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NCMA 219: Care for child at risk, Lecture notes of Nursing

Maternal and child health (MCH) care is the health service delivered to both Mothers (women in their childbearing age) and children. The objectives for MCH is all women between the ages of 15-49 years who are of reproductive age. This course It encompasses promotional and preventive measures to cater the health needs of mothers with normal health conditions.

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NCMA 219
Necrosis There is an inflammation or damage to
tissues.
Nectrotizing enterocolitis Necrotizing Enterocolitis is
the inflammation and death of intestinal tissue. It
may involve just the lining of the intestine or the
entire thickness of the intestine. In severe cases, the
intestine may even perforate. If this happens,the
bacteria normally found only in the intestine can leak
into the abdomen and cause widespread infection.
This is considered a medical emergency.
NEC is most common in premature infants.
It usually develops within two weeks of birth
Pathophysiology
The precise cause of NEC Is still uncertain, but it
appears to occur in infants whose GI tract has
suffered vascular compromise- means there is
prematurity of gastrointestinal tract leading to
hypoxia.
Bowels is compromised with oxygen Intestinal
schemia injury caused by decreases oxygen supply in
the gastrointestinal tract ; unknown case
gastrointestinal tract proliferation NEC Damage
to mucosal cells lining and bowel wall Diminised
blood suplly to these cells causes death in large
numbers Stop secreting protective, lubricating
mucus (making it prone to exotoxin), and the thin,
unprotected bowel wall is attacked by proteolytic
enzymes Unable to synthesize protected IgM, and
the mucosa is permeable to macromolecules (e.g.,
exotoxins) which further hamper intestinal defenses
Gasforming bacteria invade the damaged areas to
produce intestinal pneumatosis, air in the submucosal
or subserosal surfaces of the bowels.
Clinical Manifestations
The prominent signs of NEC are
- Distended abdomen
- Gastric residuals
- Bloos in the stools (hematochezia)
Because NEC closely resembles septicemia, the infant
may (“not look well”)
Non specific signs include:
- Lethargy
- Poor feeding
- Hypotension
- Apnea
- Vomiting (often bile-stained)
- Decreased urinary output
- Hypothermia
The onset is usually between is usually between 4
and 10 days after the initiation of feedings
But signs may be evident as early as 4 hours of age
as late as 30 days
NEC in full term infants almost always occurs in the
first 10 days of life
Diagnostic Evaluation
Radiographic studies show a sausage-shaped
dilation of the instestine that progresses to marked
distension and the characteristic intestinal
pneumatosis-“soapsuds,” or the bubbly appearance
of thickened bowel wall and ultralumina.
Air may be present in the portal circulation or free air
observed in the abdomen, indicating perforation.
Laboratory findings may include anemia, leukopenia,
leukocytosis, metabolic acidosis, and electrolyte
imbalance.
- In severe cases coagulopathy (disseminated
intravascular coagulation) or thrombocytopenia
may be evident.
- Organisms may be cultures from blood, although
bacteremia or septicemia may not be prominent
early in the course of the disease.
NECROTIZING ENTEROCOLITIS
Diseases of the Newborn
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NCMA 219

  • Necrosis – There is an inflammation or damage to tissues.
  • Nectrotizing enterocolitis – Necrotizing Enterocolitis is the inflammation and death of intestinal tissue. It may involve just the lining of the intestine or the entire thickness of the intestine. In severe cases, the intestine may even perforate. If this happens,the bacteria normally found only in the intestine can leak into the abdomen and cause widespread infection. This is considered a medical emergency.
  • NEC is most common in premature infants.
  • It usually develops within two weeks of birth Pathophysiology
  • The precise cause of NEC Is still uncertain, but it appears to occur in infants whose GI tract has suffered vascular compromise- means there is prematurity of gastrointestinal tract leading to hypoxia. Bowels is compromised with oxygen Intestinal schemia injury caused by decreases oxygen supply in the gastrointestinal tract ; unknown case gastrointestinal tract proliferation NEC Damage to mucosal cells lining and bowel wall Diminised blood suplly to these cells causes death in large numbers Stop secreting protective, lubricating mucus (making it prone to exotoxin), and the thin, unprotected bowel wall is attacked by proteolytic enzymes Unable to synthesize protected IgM, and the mucosa is permeable to macromolecules (e.g., exotoxins) which further hamper intestinal defenses Gasforming bacteria invade the damaged areas to produce intestinal pneumatosis, air in the submucosal or subserosal surfaces of the bowels. Clinical Manifestations
  • The prominent signs of NEC are
  • Distended abdomen
  • Gastric residuals
  • Bloos in the stools (hematochezia)
  • Because NEC closely resembles septicemia, the infant may (“not look well”)
  • Non specific signs include:
  • Lethargy
  • Poor feeding
  • Hypotension
  • Apnea
  • Vomiting (often bile-stained)
  • Decreased urinary output
  • Hypothermia
  • The onset is usually between is usually between 4 and 10 days after the initiation of feedings
  • But signs may be evident as early as 4 hours of age as late as 30 days
  • NEC in full term infants almost always occurs in the first 10 days of life Diagnostic Evaluation
  • Radiographic studies show a sausage-shaped dilation of the instestine that progresses to marked distension and the characteristic intestinal pneumatosis-“soapsuds,” or the bubbly appearance of thickened bowel wall and ultralumina. Air may be present in the portal circulation or free air observed in the abdomen, indicating perforation.
  • Laboratory findings may include anemia, leukopenia, leukocytosis, metabolic acidosis, and electrolyte imbalance.
  • In severe cases coagulopathy (disseminated intravascular coagulation) or thrombocytopenia may be evident.
  • Organisms may be cultures from blood, although bacteremia or septicemia may not be prominent early in the course of the disease.

NECROTIZING ENTEROCOLITIS

Diseases of the Newborn

Therapeutic Management

  • Treatment of NEC begins with prevention of perforation.
  • Oral feedings may be withheld for 24 to 48 hours from infants who are believed to have suffered birth aspyxia.
  • Breastmilk is preferrend enteral nutrient. There is evidence that human milk may have a protective effect against the development of NEC because it confers some passive immunity (IgA), macrophages, and lyzozymes that could help in immunity and strengthening the intestinal mucosa. Medical Treatment
  • Discontinuation of all oral feedings; institution of abdominal decompression via nasogastric suction; administration of IV antibiotics; and correction of extravascular volume depletion, electrilyte abnormalities, acid-base imbalances, and hypoxia.
  • Replacing oral feedings with parenteral fluid decreases the need for oxygen and circulation to the bowel.
  • Serial abdominal radiograph films (every 4 to 6 hours in te acute phase) are taken to monitor for possible progression of the disease to intestinal perforation.
  • If there is progressive deterioration under medical management or evidence of perforation, surgical resection and anastomosis are performed.
  • If damage is so intensive, may be necessitate surgical intervention and establishment of an ileostomy, jejunostomy, or colostomy. (Another way for the patient to pass their stools.)
  • Sequelae in surviving infants include short-bowel syndrome, colonic stricture with obstruction, fat malabsorption, and failure to thrive secondary to intestinal dysfunction. Nursing Care Management
  • Astute nursing care is a key factor in the prompt recognition of the early warming signs of NEC.
  • When the disease is suspected, the nurse assists with disgnostic procedures and implements the therapeutic reginmen. - Monitor vital signs, including blood pressure for changes that might indicate bowel perforation, septicemia, or cardiovascular shock. Measures are instituted to prevent possible transmission to other infants. - Avoid rectal temperatures because of the increased danger of perforation. - To avoid pressure on the distended abdomen and to facilitate continous observation, infants are often left undiapered and positioned supine or on the side. - A disorder involving immature retinal vasculature - Formerly known as “Retrolental Fibroplasia” - It is a serious Vaso proliferative disorder that affects extremely premature infants. ROP often regresses or heals but can lead to severe visual impairment or blindness. - Normally, the eye starts to develop at about 16 weeks of pregnancy, when the blood vessels of the retina begin to form at the optic nerve in the back of the eye. - It is a term use to describe retinal changes in preterm infants. The incident and severity of the disease correlate to the degree of infants maturity. This means that the younger the gestational age, the greater the likelyhood of developing ROP. - Preterm infants are mostly at risk, however, although ROP is commonly seen to premature baby there are still documented incidents that ROP can also be seen in full term infants especially those who received a higher doses of oxygen therapy. - Etiology: Hyperoxemia, Hypoxia, Hypercarbia, Hypcarbia, Prenatal complications, Exposure to light. Pathophysiology Severe vascular constriction in retinal vasculature Hypoxia in the area of the retina (decreased perfusion and oxygenation) Stimulation of vascular proliferation towars the lens (The body will try to compensate by increasing the number of veins in capillaries in the area of the retina due to hypoxia) Aqueous and vitreous humor becomes TURBID Retinal hemorrhage and edema Retinal detachmet Irreversible blindness

RETINOPATHY OF PREMATURY (ROP)

  • The primary aim of therapeutic management of isoimmunization is prevention
  • Prevention of Rh Immunization
    • Sometimes Rh negative mother continue normal pregnancy, but once she delivers that’s the time when she will develop antibodies. This means that her next baby will most likely develop erythroblastosis fetalis because of the presence of free flowing antibodies.
    • RhIG or RhoGAM will be received by the mother to eradicate maternal antibodies.
  • Intrauterine Transfusion
    • If the andibody develop during pregnancy, blood transfusion is necessary.
    • Using 22 g spinal needle infused in the umbilical vein.
  • Exchange Transfusion
    • Process of removing blood hih in bilirubin and transfusing good blood. Nursing Care Management
  • The initial nursing responsibility is recognizing the early onset of neonatal jaundice.
  • The possibility of hemolytic disease can be anticipated from the prenatal and perinatal history.
  • Prenatal evidence of incompatibility, maternal blood type O, and a positive Coombs test are cause for increase vigilance for early signs of jaundice in an infant.
  • The nursing care of the infant undergoing phototherapy:
    • If an exchange transfusion is required, the nurse prepares the infant and the family and assists the practitioner with the procedure.
    • The infant must remain NPO (“nothing by mouth”) during the procedure; therefore, a peripheral infusion of dextrose and electrocytes is established.
  • Nursing care of the infant during exchange transfusion includes the documentation of blood exchange
    • The amount of blood withdrawn and infused
    • The time of each procedure
      • The cumulative record of the total volume exchanged.
      • The nurse also evaluates vital signs frequently (monitored electronically during the procedure) and correlates them with the removal and infusion of blood.
      • If signs of cardiac or respiratory problems occur, the procedure is stopped temporarily and resumed once the infant’s cardiorespiratory function stabilizes.
      • The nurse also observes for signs of transfusion reaction (e.g., temperature instability, hypotension, tachycardia, bradycardia, rash) and maintains adequate neonatal thermoregulation, blood glucose levels, and fluid balance.
  • Tachypnea – Increased respiration of the newborn
  • Is transient respiratory distress caused by delayed resorption of fetal lung fluid. Clinical manifestations
  • Symptoms of transient tachypnea of the newborn include:
  • Intracostal and subcostal retractions
  • Grunting
  • Nasal flaring
  • Possible cyanosis Diagnostic Evaluation
  • Chest X-ray – If increase respiration is present, chest x-ray will be done to determine the reason for transient tachypnea.
  • Complete blood count (CBC) and blood cultures – To check for infection. Therapeutic Management and Outcome
  • Oxygen therapy – Supportive management for respiratory distress
  • Recovery usually ocurs within 2 to 3 days.

TRANSIENT TACHYPNEA OF THE NEWBORN

  • Down syndrome is the most common chromosomal abnormality of a generalized syndrome, occurring in 1 in 691to 1000 live births.
  • Physical and cognitive abnormalities vary.
  • Intelligence quotient (IQ) range is typically mild to moderate impairment.
  • In spite of modern medical developments, life expectancy is still shortened, with 20% dying in the first decade, and 50% by age 60 years. Etiology
  • The cause of Down syndrome is not known.
  • Recent reposrts of cytogenetic and epidemiologic studies support the concept of multiple causality.
  • Although the etiology is unclear, the cytogenetics of the disorder us well established.
  • Approximately 97% of all cases of Down syndrome are attributable to an extra chromosome 21.
  • Although children with trisomy 21 are born to parents of all ages, there is a statistically greater risk for older women, particularly those over 35 years of age. Clinical manifestations
    • Intelligence
      • Mental capacity varies from severe cognitive impairmen (CI) to low average intelligence but is generally within the mild to moderate range of CI and may be related to parental intelligence
      • Social development
        • Development may be 2 to 3 years beyond the mental age, especially during early childhood and a trend toward the easy-child pattern that may facilitate parent-child attachment and assist in integration with peers at school and in the community.
      • Congenital anomalies
        • About 40% to 45% have congenital heart disease (CHD), especiallt septal defects.
        • Other structural defects include renal agenesis, duodenal atrasia, hirschsprung disease, and tracheosophageal fistula.
        • Skeletal defects include patella dislocation, hip subluxation, and atlantaoxial instability (i.e., instability of the first and second cervical vertebrae) in some children.
      • Sensory problems
        • Ocular problems includes strabismus, nystagmus, astigmatism, myopia, hyperopia, head tilt, excessive tearing, and cataracts.
        • Hearing loss occurs in a large percentage of children with Down syndrome.
        • Conductive, sensorineural, and mized losses each account for approximately one third of the diagnoses,.
        • Frequen otitis media, narrow may contribute to the hearing problems.
      • Growth
        • Growth in both height and weight is reduced
        • But weight gain is more rapid than growth in stature, which often results in overweight by 36 months of age.
      • Sexual development
        • Development may be delayed, incomplete, or both.
        • Male genitals and secondary sexual characteristics such as facial hair may be underdeveloped.

TRISOMY 21

  • Phenylketonuria
  • Galactosemia
  • G6PD
  • Congenital adrenal Hyperplasia
  • Congenital hypothyroidism occurs when the thyroid gland fails to develop or function properly.
  • In 80 to 85% of cases, the thyroid gland is absent, severely reduced in size (hypoplastic), or abnormally located.
  • Normal functioning thyroid is vital because it secretes thyroxine which is play a role in metabolism, stress response and temperature regulation. Without enough thyroxine, the baby can have a lot of problem. Clinical manifestations
  • Signs and symptoms of congenital hypothyroidism result from the shortage of thyroid hormones.
  • Affected babies may show no features of the condition, although some babies with congenital hypothyroidism are less active and sleep more than normal.
  • They may have difficulty feeding and experience constripation.
  • If untreated, congenital hypothyroidim can lead to intellectual disability and slow growth.
  • If treatment begins in the first two weeks after birth, infants usually develop normally. Therapeutic Management
  • Treated by giving thyroid hormone medication in a pill form called levothyroxine.
  • Many children will require treatment for life.
  • Levothyroxine is a synthetic thyroxine and should be crushed and given once daily, mixed with a small amount of water, formula, or breastmilk using a dropper or syringe.
  • Phenylalanine is a amino acid found in the food we eat. It is converted to tyrosine by the hepatic enzyme called Phenyalanine hydroxylase. High phenylalanine can cause intellectual disabilities that can also cause brain damage, seizures and other skin problems.
  • Tyrosine, on the other hand, is a brain chemical or neurotransmitter that can help produce epinephrine, norepineprine, and dopamine (synthetic adrenalines). If the phenylalanine can’t be converted to tyrosine the body will not be able to produce synthetic adrenalines.
  • Phenylketonuria (PKU), is a genetic disease inherited as an autosomal recessive trait, is caused by an absence of the enzyme phenylalanine hydroxylase needed to metabolize the essential amino acid phenylalanine.
  • In PKU, the hepatic enzyme phenylalanine hydroxylase, which controls the conversion of phenylalanine to tyrosine, is absent.
  • Classic PKU is at one end of a spectrum of conditions that involve defects in amino acids phenylalanine and tyrosine metabolism known as hyperphenylalaninemia.
  • Within the spectrum of hyperphenylalaninemia are conditions with varying degrees of severity, depending on the degree of enzyme deficiency.
  • Phenylpyvuric acid in the urine
  • Cathecolamines – important for stress response, neurohormone that helps nerves sends signals to the body
  • Tryptophan – productions and maintenance of protein in the body. Important in developing neurotransmitters like serotonin.

CONGENITAL HYPOTHYROIDISM PHENYLKETONURIA

Pathophysiology Clinical Manifestations

  • Clinical manifestations include
    • Growth failure ( failure to thrive)
    • Frequent vomiting
    • Irritability
    • Hyperactivity
    • Unpredictable
    • Erratic behavior
  • Older children commonly display bizarre or schozoid behavioral patterns such as
    • Fright reactions
    • Screaming episodes
    • Head banging
    • Arm biting
    • Disorientation
    • Failure to respond to strong stimuli
    • Spasticity or catatonia-like positions
  • Many of the severely cognitively impaired children have seizures, and approximately 80% of untreated persons with PKU demonstrate abnormal electrocephalographs, regardless of whether overt seizures occur. Therapeutic Management
  • Restriction of dietary protein
  • Infants with PKU who have blood phenylalanine levels higher than 10 mg/dl should begin treatment to establish metabolic control as soon as possible, ideally by 7 to 10 days of age.
  • A restricted phenylalanine foods and low-protein products will be medically required for individuals for their entire life to maintain and achieve optimum metabolic control and outcome. Nursing Care Management
  • Teaching the family regarding dietary restrictions.
  • Foods with low phenylalanine levels (e.g., vegetables except legumes, fruits, juices, and some cereals, breads, and starches) must be measures to provide the prescribed amount of phenylalanine.
  • Most high-protein foods, such as meat and dairy products, are either eliminated or restricted to small amounts.
  • Parents can introduce solid foods such as cereals, fruits, and vegetables as usual to the infant.
  • The assistance of a registered dietition is essential.
  • Parents need a basic understanding of the disorder and practical suggestions regarding food selection and preparation. A number of support groups for parents of children with PKU are available nationwide.
  • Is a rare autosomal recessive disorder that results from various gene mutations leading to three distinct enzymatic deficiencies.
  • The most common type of galactosemia (classic galactosemis) results from a deficiency of a hepatic enzyme, galactose 1-phosphate uridyltransferase (GALT), and affects approximately 1 of 47,000 births. The other two varieties of galactosemia involve deficiencies in the enzymes galactikinase (GALK) and galactise 4’-epimerase (GALE); these are extremely rare disorders.
  • GALT, GALK, and GALE are all involved in the conversion of galactose into glucose
  • If galactosemic infant is given milk, unmetabolized milk sugars build up and damage the liver, eyes, kidneys, and brain. Clinical Manifestations
  • Appear normal at birth, but on ingestion of milk (which has high lactose content) they begin to show progreesive symptoms including:
  • Vomiting

GALACTOSEMIA

  • Adrenal gland are the glands situated on the top of kidney. It produces cortisol which is a medication that manage the food inatke, weight, and stress. A decresed cortisol in the body can lead to fatigue, weightloss, and poor appetite.
  • Cortisol is also responsible for the secretions of steroid hormone and androgen. If theres an excess production of steroid hormone this can lead to problems with growth development, metabolism, energy, and reproduction.
  • Congenital adrenal hyperplasia (CAH) is a family of disorders caused by decreased enzyme activity required for cortisol production in the adrenal cortex.
  • This deficiency is an autosomal recessive disorder that results in improper steroid hormone synthesis.
  • This occurs in approximately 1 per 12,000 to 15, births. In its most severe form, it can be life threatening. Clinical Manifestations
  • Excess production of androgens causes ambiguous genetalia in female and precocious genital development in males.
  • Other forms of CAH do not result in excess production of androgens but cause various degrees of hypoaldosteronism or hyperaldosteronism.
  • Untreated CAH results in early sexual maturation:
    • with enlargement of the external sexual organs
    • development of axillary, pubic, and facial hair
    • Deepening of the voice
    • Acne
    • Marked increase in musculature with changes toward an adult male physique.
  • In the female, breasts do not develop, and she remains amenorrheic and infertile.
  • In the male the testes remain small, and spermatogenesis does not occur.
  • In both sexes, linear growth is accelerated, and epiphyseal closure is premature, resulting in short stature by the end of puberty. Therapeutic Management Medical Management - Administration of glucocorticoids to suppress the abnormally high secretions of ACTH and adrenal androgens - The recommend oral dosage is divided to stimulate the normal diurnal pattern of ACTH secretion. - It is necessary to increase the dosage during episodes of infection, fever, or other stresses because these children are unable to rpoduce cortisol in response to stress. - Acute emergencies require immediate IV or intramuscular administration. - Emergency situations include bacterial and viral infections, vomiting, surgery, fractures, major injuries, and sometime insect stings. Nursing Care Management - Early recognition of ambiguous genitalia and diagnostic confirmation in newborns. As with any congenital defect, the parents require an edquate explanation of the condition and time to griever for the loss of perfection. In this instance they may also need to grieve for the loss of the desired-sex child. - Nursing care management regarding cortisol and aldosterone replacement. - A follow-up visit by a home health nurse may be desirable to ensure that parents understand and comply with the treatment regimen. - Nurses in well-child facilities should assume responsibility for guidance and supervision regarding this aspect of care during each visit.

CONGENITAL ADRENAL HYPERPLASIA

NCMA 219

  • Failure to thirve (FTT), or groth faiure, is a sin of inadequate growth resulting from an inability to obtain or use calories required for growth.
  • Infant is not reaching a certain development that he/she should’ve reached for certain period of time
  • FTT be classified according to pathophysiology in the following categories: → Inadequate caloric intake – Incorrect formula preparation, neglect, food fads, excessive juice consumption, poverty, breastfeeding problems, behavioral problems affecting eating, parental restriction of caloric intake, or central nervous system problems affecting intake. → Inadequate absorption – Cystic fibrosis, celiac disease, Crohn’s disease, vitamin or mineral deficiencies, cow’s milk allery, biliary atresia, or hepatic disease. → Increased metabolism – Hyperthyroidism, congenital heart disease, hyperthyroidism, or chronic immunodeficiency. → Defective utilization – Genetic anomaly such as trisomy 21 or 18, congenital infection, or metabolic storage diseases. Clinical Manifestations
  • Growth failure
  • Developmental delays – social, motor, adaptive, language
  • Undernutrition
  • Apathy – the baby shows no emotions at all
  • Withdrawn behavior
  • Feeding or eating disorders, such as vomiting, feeding resistance, anorexia, pica, rumination
  • No fear of strangers (at age when stranger anxiety is normal)
  • Avoidance of eye contact
  • Wide-eyed gaze and continual scan of he environment (“radar gaze”)
  • Stiff and unyielding or flaccid and unresponsive
    • Minimal smiling Diagnostic Examination
    • Diagnosis is initially made from evidence of FTT.
    • If FTT is recent, the weight, but not the height, is below accepted standards (usually the 5th^ percentile) Therapeutic Management
    • The primary management of FTT is aimed at reversing the cause of the growth failure. If malnutrition is severe, the initial treatment is directed at reversing malnutrition.
    • In most cases of FTT, an interdisciplinary term of physician, nurse, dietition, child life specialist, occupational therapist, pediatric feeding specialist, and social worker or mental health professional is needed to deal with the multiple problems.
    • Colic is reported to occur in 15% to 40% of all infants, yet it has no particular affinity in regard to the gender, race, or socioeconomic status.
    • An organic cause may be identified in less than 5% of infants seen by practitioners because of excessive crying.
    • The condition is generally described as abdominal pain or cramping that is manifested by loud crying and drawing the legs up to the abdomen.
    • Other definitions include variables such as duration of cry greater than 3 hours a day, occuring more than 3 day, occuring more than 3 days per week, and for more than 3 weeks and parenteral dissatisfaction with the child’s behavior.
    • Some studies report an increase in symptoms (fussiness and crying) in the late afternoon or evening. Etiology
    • Potential causes are:
      • Too rapid feeding
      • Overeating
      • Swallowing excessive air
      • Improper feeding technique (especially in positioning and burping)

FAILURE TO THRIVE

Infant and Young Infant Problem

COLIC (PAROXYSMAL ABDOMINAL PAIN)