● ACUTE MYELOGENOUS LEUKEMIA (AML)

1. 20% survival rate

● CHRONIC MYELOGENOUS LEUKEMIA (CML)
ETIOLOGY/CAUSES
LEUKEMIA
1. Chromosomal changes
● Represents a group of diseases characterized by “unregulated 2. Chemical Agents - Benzene
proliferation and incomplete maturation of the precursors to white 3. Chemotherapy - Alkylating agents
cells and lymphocytes. 4. Viruses - Retroviruses
5. Radiation
TYPES
6. Unknown Factors
1. Acute Myeloid leukemia (AML)
CLINICAL MANIFESTATIONS
2. Acute lymphoblastic leukemia (ALL)
3. Chronic Myeloid leukemia (CML) 1. Anemia
4. Chronic Lymphoblastic leukemia (CLL) 2. Fatigue & weakness
3. Bleeding
PATHOLOGY
4. Fever and infections
● Loss of regulation in cell division causes proliferation of malignant 5. Weight loss
leukocytes. 6. Joint pain
7. Mouth sores
CLASSIFICATION BASED ON PREDOMINANT CELL OF ORIGIN 8. Hepatosplenomegaly - Enlarged liver refers to swelling of the liver
beyond its normal size. Hepatomegaly is another word to describe
1. Lymphoid this problem. If both the liver and spleen are enlarged
2. Myeloid 9. Lymphadenopathy - the term for swollen glands or swelling of the
LYMPHOCYTIC LEUKEMIA lymph nodes. The lymph glands are part of the immune system and
help fight infections and other diseases. They are enlarged when the
● ACUTE LYMPHATIC LEUKEMIA (ALL) body is fighting infection or other diseases.
1. Common with pedia patients
2. 5 year survival - 80% Pedia patients survival rate | 40% TREATMENT
Adult patients survival rate CHEMOTHERAPY
● CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)
1. Most common with adults 1. Induction therapy - attempts to induce or bring about remission.
2. 73% survival rate 2. Consolidation therapy - after remission achieved-eliminate
remaining cells
MYELOGENOUS LEUKEMIA

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 1
3. Maintenance therapy - treatment with lower doses of the same Need to include:
drugs every 3-4 weeks.
4. Combination therapy - Stem cell transplant, Bone marrow transplant ● weight bearing exercises, including upper limbs
● trunk exercises
NURSING MANAGEMENT ● Ambulation - the ability to walk without the need for any kind of
assistance. It is most often used when describing the goals of a
1. Communicate treatment plan patient after a surgery or physical therapy. In order to reach a
2. Protective isolation/ Neutropenic Precautions patient's goal of ambulation, they may require assistance before they
3. Educate are able to walk around on their own.
4. Manage chemo side-effects ● muscle strengthening
NEUTROPENIA Considerations
● Severe decrease in neutrophils secondary to chemo or 1. Myelosuppression - A condition in which bone marrow activity is
immunosuppressive therapy. decreased, resulting in fewer red blood cells, white blood cells, and
platelets. Myelosuppression is a side effect of some cancer
Symptoms - Decreased immune/inflammatory response, low grade fever
treatments. When myelosuppression is severe, it is called
NURSING MANAGEMENT myeloablation.
● Anemia - a condition in which the body does not have enough
1. Neutropenic precautions healthy red blood cells. Red blood cells provide oxygen to body
2. obtain pan cultures tissues
3. start IV abx ● Thrombocytopenia - a condition that occurs when the platelet count
4. assess for septic shock in your blood is too low. Platelets are tiny blood cells that are made
in the bone marrow from larger cells. When you are injured,
IMPLEMENT A PLAN OF PHYSIOTHERAPY TREATMENT platelets stick together to form a plug to seal your wound. This plug
To maintain and improve: is called a blood clot
● Leucopenia - a decrease in the number of white blood cells, which
1. Muscle strength puts a person at risk for infection. Normally when a person has
2. 2 Respiratory and cardiac function infection or inflammation, the number of white blood cells increases
3. Joint ROM so there are more cells to fight the infection with.
4. Body’s protein reserve 2. N & V (nausea/vomiting.) - restricts activity
5. To help with the long term psychological considerations associated 3. Neurotoxicity - occurs when the exposure to natural or manmade
with long term hospitalization. toxic substances (neurotoxicants) alters the normal activity of the
nervous system. This can eventually disrupt or even kill neurons
Muscle strength (nerve cells) which are important for transmitting and processing
signals in the brain and other parts of the nervous system.
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 4. Myopathies - Myopathies are a heterogeneous group of disorders ● Bone marrow depression
primarily affecting the skeletal muscle structure, metabolism or ● Gastro-intestinal symptoms
channel function. They usually present with muscle weakness ● Specific drug-related problems
interfering in daily life activities. Muscle pain is also a common ● Psychological issues
finding and some myopathies are associated with rhabdomyolysis.
5. CNS involvement - Traditionally, CNS leukemia is defined by the Anemia
presence of at least 5 leukocytes per microliter of CSF and the
● Occurs when the Haemoglobin is <11g/dl
detection of leukemic blast cells, or by the presence of cranial nerve
● Normal for Males = 13.5 – 17.5g/dl
palsy.
● Normal for Females = 11.5 – 15.5g/dl
6. TBI - (traumatic brain injury) Somnolence syndrome
Symptoms
Respiratory and cardiac function
● Lethargy
Chest Infections
● Dyspnoea
bacterial ● Weakness
● Peripheral shutdown
● Staphylococcus ● Hypotension
● streptococcus
Thrombocytopenia
fungal
● Occurs when the platelet count is <50 x 109/l, normal values are 150
● Aspergillus – 400 x 109/l.
● candida
Symptoms:
Mucositis - inflammation of the mucosa, the mucous membranes that line
your mouth and your entire gastrointestinal tract. It's a common side effect ● Bruising (peticheae)
of cancer treatments involving radiation or chemotherapy. ● Nosebleeds (epistaxis)
● Blood in urine (haematuria)
ARDS - Acute respiratory distress syndrome (ARDS) is a serious lung ● Vomiting blood (haematemesis)
condition that causes low blood oxygen. People who develop ARDS are ● Blood in sputum (haemoptysis)
usually ill due to another disease or a major injury. In ARDS, fluid builds
up inside the tiny air sacs of the lungs, and surfactant breaks down. Gastro-Intestinal Side Effects

Respiratory failure - no ICU ● Nausea

● Vomiting
Cardiac toxicity ● Diarrhea
● Oesophagitis
The Side-Effects Of Chemotherapy ● Mucositis
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 Oncological Emergencies Septic Shock
● Tumor Lysis Syndrome ● Increasing metabolic and respiratory demand.
● Sepsis ● No response of blood pressure.
● Acute Bleed
● Disseminated Intravascular Coagulation (DIC) Severe Sepsis

Sepsis ● Multi-organ involvement.

● Global cellular damage.
● Sepsis is the body's extreme response to an infection. It is a ● Global organ damage.
life-threatening medical emergency. Sepsis happens when an ● Critical Care for respiratory, cardiac and renal support
infection you already have triggers a chain reaction
throughout your body. Infections that lead to sepsis most often Sepsis Physiotherapy Management
start in the lung, urinary tract, skin, or gastrointestinal tract
● Most valuable tool = ASSESSMENT
● Sepsis is the body's extreme response to an infection. It is a
● Often non-productive cough ⇒ positioning and relaxation
life-threatening medical emergency. Sepsis happens when an
● Be aware that respiratory techniques place further demand on tiring
infection you already have triggers a chain reaction
patient
throughout your body. Infections that lead to sepsis most often
● Treat what find
start in the lung, urinary tract, skin, or gastrointestinal tract..
● Critical Illness Myopathy
At risk
Lymph System
● neutropenic patients
Consists of: lymphatic capillaries, ducts, lymph nodes, lymph fluid
● any patient on chemotherapy
● Occur at any stage during treatment phase Function:
● Haemato-oncology patients experience profound
● neutropenia therefore more at risk ● Returns excess interstitial fluid to the blood
● Three phases ● Absorbs fatty acids
● Produces immune cells
Sepsis – Systemic Inflammatory Response Syndrome ● Lymph nodes: Filtration of bacteria and foreign particles carried by
lymph fluid.
● Pyrexia ⇒ ↓ Cardiac Output
● Tachycardia ⇒ Vasoconstriction Lymphoma – Hodgkin’s
● Low blood pressure
● Low urine pressure ⇒ Oliguria Clinical Manifestations
● ↑ metabolic demand
● ↑ respiratory rate ⇒ Poor Perfusion
● Enlargement of cervical,
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axillary or inguinal lymph ● Holistic nursing management-same as previous blood
disorders…pain control, management of SE, psychosocial support,
Nodes ● Spiritual care-multidisciplinary team
● *Wt Loss, *Fever and Multiple Myeloma
chills,*Night sweats Patho
Fatigue and weakness ● excess production of plasma cells w/resultant
● Tachycardia myeloma proteins destroys bone/bone marrow
Treatment: Based on stage of the disease Clinical manifestations (develop slowly and
● Radiation alone or with chemotherapy insidiously)
Nursing Management ● Skeletal pain (esp pelvis, spine & ribs) *Major
● pain control manifestation, presents first.
● managing side effects
● psychosocial support ● Osteolytic lesions; can see in skull, vertebrae & ribs
● Hypercalcemia from bony degeneration
Non-Hodgkin’s Lymphomas ● Anemia, thrombocytopenia, & granulocytopenia
Patho Multiple Myeloma
Prevalence Diagnosis
Categories ● Lab, x-rays, bone marrow
● Urine has Bence Jones protein
● Low grade (indolent)
● Intermediate grade (aggressive) Collaborative management:
● High grade (very aggressive)
● Affects all ages ● Radiation
● Chemo
Diagnosis/Treatment
Nursing Management
● Radiation if just stage I
● Chemotherapy involves multidose/multiagent ● Ambulation & adequate hydration
● Ambulate w/care
Regimen ● Pain control
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 ● Infection control
● Emotional/spiritual support
Wilms Tumor (Nephroblastoma)
● Wilms tumor, or nephroblastoma, is the most common childhood
abdominal malignancy.
● Wilms tumor is an adenosarcoma in the kidney region.
● The tumor arises from bits of embryonic tissue that remain after
birth.
● This tissue can spark rapid cancerous growth in the area of the
kidney.
Stages
The Children’s Oncology Group has identified the staging of Wilms tumor
as:
Stage 1. The tumor is limited to the kidney and is completely resected; the
renal capsule is intact; the tumor was not ruptured or biopsied prior to
removal; the vessels of the renal sinus are not involved, and no evidence of
tumor is present at or beyond the margins of resection.
Stage 2. The tumor is completely resected; no evidence of tumor at or
beyond the margins of resection is noted; and the tumor extends beyond the
kidnnetration of renal capsule, involvement of rena
Stage 3. A residual, non hematogenous tumor is present following surgery
and is confined to the abdomen; positive lymph nodes in the abdomen or
pelvis are noted; penetration through the peritoneal surface is observed;
peritoneal implants are present; gross or microscopic tumor remains
postoperatively, including positive margins of resection; tumor spillage is
noted, including biopsy; the tumor is treated with preoperative
chemotherapy; and the tumor is removed in more than 1 piece.
Stage 4. Hematogenous metastases (eg, lung, liver, bone, brain) or lymph
node metastases beyond the abdomen or pelvis are noted.
Stage 5. Bilateral renal involvement by the tumor is present at diagnosis.
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Pathophysiology
● There are mutations of WT1 gene on chromosome 11 and
nephroblastomatosis (persistence of renal blastema in kidney tissue.
● The tumor consists of tumor epithelial component (abortive tubules
and glomeruli) surrounded by metanephric blastema and tumor
immature spindle cell stroma.
● The stroma may include differentiated (muscle, cartilage, bone, fat
tissue, fibrous tissue) or anaplastic elements. The tumor compresses
the normal kidney parenchyma.
Statistics and Incidences
The occurrence of Wilms tumor in the United States and around the world
are as follows:
● Wilms tumor affects approximately 10 children and adolescents per
1 million before age 15 years.
● Therefore, it accounts for 6-7% of all childhood cancers in North
America.
● As a result, about 450-500 new cases are diagnosed each year on
this continent.
● Wilms tumor appears to be relatively more common in Africa and
least common in East Asia.
● Wilms tumor is relatively more common in blacks than in whites
and is rare in East Asians.
● Estimates suggest 6-9 cases per million person-years in whites, 3-4
cases per million person-years in East Asians and more than 10
cases per million person-years among black populations.
● Among patients with unilateral Wilms tumor enrolled in all NWTSG
protocols, the male-to-female ratio was 0.92:1.
CAUSES
● Wilms tumor is thought to be caused by alterations of genes
responsible for normal genitourinary development.
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 ● WT1 gene. WT1, the first Wilms tumor suppressor gene at
chromosomal band 11p13, was identified as a direct result of the
study of children with Wilms tumor who also had aniridia,
genitourinary anomalies, and mental retardation (WAGR syndrome).
● Additional genetic loci. A second gene that predisposes individuals
to develop the Wilms tumor has been identified (but has not yet
been cloned) telomeric of WT1, at 11p15; this locus was proposed
on the basis of studies in patients with both Wilms tumor and
Beckwith-Wiedemann syndrome (BWS), another congenital
Wilms-tumor predisposition syndrome linked to chromosomal band
11p15.
Clinical Manifestations
The child with Wilms tumor exhibits the following:
1. Abdominal mass. The most common manifestation of Wilms tumor is an
asymptomatic abdominal mass; an abdominal mass occurs in 80% of
children at presentation.
2. Abdominal pain. Abdominal pain or hematuria occurs in 25%.
3. Tumor Hemorrhage. A few patients with hemorrhage into their tumor
may present with hypotension, anemia, and fever.
Assessment and Diagnostic Findings
The following studies are indicated in patients with Wilms tumor:
1. Laboratory studies. CBC, chemistry profile, U/A, coagulation
studies, and cytogenic studies are made to determine Wilms tumor;
results may reveal an 11p13 deletion, as in WAGR syndrome, or a
duplication of the paternal allele 11p15, as in Beckwith-Wiedemann
syndrome (BWS).
2. Renal UTZ, the initial study because = children no exposure to the
detrimental effects of radiation.
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3. CT scanning. Abdominal = determining the origin of the tumor,
involvement of the lymph nodes, bilateral kidney involvement, invasion
into major vessels (eg, inferior vena cava), and liver metastases.
4. MRI scanning. the most sensitive imaging modality for determination of
caval patency and may be important in determining whether the inferior
vena cava is directly invaded by the tumor.
Medical Management
Tx consists of surgical removal ASAP, after the growth is discovered,
combined w/ radiation & chemotherapy
Focal anaplastic stage I-III Wilms tumors and diffuse anaplastic stage I
Wilms tumors. Nephrectomy followed by vincristine, actinomycin-D, and
doxorubicin in addition to local radiotherapy
Focal anaplastic stage IV Wilms tumors and diffuse anaplastic stage II-III
tumors. Patients undergo the same treatment, with the addition of
cyclophosphamide, etoposide, and carboplatin.
Stage IV diffuse anaplastic Wilms tumors. More aggressive tx is delivered;
nephrectomy then initial irinotecan & vincristine admn., w/c in turn is
followed by actinomycin-D, doxorubicin, cyclophosphamide, carboplatin,
etoposide, and radiotherapy.
Activity. No precs regarding activity are advised, the pt and his or her
parents should be aware that the pt will have only 1 kidney after therapy;
activities that carry an inherent risk of kidney injuries, such as boxing &
hockey, should be avoided.
Pharmacologic Management
As previously stated, several cytotoxic agents may cause liver damage in
patients treated for Wilms tumor.
● Antineoplastics. Chemotherapeutic agents used to treat pts
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w/ Wilms tumor depend on the stage & histology of ds; commonly used
agents include dactinomycin, vincristine, doxorubicin, cyclophosphamide,
etoposide, and carboplatin; the dosage depends on the particular stage of the
ds & on the child.
Nursing Management
Nursing Assessment
Assessment of the child with Wilms tumor include:
● Assess for bleeding. Assess for bleeding from any site and febrile
episodes; Monitor WBC, platelet count, hematocrit, absolute
neutrophil count.
● Assess the oral cavity. Assess oral cavity for pain ulcers, lesions,
gingivitis, mucositis or stomatitis and effect on the ability to ingest
food and fluids.
● Assess for anxiety. Assess the source and level of anxiety and need
for information and support that will relieve it.
Nursing Diagnoses
Based on the assessment data, the major nursing diagnoses are:
● Ineffective protection related to antineoplastic agents, radiation
therapy, or leukopenia.
● Impaired oral mucous membrane related to chemotherapy.
● Anxiety related to change in health status and threat of death.
● Risk for injury related to side effects of medications and
complications.
Nursing Care Planning and Goals
Main Article: 4 Wilms Tumor (Nephroblastoma) Nursing Care Plans
The major nursing care planning goals for a child with Wilms tumor are:
● Child will be protected from illness or injury.
● Child will be free of oral mucous membrane irritation.
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● Clients will experience decreased anxiety.
● Child will not experience injury.
Nursing Interventions
Nursing interventions appropriate for the child are:
● Prevent transfer of microorganisms. Perform hand washing prior
giving care, utilize mask & gown when needed, provide a private
room, monitor for any signs and symptoms of infection.
● Prevent oral trauma. Instruct the use of a soft-sponge toothbrush or
sponge toothette or gauze when rinsing the mouth; instruct to avoid
foods which are hot, spicy, or high in ascorbic acid (vitamin C);
provide oral hygiene 30 minutes prior or after meals; instruct to
refrain from eating or drinking for 30 minutes after completion of
oral hygiene; and offer moist, soft, bland foods.
● Prevent anxiety. parents to stay with the child or encourage open
visitation, provide cp# to call for information; explain all procedures
& care in simple, direct, honest terms & repeat as often as prn;
reinforce physician information if needed & provide sp information
as needed; & provide consistent nurse assignment with the same
personnel; encourage parents to participate in care.
● Prevent injury. Avoid any palpation of abdominal mass; post sign on
bed stating not to palpate preoperatively; assess incision site for
redness, swelling, drainage, intactness, and healing and change
dressing when soiled or wet; assess oral and perineal area; and
encourage parents to appropriately dress child based on weather
conditions and to refrain from participating on rough activities or
sports.
Evaluation
Goals are met as evidenced by:
● Child is protected from illness or injury.
● Child is free of oral mucous membrane irritation.
● Clients experienced decreased anxiety.
● Child did not experience injury.
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 Documentation Guidelines
Documentation in a child with Wilms tumor include:
● Cultural and religious beliefs, and expectations.
● Plan of care.
● Teaching plan.
● Responses to interventions, teaching, and actions performed.
● Postoperative care.
● Modifications to the plan of care.
● Attainment or progress toward desired outcomes.
Juvenile Rheumatoid Arthritis
Juvenile rheumatoid arthritis (JRA), also known as Juvenile Idiopathic
Arthritis (JIA), is the most common chronic rheumatologic disease in
children and is one of the most common chronic diseases of childhood.
What is Juvenile Rheumatoid Arthritis?
● It represents a group of disorders that share the clinical
manifestation of chronic joint inflammation.
● Connective tissues are those that provide a supportive framework
and protective covering for the body, such as the musculoskeletal
system and skin and mucous membranes.
Pathophysiology
Genetically complex disorder in which multiple genes are important
for disease onset and manifestations.
● Humoral and cell-mediated immunity
● T lymphocytes have a central role, releasing proinflammatory
cytokines (eg, tumor necrosis factor–alpha [TNF-α], interleukin
[IL]-6, IL-1) and favoring a type-1 helper T-lymphocyte response.
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● Studies of T-cell receptor expression confirm recruitment of
T-lymphocytes specific for synovial nonself antigens.
● Abnormalities = humoral immune system (↑’d autoantibodies (esp.
antinuclear antibodies), ↑’d serum immunoglobulins, circulating
immune complexes, and complement activation.
● Chronic inflammation of synovium is characterized by
B-lymphocyte infiltration and expansion.
● Macrophages and T-cell invasion are asso’d w/ release of cytokines,
which evoke synoviocyte proliferation.
● Some pediatric rheumatologists view systemic-onset JRA as
autoinflammatory disorder, such as familial Mediterranean fever
(FMF) or cryopyrin-associated periodic fever syndromes, rather than
a subtype of JRA.
● Theory is similar expression patterns of a phagocytic protein
(S100A12) in systemic-onset JRA and FMF, as well as the same
marked responsiveness to IL-1 receptor antagonists.
Statistics and Incidences
● The occurrence of Juvenile rheumatoid arthritis appears to
● peak at two age levels: 1 to 3 years and 8 to 12 years.
● Approximately 300,000 children in the United States are
● estimated to have some type of arthritis.
● For JRA, the prevalence has ranged from 1.6 to 86.1
● cases per 100,000.
● Worldwide, JRA appears to occur more frequently in
● certain populations (eg, indigenous peoples) from such disparate
areas as British Columbia and Norway.
● Disease-associated mortality for JRA is difficult toquantify, but it is
estimated to be less than 1% in Europe and less than 0.5% in North
America.
● Most deaths associated with JRA in Europe are related to
amyloidosis, and most in the United States are related to infections.
● Girls with an oligoarticular onset outnumber boys by a ratio of 3:1.
In children with uveitis, the ratio of girls to boys is 5-6.6:1, and in
children with polyarticular onset, girls outnumber boys by 2.8:1.
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 Causes
● Etiology = unknown, & gen's component= complex, making clear
distinctions between the various subtypes are difficult.
Clinical Manifestations
● Arthritis=intra-articular swelling or as limit’n of joint motion in
asso’n w/ pain, warmth, or erythema of the joint.
● Loss of motion. The hips, temporomandibular joint, and small joints
in the spine do not demonstrate swelling when affected by synovitis
but demonstrate the combination of loss of motion and pain.
● Synovitis. In synovitis, the fingers may appear swollen, and the
range of motion becomes painful.
● Swelling. A soft, boggy swelling is appreciated in the popliteal
fossa.
● Joint inflammation. Joint inflammation occurs first; if untreated,
inflammation leads to irreversible changes in joint cartilage,
ligaments, and menisci.
Assessment and Diagnostic Findings
● Inflammatory markers. The erythrocyte sedimentation rate (ESR) or
C-reactive protein (CRP) level is usually elevated in children with
systemic-onset JRA (with a disproportionate increase in the CRP)
and may be elevated in those with polyarticular disease; however, it
is often within the reference range in those with oligoarticular
disease; other markers of inflammation include thrombocytosis,
leukocytosis, complement, and, in a reverse fashion, albumin and
hemoglobin.
● Complete blood count and metabolic panel. A complete blood
count, liver function tests (to exclude the possibility of viral or
autoimmune hepatitis), and assessment of renal function with serum
creatinine levels should be done before starting treatment with
nonsteroidal anti-inflammatory drugs (NSAIDs), methotrexate
(MTX), or tumor necrosis factor–alpha inhibitors.
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● Antinuclear antibody test. + ANA is ↑’d risk of anterior uveitis;
child’n < 6 yrs at arthritis onset w/ + ANA finding are highest risk
category for dev’t of uveitis & need slit lamp screening ꝗ 3-4 mos.
● Radiography. When only a single joint is affected, radiography is
important to exclude other diseases, such as osteomyelitis.
● CT & MRI. CT scanning is the best method for analyzing bony
abnormalities, but superseded by MRI in overall assessment of JRA;
& MRI =most sensitive radiologic indicator of ds activity.
● UTZ. inflamed synovium can appear as an area of mixed
echogenicity lining the articular cartilage; the vascularity of the
synovium can be assessed with Doppler flow studies.
Medical Management
Prevent or control joint damage, to prevent loss of function, and to decrease
pain.
● Exercise. preserves joint ROM & muscular strength, & protects joint
integrity =providing better shock absorption; muscle-strengthening
program, ROM activity, stretching of deformities, and endurance
and recreational exercises.
● Synovectomy is rarely needed, and long-term outcome is poor;
however, it may be used in children in whom a single joint or just a
few joints are involved and who have very active, proliferative
synovitis.
● Osteotomy and arthrodesis. Osteotomy and arthrodesis are salvage
procedures for patients whose JIA is associated with severe joint
destruction or deformity.
● Total hip and knee replacements. Total hip and knee replacements
provide excellent relief of pain and restore function in a functionally
disabled child with debilitating Disease.
Pharmacologic Management
Treatment is aimed at inducing remission with the least toxicity from
medications with hopes of inducing a permanent remission.
● Nonsteroidal anti-inflammatory drugs (NSAIDs). Nonsteroidal
anti-inflammatory drugs (NSAIDs) interfere with prostaglandin
synthesis through inhibition of the enzyme cyclooxygenase (COX),
thus reducing swelling and pain; NSAIDs are used to treat all
subtypes of JIA; they may help with pain and decrease swelling.
● Disease-modifying antirheumatic drugs (DMARDs).
Disease-modifying antirheumatic drugs (DMARDs) can retard or
prevent disease progression and, thus, joint destruction and
subsequent loss of function.
● Corticosteroids. Corticosteroids are potent anti-inflammatory drugs
used in patients with JIA to bridge the time until DMARDs are
effective.
● Immunomodulators. The recognition of tumor necrosis factor-alpha
(TNF-alpha) and interleukin (IL)–1 as central proinflammatory
cytokines has led to the development of agents that block these
cytokines or their effects.
Nursing Management
Tx & nsg mgt goal for juvenile rheumatoid arthritis is to maintain mobility
and preserve joint function.
● The most important steps are medical history and physical exam.
Medical history. Assess for the duration of symptoms, onset,
affected joints, pain description, changes in physical activity, general
health, history of arthritis, previous illness, and other symptoms
associated with JRA.
● Physical exam. Assess the vital signs, auscultate the heart and lungs,
palpate the abdomen, and examine the skin.
Nursing Diagnosis
Based on assessment data, the major nsg diagnosis are:
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● Acute pain related to tissue distension by fluid accumulation /
inflammation, joint destruction.
● Impaired physical mobility related to skeletal deformities, pain,
discomfort,activity intolerance, decreased muscle strength.
● Disturbed body image related to changes in ability to perform usual
tasks.
● Self-care deficit related to musculoskeletal impairment.
● Deficient knowledge related to lack of exposure/recall.
Nursing Care Planning and Goals
Focus on ff nursing care planning goals for the child with juvenile
rheumatoid arthritis:
● Report pain is relieved/controlled.
● Appear relaxed, able to sleep/rest and participate in
activities appropriately.
● Follow prescribed pharmacological regimen.
● Incorporate relaxation skills and diversional activities into a pain
control program.
● Maintain position of function with absence/limitation of
contractures.
● Maintain or increase strength and function of affected and/or
compensatory body part.
● Demonstrate techniques/behaviors that enable
resumption/continuation of activities.
● Verbalize increased confidence in ability to deal with illness,
changes in lifestyle, and possible limitations.
● Verbalize understanding of condition/prognosis, and potential
complications.Formulate realistic goals/plans for future.
Nursing Interventions
Nsg intervention appropriate for a child with JRA are:
 ● Physical therapy. Physical therapy includes exercise, application of
splints, and heat.
● Activity. Stress to the caregivers the importance of encouraging the
child to perform activities of daily living to maintain function and
independence.
● Pain relief. Recommend or provide firm mattress or bedboard, small
pillow; elevate linens with bed cradle as needed; and suggest patient
assume position of comfort while in bed or sitting in a chair.
● ROM exercises. Assist with active and passive ROM and resistive
exercises and isometrics when able.
● Emotional support. Encourage verbalization about concerns of
disease process, future expectations; give positive reinforcement for
accomplishments; and acknowledge and accept feelings of grief,
hostility, dependency.
● Health education. Review disease process, prognosis, and future
expectations; discuss patient’s role in management of disease
process through nutrition, medication, and balanced program of
exercise and rest; and assist in planning a realistic and integrated
schedule of activity, rest, personal care, drug administration,
physical therapy, and stress management.
Evaluation
Goals are met as evidenced by:
● Reported pain is relieved/controlled.
● Appeared relaxed, able to sleep/rest and participate in
activities appropriately.
● Followed prescribed pharmacological regimen.
● Incorporated relaxation skills and diversional activities into a pain
control program.
● Maintained position of function with absence/limitation of
contractures.
● Maintained strength and function of the affected and/or
compensatory body part.
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● Demonstrated techniques/behaviors that enable
resumption/continuation of activities.
● Verbalized increased confidence in ability to deal with illness,
changes in lifestyle, and possible limitations.
● Verbalized understanding of condition/prognosis, and potential
complications.Formulate realistic goals/plans for future.
Diabetes Mellitus Type 1 (Juvenile Diabetes)
● Diabetes mellitus (DM) is a chronic metabolic disorder caused by an
absolute or relative deficiency of insulin, an anabolic hormone.
● Type 1 diabetes or (also known as insulin-dependent diabetes
mellitus (IDDM) and juvenile diabetes mellitus) is a chronic illness
characterized by the body’s inability to produce insulin due to the
autoimmune destruction of the beta cells in the pancreas.
● Insulin is produced by the beta cells of the islets of Langerhans
located in the pancreas, and the absence, destruction, or other loss of
these cells results in type 1 diabetes (insulin-dependent diabetes
mellitus [IDDM]).
● Diabetes mellitus is often considered an adult disease, but at least
5% of cases begin in childhood, usually at about 6 years of age or
around the time of puberty.
Pathophysiology
Insulin is essential to process carbohydrates, fat, and protein; it reduces
blood glucose levels by allowing glucose to enter muscle cells and by
stimulating the conversion of glucose to glycogen (glycogenesis) as a
carbohydrate store; it also inhibits the release of stored glucose from liver
glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides,
free fatty acids, and ketones; it stimulates fat storage; additionally, insulin
inhibits the breakdown of protein and fat for glucose production
(gluconeogenesis) in the liver and kidneys.
● Hyperglycemia (ie, random blood glucose concentration of more
than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads
 to uninhibited gluconeogenesis and prevents the use and storage of
circulating glucose.
● The kidneys cannot reabsorb the excess glucose load, causing
glycosuria, osmotic diuresis, thirst, and dehydration; increased fat
and protein breakdown leads to ketone production and weight loss.
● The brain depends on glucose as a fuel; as glucose levels drop below
65 mg/dL (3.2 mmol/L) counterregulatory hormones (eg, glucagon,
cortisol, epinephrine) are released, and symptoms of hypoglycemia
develop.
● The glucose level at which symptoms develop varies greatly from
individual to individual (and from time to time in the same
individual), depending in part on the duration of diabetes, the
frequency of hypoglycemic episodes, the rate of fall of glycemia,
and overall control.
Statistics and Incidences
The occurrence of diabetes mellitus type 1 in the United States and
worldwide are as follows:
● annual incidence of DM Type 1 is 24.3 cases per 100,000
person-years.
● approximately 15,000 annually), increasing numbers of older
children are being diagnosed with type 2 diabetes mellitus,
especially among minority groups (3700 annually).
● A study by Mayer-Davis et al indicated that between 2002 and 2012,
the incidence of type 1 and type 2 DM significant rise among youths
in the US; according to the report, after the figures were adjusted for
age, sex, and race or ethnic group, the incidence of type 1 (in
patients aged 0-19 years) and type 2 diabetes mellitus (in patients
aged 10-19 years) during this period underwent a relative annual
increase of 1.8% and 4.8%, respectively.
● Type 1 DM has wide geographic variation in incidence and
prevalence.
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● Annual incidence varies 0.61 cases/100,000 pop’n China to 41.4
cases/100,000 pop’n Finland.
● Whites highest reported incidence, but Chinese ind’ls have the
lowest.
● T1 DM is 1.5 x more in American whites than American blacks/
Hispanics.
● Males at greater risk in regions of high incidence, esp older males,
whose incidence rates often show seasonal variation; females appear
to be at a greater risk in low-incidence regions.
● Onset 1st yr of life, type 1 DM must be considered in any infant or
toddler bcoz these child’n have greatest risk for mortality if Dx is
delayed.
Clinical Manifestations
● Most easily recognized symptoms of type 1 diabetes mellitus
(T1DM) are secondary to hyperglycemia, glycosuria, & DKA.
● Hyperglycemia: general malaise, headache, and weakness; children
may also appear irritable and become ill-tempered.
● Glycosuria.
● Polydipsia.
● Polyuria.
● Diabetic ketoacidosis (DKA). DKA is characterized by drowsiness,
dry skin, flushed cheeks, and cherry-red lips, acetone breath with a
fruity smell, and Kussmaul breathing.
Assessment and Diagnostic Findings
Early detection & control are critical in postponing or minimizing
later complications of diabetes.
● Fingerstick glucose test. Children w/ fam hx of DM should be
monitored for glucose using a fingerstick glucose test.
● Urine dipstick test=ketones in the urine,
 ● FBS If elevated or ketonuria is + , fbs be performed; an FBS result
of 200 mg/dl or higher almost certainly is diagnostic for diabetes
when other signs are present.
● Lipid profile. inc’d circ’g triglycerides caused by gluconeogenesis.
● Glycated hemoglobin. Glycosylated hemoglobin derivatives
(HbA1a, HbA1b, HbA1c) are the result of a nonenzymatic reaction
between glucose and hemoglobin; a strong correlation exists
between average blood glucose concentrations over an 8- to
10-week period and the proportion of glycated hemoglobin.
● Microalbuminuria. Microalbuminuria is the first evidence of
nephropathy; the exact definition varies slightly between nations,
but an increased AER is commonly defined as a ratio of first
morning-void urinary albumin levels to creatinine levels that exceed
10 mg/mmol, or as a timed, overnight AER of more than 20
mcg/min but less than 200 mcg/min.
Medical Mgt
● Insulin therapy. Insulin therapy is an essential part of the treatment
of diabetes in children; the dosage of insulin is adjusted according to
blood glucose levels so that the levels are maintained near normal;
many children are prescribed with an insulin regimen given at two
times during the day: one before breakfast and the second before the
evening meal.
● Diet. Current dietary management of diabetes emphasizes a healthy,
balanced diet that is high in carbohydrates and fiber and low in fat.
● Activity. Type 1 diabetes mellitus requires no restrictions on
activity; exercise has real benefits for a child with diabetes; current
guidelines are increasingly sophisticated and allow children to
compete at the highest levels in sports.
● Continuous glucose monitoring. The American Diabetes
Association’s Standards of Medical Care in Diabetes-2018
recommend consideration of continuous glucose monitoring for
children and adolescents with type 1 diabetes, whether they are
using injections or continuous subcutaneous insulin infusion, to aid
in glycemic control.
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Pharmacologic Management
Insulin is always required to treat type 1 diabetes mellitus; these agents are
used for the treatment of type 1 diabetes mellitus, as well as for type 2
diabetes mellitus that is unresponsive to treatment with diet and/or oral
hypoglycemics.
● Insulin aspart. Rapid-acting insulin; insulin aspart is approved by the
FDA for use in children aged >2 y with type 1 DM for SC daily
injections and for SC continuous infusion by external insulin pump;
however, it has not been studied in pediatric patients with type 2
DM; onset of action is 10-30 minutes, peak activity is 1-2 h, and
duration of action is 3-6 h.
● Insulin glulisine. Rapid-acting insulin; the safety and effectiveness
of SC injections of insulin glulisine have been established in
pediatric patients (aged 4-17 y) with type 1 DM; however, it has not
been studied in pediatric patients with type 2 DM; onset of action is
20-30 minutes, peak activity is 1 h, and duration of action is 5 h.
● Insulin lispro. Rapid-acting insulin; only lispro U-100 is approved
by the FDA to improve glycemic control in children aged >3 y with
type 1 DM; however, it has not been studied in children with type 2
DM; onset of action is 10-30 minutes, peak activity is 1-2 h, and
duration of action is 2-4 h.
● Regular insulin. Short-acting insulin. Novolin R has been approved
by the FDA to improve glycemic control in pediatric patients aged
2-18 y with type 1 DM; however, it has not been studied in pediatric
patients with type 2 DM; Humulin R is indicated to improve
glycemic control in pediatric patients with diabetes mellitus
requiring more than 200 units of insulin per day; however, there are
no well-controlled studies of use of concentrated Humulin R U-500
in children.
● Insulin NPH. Intermediate-acting insulin; it is indicated to improve
glycemic control in pediatric patients with type 1 diabetes mellitus;
onset of action is 3-4 h, peak effect is in 8-14 h, and usual duration
of action is 16-24 h.
 ● Insulin glargine. Long-acting insulin; the safety and effectiveness of
glargine U-100 have been established in pediatric patients (6-15 y)
with type 1 DM; however, it has not been studied in pediatric
patients with type 2 DM.
● Insulin detemir. Long-acting insulin. Insulin detemir is indicated for
once- or twice-daily SC administration for the treatment of pediatric
patients (aged 6-17 years) with type 1 DM; however, detemir has
not been studied in pediatric patients with type 2 DM; onset of
action is 3-4 h, peak activity is 6-8 h, and duration of action ranges
from 5.7 h (low dose) to 23.2 h (high dose).
● Insulin degludec. Ultra-long-acting insulin; insulin degludec is
approved by the FDA to improve glycemic control in pediatric
patients aged >1 y with type 1 or type 2 DM; it usually takes 3-4
days for insulin degludec to reach steady state, peak plasma time is
9 h and the durations of action is at least 42 h; it is highly protein
bound, and following SC, the protein-binding provides a depot
effect.
NSG MGT
Nursing assessment for patients with diabetes mellitus type 1
involves:
Nursing Diagnoses
● Imbalanced nutrition: less than body requirements related to
insufficient caloric intake to meet growth and development needs
and the inability of the body to use nutrients.
● Risk for impaired skin integrity related to slow healing process and
decreased circulation.
● Risk for infection related to elevated glucose levels.
● Deficient knowledge related to complications of hypoglycemia and
hyperglycemia.
● Deficient knowledge related to appropriate exercise and activity.
Nursing Care Planning and Goals
The major nursing care planning goals for diabetes mellitus type 1 the
child include:
● Maintaining adequate nutrition.
● Promoting skin integrity.
● Preventing infection.
● Regulating glucose levels.
● Learning to adjust to having a chronic disease.
● Learning about and managing hypoglycemia and hyperglycemia,
insulin administration, and exercise needs for the child.

● Hx. ask about the child’s appetite, weight loss or gain, evidence of
polyuria or enuresis in a previously toilet-trained child, polydipsia,
dehydration, irritability and fatigue; include the child in the
interview and encourage him or her to contribute info.
● PE. Measure the height and weight and examine the skin for
evidence of dryness or slowly healing sores; note signs of
hyperglycemia, record vital signs, and collect a urine specimen;
perform a blood glucose level determination using a bedside glucose
monitor.

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