Professional Documents
Culture Documents
SUSAN MONTERO
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
2 3 years
4 -5 years From 6 years 10 19 years
Pre-school
School age
Adolescence
Social/Cognitive
Social Smile Laughs
Stranger anxiety
9 12
Holds head up Rolls over; grasps object Sits without support Crawls Walks
Says Mama/Dada
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
Recommended Schedule for Routine Active Immunization of Normal Infants & Children
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
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
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
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
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
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
Psychoanalytic Concepts of Personality Development (Freud) Eriksons Psychosocial Theory Piagets Theories on Cognition
Birth 3 months; marked passivity on the part of the infant 3 18 months; dependency
Symbiotic phase
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
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
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
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
Effects of excess
Overweight, atherosclerosis
Fats
Source
Plant: margarine, nuts, salad oils, vegetable oils Animal: breast milk, butter, cream, fats from meat, lard
Vitamin A
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
Vitamin D
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
Sources
Citrus fruits, quava, anonas, guyabano, strawberries, tomato, melon, pinya, leafy vegetables, ampalaya (destroyed by prolonged heating)
RDA: 0.5 mg/day Sources: unpolished rice, whole grain and cereals, soybeans, lean pork, egg yolk, int. organs
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
Niacin
Coenzyme in glycolysis, protein, amino acid, lipid metabolism Deficiency is found in exclusive corn diet Manifestations
RDA: 1 2 mg/day Sources: whole grain cereals, legumes, vegetable oils, lard, meat, internal organs
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
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
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
Bleeding gums
Vitamin C deficiency
Glossitis, cheilosis
Vitamin B2 deficiency
Strawberry tongue
Scarlet fever
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
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
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
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
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
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
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
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
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
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
Severe mental retardation, rocker bottom feet, lowset ears, CHD, clenched hands, prominent occiput
Pataus Syndrome
Tetralogy of Fallot
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
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
P.E. findings
Cyanosis, tachypnea, and progressive respiratory failure Some may present with signs of CHF
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
Angiography is diagnostic, showing the single great vessel ECG usually shows normal axis Surgical repair is necessary
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
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
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
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
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
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
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)
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