accessible
• Do not use your thumb because you may feel your own pulse
PULSE CHECK! ADULT: carotid, CHILD (1yr- puberty); Carotid/ Femoral,
INFANT: Brachial/Femoral

If there is no pulse, give chest compressions

Find hand position.

Child: 1-2 hands, center of breastbone, between nipples
 Infant: 1 rescuer: 2 finger technique
Place the heel of one hand over the center of the person’s chest, between the nipples.
Place your other hand on top of the first hand.
Interlace, hold or extend fingers up.
Use your upper body weight (not just your hand) as you push straight down on (compress) the chest at
least at least 2 inches (approximately 5 centimeters)
Push hard at a rate of about 100 compressions per minute

Adults: 2 inches
Child: (1 yr- puberty): approximately 1/3 to ½ depth of the chest or 1 in-1 ½
Infant: approximately 1/3 to ½ of the depth chest or ½ to 1 inch
Allow chest to recoil to increase preload and afterload of blood circulation. Do 30 chest compressions.

Open airway (use head tilt-chin lift method)

Place hand nearest victim’s forehead and apply backward pressure to tilt head back
Place fingers of other hand under bony of jaw near chin then lift. Avoid pressing on soft tissues under jaw.
Tilt head backward without closing victim’s mouth.
Do not use your thumb to lift the chin.
If you suspect head injury, do not move victim’s head or neck. First try lifting chin without titling head back.
If breaths do not go in, slowly and gently tilt the head back until breaths can go in. if you suspect trauma:
Jaw thrust

Give 2 slow breaths

• Keep head tilted back with head tilt- chin lift to keep airway open.
• Pinch nose shut.
• Take a deep breath and seal your lips tightly around victim’s mouth.
• If on infants, rescuer places mouth over the infant’s mouth and nose, exhales less with force to
prevent damage to the lungs.
• Give 2 slow breaths (1 second/breath).
Adult: 8-10 breaths/min, child (1yr-puberty) & Infants: 12-20 breaths/min
• Watch chest rise to see if your breaths go in.
• Allow for the chest deflation after each breath.
• If neither of the 2 breaths went in, retilt the head and try 2 more breaths. If still unsuccessful,
suspect choking.
• Give 2 slow breaths after each cycle.
Adult: 30:2 child (1 yr-puberty) & infant: 15:2
• Complete 5 cycles. If there is still no pulse, restart CPR with chest compressions.
• If there is pulse, give rescue breathing.

Use the recovery position for an unconscious, breathing victim

• Roll victim onto side (if no evidence of head or neck injury)

• Place hand under chin to support head and flex leg.
• CPR serves as a holding action until such medical care provided.

PRECAUTIONS
There are certain important precautions to remember in order to protect the victim and get the best result
from CPR. These include:
• Do not leave victim alone.
 • Do not chest compressions if the victim has a pulse. Chest compression when there is normal
circulation could cause the heart to stop beating.
• Do not give the victim anything to eat or drink.
• Avoid moving victim’s head or neck if spinal injury is a possibility. The person should be left as
found if breathing freely. To check for breathing when spinal injury is suspected, the rescuer
should only listen for by the victim’s mouth and watch the chest for movement.
• Do not slap the victim’s face, or throw water on the face, to try and revive the person.
• Do not place a pillow under the victim’s head.

When to Stop CPR

• Victim’s revives (regains pulse and breathing). Though most victims also require advanced cardiac
procedures before they regain their heart and lung functions.
• Replaced by either another trained rescuer or EMS system.
• Too exhausted to continue
• Scene becomes unsafe
• A physician tells you to stop

When Not to Start CPR

Do not start CPR when positive signs of death appear such as:
Severe injury and/ or decapitation

• Rigor mortis (stiffness of the muscles which sets in after death)

• Evidence of tissue decomposition
• Lividity (purple-reddish color showing on parts of body closest to ground)
• Obvious massive head or trunk trauma which is incompatible with life (provided the patient does
not have vital signs).

Do not start CPR

• When DNR “do not resuscitate” orders apply usually in writing and decided upon by the victim’s
family.
• In an unsafe environment or situation. In such cases if possible, move the victim to a safe location
and then begin CPR.

Rescue breathing mistakes

• Inadequate head tilt
• Failing to pinch nose shut
• Not giving slow breaths
• Failing to maintain tight seal around victim’s mouth and/ or nose

EMERGENCY CART
EMERGENCY CARTs are valuable hospital tools that are designed to store and transport critical emergency
equipment to be used for patients care. In the fast-paced medical field, it is crucial that tasks be performed
in a timely manner. Medical tools must be readily available and easily accessible so that no time is lost and
patients’ lives can be saved.
External contents:
 • Portable monitor/defibrillator unit with charged batteries, multi-function cable, multi-function pads
(pedia, adult or both as appropriate), pacer cable (if pacer capable machine), EKG electrodes,
appropriate sized paddles (adult, pediatrics), defibrillation gel, monitor paper, blood pressure cuff
(adult carts)
• Spo2 probe
• Sharps container
• Cardiopulmonary resuscitation records
• Emergency crash cart check sheet
• List of cart contents
• Emergency drug information sheets as appropriate for unit
• Cardiac board

• OPTIONAL PEDIATRIC/ NEWBORN SUPPLIES FOR ADULT AREAS

• Pediatric bag valve mask
• Pediatric incubation tray
• Pediatric Stylet
• Nasal Cannula: infant and pedia
• Non-breather mask
• Oral airways: 2 child, 2 infant
• Endotracheal tubes, 1 each: 3.0, 3.5, 4.0, 4.5, 5.0
• Suction catheters: 1 14 Fr. 1 10 Fr, 1 8 Fr, 1 6 Fr.
• Feeding tubes: 1 x 8 Fr, 1 x 5 Fr
• Syringes: 4x TB, 2 x 20 cc
• 2 Intraosseous needles 15G
• 4 Angiocaths: 2 x 22G, 2 x 24G
• Bulb Syringe
• 2 Blankets
• Cord Clamp

American Academy of pediatrics care

Retrieved: September 2,2021
https://pediatrics.aapublications.org

Philippine Pediatric Society

Retrieved: September 8,2021
https://www.philippinemedical association.org

Moses-Kolko EL, Bogen D, Perel J, et al. Neonatal signs

after late in utero exposure to serotonin reuptake inhibitors.
JAMA. 2005;293:2372–83. [PubMed] [Google Scholar]
Philippine Journal for obstetrics and gynecology (2016)
Retrieved date: July 2020
Website: pjog.org

WHO Health Topics

Retrieved: August 30,2021
https:// www.who.int.

Acute- come on rapidly, and are accompanied by distinct symptoms that require urgent or short
term care.
Acutely Ill-These patient has typically developed life threatening ,neurologically and
cardiorespiratory instability.

Chronic- A long term health condition that may not have a cure.

Emergency- A person with a medical condition requiring immediate treatment

Life Threratening- is very seriously dangerous , and it might even result in death.

Case Study ( 100 Points)

A newborn boy get rushed in emergency department after 2 hours of life with respiratory distress and
jitteriness.
He was born at term to a G1P0 mother who had an unremarkable pregnancy, protective serologies and no
diabetes. She tested negative for group B streptococcus, and had no history of maternal herpes simplex
virus infection. She denied smoking, alcohol and recreational drug use during pregnancy. The baby was
born at home following an uncomplicated vaginal delivery. At 2h of life, the baby was still grunting and
jittery, and was brought to the emergency department.
In the emergency department, he was in moderate respiratory distress. His respiratory rate was 76
breaths/min, with visible subcostal indrawing and nasal flaring. His heart rate was 150 beats/min,
O2 saturation was 92% on room air and his rectal temperature was 36.8°C. The infant was alert, appeared
warm and pink, but demonstrated fine tremor in all four limbs, which was suppressed by holding his limbs
firmly. There were no dysmorphic features, fontanelles were flat, and the infant’s cardiorespiratory
examination was normal. Neurological examination revealed normal primitive reflexes, but significantly
increased tone to all four limbs.
The infant’s bedside glucose level measured 0.34 g/L, which was normalized with a bolus of 10% dextrose
in water. Jittery movements and hypertonia persisted despite correction of hypoglycemia. Full septic work-
up was performed, and the infant was started on broad-spectrum antibiotics and admitted to the neonatal
intensive care unit.
1. If you are the nurse on duty (NOD) what is your immediate interventions to the patient?
2. What is your diagnosis?
3. Make a Nursing Care Plan for your diagnosis.

Wong Essentials of Pediatric Nursing -Marilyn Hockenberry and David Wilson 9th Edition.

Essential guide for the practice of Obstetrics and Gynecology, Oxford handbooks of obstetrics and
gynecology 3rd Edition ( S. Kollins,S. et all. ).

International Liaison Committee on Resuscitation

Council Guidelines for Resuscitation (2021)

Philippine Heart Center

BLS-ACLS
Https://www.philheart.org

Care New England Health System

Reviewed date: July 2020
Website: https:// www.womenandinfants.org.

Department of health & human services

Copyright State of Victoria 2020
www.betterhealth.vic.gov.au

Prepared by: ACR : )

BACHELOR OF SCIENCE IN NURSING:
CARE OF MOTHER AND CHILD AT RISK OR
WITH PROBLEMS (ACUTE AND CHRONIC):
COURSE MODULE COURSE UNIT WEEK
3 15 17

Integrated Management of Childhood Illness

Read course and unit objectives

Read study guide prior to class attendance
Read required learning resources; refer to unit
terminologies for jargons
Proactively participate in classroom discussions
Participate in weekly discussion board (Canvas)
Answer and submit course unit tasks

At the end of this unit, the students are expected to:

Cognitive:
1. Enhance the skills in managing illness in infants and children using case management process.
2. Check and identify the general danger signs prescribed by a child and use good communication skills in
assessing the general danger signs presented by a sick child.
3. Know the Major conditions/symptoms & routinely assess them using the IMCI procedure.
 4. Check the child’s nutrition and immunization status & assess other problems that child may have.
5. Know the clinical signs and symptoms used in algorithm and know how to assess them.
6. Classify the illness and identify the appropriate treatments for infants and children.
7. Give important pre- referral treatments and referring the child to a specialist.
Affective:
1. Listen attentively during class discussions
2. Demonstrate tact and respect when challenging other people’s opinions and ideas
3. Accept comments and reactions of classmates on one’s opinions openly and graciously.
4. Develop heightened interest in studying Maternal and Child Nursing.
Psychomotor:
1. Participate actively during class discussions and group activities
2. Express opinion and thoughts in front of the class

Department of Health. (2011). IMCI chart booklet Integrated management of childhood illness. Manila :
Department of Health. F 618.92 I1 2011, c3

Integrated Management of Childhood Illness (IMCI)

• IMCI is an integrated approach to child health that focuses on the well-being of the whole child.
• IMCI aims to reduce death, illness and disability, and to promote improved growth and
development among children under five years of age.
• IMCI includes both preventive and curative elements that are implemented by families and
communities as well as by health facilities.

Steps in IMCI case management process:

1. ASSESS - Taking the history of the patient is one way of getting information about the disease
condition. This can be done by asking and observing the patient’s condition to explore the
possible causes.
a. Check for General Danger Signs: LETHARGY
UNCONSCIOUSNESS
C - convulsion
U - unable to drink or breastfeed
V - vomiting
A - abnormally sleepy/ Lethargic
VOMITING
DANGER CONVULSIONS
C - Chest indrawing
S - Stridor
SIGNS

INABILITY TO DRINK
OR BREASTFEED
 b. Assess for Main Symptoms:
C - cough/ difficulty breathing
D - diarrhea
F - fever
E - ear problem
c. Assess NUTRITION and IMMUNIZATION STATUS and POTENTIAL FEEDING
PROBLEMS
d. Check for OTHER PROBLEMS

CLASSIFY - A thorough assessment supported with laboratory results is necessary for

classification of illnesses and confirmation of the disease.

2. IDENTIFY THE TREATMENT - write the treatments identified for each classification on the
reverse side of the case recording form.
3. TREATMENT - A curative method of treating diseases. This vary on the condition of the patient.
The IMCI chart titled TREAT THE CHILD shows how to do the treatment steps identified on the
ASSESS AND CLASSIFY chart. TREAT means giving treatment in clinic, prescribing drugs or
other treatments to be given at home, and also teaching the caretaker how to carry out the
treatments.
4. COUNSEL - Providing health education to clients promotes health and avoid risk of infection.
These are important for parents/caregivers especially who lack knowledge on health practices
and risks factors that contribute to disease ailments. Recommendations on feeding, fluids and
when to return are given on the chart titled COUNSEL THE MOTHER. For many sick children,
you will assess feeding and counsel the mother about any feeding problems found. For all sick
children who are going home, you will advise the child’s caretaker about feeding, fluids and when
to return for further care.
5. FOLLOW UP - Several treatments in the ASSESS AND CLASSIFY chart include a follow-up visit.
 At a follow-up visit you can see if the child is improving on the drug or other treatment that was
prescribed. The GIVE FOLLOW-UP CARE section of the TREAT THE CHILD chart describes
the steps for conducting each type of follow-up visit.

MANAGEMENT OF SICK CHILD AGED 2 MONTHS TO 5 YEARS

ASSESS MAIN SYMPTOMS:
COUGH OR DIFFICULT BREATHING
• Respiratory infections can occur in any part of the respiratory tract such as the nose, throat,
larynx, trachea, air passages or lungs.
• A child with cough or difficult breathing may have pneumonia or another severe respiratory
 infection.

Pneumonia is an infection of the lungs. Both bacteria and viruses can cause pneumonia. In
developing countries, pneumonia is often due to bacteria.The most common are Streptococcus
pneumoniae and Hemophilusinfluenzae. Children with bacterial pneumonia may die from hypoxia
(too little oxygen) or sepsis (generalized infection).
• TWO CLINICAL SIGNS OF PNEUMONIA:
o Fast breathing – PNEUMONIA
o Chest indrawing – SEVERE PNEUMONIA
• Assessment
o > 30 days = chronic cough
o Fast breathing –
▪ Count the breath in one minute – Respiratory rate
▪ cut-off for fast breathing:
If the child is: Fast breathing is:
2 months up to 12 months 50 breaths/ minute or more
12 onths up to 5 years 40 breaths/ minute or more
o Chest indrawing – the lower chest wall goes IN when the child breaths IN
o Look or listen for stridor.
Stridor – harsh noise made when the child breaths IN that happens when there is
swelling of the larynx, trachea, or epiglottis.
• Classification
o Severe Pneumonia or Very Severe Disease (PINK)
Signs – at least one sign to classify it under the pink category or severe classification.
▪ Any general danger sign
▪ Chest indrawing
▪ Stridor in calm child
Treatment:
▪ Give the first dose of an appropriate antibiotic (give an intramuscular antibiotic:
ampicillin (50 mg/kg) and gentamicin (7.5 mg/kg)
▪ IF REFERRAL IS NOT POSSIBLE OR DELAYED, repeat the ampicillin
injection every 6 hours, and the gentamicin injection once daily
▪ Refer URGENTLY to hospital
o Pneumonia (YELLOW)
Signs
▪ Fast breathing – 2 months up to 12 months (50 breaths/ minute or more)
12 months up to 5 years (40 breaths/ minute or more)
Treatment:
▪ Give an appropriate oral antibiotic for 5 days
▪ First line antibiotic: Amoxicillin
▪ Second line antibiotic : Cotrimoxazole
▪ Soothe the throat and relieve the cough with safe remedy
▪ Breastmilk for exclusive breastfed infant
▪ Tamarind, calamansi and ginger
 ▪ Advise mother when to return immediately
▪ Follow up in 2 days
o No Pneumonia: Cough or colds (GREEN)
Signs
▪ No signs of pneumonia or very severe disease
Home management:
▪ If coughing for more than 30 days, refer for assessment
▪ Soothe the throat and relieve the cough with safe remedy
▪ Advice mother when to return immediately
▪ Follow up in 5 days if not improving

Diarrhea
• Assessment
o How long the child has diarrhea ?
▪ To determine the type of diarrhea
▪ Acute Diarrhea- diarrhea lasts for less than 14 days
▪ Persistent Diarrhea- diarrhea last for 14 days or more
o Is there blood in the stool?
▪ Diarrhea with blood in the stool, with or without mucus is called dysentery
▪ The most common cause of dysentery is Shigella bacteria
o Check for signs of dehydration
▪ Restless and irritable
▪ Abnormally sleepy or difficult to awaken
▪ Sunken eyes
▪ Child is not able to drink or drinking poorly or drinking eagerly , thirsty
o Slowly Pinch the skin of the abdomen. Does it goes back: Very slowly(longer than 2
seconds);
• Classification
o Classifying Diarrhea:
▪ All children with diarrhea are classified for dehydration
▪ If the child has had diarrhea for 14 days or more, classify the child for persistent
diarrhea
▪ If the child has blood in the stool, classify the child for dysentery
o Classifying Diarrhea with Dehydration
▪ Severe Dehydration
▪ Some dehydration
▪ No Dehydration
o CLASSIFICATION: for diarrhea 14 days or more
▪ Severe Persistent Diarrhea (Pink) – dehydration present
▪ Persistent Diarrhea (Yellow) – no dehydration
o CLASSIFICATION: Dysentery (Yellow)
Signs : blood in the stool
Treatment:
▪ Treat for 5 days with oral antibiotic recommended for shigella in your area.
• First line antibiotic for shigella: COTRIMOXAZOLE
 • Second-line antibiotic for shigella: NALIDIXIC ACID
▪ Follow up in 2 days
• Treatment
o Treat for severe dehydration quickly (PLAN C)
▪ If you can give Intravenous fluid immediately:
• Start IV fluid immediately
• If the child can drink, give ORS by mouth while the drip is set up.
• Give 100 ml/kg Ringer’s Lactate Solution (or, if not available, normal
saline), divided as follows:
o Infants (under 12 mos.)
▪ Give 30ml/ kg in 1 hour
▪ Then give 70ml/ kg in 5 hours
o Children (12 months to 5 years)
▪ Give 30ml/ kg in 30 minutes
▪ Then give 70ml/ kg in 2 1/2 hours
• Reassess the child every 1- 2 hours. If hydration status is not improving,
give the IV drip more rapidly.
• Also give ORS (about 5 ml/kg/hour) as soon as the child can drink: usually
after 3-4 hours (infants) or 1-2 hours (children).
• Reassess an infant after 6 hours and a child after 3 hours. Classify
dehydration. Then choose the appropriate plan (A, B, or C) to continue
treatment.
▪ If IV treatment available nearby within 30 minutes:
• Refer URGENTLY to hospital for IV treatment.
• If the child can drink, provide the mother with ORS solution and show her
how to give frequent sips during the trip or give ORS by naso-gastic tube.
▪ Is the health care provider trained to use NGT for rehydration/ Can the child drink
• Start rehydration by tube or mouth with ORS solution : give 20 ml/kg/hr for
6 hrs ( total of 120 ml/kg)
• Reassess the child every 1-2 hours while waiting for transfer:
o If there is repeated vomiting or abdominal distension, give the fluid
more slowly.
o If the hydration status is not improving after 3 hours, send the child
for IV therapy.
• After 6 hours reassess the child. Classify dehydration. Then choose the
appropriate plan (A, B, or C) to continue treatment.
o Treat for Some Dehydration with ORS (PLAN B)
▪ In the clinic, give recommended amount of ORS over 4-hour period
• Determine amount of ors to give during first 4 hours
 • Use the child’s age only when you do not know the weight. The
approximate amount of ORS required (inml) can also be calculated by
multiplying the child’s weight in kg times 75.
• If the child wants more ORS than shown, give more.
• For infants below 6 months who are not breastfed, also give 100-200ml
clean water during this period
• Show the mother how to give ors solution:
o Give frequent small sips from a cup
o If the child vomits, wait 10 minutes then continue - but more slowly
o Continue breastfeeding whenever the child wants
• After 4 hours:
o Reassess the child and classify the child for dehydration
o Select the appropriate plan to continue treatment
o Begin feeding the child in clinic
• If the mother must leave before completing treatment:
o Show her how to prepare ORS solution at home
o Show her how much ORS to give to finish 4-hour treatment home
o Give her instructions how to prepare salt and sugar solution for use
at home
o Explain the 4 Rules of Home Treatment:
▪ Give extra fluid
▪ Give zinc (age 2 months up to 5 years)
▪ Continue feeding (exclusive breastfeeding if age less than
6 months)
▪ When to return
o Treat for Diarrhea at Home (PLAN A)
▪ Counsel the mother on the 4 Rules of Home Treatment:
• Give Extra Fluid (as much as the child will take)
o Tell the mother:

▪ Breastfeed frequently and for longer at each feed

▪ If the child is exclusively breastfed, give ors or clean water
in addition to breast milk
▪ If the child is not exclusively breastfed, give one or more of
 the following: food-based fluids (such as soup, rice water,
and yoghurt drinks), or ors
▪ It is especially important to give ors at home when:
• The child has been treated with plan b or plan c
during this visit
• The child cannot return to a clinic if the diarrhea gets
worse
o Teach the mother how to mix and give ors. Give the mother 2
packets of ors to use at home.
o Show the mother how much fluid to give in addition to the usual
fluid intake:
▪ Up to 2 years: 50 to 100 ml after each loose stool
▪ 2 years or more: 100 to 200 ml after each loose stool
o Tell the mother to:
▪ Give frequent small sips from a cup.
▪ If the child vomits, wait 10 minutes then continue - but more
slowly
▪ Continue giving extra fluid until the diarrhea stops
• Give Zinc Supplements (age 2 months up to 5 years)
o Tell the mother how much zinc to give (20 mg tab) :
▪ 2 months up to 6 months — 1/2 tablet daily for 14 days
▪ 6 months or more ——- 1 tablet daily for 14 days
o Show the mother how to give zinc supplements
▪ Infants—dissolve tablet in a small amount of expressed
breast milk, ORS or clean water in a cup
▪ Older children - tablets can be chewed or dissolved in a
small amount of clean water in a cup
• Continue Feeding (exclusive breastfeeding if age less than 6 months)
• When to Return
FEVER
A child with fever may have the following conditions: Malaria, Measles, Dengue Hemorrhagic
Fever(DHF), another severe disease, and simple cough or cold or another viral infection.

Malaria
Malaria is caused by parasites in the blood called “plasmodia”. It is transmitted through the bite of
anopheles mosquitoes. Four species of plasmodia can cause malaria, but the only dangerous one is
Plasmodium Falciparum. Fever is the main symptom of malaria. Other signs of falciparum malaria are
shivering, sweating, and vomiting.

In most areas in the Philippines where there is malaria transmission, malaria is a significant cause of
death of children. The child is considered to be MALARIA RISK if the child visited or stayed overnight in
a malaria area in the past 4 weeks.
HIGH MALARIA RISK
• Very Severe Febrile Disease (PINK)

o Signs
▪ Any danger sign
▪ Stiff neck

o Treatment
▪ In giving the first dose of Quinine it should be under medical supervision or if a
hospital is not accessible within 4 hours
▪ Give first dose of an appropriate antibiotic.
▪ Treat the child to prevent low blood sugar
• If the child is able to breastfeed:
o Ask the mother to breastfeed the child
• If the child is not able to breastfeed but is able to swallow
o Give expressed breastmilk or breastmilk substitute
• If neither of these is available, give sugar water
o Give 30-50 ml of milk or sugar water before departure
• If the child is not able to swallow
o Give 50 ml of milk or sugar water by NGT
• If the child is difficult to waken or unconscious, start IV infusion
o Give 5 ml/kg of 10% of dextrose solution ( D10) over a few minutes
o Or give 1 ml/kg of 50% (D50) by slow push
▪ Give one dose of paracetamol in clinic for high fever (38.5 C or above)
▪ Refer URGENTLY to hospital.
▪ Send a blood smear with the patient

• Malaria (YELLOW)

o Signs – Fever (37.5 C or above)

o Treatment
▪ If no cough with fast breathing, treat with oral antimalarial
▪ If cough with fast breathing, treat with cotrimoxazole for 5 days
▪ Give one dose of paracetamol in clinic for high fever (38.5 C or above)
▪ Advise mother when to return immediately
▪ Follow up in 2 days if fever persists
▪ If fever is present every day for more than 7 days, REFER for assessment.
LOW MALARIA RISK

NO MALARIA RISK
Measles
• Signs and symptoms include generalized rash, cough, runny nose, red eyes and corneal clouding
due to vitamin A deficiency that may lead to blindness.

Ear Problem
A child with ear problem may have ear infection. The main cause of deafness in low-income area which
leads to learning problems. Clinical Assessment include:
• Tender Swelling behind the ear - this is a manifestation of deep infection in the mastoid bone
in infants can also be above the ear
• Ear pain - can be seen in early stage of acute otitis causing the child to become irritable and
rub ear
• Ear discharge or pus - check for pus drainage from the ears. Find out how long the discharge
has been present.

• Classification
• Mastoiditis (PINK)
• Signs
• Tender swelling behind the ear
• Treatment
• Give the first dose of an appropriate antibiotic
• Give the first dose of paracetamol for pain
• Refer URGENTLY to hospital
 • Acute ear infection (YELLOW)
• Signs
• Ear pain
• Pus is seen draining from the ear, and discharge is reported for less than 14
days.
• Treatment
• Give an antibiotic for 5 days
• Give paracetamol for pain
• Dry the ear by wicking
• Follow up in 5 days
• Advise mother when to return immediately

• Chronic ear infection (YELLOW)

• Signs
• Pus is seen draining from the ear, and discharge is reported more than 14
days.
• No antibiotic must be given
• Treatment
• Dry the ear by wicking
• Follow up in 5 days
• Advise mother when to return immediately
• Check immunization and vitamin status

• No ear infection (GREEN)

• Signs
• No ear pain and no ear discharge seen draining from the ear
• Treatment
• No treatment
• Move to the next assessment

Malnutrition and Anemia

Look for visible wasting in the child. A child with visible wasting has Marasmus, a form of severe
malnutrition. The child is very thin, has no fat, and looks like skin and bones. The face of the child with
visible severe wasting may still look normal. The child’s abdomen may be large or distended. Check also
if the child has for edema of both feet. A child with edema of both feet may have Kwashiorkor, another
form of severe malnutrition. Signs of kwashiorkor include thin, sparse and pale hair which easily falls out;
dry, scaly skin especially on the arms and legs; and a puffy or “moon” face. Look for palmar pallor. Pallor
is unusual paleness of the skin. It is a sign of anemia. Determine weight for age. Weight for age compares
the child’s weight with the weight of other children who are of the same age.
Immunization Status
OBSERVE CONTRAINDICATIONS TO IMMUNIZATION
• There are only three situations at present that are contraindications to immunization:
• Do not give BCG to a child known to have AIDS.
• Do not give DPT 2 or DPT 3 to a child who has had convulsions or shock within 3 days of the
most recent dose.
• Do not give DPT to a child with recurrent convulsions or another active neurological disease
of the central nervous system.
• In all other situations, here is a good rule to follow:
• There are no contraindications to immunization of a sick child if the child is well enough to go
home

MANAGEMENT OF SICK YOUNG INFANT AGED 1 WEEK UP TO 2 MONTHS

Young infants have special characteristics that must be considered when classifying their illnesses.
They can become sick and die very quickly from serious bacterial infections. They frequently have only
general signs such as few movements, fever, or low body temperature. In the first week of life, newborn
infants are often sick from conditions related to labor and delivery or have conditions which require
special management. Newborns may be suffering from asphyxia, sepsis from premature ruptured
membranes or other intrauterine infection, or birth trauma. Or they may have trouble breathing due to
immature lungs. For all these reasons, management of a sick newborn is somewhat different from caring
for a young infant age 1 week up to 2 months.

Check for serious bacterial infection

• Assessment
o Ask: Has the infant had convulsions
o Look: Count the breaths in one minute, repeat the count if elevated.
▪ The breathing rate of a healthy young infant is commonly more than 50 breaths
per minute.
▪ Therefore, 60 breaths per minute or more is the cutoff used to identify fast
breathing in a young infant
▪ If the first count is 60 breaths or more, repeat the count. This is important because
the breathing rate of a young infant is often irregular.
▪ The young infant will occasionally stop breathing for a few seconds, followed by a
period of faster breathing.
▪ If the second count is also 60 breaths or more, the young infant has fast breathing.
o Look for severe chest indrawing
▪ Look for chest indrawing as you would look for chest indrawing in an older infant
or young child. However, mild chest indrawing is normal in a young infant because
the chest wall is soft.
▪ Severe chest indrawing is very deep and easy to see. Severe chest indrawing is
a sign of pneumonia and is serious in a young infant.
o Look for nasal flaring
▪ Nasal flaring is widening of the nostrils when the young infant breathes in.
o Look and listen for grunting
▪ Grunting is the soft, short sounds a young infant makes when breathing out.
Grunting occurs when an infant is having trouble breathing
o Look and feel for bulging fontanelle
▪ The fontanelle is the soft spot on the top of the young infant’s head, where the
bones of the head have not formed completely.
▪ Hold the young infant in an upright position.
▪ The infant must not be crying.
▪ Then look at and feel the fontanelle. If the fontanelle is bulging rather than flat, this
may mean the young infant has meningitis.
o Look for pus draining from the ear
▪ Pus draining from the ear is a sign of infection.
▪ Look inside the infant’s ear to see if pus is draining from the ear.
o Look at the umbilicus—is it red or draining pus? Does the redness extend to the skin?
▪ There may be some redness of the end of the umbilicus or the umbilicus may be
draining pus.
▪ The cord usually drops from the umbilicus by one week of age.
▪ How far down the umbilicus the redness extends, determines the severity of the
infection
▪ If the redness extends to the skin of the abdominal wall, it is a serious infection.
o Feel: measure temperature (or feel for fever or low body temperature)
▪ Fever (axillary temperature more than 37.5 °c or rectal temperature more than 38
°c) is uncommon in the first two months of life.
▪ If a young infant has fever, this may mean the infant has a serious bacterial
infection.
▪ In addition, fever may be the only sign of a serious bacterial infection.
▪ Young infants can also respond to infection by dropping their body temperature to
 below 35.5 °c (36 °c rectal temperature).
▪ Low body temperature is called hypothermia.
▪ If you do not have a thermometer, feel the infant’s stomach or axilla (underarm)
and determine if it feels hot or unusually cool.
o Look for skin pustules. Are there many or severe pustules?
▪ Examine the skin on the entire body.
▪ Skin pustules are red spots or blisters that contain pus.
▪ A severe pustule is large or has redness extending beyond the pustule.
▪ Many or severe pustules indicate a serious infection.
o Look: see if the young infant is lethargic or unconscious
▪ A lethargic young infant is not awake and alert when he should be.
▪ He may be drowsy and may not stay awake after a disturbance.
▪ An unconscious young infant cannot be wakened at all.
▪ He does not respond when he is touched or spoken to.
o Look at the young infant’s movements. Are they less than normal?
▪ A young infant who is awake will normally move his arms or legs or turn his head
several times in a minute if you watch him closely.
▪ Observe the infant’s movements while you do the assessment.

• Classification of possible bacterial infection:

Check for Diarrhea
• Assessment
o Ask: Does the young infant have diarrhea?
o If yes: assess and classify the young infant’s diarrhea.
o Then check for feeding problem or low weight, immunization status and other problems.

• Classification:
Two of the following • Give fluid and
signs are present: food for some
• Restless, dehydration (Plan B).
irritable • If infant also
• Sunken eyes Some has Possible Serious
• Skin pinch Dehydration Bacterial Infection or
goes back Dysentery: Refer
slowly URGENTLY to
hospital with sips of
ORS.

Check about feeding and determine weight for age

• Assessment
o Ask: is there any difficulty feeding?
▪ Any difficulty mentioned by the mother is important.
▪ This mother may need counselling or specific help with a difficulty.
▪ If a mother says that the infant is not able to feed, assess breastfeeding or watch
her try to feed the infant with a cup to see what she means by this.
▪ An infant who is not able to feed may have a serious infection or other life-
threatening problem and should be referred urgently to hospital
o Ask: is the infant breastfed? If yes, how many times in 24 hours?
▪ The recommendation is that the young infant be breastfed as often and for as long
as the infant wants, day and night. This should be 8 or more times in 24 hours.

Stridor – harsh noise made when the child breaths IN that happens when there is swelling of the larynx,
trachea, or epiglottis.
World Health Organization (2005). Handbook: IMCI Integrated Management of Childhood Illness. Retrieved
at: https://apps.who.int/iris/bitstream/handle/10665/42939/9241546441.pdf;sequence=1. WHO
Library Cataloguing-in-Publication Data.

Study Questions

• Assess, classify and make a treatment plan for the following cases:
1. A 6-month old boy does not have general danger signs. He is with fever, ear pain and ear
discharges for a week, no anemia, not very low weight.
2. A 7-month old girl with cough and cold, no dehydration, persistent diarrhea, no anemia, not
very low weight
3. A 9-month old boy is lethargic, with severe dehydration, no anemia, not very low weight
4. A 2-year old girl does not have general danger signs. She is with severe dehydration,
severe malnutrition and severe anemia.

Ang, Beverly. (2009). Easy IMCI for Nurses & student Nurses. Mla:
Educational Publishing. F 610.7362 A4 2009

Department of Health. (2011). IMCI chart booklet Integrated

management of childhood illness. Manila: Department of Health.
F 618.92 I1 2011, c3

Padilla, Ma. Teresa C.. (2008). Integrated management of childhood

illness : a textbook for Filipino healthcare students. Manila:
Educational Publishing House. F 618.92 P13 2008

Villarama, Rouena S. (2009). Integrated management of childhood

Illness (IMCI): a condensed module for nurses, revised edition. QC:
C&E. F 618.92 V71 2009