PEDIATRIC DISTURBANCES

SUSAN MONTERO

Normal Growth & Development

Age Groups

Perinatal period

From the 20th week of gestation to the first six days after birth
The first 28th days after birth Under 1 month to 1 year

Neonatal period

Early infancy

Age Groups

Later infancy (toddlers)

2 3 years
4 -5 years From 6 years 10 19 years

Pre-school

School age

Adolescence

Growth & Development

Age (months) Motor
2 45
7

Social/Cognitive
Social Smile Laughs
Stranger anxiety

9 12

Holds head up Rolls over; grasps object Sits without support Crawls Walks

Says Mama/Dada

Growth & Development

Age (months) Motor
18 24 Runs

Social/Cognitive

36

Names common objects Walks up & Uses 2 word down stairs combinations; Understands 2-step commands Pedals a tricycle; Uses plurals & copies a circle 3-word combination

At the playground

Stranger anxiety Separation anxiety Parallel play Group play

0 1 years 1 3 years 2 3 years 3 4 years

Recommended Schedule for Routine Active Immunization of Normal Infants & Children

BCG (Bacille Calmette-Guerin)

Live attenuated M.bovis Direct vaccination at any age usually between 3 14 months of age 0.05 mL intradermally over deltoid area Booster: 1st grade school entrants (0.1 mL ID) Possible reaction:

Keloid scar, regional adenitis, dessseminated BCG infection, osteomyelitis among immunocompromise

DPT (Diphtheria, Pertussis & Tetanus Toxoids)

Given at age 2, 4 & 6 months or thereafter Below 6 years: 3 doses with intervals of 4 weeks 3 doses of 0.5 mL IM 1st Booster: 1 year after completion of primary immunization (0.5 mL) 2nd Booster: 4 6 years

DPT (Diphtheria, Pertussis & Tetanus Toxoids)

Subsequent booster using DT at 10 year interval Possible reaction:

Fever, restlessness, irritability, local signs of inflammation

DT or Td (Diphtheria & Tetanus Toxoids)

For over 6 years & those with severe reaction to DPT 3 doses of 0.5 mL IM at monthly interval Booster: 1 year after primary & every 10 years thereafter (0.5 mL IM)

Tetanus Toxoid

Over 2 months when DPT or DT are not available 2 doses 0.5 mL IM at 6 8 weeks interval Booster: 1 year after primary immunization & every 10 years thereafter (0.5 mL IM)

Tetanus Toxoid

Pregnant women: 2 doses 0.5 mL IM at 8 weeks interval after 5 months of gesttion 2nd dose is given not later than 1 month prior to EDC

Poliomyelitis Vaccine (OPV)

Given at age 2, 4 & 6 months or 3 doses at 6 8 weeks interval (at later age) 0.5 mL orally for single dose preparation or 3 drops for multiple dose preparation 1st Booster: 1 year after primary 2nd Booster at age 4 6 years Possible reaction: paralytic polio

Poliomyelitis Vaccine (IPV)

Age indication is the same as for OPV 3 doses subcutaneous

1st 3 doses at 4 weeks interval 4th dose 6 12 months after

Booster dose upon entering school No possible reaction

Measles Vaccine

Live attenuated virus 9 months later but may be given as early as 6 months 1 dose SC 2nd dose given at 15 months if 1st dose is given below 1 year 3rd dose given at 5 12 years as part of MMR

Measles Vaccine

Possible reaction
Fever Rash 5 10 days after dose

95% Efficacy May last for 12 years

Rubella Vaccine

Live attenuated virus <1 year or older or non-pregnant adults 1 mL SC Booster: 5 12 years if 1st dose is given at infancy (as MMR) Arthralgia, LAD, mild rash 2 4 weeks later time

Mumps Vaccine

Live attenuated virus 1 year or older to 21 years 0.5 mL SC Booster: 5 12 years if 1st dose is given at infancy Possible reaction: febrile seizures, nerve deafness, encephalitis, rash, pruritus

MMR

Live attenuated viruses of measles, mumps & rubella 12 months or older 0.5 mL SC 5 12 years if 1st dose is given at infancy Possible reaction is the same as those cited for individual components

HBV

From birth to adult in endemic areas 3 doses by IM at 1 month intervals Booster: probably 5 years after primary which may not be necessary Possible reaction: arthralgia & neurologic reactions

Child Development: Principles & Norms

Psychoanalytic Concepts of Personality Development (Freud) Eriksons Psychosocial Theory Piagets Theories on Cognition

The Psychoanalytic Concepts of Personality Development

Oral Stage The erotic zone or source of security and satisfaction during this stage is the mouth Autistic phase

Birth 3 months; marked passivity on the part of the infant 3 18 months; dependency

Symbiotic phase

The Psychoanalytic Concepts of Personality Development

Oral Stage Aggression may appear during this stage and is manifested mainly by biting Weaning taking the child off the nipple and transferring him to the cup for his milk supply Oral person an individual who continues to be mouth-centered far beyond the age when the mouth should have ceased to be a source of satisfaction

The Psychoanalytic Concepts of Personality Development

Anal Stage The mouth shares its pleasure-giving role with the anus 12 36 months There is decreasing dependency on the parents terrible twos a 2-year-old child is usually pictured as a scowling, angry child

The Psychoanalytic Concepts of Personality Development

Anal Stage The anal type of personality is usually seen in the obstinate and parsimonious adult A child is toilet-trained only when he shows signs of being ready
18 24 months for day control 2 - 3 years for night control

The Psychoanalytic Concepts of Personality Development

Phallic Stage It usually begins at 3 4 years and ends at 5 7 years The child still exhibits ambivalence plus curiosity & exhibitionism He continues to believe readily in magic and becomes preoccupied with the genitals and sex differences

The Psychoanalytic Concepts of Personality Development

Phallic Stage The boy fears that he might lose his penis while the girl feels that she has lost hers For the boy castration anxiety For the girl penis envy Oedipus complex attraction to the parent of the opposite sex Formal sex education should be started at this age

The Psychoanalytic Concepts of Personality Development

Latency Stage The erogenous area remains in the phallic area This encompasses the ages from 5 7 years to 8 12 years There is an increasing accumulation of knowledge and development of physical ability Good reality adaptation and has a conscious fear of death and a relative decrease in sex interest

The Psychoanalytic Concepts of Personality Development

Adolescence The primary erotic zone still is focused on the sexual parts 10 12 years to 16 18 years Rapid development of the sex organs and maturation of sexual reproductive capacities Inconsistencies in behavior, vacillation in moods, intense interest in peer groups, fads involving clothing, hair & music

Eriksons Psychosocial theory

Stage 1 (trust vs. mistrust) The focus is on infant parent interaction With consistency & reliability in handling the child, he develops trust Stage 2 (autonomy vs. shame) NO stage the child must show that he is an individual in his own right at the same time he worries if he is capable of being so

Eriksons Psychosocial theory

Stage 3 (initiative vs. guilt) This takes place during the preschool period One of his ambitions is to win his mother away from his father but feels that he is wrong to wish to possess his mother and thus experiences guilt Stage 4 (industry vs. inferiority) It is the period when children industriously apply themselves to learn the skills that society requires of them

Eriksons Psychosocial theory

Stage 5 (identity vs. ego confusion) Who am I? Adolescents must learn to develop an identity of their own & face a rapidly changing physical appearance

Piagets Theories on Cognition

Stage I (birth 1 month) Neonatal reflexes and the infant responding to the environment in an uncoordinated manner Stage II (1 4 months) New response patterns occurs as a result of chance combination of primitive reflexes Stage III (4 8 months) Response patterns are intentionally formed and repeated

Piagets Theories on Cognition

Stage IV (8 12 months) Anticipatory & intentional behavior are more apparent including search for vanished objects Stage V (12 18 months) Variations occur in behavior patterns to achieve different effects Stage VI (1 2 years) Symbolic representation begins

Basic Food Elements

Water

Is an important part of the cellular structure, vehicle for cellular exchanges, temperature regulation Effects of deficiency

Thirst, dryness of the skin & mucous membranes, dehydration, decreased urine output, impaired kidney function

Water

Effects of excess

Cramps, water intoxication, headache, convulsions, edema and circulatory failure

Sources: water and other liquids; all foodstuffs

Proteins

Supplies amino acids for building and repairing body tissues It supplies heat and energy when there is shortage of fats and carbohydrates Effects of deficiency

Weakness, prominent abdomen, edema, retarded growth, slow recovery from disease, loss of weight, reduced resistance to infection

Protein

Effects of Excess

Azotemia, acidosis, hyperammonemia

Sources:
Plant: garbanzos, tokwa, peanut butter, munggo, dried beans and nuts Animal: milk, meat, liver, heart, kidney, poultry, eggs, fish and shelfish

Carbohydrates

It is an important energy source; storage of calories as glycogen and conversion to fat, amino acids synthesis Effects of deficiency
Underweight if total calories are low, ketosis, general weakness In severe cases, fainting, collapse and seizures

Carbohydrates

Effects of excess

Obesity, diarrhea, syndromes due to inborn errors of sugar metabolism

Sources
Plant: starch, bread, cereals, rice, potatoes Animals: milk Sugars: fruits, jams, preserves, cakes, jellies, cookies

Fats

Reserve energy source, protects organs and vessels, maintains body heat, supplies essential fatty acids, spares proteins Effects of deficiency

Underweight, lack of satiety, skin changes, hair loss

Effects of excess

Overweight, atherosclerosis

Fats

Source
Plant: margarine, nuts, salad oils, vegetable oils Animal: breast milk, butter, cream, fats from meat, lard

Vitamins of Nutritional Importance

Vitamin A

Retinol (an alcohol) Function

Retinal pigment formation Formation and maturation of epithelium Development of bones and teeth Regulation of membrane function

Deficiency may be produced by decreased intake or absorption, increased consumption & loss through diarrhea

Vitamin A

Effects of deficiency
Eye symptoms and signs (nyctalopia, photophobia, xerophthalmia, keratomalacia Keratinization of mucous membranes and skin Growth failure

Excess

Carotenemia; anorexia, slow growth, dryness & cracking of skin, swelling and pain of long bones

Vitamin A

RDA: 1800 IU/day Sources

Plant: leafy vegetables Animal: liver and fish liver oils, whole milk, dried and evaporated, cheese, butter, margarine, cream and egg yolk

Vitamin D

Steroid alcohols Functions

It regulates absorption of Ca and P Regulates concentration of ALP (deposition of Ca and P in bones and teeth) Renal conservation of Ca & P

Deficiency is produced by inadequate exposure to sunlight

Vitamin D

Manifestations of deficiency

Rickets, infantile tetany, osteomalacia, cranial bossing, bowed legs, persistently open anterior fontanelle

Excess: hypercalcemia (vomiting, mental retardation, bone changes RDA: 400 IU/day Sources: Fish liver oils, milk & margarine, intestinal organs, exposure to sunlight

Vitamin E

Functions
Muscle metabolism and RBC wall stability Synthesis of blood pigments, cell maturation

Deficiency is produced by loss through steatorrhea growth disturbance RDA: 4 -5 IU/day Sources: green leafy vegetables, whole grains, olive oil, beans and legumes, egg yolk, fish liver oil, salmon and sardines

Vitamin K

Necessary for blood clotting Found in lesser amount in breast milk Deficiency may due to lack of bacterial synthesis, prolonged use of sulfonamides and salicylates Manifestations: bleeding tendencies, cirrhosis

Vitamin K

Excess of vitamin K may cause jaundice, hemolytic anemia and cranial nerve palsy RDA: 1 2 mg/day Sources:
Plant: green cabbage, spinach, cauliflower, carrots, soybean oil, seaweed Animal: pork, liver, egg yolk

Vitamin C

Ascorbic acid It is important for the maintenance of intercellular material Deficiency is produced by dietary inadequacy; increased need in febrile illness
Scurvy skin hemorrhages, irritability, tenderness of legs Poor wound healing

Vitamin C

Its value as cold remedy unproven (? Nasal decongestant) RDA:

1st year: 30 mg/day 1 12 years: 35 mg 75 mg/day

Sources

Citrus fruits, quava, anonas, guyabano, strawberries, tomato, melon, pinya, leafy vegetables, ampalaya (destroyed by prolonged heating)

Thiamine (Vitamin B1)

It promotes normal functioning of the nervous system Manifestations of deficiency

Polyneuritis, edema, cardiac failure (beriberi) Early manifestations: irritability, constipation, tachycardia

RDA: 0.5 mg/day Sources: unpolished rice, whole grain and cereals, soybeans, lean pork, egg yolk, int. organs

Riboflavin (Vitamin B2)

Functions
Coenzyme in cellular oxidation Retinal pigment for light adaptation

Deficiency is produced by inadequate intake, faulty absorption in hepatitis Eye changes (photophobia, blurring of vision, burning sensation of eyes) Seborrheic skin changes and mucocutaneous lesions, magenta tongue, anemia

Riboflavin (Vitamin B2)

RDA: 6 mg/day Sources:

Plant: enriched rice and whole wheat bread, peanut butter, dried fruits, potatoes, beans and mushrooms Animal: lean pork, internal organs, beef, turkey, chicken and fish

Niacin

Coenzyme in glycolysis, protein, amino acid, lipid metabolism Deficiency is found in exclusive corn diet Manifestations

Pellagra, cheilosis, angular stomatitis, inflammation of mucous membranes, weakness

RDA: 6 mg/day Excess: flushing, vasodilatation, vasomotor instability

Pyridoxine (Vitamin B6)

Coenzyme of amino acid metabolism Deficiency is manifested by:

Irritability, convulsions, anemia, abdominal distress, vomiting Peripheral neuritis (INH administration in adults)

RDA: 1 2 mg/day Sources: whole grain cereals, legumes, vegetable oils, lard, meat, internal organs

Cobalamine (Vitamin B12)

Maturation of RBC in bone marrow Deficiency is produced in defective absorption due to lack of intrinsic factor Manifestations: pernicious anemia, neurologic deficits RDA: 0.3 mcg/day Sources: internal organs, fish, eggs, milk, cheese

Growth and Development: Nutrition

Breast milk

Compared to cows milk it has more fat, CHO but lacks vitamin D

Supplementation
Iron (start at 4-6 months) Vitamin B12 for breastfed infants if mother is vegetarian Fluoride is recommended for all breastfed infants Calcium, vitamin D for breastfed infants at risk (little sunlight)

Nutrition
Commercial formulas Cow milk based

With added whey protein

Soy protein formulas

hypoallergenic Useful after diarrhea (transient lactase deficiency)

Alteration in Nutrition

Marasmus

Severe malnutrition Watch for electrolyte imbalances Do not refeed too rapidly!

Kwashiorkor

Alteration in Nutrition

Obesity

Behavior modification, diet and exercise Surgery (gastroplasty, gastric bypass) only for severe obesity

Alteration in Nutrition

Anorexia Nervosa

Psychiatric disease Psychotherapy Restore normal eating pattern/caloric intake Force feeding only in life-threatening situation

Mouth: Signs and Symptoms

Bleeding gums

Vitamin C deficiency

Glossitis, cheilosis

Vitamin B2 deficiency

Mouth: Signs and Symptoms

Beefy red tongue

Vitamin b12 deficiency

Strawberry tongue

Scarlet fever

Mouth: Signs and Symptoms

Kopliks spots

Measles

Oral thrush

Systemic candidiasis

Failure to Thrive
Slow growth and mental development in 1st 3 years of life Assessment Growth is 2 standard deviations below normal Apathy, weakness, irritability Lack of social responses (eye contact, smiles)

Failure to Thrive
Assessment Provide sensory stimulation
Cuddling, rocking, talking Colorful toys

Observe parent-child interaction Client education Develop home-care plan with parents Referral for financial or mental health assistance

Gastroesophageal Reflux Disease

GERD is the backflow of gastric contents into the esophagus It usually results from relaxation or incompetence of the lower esophageal sphincter It is the most common esophageal problem in infancy

Gastroesophageal Reflux Disease

It is deemed pathologic when it is severe, persists into late infancy, or is associated with complications It is common in children with TEF, prematurity, BPD, cerebral palsy, scoliosis, asthma, or neurologic disorders The cause is unknown but may result from delayed maturation of lower esophageal neuromuscular function

Gastroesophageal Reflux Disease

Pathophysiology Inappropriate relaxation or failure of cardiac sphincter contraction leads to increased gastric pressure and reflux of gastric contents Delayed gastric emptying may be a contributing factor Repeated reflux can damage delicate esophageal mucosa

Gastroesophageal Reflux Disease

Clinical Manifestations Forceful vomiting, possibly hematemesis Weight loss, aspiration and recurrent respiratory infections Cyanotic and apneic episodes Esophagitis and bleeding from repeated irritation Melena, heartburn, abdominal pain and bitter taste in mouth

Gastroesophageal Reflux Disease

Laboratory Findings Upper GI study will reveal reflux following barium swallow and absence of gastric or duodenal obstruction CBC may reveal anemia secondary to blood loss

Gastroesophageal Reflux Disease

Nursing Management Promote adequate hydration Assess the amount, frequency, and characteristics of emesis Improve nutritional status through feeding techniques

Administer small, frequent feedings and burp the infant frequently

Gastroesophageal Reflux Disease

Nursing Management Administer prescribed medications
Antacids and H2 blockers Prokinetic medications which may decrease reflux Drugs that promote gastric emptying and increases lower esophageal sphincter

Pyloric Stenosis
Is the narrowing of the pyloric sphincter at the outlet of the stomach The exact cause is unknown; heredity Pathophysiology The pylorus narrows because of progressive hypertrophy and hyperplasia of the pyloric muscle obstruction

Pyloric Stenosis
Clinical Manifestations No abnormal signs in the first weeks after birth Regurgitation or nonprojectile vomiting beginning by 3 weeks of age Emesis is not bile stained and contains only gastric contents but may be blood tinged No signs of anorexia; good appetite and feeding habits

Pyloric Stenosis
Clinical Manifestations No evidence of pain, weight loss may occur Upper abdominal distention Palpable olive-shaped mass in the epigastrium just to the right of the umbilicus Decreased frequency and volume of stolls Signs of malnutrition and dehydration

Pyloric Stenosis
Laboratory Findings UTZ and upper GI study may reveal delayed gastric emptying, an elongated pylorus, or a pyloric mass ABGs will reveal increased serum pH and bicarbonate levels metabolic alkalosis Decreased serum CL, Na, and K CBC will reveal hemoconcentration

Pyloric Stenosis
Nursing Management Monitor feeding pattern and association between feedings and vomiting Assess the amount, character, and frequency of emesis Promote adequate hydration Prevent aspiration

Hirschsprung Disease

Is a congenital anomaly characterized by absence of nerves to a segment of the intestines It may result to obstruction due to inadequate motility in an intestinal segment It is four times more common in boys than in girls More commonly seen in patients with Down syndrome

Hirschsprung Disease
Pathophysiology Absence of nerve innervation in one segment of the colon

Absence of propulsive movements

Accumulation of intestinal contents and distention of the bowels

Hirschsprung Disease
Pathophysiology Enterocolitis is the leading cause of death in children with Hirschsprung disease It occurs as a result of intestinal distention and ischemia secondary to bowel distention

Hirschsprung Disease
Clinical Manifestations Newborns

Failure to pass meconium, reluctance to ingest fluids, abdominal distention, and bile-stained emesis Failure to thrive, constipation, abdominal distention, vomiting and episodic diarrhea

Infants

Hirschsprung Disease
Clinical Manifestations Older children
Anorexia, chronic constipation, foul-smelling ribbon-like stools Abdominal distention, visible peristalsis, palpable fecal mass Malnourishment, signs of anemia and hypoproteinemia

Hirschsprung Disease
Clinical Manifestations Rectal examination typically reveals a rectum empty of stool, tight anal sphincter and stool leakage Ominous sign signifying enterocolitis include explosive, bloody diarrhea, fever, and severe prostration

Hirschsprung Disease
Laboratory Findings Barium enema reveals megacolon Rectal biopsy will reveal absence of ganglionic cells Nursing Management Assess for signs of enterocolitis Promote adequate hydration Assess bowel functioning

Hirschsprung Disease
Nursing Management Promote adequate nutrition Administer enemas Administer the prescribed medications

Antibiotics and stool softeners

Decrease discomfort due to abdominal distention

Intussuseption

Is an invagination or telescoping of one portion of the intestine into an adjacent portion, causing obstruction It is one of the most frequent causes of intestinal obstruction in children It affects children between 3 months and 5 years of age; more commonly between 3 12 months

Intussuseption

If treatment is delayed for longer than 24 hours, bowel strangulation may occur necrosis, obstruction, perforation and peritonitis, and shock The cause is unknown It may be associated with viral infections, intestinal polyps, Meckel diverticulum and lymphoma

Intussuseption
Pathophysiology Invagination typically begins with hyperperistalsis in an intestinal segment, most often at the ileocecal valve Peristalsis continues to pull the invaginated segment along the bowel intestinal edema, obstruction and loss of blood supply

Intussuseption
Clinical Manifestations Severe paroxysmal abdominal pain, causing the child to scream and draw his knees to the abdomen Vomiting of gastric contents Tender, distended abdomen with a palpable mass Currant jelly stools, bile-stained emesis, shocklike syndrome death

Intussuseption
Laboratory Findings An enema may be used for diagnosis or therapeutic treatment tool Electrolyte studies will reveal electrolyte loss relative to symptoms

Intussuseption
Nursing Management Promote adequate hydration Promote adequate nutrition Monitor bowel elimination status Monitor infection

Infectious & Immunologic Disorders of Infancy & Childhood

HIV and AIDS

HIV It causes a broad spectrum of diseases and varied clinical course AIDS is the most severe end of the spectrum AIDS in children and adolescents accounts for approximately 2% of all reported cases The majority of children with HIV infection are less than 7 years of age

HIV and AIDS

ETIOLOGY The predominant modes of transmission in children and adolescents are: Mother-to-infant transmission Sexual contact Blood transfusion

HIV and AIDS

Mother-to-infant transmission The risk of contracting HIV for an infant of an HIV-positive mother is 15% to 30% Transmission occurs through one of the ff. ways Via placental spread Exposure to blood & mucous membranes Breast-feeding (possibly)

HIV and AIDS

Sexual contact Both homosexual and heterosexual

Transfusion of blood This is now a rare mode of transmission 11% to 13% of HIV-infected children were infected by blood transfusions before 1985

HIV and AIDS

Etiology Most infected children are born to families where one or both parents are infected with HIV The remainder includes children who received contaminated blood, children who have been sexually abused, or adolescents with adult risk factors

HIV and AIDS

Pathophysiology AIDS is caused by infection with HIV HIV is a retrovirus that produces lymphophenia A decrease in the number of CD4+ T cells may lead to immunosuppression T cells controls B cell function

HIV and AIDS

Pathophysiology Young children with HIV are deficient in both cellular and humoral immunity Immunoglobulins are nonfunctional recurrent bacterial infections Children are also unable to form antibodies after immunizations

HIV and AIDS

Pathophysiology

Infection with HIV Destruction of CD4+ T cells

Lymphopenia

HIV and AIDS

Pathophysiology

Destruction of T cells Abnormal B cell function

Inability to produce immunoglobulins

HIV and AIDS

Clinical manifestations The incubation period of symptomatic HIV is variable and ranges from months to years Perinatally infected individuals are symptomatic by 18 to 24 months of age About 20% of prenatally infected children are symptomatic in the first year Most of this children die by 4 years of age

HIV and AIDS

Clinical manifestations Failure to thrive & nutritional deficiencies Organomegaly & recurrent bacterial infection Pulmonary diseases occur in 2/3 of HIVinfected children and include: Pneumocystis carinii pneumonia Interstitial pneumonitis pulmonary Lymphoid hyperplasia

HIV and AIDS

Clinical manifestations Chronic diarrhea may be primary or secondary to oppotunistic GI infections Neurologic problems occur in 75% to 90% of HIV children and include: Developmental delays, loss of reflexes Memory loss and lack of coordination Ataxia, visual disturbances, microcephaly

HIV and AIDS

Laboratory findings Viral assays will detect HIV in virtually all infected infants by 6 months of age PCR: a positive test indicates possible HIV infection ELISA and Western blot: used in children over 18 months

HIV and AIDS

Laboratory findings Early peripheral smear may be normal; lymphopenia is noted later Immune function tests will reveal decreased CD4 counts

HIV and AIDS

Nursing management Prevent opportunistic infections Assess for signs of infection Administer prescribed medications antiretrovirals and other medications used to prevent infection Zidovudine (AZT) should begin as soon as possible after birth

HIV and AIDS

Prevent opportunistic infections Administer immunizations against childhood infections all are recommended except for varicella IPV is used instead of OPV MMR is given unless the child is severely immunocompromised

HIV and AIDS

Provide adequate nourishment Offer high-calorie, high-protein foods that the child likes Nutritional supplements may be given Children should only eat peeled or cooked fruits and vegetables to avoid infection Provide mouth care

Juvenile Rheumatoid Arthritis

JRA It is an autoimmune inflammatory disorder It is one of the more common chronic diseases in children It is rarely life-threatening even in its most severe form

Juvenile Rheumatoid Arthritis

There are 3 major forms of JRA Systemic Pauciarticular This form involves a few joints, usually less than 5 Polyarticular This form involves 4 or more joints

Juvenile Rheumatoid Arthritis

Pathophysiology The cause is unknown The synovial joints are primarily involved Immune complexes initiate the inflammatory response Inflammatory response may damage the joints causing it to swell

Juvenile Rheumatoid Arthritis

Clinical manifestations Systemic Any joint can be involved Extra-articular manifestations include: fever, malaise, myalgia, rash, pericarditis, pleuritis, hepatosplenomegaly

Juvenile Rheumatoid Arthritis

Clinical manifestations Pauciarticular Joint involvement is usually confined to the lower extremities Extra-articular manifestations include: iridocyclitis, sacriliitis, ankylosing spondylitis

Juvenile Rheumatoid Arthritis

Clinical manifestations Polyarticular Any joint can be involved; smaller joints are usually affected Systemic symptoms are mild and may include: low-grade fever, fatigue, and slowed growth

Juvenile Rheumatoid Arthritis

Laboratory findings Systemic CBC reveal leukocytosis and anemia ESR will be elevated Rheumatoid factor is negative Antinuclear antibody is negative

Juvenile Rheumatoid Arthritis

Laboratory findings Pauciarticular CBC will reveal leukocytosis ESR will be elevated Antinuclear antibody may be positive

Juvenile Rheumatoid Arthritis

Laboratory findings Polyarticular ESR will be elevated Rheumatoid factor is positive

Juvenile Rheumatoid Arthritis

Nursing management Assess joint function and extra-articular manifestations Administer prescribed medications Relieve pain Promoting adequate joint function Promote self-care

Allergy

Allergic disorders include, but not limited to: Allergic rhinitis Allergic asthma It tends to have a familial predisposition Allergic exposure is necessary to trigger an allergic response

Allergic Rhinitis
Clinical manifestations Water rhinorrhea Nasal obstruction Sneezing Nasal pruritus Allergic facies

Infantile Eczema
Clinical manifestations Generalized on the scalp, cheeks, trunk, and extensor surfaces of the extremities Characterized by erythema, vesicles, papules, weeping, oozing, crusting lesions, and scaling Lesions are often symmetrical

Childhood Eczema
Clinical manifestations Is commonly seen on the flexor areas, wrists, ankles, and feet Characterized by symmetrical involvement, papules or scaly patches, dry, hyperpigmented areas, lichenification and keratosis

Adolescent Eczema
Clinical manifestations Is commonly seen on the face, sides of neck, hands, feet, and antecubital and popliteal area Characterized by the same signs seen during childhood with addition of lichenified plaques and confluent papules

Allergy
Laboratory findings CBC will reveal increased eosinophil count Radioallergosorbent test may be positive for the childs particular allergies

Allergy
Nursing management Minimize itching Use distraction Administer antihistamines, antipruritus, or topical steroid Dress the child in soft clothing; wash clothes in mild detergents Bathe the child in an oatmeal solution

Allergy
Nursing management Prevent infection Keep nails trimmed to prevent scratching and secondary infection Use elbow restraints if scratching is difficult to prevent Maintain good skin hygiene

Asthma

Is a chronic, reversible, obstructive airway disease Characterized by wheezing caused by spasm of the bronchial tubes after exposure to various stimuli It is the most common chronic disease in childhood

Asthma
Etiology It commonly results from hyperresponsiveness of the airways to irritants Common irritants include Allergen exposure, viral infections Irritants, certain foods, rapid changes in temperatures, exercise and stress

Asthma
Pathophysiology Three events contribute to clinical manifestations: Bronchial spasm Inflammation and edema of the mucosa Production of thick mucus increased airway resistance

Asthma
Pathophysiology If not treated promptly, status asthmaticus may occur Status asthmaticus is an acute, severe, prolonged asthma attack that is unresponsive to usual treatment requiring hospitalization

Asthma
Mild, Intermittent Asthma Symptoms < 2 times per week Brief exacerbations Nighttime symptoms < 2 times a month Asymptomatic with normal PEF between exacerbations

Asthma
Mild, Persistent Asthma Symptoms > 2 times a week, but less than once a day Exacerbations may affect activity Nighttime symptoms > 2 times a month

Asthma
Moderate, Persistent Asthma Daily symptoms Exacerbations affects affect activity Exacerbations > 2 times a week Exacerbations may last days Nighttime symptoms > once a week

Asthma
Severe, Persistent Asthma Continual symptoms Frequent exacerbations Frequent nighttime symptoms Limited physical activity

Asthma
Clinical manifestations Increased respiratory rate Wheezing, productive cough, dyspnea Use of accessory muscles Fatigue, moist skin Anxiety and apprehension

Asthma
Laboratory findings CBC will reveal leukocytosis with eosinophilia Decreased forced expiratory volume Diminished vital capacity Diminished inspiratory capacity

Asthma
Nursing management Assess respiratory status Administer prescribed medications such as bronchodilators, anti-inflammatories and antibiotics Promote adequate oxygenation and normal breathing pattern

Fever

Is an abnormally elevated body temperature of atleast 37.8C It is a sign of an underlying problem Common causes: Upper & lower respiratory tract infection Vaccination reactions, overdresing UTI, pneumonia, bacteremia, meningitis, arthritis, cancer, dehydration

Fever
Clinical manifestations Temperature over 37.8C measured by axillary route Skin flushing, diaphoresis, and chills Restlessness and lethargy

Fever
Nursing management Maintain stable body temperature Administer prescribed medications including antipyretics, acetaminophen, or ibuprofen Teaching parents how to take the childs temperature and implement fever control measures

Febrile Seizures

Are seizures associated with an illness characterized by a high fever lasting less than 15 minutes, occurring in children with neurologic disability It affects 3% to 5% of children, occurring after 6 months and before 3 years of age Febrile convulsions are unusual after the child is 5 years old

Febrile Seizures
Etiology The exact cause in unknown Febrile convulsions are usually associated with upper respiratory tract infections, urinary tract infections, and roseola

Febrile Seizures
Pathophysiology The seizure is characterized by an active tonicclonic pattern It usually last less than 1 minute and is associated with an acute, benign febrile illness The convulsion usually result from the rapid rise in temperature, with initial fever

Febrile Seizures
Clinical manifestations Most seizure activity ceases by the time the child is brought in for medical attention, but the child may be unconscious Tonic: contraction of muscles, extension of extremities, loss of bowel and bladder control, cyanosis and loss of consciousness

Febrile seizures
Clinical manifestations Clonic: rhythmic contraction and relaxation of extremities Postictal phase: characterized by persistent unconsciousness There is often a family history of febrile convulsions

Febrile Seizures
Laboratory findings EEG is usually normal, ruling out the likelihood of seizure disorder Lumbar puncture may be done to rule out meningitis CT scan and MRI may be performed to rule out abnormalities

Febrile Seizures
Nursing management Maintain a stable body temperature Prevent injury and recurrences of seizures Administer anticonvulsant therapy if prescribed

Sepsis

Is a generalized bacterial infection that usually occurs in the first month of life Neonates are highly susceptible due to immature immune response Risk factors include: prematurity, invasive procedures, chronic use of steroids for lung problems, nosocomial exposure Breast-feeding has a protective benefit against infection

Sepsis
Etiology All neonatal infections are considered opportunistic and any bacteria are capable of causing sepsis Group B streptococcus is the most common cause of sepsis, followed by Eschericia coli, Grup A strep, and Streptococcus viridans

Sepsis
Pathophysiology Immune defense mechanisms are immature, posing for rapid invasion, spread, and multiplication of infecting organisms The newborn is unable to localized infections

Sepsis
Clinical manifestations Initial signs and symptoms include: Poor sucking and feeding Weak cry Lethargy Irritability

Sepsis
Clinical manifestations Subsequent signs and symptoms may include: Pallor, cyanosis, mottling Hypotension, tachycardia, irregular respirations Jaundice, dehydration, temperature instability GI disturbances, seizures, tremors Full fontanelle

Sepsis
Laboratory findings Blood culture may reveal the offending organism Urine culture and CSF analysis will detect organism CBC will reveal leukocytosis with neutrophilia ESR and CRP will be increased

Sepsis
Nursing management Promote normal physiologic functioning Maintain a patent airway Provide neutral thermal environment Provide adequate nutrition Administer prescribed medications Monitor impending shock

Meningitis

Is an infection of the meninges usually caused by bacterial invasion Bacterial meningitis is fatal if it is not treated immediately Most cases occur between 1 month and 5 years of age Infants younger than 12 months of age are the most susceptible

Meningitis
Etiology E. coli, Group B streptococcus, and Listeria monocytogenes are the most common organisms that cause meningitis in the neonate Haemophilus influenza, Neisseria meningitidis are the most common cause of meningitis in infants and children

Meningitis
Etiology Other causative organisms include -hemolytic streptococcus and Staphylococcus aureus Viral meningitis is a self-limiting disease lasting for 7 to 10 days

Meningitis
Clinical manifestations Children younger than 2 years old exhibit: Poor feeding, irritability and lethargy High-pitched cry, bulging fontanelle Fever or low temperature Opisthotonus

Meningitis
Clinical manifestations Older children may exhibit: Respiratory or GI problems Nuchal rigidity (stiff neck) Headache Kernig and Brudzinski signs Petechial rash

Meningitis
Laboratory diagnosis CSF analysis establishes both the diagnosis and causative agent CBC reveals an increased WBC count Blood culture may also identify the causative agent

Meningitis
Nursing management Perform careful assessments to note clinical characteristics in the early stages Monitor temperature and vital signs frequently Check neurologic signs and monitor the level of consciousness Administer prescribed medications Provide supportive interventions

Autosomal Trisomies

Downs Syndrome

Trisomy 21 (1:700) Most common chromosomal disorder and cause of congenital mental retardation Findings:

Mental retardation, flat facial profile, prominent epicanthal folds, simian crease, duodenal atresia, CHD

Edwards Syndrome

Trisomy 18 (1:8000) Findings:

Severe mental retardation, rocker bottom feet, lowset ears, CHD, clenched hands, prominent occiput

Deah usually occurs within 1 year of birth

Pataus Syndrome

Trisomy 13 (1:6000) Findings:

Severe mental retardation, microphthalmia, microcephaly, Cleft lip/palate, abnormal forebrain structures, polydactyly, CHD

Death usually occurs within 1 year of birth

Genetic Gender Disorders

Klinefelters syndrome Male (XXY); 1:850 Testicular atrophy, tall, long extremities, gynecomastia, female hair distribution Turners syndrome Female (XO); 1:3000 Short stature, ovarian dysgenesis, webbing of neck, coarctation of aorta, amenorrhea

Congenital Heart Disease

Right to left shunts - early cyanosis; blue babies

Tetralogy of Fallot Transposition of great vessels Truncus arteriosus

Left to right shunts - late cyanosis; blue kids

Ventricular septal defect Atrial septal defect Patent ductus arteriosus

Tetralogy of Fallot

Most common cause of early cyanosis It consists of:

Pulmonary stenosis Right ventricular hypertrophy Overriding of the aorta Ventricular septal defect

Risk factors include Downs syndrome & trisomy 13/18

Tetralogy of Fallot

Patients present during infancy with cyanosis, dyspnea, and easy fatigability Children often squat for relief during hypoxemic episodes failure to thrive or mental status changes P.E. findings: systolic ejection murmur at the left sternal border Evaluation: Echocardiography & catheterization

Tetralogy of Fallot
CXR shows a boot-shaped heart ECG shows right-axis deviation and RVH Treatment Administer PGE1 to keep the ductus arteriosus open Treat cyanotic spells with oxygen, propanolol, knee-chest position, fluids and morphine Surgical correction: balloon atrial septostomy

Transposition of Great Vessels

A condition in which the pulmonary and systemic circulations exist in parallel

The aorta is connected to the right ventricle and the pulmonary artery to the left ventricle

Patients usually present immediately after birth with cyanosis and are critically ill These condition is fatal without correction unless the patient has PDA or VSD

Transposition of Great Vessels

P.E. findings
Cyanosis, tachypnea, and progressive respiratory failure Some may present with signs of CHF

Evaluation: 2D-echo; CXR may show narrow heart base Treatment

Keep the ductus open with PGE1 Surgical correction (arterial switch)

Truncus Arteriosus

A congenital heart defect in which a failure of separation leads to a single great vessel supplying both systemic & pulmonary arterial beds Patients usually presents with cyanosis shortly after birth Further symptoms develop in the 1st weeks to months; dyspnea, easy fatigability, failure to thrive

Truncus Arteriosus

P.E. findings

Harsh systolic murmur, cardiomegaly, bounding pulses

Angiography is diagnostic, showing the single great vessel ECG usually shows normal axis Surgical repair is necessary

Ventricular Septal Defect

A congenital hole in the ventricular septum It is the most common congenital heart defect Usually asymptomatic at birth if the defect is small May present with frequent respiratory infections, FTT, dyspnea, exercise intolerance, shortness of breath, cardiac failure

Ventricular Septal Defect

P.E. findings
Pansystolic murmur at the lower left sternal border Cardiomegaly, crackles

Diagnosis is made by clinical presentation and echocardiogram ECG may be normal if small; may reveal RVH or LVH

Atrial Septal Defect

An opening in the atrial septum that allows the flow of blood between the atria It usually begins as a left to right shunt but may reverse if pulmonary hypertension develops It may present at any age, but usually not until late childhood or early adulthood Other symptoms include dyspnea, easy fatigability and FTT

Atrial Septal Defect

2D-echo will show blood flow between the atria and a dilated right ventricle ECG shows right axis deviation CXR shows cardiac enlargement and increased pulmonary vascular markings Small defects do not require treatment but should undergo preventive measures such as antibiotics before dental procedures

Patent Ductus Arteriosus

Failure of the ductus arteriosus to close within the first few days of life Risk factors include prematurity, high altitude and maternal first trimester rubella infection It is more common in females and preterm infants Asymptomatic or may present with symptoms of heart failure, lower extremity clubbing, dyspnea

Patent Ductus Arteriosus

machinery murmur at the 2nd ICSLPL Echocardiography shows left atrial and ventricular enlargement ECG may show LVH; CXR cardiomegaly Treat with indomethacin Surgical closure is preferred if indomethacin fails or if child is 6 8 months old

Communicable Diseases with Rashes

Diphtheria Whooping cough Poliomyelitis Parotitis

Diphtheria

The infectious agent is Corynebacterium diphtheriae Modes of transmission: Direct contact, air and personal articles Incubation period: 2 to 5 days or longer Period of communicability: 2-4 weeks w/o treatment or 1-2 days after the start of treatment

Diphtheria

Clinical manifestations Nasal: common colds, foul-smelling, serous to purulent discharge Tonsillopharyngeal: malaise, anorexia, sore throat, fever, and lymphadenitis; toxemia, septic shock and death Laryngeal: fever, hoarseness and airway obstruction

Diphtheria

Complications: myocarditis and neuritis Nursing implications: Maintain strict isolation Maintain patent airway & observe for signs of obstruction Promote hydration, administer antibiotics, and maintain bed rest Institute antitoxin and antibiotics

Diphtheria

Prevention: vaccination with DPT and is maintained by boosters (DaPT, DT, dT)

Whooping Cough

The infectious agent is Bordetella pertussis Modes of transmission: Direct contact, air, and personal objects Incubation period: 5 to 21 days (average 10) Period of communicability: catarrhal stage through 4th week

Whooping Cough

Clinical manifestations: Catarrhal stage: Symptoms of URTI It continues for 1-2 weeks at which point the hacking cough becomes more severe

Whooping Cough

Clinical manifestations: Paroxysmal stage: Generally 4-6 weeks Whoophing cough develops (usually at night) Flushed/cyanotic cheeks, bulging eyes, protruding tongue Posttussive vomiting

Whooping Cough

Clinical manifestations: Convalescent stage: The cough gradually decreases The vomiting stops Patients strength returns

Whooping Cough

Complications: Pneumonia, atelectasis, OM, Convulsions, weight loss, dehydration Rectal prolapse Apnea and respiratory arrest Prevention is through vaccination (DPT)

Whooping Cough

Nursing implications: Institute isolation and bed rest when febrile Provide quite environment to decrease paroxysms Encourage fluids, provide humidity, observe for signs of obstruction, administer antibiotics and Ig

Poliomyelitis

The infectious agents are enteroviruses Modes of transmission: direct contact & fecaloral route Incubation period: 7-14 days Period of communicability: the virus is in the throat for 1 week after onset and in the feces intermittently for 3 to 4 weeks

Poliomyelitis

Clinical manifestations: Abortive or apparent: brief fever, anorexia, nausea, vomiting, constipation, headache & abdominal pain Nonparalytic: more severe pain nuchal & spinal rigidity Paralytic: muscular weakness progressing to paralysis (bowel, bladder & respiratory)

Poliomyelitis

Complications: Permanent paralysis Respiratory arrest Hypertension Kidney stones Pulmonary edema and emboli Prevention is through vaccination (OPV)

Poliomyelitis

Nursing implications: Participate in physiotherapy techniques, maintain body alignment Observe for respiratory paralysis Supportive treatment with airway maintenance and bowel and bladder programs Prevent contractures and decubiti

and

Parotitis

The infectious agent is the paramyxovirus Modes of transmission: direct contact and droplet spray Incubation period: 14-21 days Period of communicability: immediately before and immediately after swelling appears

Parotitis

Clinical manifestations: Prodromal stage: fever, headache & anorexia; earache aggravated by chewing Acute stage: glandular swelling by the 3rd day accompanied by pain & tenderness Other symptoms: malaise, anorexia & lymphadenopathy

Parotitis

Complications Meningoencephalitis Orchitis, epididymitis & sterility in males Arthritis Obstructive laryngitis OM and pneumonia

Parotitis

Nursing implications Isolation, respiratory precautions & bed rest Administer analgesics and fluids Provide warmth and support for orchitis Dim the lights Prevention is through vaccination (MMR)

Communicable Diseases with Rashes

Rubeola (measles) Rubella (German measles) Varicella Erythema infectiosum (fifth disease) Erythema subitum

Rubeola

The infectious agent is a virus Mode of transmission: direct contact with droplets Incubation period: 10-20 days Period of communicability: 4 days before to 5 days after the rash appears

Rubeola

Clinical manifestations Prodromal stage: Fever and malaise Coryza, cough and conjunctivitis Photophobia in 24 hours Koplik spots on the inside of the cheek

Rubeola

Clinical manifestations: Rash It appears 3-4 days after the onset of the prodromal stage Usually on the face and gradually spreads downward More severe in earlier sites It turns brownish after 3-4 days when fine desquamation occurs

Rubeola

Complications: Otitis media, Pneumonia, laryngotracheitis, encephalitis Nursing implications: Show parents how to provide supportive management for fever and discomfort Use dimly lit room or sunglasses

Rubella

The infectious agent is the rubella virus Mode of transmission: direct & indirect contact Incubation period: 14-21 days Period of communicability: 7 days before to about 5 days after the rash appears

Rubella

Clinical manifestations: There is no prodromal stage The rash starts on the face & rapidly spreads downward & disappears in the same order as it appeared Other symptoms include low-grade fever, headache, malaise & lymphadenopathy

Rubella

Complications include possible teratogenic effects on a fetus Nursing implications: provide supportive care Prevention is through vaccine (MMR)

Varicella

The infectious agent is the varicella-zoster virus Modes of transmission: direct contact or contact with contaminated objects Incubation period: 2-3 weeks Period of communicability: 1-2 days before the rash develops until all lesions are crusted

Varicella

Clinical manifestations: Prodromal stage: low-grade fever,malaise & anorexia Rash: macules, papules, vesicles, pustules & crusts; spreading from face & extremities, very pruritic General symptoms: fever, lymphadenopathy & irritability from pruritus

Varicella

Complications Secondary infections, encephalitis, pneumonia Hemorrhagic varicella Nursing implications: Maintain strict isolation; provide cool baths Provide skin care, administer antipyretics & antihistamines, Acyclovir and Ig

Erythema Infectiosum

The infectious agent is the HPV B19 Modes of transmission: possibly via respiratory tract and blood Incubation period: 4-14 days, may be as long as 20 days Period of communicability: before the onset of symptoms and approx. 1 week after onset of symptoms

Erythema Infectiosum

Clinical manifestations: Three-stage rash Stage I Erythema on the face that gives the cheeks a slapped face appearance Facial rash disappears in 1-4 days

Erythema Infectiosum

Clinical manifestations: Three-stage rash Stage II It begins approximately 1 day after the facial rash appears It is symmetrical, red, maculopapular that appears on upper and lower extremities Proximal to distal progression

Erythema Infectiosum

Clinical manifestations: Three-stage rash Stage III The rash subsides but it can resurface if skin is irritated or traumatized Prodromal symptoms: lethargy, fever, myalgia, nausea, vomiting, abdominal pain

Erythema Infectiosum

Complications: Arthritis and arthralgia Myocarditis, encephalitis, fetal death Nursing implications: Administer antipyretics and analgesics Prevention: there is no vaccine at present

Erythema Subitum

The infectious agent is HSV type 6 Modes of transmission: unknown Incubation period; 5-15 days Period of communicability: unknown Prevention: there is no vaccine at present

Erythema Subitum

Clinical manifestations: General symptoms: high fever persisting for 3-4 days followed appearance of rashes upon drop of fever The rash is discrete, nonpruritic, pink, maculopapular, first appearing on trunk then face, neck & extremities; fades on pressure & lasts 1-2 days

Erythema Subitum

Complications: Recurrent febrile seizures Encephalitis Nursing implications Teach parents temperature regulation measures Discuss seizure precautions

Scarlet Fever

The infectious agent is group A -hemolytic streptococci Modes of transmission: direct & indirect contact, droplet spread Incubation period: 2-4 days or 1-7 days Period of communicability: incubation phase & clinical illness & during the 1st 2 weeks of the carrier phase

Scarlet Fever

Clinical manifestations: Prodromal stage: Sudden high fever, headache, vomiting, general malaise, abdominal pain & chills The rash appears within 12 hours after prodromal stage being more intense in joint folds; skin desquamation lasting for 3 weeks

Scarlet Fever

Clinical manifestations: General symptoms: Tonsils are enlarged, rd, swollen with exudates The pharynx is beefy red & palate is covered with red, punctate lesions The tongue is coated & papilla are red & swollen (white strawberry tongue)

Scarlet Fever

Complications: OM, peritonsillar abscess, sinusitis Nephritis, carditis & polyarthritis Nursing implications: Administer full course of antibiotics, analgesics & antipyretics Encourage fluids & initiate respiratory precaution