This legal document is a private property of Mr.

Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher.

Preterm/Premature
A neonate born before 37 weeks of gestation Primary concern relates to immaturity of all body systems. Most pregnancies last about 40 weeks. By definition, a premature birth takes place more than three weeks before the due date. A premature birth gives a baby less time to develop and mature in the womb. The result is an increased risk of various medical and developmental problems, including trouble breathing and bleeding in the brain. If you go into labor too early, your doctor may try to delay your baby's birth. Even if premature birth is inevitable, a few extra days in the womb can promote significant development. Although the rate of premature birth seems to be on the rise, there's good news. A healthy lifestyle can go a long way toward preventing preterm labor and premature birth. Risk factors The most common risk factors include: Having a previous preterm labor or premature birth Pregnancy with twins, triplets or other multiples Problems with the uterus, cervix or placenta Smoking cigarettes, drinking alcohol or using illicit drugs Some infections, particularly of the amniotic fluid and lower genital tract Some chronic conditions, such as high blood pressure and diabetes Being underweight or overweight before pregnancy Stressful life events, such as the death of a loved one or domestic violence Multiple miscarriages or abortions When to seek medical advice Proper prenatal care can help you prevent preterm labor and premature birth. If you're at risk of preterm labor or premature birth, your health care provider may recommend more frequent visits. Clinical Manifestations 1. Irregular respirations w/ periods of apnea

Body temperature is below normal NB has poor suck & swallow reflexes Diminished bowel sounds Increased or decreased urinary output Extremities are thin, with minimal creasing on soles & palms 7. NB extends extremities & does not maintain flexion 8. Lanugo on skin & in the hair on the NB s head is present in woolly patches 9. Skin is thin w/ visible blood vessels & minimal subcutaneous fat pads 10. Skin may appear jaundiced 11. Testes are undescended in boys 12. Labia are narrow in girls Complications The risks of premature birth vary depending on how soon a baby is born. Although survival is possible for babies born as early as 23 to 26 weeks, the risks are greatest for the youngest babies. Complications of premature birth may include: Difficulty breathing Episodes of stopped breathing (apnea) Bleeding in the brain (intracranial hemorrhage) Fluid accumulation in the brain (hydrocephalus) Cerebral palsy and other neurological problems Vision problems Intestinal problems Developmental delays Learning disabilities Less serious complications may include: Yellowing of the skin and whites of the eyes (jaundice) Lack of red blood cells (anemia) Low blood pressure For some premature babies, difficulties may not appear until later in childhood or even adulthood. Not performing well in school is often a prime concern. Some studies suggest that premature babies may face an increased risk of type 2 diabetes and cardiovascular disease in adulthood. But not all preemies have medical or developmental problems. By 28 to 30

2. 3. 4. 5. 6.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. weeks, the risk of serious complications is much lower. And for babies born between 32 and 36 weeks, most medical problems related to premature birth are short term. Physical Features of a Premature Newborn Small size Large head relative to rest of the body Little fat under the skin Thin, shiny, pink skin Veins visible beneath the skin Few creases on soles of feet Scant hair Soft ears, with little cartilage Underdeveloped breast tissue Boys: Small scrotum with few folds. Testes may be undescended in very premature newborns Girls: Labia majora not yet covering labia minora Rapid breathing with brief pauses (periodic breathing), apnea spells (pauses lasting longer than 20 seconds), or both Weak, poorly coordinated sucking and swallowing reflexes Reduced physical activity and muscle tone (a premature newborn tends not to draw up the arms and legs when at rest as does a full-term newborn) Sleeping for most of the time Alteration in Respiratory Physiology: - Preterm NB is at risk for respiratory problems because the lungs are not fully mature & not fully ready to take over the process of oxygen & carbon dioxide exchange w/o assistance until 37 to 38 week s gestation. Critical factors in the development of respiratory distress includes: 1. The preterm infant is unable to produce adequate amounts of surfactant. - Inadequate surfactant lessens compliance (ability of the lung to fill with air easily) - the inspiratory pressure needed to expand the lungs with air is higher. - The collapsed or atelectatic alveoli will not exchange oxygen & carbon dioxide - The infant becomes hypoxic, pulmonary blood flow is not sufficient - The preterm NB available energy is depleted. 2. The muscular coat of pulmonary blood vessels is incompletely developed. - The pulmonary arterioles do not constrict as well in response to decrease oxygen levels. - Lower pulmonary vascular resistance leads to left to right shunting of blood through the ductus arteriosus back into the lungs Alteration in Thermoregulation: - Major problems in preterm NB s is heat loss. Two factors limiting heat production: a. The availability of glycogen in the liver & b. The amount of brown fat available for metabolism. Physiologic & Anatomic factors causes heat loss in the preterm infant: 1. The preterm baby has a higher ratio of body surface to body weight. 2. The preterm baby has very little subcutaneous fat. 3. The preterm baby has thinner, more permeable skin than the term infant. 4. The posture of the preterm baby. 5. The preterm baby has a decreased ability to vasoconstrict superficial blood vessels & conserve heat in the body core. Alteration in Gastrointestinal Physiology Ingestion, digestive & absorption problems: 1. Aspiration 2. Difficulty in meeting high caloric & fluid needs for growth 3. Limited ability to convert certain essential amino acids to nonessential amino acids. 4. Inability to handle the increased osmolarity of formula protein d/t kidney immaturity. 5. Difficulty absorbing saturated fats. 6. Difficulty w/ lactose digestion 7. Rickets & significant bone demineralization. 8. Increased basal metabolic rate & increased oxygen requirement. 9. Feeding intolerance & necrotizing enterocolitis. Alteration in Renal Physiology: Specific Characteristics: 1. GFR is lower because of decreased renal blood flow.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 2. Preterm infant s have limited ability to concentrate urine or to excrete excess amounts of fluids. 3. Kidney s of the preterm infant begin excreting glucose at a lower serum glucose level. 4. The kidneys buffering capacity is reduced, predisposing the infant to metabolic acidosis. 5. The immaturity of the renal system affects the preterm infant s ability to excrete drugs. f Nursing Management Nursing Assessment: - Assess the physical characteristics & gestational age of the preterm NB accurately to anticipate the special needs & problems of the baby. Physical characteristics: a. Color b. Nails c. Skin d. Genitals e. Vernix caseosa f. Resting position g. Lanugo h. Cry i. Head size j. Reflexes f. Ears g. Activity Nursing Management 1. Monitor vital signs 2. Maintain cardiopulmonary functions 3. Administer oxygen & humidification as prescribed 4. Monitor I &O & electrolyte balance 5. Monitor daily weight 6. Maintain NB in a warming device 7. Position every 1-2 hours & handle NB carefully 8. Avoid exposure to infections 9. Provide NB with appropriate stimulation Nursing Diagnoses: a. Impaired gas exchange b. Altered nutrition c. Ineffective thermo regulation d. Fluid volume deficit e. Ineffective family coping Planning & Implementation Maintenance of respiratory function Signs of respiratory distress: Cyanosis Tachypnea Retractions Expiratory grunting Nasal flaring Apneic episodes Presence of rales or ronchi on auscultation Diminshed air entry Maintenance of neutral thermal environment 1. Allow skin to skin contact between mother & NB Kangaroo Care 2. Warm & humidify oxygen 3. Place the baby in a double-walled incubator 4. Avoid placing the baby in cold surfaces 5. Used warmed ambient humidity. 6. Keep the skin dry & place a cap on the baby s head 7. Keep radiant warmers, incubators & cribs away from windows& cold external walls & out of drafts 8. Open incubator portholes & doors only when necessary. 9. A skin probe is used to monitor the NB temperature. 10. Warm formula or stored breast milk before feeding. 11. Use reflector patch over the skin temperature probe when using a radiant warmer bed. Maintenance of fluid & electrolyte status Signs of Dehydration: Sunken fontanelle Poor skin turgor Dry oral mucus membranes Decreased urine output Increased specific gravity (>1.013) Provision of adequate nutrition & prevention of fatigue during feeding Treatments and drugs Hospital neonatal intensive care units (NICUs) are designed to provide round-the-clock care for premature babies and full-term babies who develop problems after birth. In the NICU, your baby will

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. probably be kept in an incubator an enclosed plastic bassinet that's kept warm to help your baby maintain normal body temperature. Because preemies have immature skin and very little body fat, they often need such care to stay warm. 5. Seizure 6. Cold stress Nursing Management Nursing assessment: 1. Appears alert, wide eyed 2. Dry, cracking, parchment like skin 3. Infants body appears long & thin 4. Meconium stained Planning & Implementation - Nursing intervention are primarily supportive. 1. Monitor cardiopulmonary status 2. Provide warmth 3. Frequently monitor blood glucose per agency protocol 4. Obtain a central line hematocrit Treatment 1. Postmature newborns who experience low oxygen levels and fetal distress may need resuscitation at birth. 2. If meconium is present in the amniotic fluid and the newborn is lethargic, a tube is passed into the windpipe (trachea) to suction as much meconium as possible from the respiratory tract. 3. If meconium has been breathed into the lungs, a ventilator may be needed to support breathing. 4. Intravenous sugar (glucose) solutions or frequent breast milk or formula feedings are given to prevent hypoglycemia. Nursing Diagnoses 1. Hypothermia 2. Altered nutrition: less than body requirement 3. Impaired gas exchange in the lungs & at the cellular level

Postmaturity/Postmature
d A postmature newborn is delivered after more than 42 weeks in the uterus. d Near the end of a term pregnancy, placental function decreases, providing fewer nutrients and less oxygen to the fetus. d Postmature newborns have dry, peeling, loose skin and may appear emaciated because they have not received sufficient nutrition. d Some postmature newborns require resuscitation, but generally treatment focuses on providing good nutrition and general care. d Postmature (post-term) delivery is much less common than premature (preterm) delivery. Clinical Manifestations 1. Hypoglycemia 2. Parchment-like skin 3. Fingernails are long & extended over ends of fingers 4. Profuse scalp hair 5. Body is long & thin 6. Extremities show wasting of fat & muscle 7. Meconium staining may be present on nails & umbilical cord Symptoms 1. Postmature newborns have dry, peeling, loose skin. 2. May appear emaciated, especially if the function of the placenta was severely reduced. 3. The fingernails and toenails are long. 4. The umbilical cord and nails may be stained green if meconium was present. Complications 1. Hypoglycemia 2. Meconium aspiration 3. Polycythemia 4. Congenital anomalies

Small for gestational age

A newborn, whether delivered preterm, term, or postterm, whose weight is less than that of 90% of newborns of the same gestational age at birth (below the 10th percentile) is considered small for gestational age. Clinical Manifestation 1. Fetal distress

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 2. Gestational age & physical maturity 3. Lowered or elevated body temperature 4. Physical abnormalities 5. Hypoglycemia 6. Signs of polycythemia 7. Signs of infection 8. Signs of aspiration of meconium Intrauterine Growth Restriction Factors Contributing to IUGR 1. Maternal factors 2. Maternal disease 3. Environmental factors 4. Placental factors 5. Fetal factors Risk Factors In many cases, newborns are small simply because of genetic factors, such as having small parents (less commonly, a specific genetic syndrome associated with small stature may be involved). The placenta (the organ that connects the fetus to the uterus and provides nourishment to the fetus) may have functioned poorly so that the fetus did not receive adequate nutrients, impairing growth. A poorly functioning placenta may occur if the mother has high blood pressure, preeclampsia, kidney disease, or longstanding diabetes. A viral infection, such as cytomegalovirus infection acquired before birth, may be responsible. Fetal growth may also have been impaired if the mother smoked or used alcohol or illicit drugs during the pregnancy Complications Meconium aspiration Excess red blood cells (polycythemia) Low blood sugar levels (hypoglycemia) Difficulty regulating body temperature An impaired immune system Nursing Management - Assess gestational age & identify signs of potential complications. - All body parts of the symmetric IUGR infant are in proportion, but they are below the normal size for the NB s gestational age; generally vigorous The head does not appear overly large or the length excessive in relation to the other body parts. - Asymmetric IUGR infant appears long, thin, & emaciated, with loss of subcutaneous fat & muscle mass. - NB may have loose skin folds; dry desquamating skin; & a thin & often meconium-stained cord. - Head appears relatively large- because the chest size & abdominal girth are decreased. - NB may have vigorous cry & appears alert & wide eyed Nursing Management 1. Maintain airway 2. Maintain body temperature 3. Observe for signs of respiratory distress 4. Monitor for infection & initiate measures to prevent sepsis 5. Monitor blood glucose levels & for signs of hypoglycemia 6. Initiate early findings & monitor for signs of aspiration 7. Provide stimulation Nursing Diagnoses 1. Risk for impaired gas exchange 2. Risk for ineffective thermoregulation & cold stress 3. Risk for injury to tissues 4. Altered nutrition: less than body requirements 5. Risk for altered parenting -

Large for Gestational Age (LGA)

g A newborn, whether delivered preterm, term, or postterm, whose weight is above that of 90% of newborns of the same gestational age at birth (above the 90th percentile) is considered large for gestational age. Factors other than genetic influences that cause accelerated intrauterine growth includes: Maternal diabetes mellitus Beckwith s syndrome Clinical Manifestations: 1. Gestational age 2. Birth trauma or injury

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 3. Respiratory distress 4. Hypoglycemia g The reason for excessive growth of the fetus varies but primarily results from an abundance of nutrients. In pregnant women with diabetes, a large amount of sugar (glucose) crosses the placenta (the organ that connects the fetus to the uterus and provides nourishment to the fetus) and results in high levels of glucose in the fetus's blood. The high levels of glucose trigger the release of increased amounts of insulin from the fetus's pancreas, resulting in accelerated growth of the fetus, including almost all organs except the brain, which grows normally. Common Complications of the IDM 1. Hypoglycemia this NB continues to produce high levels of insulin, w/c deplete the blood glucose w/in hours after birth. 2. Hypocalcemia tremors are the clinical signs of hypocalcemia, may be d/t difficult pregnancy, labor & birth w/c predispose any infant to hypocalcemia. Symptoms and Complications Symptoms depend on which complications occur. Common complications include the following: 1. Excess amount of red blood cells (polycythemia): Large-for-gestational-age newborns may have a ruddy complexion because too many red blood cells are produced. As the excess red blood cells are broken down, bilirubin is formed, which, along with poor feeding, results in jaundice 2. Low blood sugar levels (hypoglycemia): In newborns of mothers with diabetes, the oversupply of glucose from the placenta stops abruptly at delivery when the umbilical cord is cut and the continuing rapid production of insulin by the newborn's pancreas leads to low levels of sugar in the blood (hypoglycemia). Often hypoglycemia causes no symptoms. Sometimes, newborns are listless, limp, or jittery. Despite their large size, newborns of mothers with diabetes often do not feed well for the first few days. 3. Lung problems: Lung development is delayed in newborns whose mothers have diabetes. When these newborns are delivered by cesarean, they are at risk of developing lung problems. Newborns born prematurely are more likely to have immature diabetes are more likely to have immature lungs and to develop respiratory distress syndrome 4. Increased risk of birth injuries: Newborns who are large for gestational age are at increased risk of birth injuries such as stretching of the nerves in the shoulder (brachial plexus injuries) and collarbone (clavicle) fractures. Vaginal delivery, especially breech deliveries, may be difficult when the fetus's head is large in comparison with the mother's pelvic measurements, which increases the risk of birth injury. Therefore, such a fetus may have to be delivered by caesarean. Nursing Management 1. Monitor vital signs 2. Monitor blood glucose levels & for signs of hypoglycemia 3. Initiate early feeding 4. Monitor for infections & initiate measures to prevent sepsis 5. Provide stimulation f To treat hypoglycemia in newborns, intravenous glucose or frequent feedings by mouth or by tube into the stomach are often needed. f Treatment of respiratory distress syndrome may require supplemental oxygen through a tube placed in the nose or intense intervention, such as respiratory support with a ventilator Nursing Diagnoses: 1. Altered nutrition: less than body requirements 2. Impaired gas exchange 3. Ineffective family coping: compromise

Respiratory distress syndrome

(hyaline membrane disease) is a breathing disorder of premature newborns in which the air sacs (alveoli) in a newborn's lungs do not remain open because the production of a substance that coats the alveoli (surfactant) is absent or insufficient. Sings & Symptoms

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 1. visibly labored breathing, including retractions of the chest below the rib cage 2. flaring of the nostrils during breathing in 3. grunting while breathing out 4. bluish discoloration to the skin (cyanosis) Complications pneumothorax brain damage Nursing Management Nursing Intervention:  Assess for increasing cyanosis, tachypnea, grunting respirations, nasal flaring, significant secretions & apnea.  Support respiration as prescribed  Monitor arterial blood gases & oxygen saturation levels  Suction every 2 hours or more often as necessary  Position NB side or back w/ neck slightly extended  Prepare to administer surfactant replacement therapy  Provide nutrition  Support bonding  Prepare parents for short to long term period of oxygen dependency if necessary  Encourage as much as parental participation in NB care as condition allows. plastic hood (oxygen hood) filled with oxygen, which is placed over the head. 3. Newborns with severe respiratory distress syndrome may require oxygen delivered by continuous positive airway pressure (CPAP a technique that allows newborns to breathe on their own while being given slightly pressurized oxygen or air given through prongs placed in both nostrils). 4. In newborns with severe respiratory distress syndrome, a tube (endotracheal tube) may need to be passed into the windpipe (intubation), and the newborn's breathing may need to be supported with mechanical ventilation. 5. Use of a surfactant preparation The presence of meconium in the amniotic fluid indicates that the fetus may be suffering asphyxia. Meconium may be aspirated into the tracheobronchial tree in utero or during the first few breaths taken by the NB. Meconium in the lungs produces a ball valve action so that the alveoli over distend & rupture, resulting in air leaks such as pneumomediastenum or pneumothorax. Diagnosis: 1. based on meconium in the amniotic fluid at birth 2. respiratory distress in the newborn abnormal 3. chest x-ray results. Risk Factors: Term SGA Post Term newborns Those who have experienced a long labor Clinical Manifestations: 1. Fetal hypoxia in utero a few days or a few minutes before birth. 2. Signs of distress at birth. *the severity of clinical symptoms depends on the extent of aspiration Assessment Auscultation reveals diminished air movement with prominent rales & ronchi.

Nursing Diagnoses: Risk for ineffective breathing pattern Ineffective thermoregulation Altered nutrition: less than body requirements Risk for fluid volume deficit Planning & Implementation: Hospital based nursing care Oxygen monitoring Mechanical ventilation Prevention and Treatment 1. When premature birth cannot be avoided, obstetricians may give the mother injections of a corticosteroid. 2. oxygen is given through prongs placed in the newborn's nostrils or through a small

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Abdominal palpation may reveal a displaced liver caused by diaphragmatic depression resulting from an over expansion of the lungs Yellowish staining on the skin, nails & umbilicus CXR reveals non-uniform, coarse patchy densities & hyperinflation. Clinical Therapy 1. After the head is born the baby s oropharynx & the nasopharynx are suctioned. 2. Direct tracheal suctioning if absent or depressed respirations, heart rate less than 100 BPM or poor muscle tone. *According to De Ungria & Steinborn (2003) if infant is vigorous even if there is thick or thin meconium in the amniotic fluid, no subsequent special resuscitation is indicated. Nursing Management Nursing Assessment: 1. During intrapartum period observe for signs of fetal hypoxia & meconium staining in amniotic fluid 2. Assess signs of distress 3. Observe for complications a. Pulmonary air leaks b. Anoxic cerebral injury c. Anoxic renal damage d. Sepsis secondary to bacterial pneumonia e. Intestinal necrosis from ischemia Nursing Diagnoses 1. Impaired gas exchange 2. Altered nutrition 3. Ineffective family coping Panning & Implementation: *hospital based nursing care 1. Maintain appropriate gas exchange 2. Maintain adequate oxygenation & ventilation 3. Regulation of temp. 4. Glucose testing & monitoring 5. Intravenous fluid administration 6. Providing caloric requirement 7. Intravenous antibiotic therapy Treatment  High levels of oxygen & high pressure ventilation.  Surfactant replacement  Chest physiotherapy  Prophylactic intravenous antibiotics NB up to 1 month of age are particularly susceptible to an infection caused by organisms that do not cause significant disease in older children. Once any infection occurs in the NB it can rapidly spread through the bloodstream regardless of its primary site. The frequency of nosocomial infection is less in normal NB infants & increase for infants in the NICU. Risk Factors signs/symptoms f subtle behavioral changes  Lethargic or irritable  Hypotonic  Color changes: pallor, duskiness, cyanosis or Shocky  Appearance: skin is cool & clammy f temperature instability  Hypothermia/hyperthermia f feeding intolerance  Decrease in total intake  Abdominal distention  Vomiting  Poor sucking  Lack of interest in feeding  Diarrhea f hyperbilirubinemia f initial tachycardia followed by spells of apnea or bradycardia. Signs & Symptoms may suggest: CNS disease jittereness, tremors, seizure activity Respiration tachypnea, labored respiration, apnea, cyanosis Hematologic jaundice, petechiae, hemorrhage, hepatospleenomeggaly Gastrointestinal diarrhea, vomiting, bile stained aspirate, hepatomegaly Most Nosocomial Infections in the NICU: 1. Bacteria 2. sepsis 3. UTI 4. Meningitis 5. Pneumonia Maternal Antepartal Infections: 1. Rubella 2. Toxoplasmosis

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 3. Cytomegalic inclusion disease 4. Herpes Intrapartum Maternal Infections: 1. Amnionitis 2. Precipitous birth 3. Passage through the birth canal & in contact with the vaginal flora.

Cytomegalovirus infection - The virus is thought

to cross the placenta from the mother during pregnancy or during delivery. After birth, newborns may become infected if breast milk contains the virus or if they are given a contaminated blood transfusion. Symptoms: Most newborns do not have symptoms. About 10% of newborns infected at birth are premature and have a low birth weight, a small head, growth delay, jaundice, small bruises, inflammation of the lungs or eyes, and an enlarged liver and spleen. Newborns infected after birth can have an enlarged liver and spleen, hepatitis, a low platelet count, a high number of white blood cells, or all of these symptoms. Hearing loss, vision loss, and intellectual disability may occur. Treatment and Prevention: The infection cannot be cured. Ganciclovir CYTOVENE may help relieve some symptoms.Newborns should have repeated hearing evaluations during the first year.

Some Infections of Newborns

Causative Agents: 1. Gram negative organisms a. Escherichia coli b. Enterobacter c. Klebsiella d. Enterococci e. Staphylococci aureus 2. Gram positive organisms Group B hemolytic streptococcus

1. Pseudomonas
Conjunctivitis - The bacteria Chlamydia or Neisseria gonorrhoeae infect the fetus during delivery. Symptoms: Chlamydia: Conjunctivitis usually begins 5 to 14 days after delivery but sometimes 6 weeks after. Newborns have swollen eyelids and a watery discharge from the eyes that contains increasing amounts of pus. Neisseria gonorrhoeae: Conjunctivitis usually begins 2 to 5 days after delivery. Newborns have severe inflammation of the eyelids and discharge of pus from the eyes. Without treatment, blindness may occur. Treatment and Prevention: Chlamydia: Erythromycin E-MYCINERYTHROCIN is given as an eye ointment for prevention and by mouth for treatment. Neisseria gonorrhoeae: An eye ointment containing polymyxin and bacitracin, BACIIM, erythromycin, or tetracycline SUMYCIN is used for prevention, and the antibiotic ceftriaxone ROCEPHIN given by injection is used for treatment.

Hepatitis B - The infection can occur during

delivery if the mother is infected. The infection can occur during delivery if the mother is infected. Symptoms: Chronic liver disease (such as chronic hepatitis or cirrhosis) develops but usually does not cause symptoms until young adulthood. Treatment and Prevention: All newborns are given hepatitis B virus vaccine before hospital discharge. A newborn born to an infected mother is given hepatitis B virus vaccine and hepatitis B immune globulin within 12 hours of birth.

Herpes - Usually, the virus (herpes simplex) is

transmitted during delivery through the mother's infected genital tract. Symptoms: Usually, a rash of small fluid-filled blisters appears. Infection may be widespread, affecting many organs, such as the eyes, lungs, liver, brain, and

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. skin. Other symptoms include sluggishness, diminished muscle tone, respiratory distress, pauses in breathing (apnea), and seizures. Treatment and Prevention: The antiviral drug acyclovir ZOVIRAX is given intravenously. Eye infections are treated with trifluridine VIROPTIC drops and acyclovir heart defects, an enlarged liver and spleen, bruising, bluish red spots, enlarged lymph nodes, and pneumonia. Treatment and Prevention: No specific treatment is available. Vaccinating all women of childbearing age before pregnancy can prevent the infection. If an expectant mother who has not been immunized comes into close contact with an infected person early in pregnancy, she may be given an injection of immune globulin.

Human immunodeficiency virus infection - The

virus is transmitted from mother to fetus during pregnancy or to the newborn during labor and delivery or after birth through breastfeeding. Symptoms: Symptoms range from none to very severe (AIDS).The lymph nodes may swell.Infection can affect many organs such as the liver, spleen, heart, kidneys, brain, and spinal cord.Symptoms can also include recurrent diarrhea, poor weight gain, invasive bacterial infections, and viral infections. Treatment and Prevention: Antiretroviral drugs are used, and consultation with a specialist and enrollment in a clinical trial is advised.Early diagnosis and treatment of infections can help.

Syphillis - The bacteria (Treponema pallidum) cross

the placenta during pregnancy if the mother acquires syphilis during pregnancy or if she has been inadequately treated for syphilis in the past. Symptoms: Stillbirth or premature birth may occur.Newborns may have no symptoms.During the first month of life, large blisters or a flat coppercolored rash may develop on palms and soles Raised bumps may develop around the nose and in the diaper area. Newborns may not grow well. They may have cracks around the mouth, or mucus, pus, or blood may run from the nose.Usually, the lymph nodes, liver, and spleen are enlarged.Rarely, inflammation of the eye or brain, seizures, meningitis, or intellectual disability occurs, but these symptoms may not appear until the child is age 2 years or older. Treatment and Prevention: Before birth, the mother is treated with penicillin.After birth, the mother, if still infected, and newborn are treated with penicillin.

Human papillomavirus infection - Usually,

newborns become infected during delivery. Symptoms: Warts grow in the windpipe and can alter the newborn's cry and sometimes cause difficulty breathing or even block the airways.The lungs may become infected. Treatment and Prevention: Warts are removed surgically.The drug interferon can reduce the risk of recurrent infections.Females aged 9 to 26 should be vaccinated.

Rubella - The virus may cross the placenta during

pregnancy. Infection is now rare because vaccination is routine. Infection is more severe if the fetus is infected early in pregnancy. Symptoms: Effects on the fetus range from death before birth to birth defects or to hearing loss without other symptoms.Newborns may have a low birth weight, brain inflammation, cataracts, damage to retina,

Toxoplasmosis - The parasite (Toxoplasma gondii) may cross the placenta from the mother to the fetus during pregnancy.Infection is more severe if the fetus is infected early in pregnancy. Symptoms: The fetus may grow slowly and be born prematurely.Newborns may have a small head, brain inflammation, jaundice, an enlarged liver and spleen, and inflammation of the heart, lungs, or eyes.Rashes may occur. Treatment and Prevention: Avoiding handling cat litter during pregnancy is recommended. Transmission from the mother to the fetus may be prevented if the mother MC publishing com.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. takes spiramycin. Pyrimethamine DARAPRIM and sulfonamides may be taken later in pregnancy if the fetus is infected. Infected newborns with symptoms are treated with pyrimethamine, sulfadiazine, and leucovorin. Inflammation of heart, lungs, or eyes is treated with corticosteroids. Prenatal Prevention Maternal screening for sexually transmitted infections Rubella titer Intrapartum Sterile technique Genital lesions, placental & amniotic fluid smears to obtain culture Genital herpes is present towards the term C-sec. is indicated. All NB eyes should be treated with an antibiotic Prophylactic antibiotic therapy for asymptomatic women who test positive from group B streptococcus Clinical Therapy 1. Blood culture 2. Spinal fluid 3. urine culture 4. Skin culture 5. Nasopharyngeal cultures 6. CBC 7. X-ray films Treatment 1. Two broad spectrum antibiotics 2. Supportive physiologic care required to maintain: a. Respiratory b. Hemodynamic c. Nutritional d. Metabolic homeostasis Provision of Antibiotic Therapy 1. Proper dose to be administered 2. Appropriate route of administration 3. Admixture incompatibilities 4. Side effects & toxicity Provision of Supportive Care 1. Observe for resolution of symptoms or development of other symptoms of sepsis. 2. Maintain neutral thermal environment with accurate regulation of humidity & oxygen administration. 3. Provide respiratory report Provide cardiovascular support Provide adequate calories Provide fluids & electrolytes Observe for the development of hypoglycemia Nursing Diagnoses 1. Risk for infection 2. Fluid volume deficit 3. Ineffective family coping 4. 5. 6. 7.

Hyperbilirubinemia
 Most common abnormal physical finding in the NB.  Yellowish coloration of the skin & sclera that develops from deposits of the yellow pigment bilirubin in lipid tissues.  Normally the placenta clears fetal unconjugated bilirubin in utero, so total bilirubin at birth is usually less than 3 mg/dL unless an abnormal hemolytic process has been present.  Post-natally the infant must conjugate bilirubin in the liver. Rate & Amount of Conjugation 1. Rate of hemolysis 2. Bilirubin load 3. Maturity of the liver 4. Presence of albumin binding sites. Physiologic Jaundice Neonatal jaundice is a normal process that occurs during transition from intrauterine to extra uterine life & appears after 24 hours of life. Some degree of jaundice occurs in a bout half of all healthy terms NB & in 80% of preterm NB. This is due to: NB shortened cell life span Slower up take by the liver Lack of intestinal bacteria Poorly established hydration Treatment: Phototherapy Certain conditions decrease the number of sites available: 1. Fetal or neonatal asphyxia 2. Neonatal drugs 3. Hypothermia & hypoglycemia

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 4. Maternal use of sulfa drugs or salicylates 5. Premature infants have less albumin available for binding 6. Neurotoxicity Clinical Therapy Criteria: 1. Clinically evident jaundice 2. Serum bilirubin concentration 3. Total serum bilirubin exceeding the 95th percentile on the nomogram. 4. Signs of underlying illness in any infant 5. Clinical jaundice persisting for more than 2 weeks in a term NB. 6. Conjugated bilirubin concentration greater than 2 mg/dL or more than 20% of the TSB concentration. Coombs test determines whether jaundice is due to Rh or ABO incompatibilities. Indirect Coombs test measures amount of Rh positive antibodies in the mother s blood. Direct Coombs test reveals antibody coated Rh positive in the NB. Therapeutic Management Variables in determining the appropriate Management: 1. Serum bilirubin level 2. Birth weight 3. Age in hours Exchange Transfusion if NB has hemolytic w/ unconjugated bilirubin level of 14 mg/dL., weight less than 2500 g, 24 hours of age or less Phototherapy over 24 hours of age. Nursing Management 1. Note changes in behavior & observe evidence of bleeding. a. Neurologic signs b. Hypotonia c. Diminished reflexes d. Lethargy e. seizures 2. Check the NB for jaundice q 2 & record observations. a. Increase of in depth of color b. Time of on set 3. Day light assessment is recommended. 4. Visually inspecting the NB w/ the use of reflectance photometers. 5. The use of a end-tidal carbon monoxide device. Nursing Daignoses

Kernicterus
- yellow nucleus, deposits of indirect or unconjugated bilirubin in the basal ganglia of the brain & to the permanent neurologic sequelae of untreated hyperbilirubinemia. Causes 1. Hemolytic disease secondary to Rh incompatibilities. Dx. Prenatal amniocentesis w/ spectrophotographic examination Alloimmune hemolytic disease/ erythroblastosis fetalis Occurs when the Rh negative mother is pregnant w/ an Rh positive fetus & maternal antibodies cross the placenta. Hydrops fetalis  Most severe form of erythroblastosis fetalis.  The maternal antibodies attach to the Rh site of the fetal RBC  This is the common cause of IUFD among infants w/ Rh disease. 2. ABO incompatibility 3. Prenatal & perinatal factors During pregnancy: a. Hereditary sphenocytosis b. DM c. Intrauterine infections d. Gram negative bacilli infections Other conditions w/c predispose the NB to hyperbilirubinemia a. Polycythemia b. Pyloric stenosis c. Atresia of the biliary ducts d. Lower bowel obstruction e. UTI f. Sepsis g. Hypothyroidism h. Hemorrhage i. Hypothermia j. Acidemia k. Hypoglycemia l. Neonatal hepatitis

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 1. 2. 3. 4. Risk for fluid volume deficit Potential for injury Sensory perceptual alterations Risk for altered parenting  This may involve segment of small intestines or colon Etiology Virus infection Use of medications that influence gut motility Body s inflammatory mediators Common site of intussusception - ileocecal valve Complications: 1. Necrosis 2. Perforation 3. Hemorrhage 4. Peritonitis Clinical manifestations: 1. Acute abdominal pain 2. Vomiting 3. Passage of brown stools 4. Then the stools become red 5. Palpable mass on the URQ Diagnoses: 1. History taking 2. Confirmed radiographs & UTZ of abdomen 3. Barium enema 4. Abdominal x-ray, CBC Treatment: 1. Enema w/ saline aqueous contrast material 2. Surgical intervention Nursing Management 1. Maintenance of fluid & electrolyte balance 2. Post operative care a. Monitor for any signs of infection b. Manage the child s pain c. Maintaining nasogastric tube patency d. Assess vital signs e. Check for abdominal distention f. Monitor all stools Nursing Diagnosis 1. Alteration in comfort 2. Risk for injury 3. Fluid volume deficit

Sudden infant death syndrome (SIDS)

is the sudden, unexpected death of a seemingly healthy infant during sleep, in whom a thorough postmortem examination does not show a cause. The cause of sudden infant death syndrome (SIDS) is not known. Putting infants to sleep on their back; removing pillows, bumper guards, and toys from the crib; protecting infants from overheating; and preventing infants from breathing second-hand cigarette smoke may help prevent SIDS. sudden infant death syndrome is one of the most common causes of death in infants between the ages of 2 weeks and 1 year. Reducing the Risk of Sudden Infant Death Syndrome Position: Always place the infant on the infant's back to sleep, for naps and at night. Surface: Place the infant on a firm sleep surface, such as a safety-approved crib mattress, covered by a fitted sheet. Location: Set up the infant's sleep area close to but separate from the sleep area of the parents and other children. Pacifiers: Consider offering the infant a clean, dry pacifier when placing the infant down to sleep. Common health problems that develop during infancy Intussusception  Occurs when one portion of the intestine prolapses & then invaginates or telescopes into another.  Common cause of intestinal obstruction during infancy  Most cases occurs in boys between the ages of 3 months & 6 years

Failure to Thrive

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Syndrome in w/c infants or young children fail to eat enough food to be adequately nourished. Etiology 1. Organic a. Congenital AIDS b. Inborn errors of metabolism c. Congenital heart defect d. Neurologic diseases e. Esophageal reflux 2. Nonorganic cause Risk Factors: a. Prematurity b. SGA Clinical Manifestations: 1. Persistent failure to eat 2. Refuse food 3. erratic sleep patterns 4. Irritable & difficult to soothe 5. Often developmentally delayed Clinical therapy: 1. may be hospitalized 2. Provide adequate & caloric, nutritional intake 3. Promote normal growth & development 4. Assist parents in developing feeding routines & responding to the infant s cues of physiological & psychologic hunger Nursing Management 1. Accurate weight & height 2. Child s activity level, developmental milestones interaction patterns 3. Observe how the child indicate hunger 4. Ability of the child to be soothed, general interaction patterns, eye contact, touch & cuddliness 5. Ask parents about: a. Stresses in their lives b. Disturbances about child parent relationship c. Children w/ eating disorder in the family 6. Observe the child & parent behavior during feeding Nursing Diagnosis 1. Imbalance nutrition less than body requirements 2. Delayed growth & development related to inadequate intake 3. Risk for impaired parenting related to lack of knowledge about nutritional needs 4. Fatigue related to malnutrition

Colic
Feeding disorder characterized by paroxysmal abdominal pain of intestinal origin & severe crying. Onset of colic is between the second & sixth weeks of life Etiology: 1. Unknown 2. Proposed causes includes: a. Feeding to rapidly b. Swallowing large amount of air Clinical Manifestations: 1. Infant cries loudly & continuously for several hours. 2. Infants face becomes flushed 3. Distended & tense abdomen 4. Draws up legs & clenches the hands 5. Episodes occurs same time each day 6. Symptoms resembles intestinal obstruction or peritoneal infection Treatment: Supportive Nursing Management: 1. Infants thorough history of diet & daily schedule & events surrounding episodes of colicky behavior. 2. Assess infants feeding patterns. 3. Assess episodes of colic 4. Measures to relieve crying 5. Observe feeding method 6. Alleviate symptoms & discomfort

Trisomy 21
  Formerly called mongolism Trisomies are the product of the union of a normal gamete with a gamete that contains an extra chromosome.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. The most common abnormality seen in children Characteristics : Central nervous system: Mental retardation Hypotonia at birth Clinical Manifestations: 1. Small head 2. Depressed nasal bridge 3. Mongoloid slant eyes 4. Brushfield spots 5. Small low set ears 6. Protruding tongue 7. Short broad hands 8. Simian line 9. Wide space between first & second toes 10. Hearing loss 11. Increased incidence of diabetes, congenital heart defect, leukemia 12. Hypotonia Clinical therapy Multi step process Involves multidisciplinary team Developmental screening Denver II Neurologic examination Observe the child for facial symmetry Nursing Management 1. History taking 2. Developmental assessment 3. Assess adaptive functioning 4. Assess language, sensory & psychomotor functioning 5. Safety hazards home & community 6. Observe how the family is managing the child, community & school 7. Availability of services, special education opportunities 8. Evaluate the coping skills of the family members Nursing Diagnosis 1. Delayed growth & development 2. Imbalanced nutrition 3. Self care deficit 4. Impaired verbal communication 5. Risk for injury 6. Compromised family coping 

Cleft palate
A structural defect Cleft lip and cleft palate are two distinct facial defects that can occur singly or in combination Etiology The maxillary process fail to fuse with the elevations on the frontal prominence during the sixth week of gestation. Failure of the tongue to move downward at the correct time prevents the palatine process from fusing Causes Multifactorial combination of environmental & genetic influences Clinical Manifestations Cleft lip may bee seen on UTZ by 13-16 weeks of AOG Cleft lip apparent at birth; simple dimple in the vermilion border of the lip, complete separation extending to the floor of the nose Unilateral or bilateral or combination with varying degrees of nasal deformity Cleft palate less obvious when they occur without a cleft lip & may not be detected at birth Cleft of the hard palate form continuous opening between mouth & nasal cavity involves the soft palate or both soft & hard palate Clinical Therapy 1. Diagnostic at birth or during the NB assessment 2. Multidisciplinary team 3. Child is medicated to minimize crying 4. Special feeding devices 5. Antibiotics 6. Continuous intervention to prevent complications 7. Orthodontic care Nursing management Physiologic assessment: 1. Cleft lip observable at birth Cleft palate NB assessment by palpation of the hard palate w/ the finger; description of the location & extent of the defects helps the nurse determine the correct method of feeding. 1. Through & complete physical assessment Psychosocial assessment

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 1. Assessment of the family s reaction 2. A poorly corrected defect can lead to low self esteem in the older child. 3. Assess the child s developmental level & social interaction w/ peers. Nursing Diagnoses: 1. Anxiety (parent) 2. Ineffective infant feeding pattern 3. Risk for caregiver role strain 4. Risk for impaired home maintenance management Kidney & urinary tract malformations Congenital heart defects Tracheal & esophageal defects Limb defects, particularly forearms Down syndrome, hirschsprung s disease & duodenal atresia Diagnostics: 1. Thorough physical examination 2. Abdominal x-ray 3. Abdominal UTZ & spinal UTZ 4. Echocardiogram 5. MRI Treatment 1. Anoplasty 2. Colostomy fro infants w/ imperforated anus w/o fistula 3. Anal dilatation after surgery Nursing Management 1. Colostomy care 2. Anal dilatation 3. For constipation high fiber diet 4. Severe constipation bowel management program 5. Toilet training 2. 3. 4. 5. 6.

Imperforated anus
The anus and the rectum do not develop properly It s a defect that occurs during the fifth to seventh week of fetal development Slightly more common in male babies. Cause: 1. Unknown 2. Environmental factors 3. Drug exposure The following abnormalities can occur with an imperforate 1. Anal passage may be narrow or misplaced in front of where it should be located. 2. A membrane may be present over the anal opening 3. The rectum may not connect to the rectum 4. The rectum may connect to the urinary tract or the reproductive system though a passage called fistula & an anal opening is not present Cause for Concern: 1. When the anal passage is narrow or misplaced in front of the correct location. 2. If there is a membrane over the anal opening the maybe may be unable to have a bowel 3. If the rectum is not connected to the anus & no fistula 4. When the rectum is not connected tot eh anus but a fistula is present Risk: Previous family history Coexisting Abnormalities with Imperforate Anus: 1. Spinal abnormalities

Hirschsprung s disease
Also known as the congenital aganglionic megacolon  It is a congenital anomaly in which inadequate motility causes mechanical obstruction of the intestine  Common in males  Absence of autonomic parasympathetic ganglion cells in the colon prevents peristalsis Clinical Manifestations 1. Failure to pass meconium 2. Refusal to suck 3. Abdominal distention 4. Bile stained emesis Clinical Manifestations in Older Children: 1. Failure to gain weight & delayed growth 2. History of abdominal distention 3. Severe constipation alternating w/ diarrhea & vomiting 4. Ribbon like stool appearance 

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Complications: 1. Complete obstruction 2. Respiratory distress 3. Shock Diagnostics: 1. Bowel patterns, anorectal manometry 2. Radiographic contrast studies 3. Rectal biopsy Treatment  Surgical removal of the aganglionic bowel  Colostomy  For child w/ milder defect:  Management: dietary modification, stool softeners, isotonic irrigations to prevent impaction. Nursing Management 1. Observance for the passage of meconium 2. Thorough history of weight gain, nutritional intake & bowel habits 3. Fluid & electrolyte balance 4. Teach parents how to ensure regular bowel movements 5. Daily rectal irrigations w/ normal saline 6. Prevent skin breakdown in the rectal area 7. Protective ointment at each diaper change  Results from a blockage in the ventricular system that prevents CSF from entering the subarachnoid space  Enlargement of ventricles, obstruction can be caused by infection, hemorrhage, tumor and structural deformity Clinical Manifestations Cause: Congenital structural defect in infancy Dandy-Walker syndrome Chiari II Malformation Intraventricular hemorrhage Sylvius stenosis Early Signs: 1. Rapidly increasing head circumference 2. Bossing 3. Cracked-pot sign 4. Prominent, distended scalp veins, translucent scalp skin 5. Sun setting eyes 6. Increased tone 7. Irritability or lethargy and poor feeding 8. Decline in level of consciousness 9. Difficulty holding head up Late Signs 1. Apnea 2. Shrill, high pitch cry 3. Difficulty swallowing or feeding 4. Vomiting 5. Cardiopulmonary depression Acquired hydrocephalus on older child after closure of sutures post infectious, tumor, hemorrhage 1. No head enlargement 2. Headache upon arising w/ vomiting 3. Fussiness, sleepiness, confusion, apathy or altered LOC 4. Personality change, loss of interest in daily activities 5. Poor judgment or verbal incoherence, worsening school performance, memory loss 6. Ataxia, spasticity or other alterations in motor development 7. Visual defects 8. Signs of increased intracranial pressure Diagnostics 1. UTZ

Hydrocephalus
It s the body s response to an imbalance between the production & absorption of cerebrospinal fluid The condition is often congenital associated w/ other CNS malformations Commonly associated with myelomeningocele Etiology Communicating the CSF flows freely between normal channels & pathways, but absorption of the CSF in the subarachnoid space & the arachnoid villi is impaired.  Can be acquired from past infectious meningitis or intraventricular hemorrhage  d/t congenital malforamation in the subarachnoid spaces Non communicating

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 2. Sonograpgy 3. Daily measurement of head circumference 4. CT scan 5. MRI Nursing Management 1. Ensure prompt identification and treatment 2. Assess the child w/a ventriculoperitoneal shunt for signs & symptoms of shunt failure & infection  Mechanical Complication:  Blockage at either proximal or distal end of the cath.  Kinking of the tubing  Valve breakdown 3. Watch out for changes in responsiveness & irritability 4. Measure head circumference daily 5. Report any abnormality to the physician immediately Nursing Diagnoses: 1. Risk for infection 2. Impaired physical mobility 3. Risk for caregiver role strain 4. Anxiety 5. Risk for injury 3. Upper respiratory infection precedes otitis media 2 Air that normally flows to the middle ear is blocked, the air is reabsorbed into the blood stream. 2 Fluid is pulled from the mucosal lining into the former air space, providing a medium for the rapid growth of pathogens 2 Tympanic membrane & fluid behind it become infected Causative Agent: Streptoccus pneumonia Haemophilus influenzae Moraxella catarrhalis *Enlarged adenoids or edema from allergic rhinitis can also obstruct the eustachian tube and can lead to otitis media Clinical Manifestations Acute Otitis Media bacterial infection in the middle ear from pathogens transferred from the nasopharynx, most common infectious agents Behavioral: ear pain pulling at ear rapid onset irritability malaise and poor feeding Examination: bulging tympanic membrane Air fluid bubbles present behind tympanic membrane Immobile or poorly mobile tympanic membrane Red, white, gray or yellow as long as bulging tympanic membrane Reduced visibility of tympanic membrane landmarks w/ displaced light reflex Clinical Therapy 1. Treat ear pain w/ local anesthetic 2. Observe child s condition for 48-72 hours if not improved treat w/ course of antibiotics Clinical Manifestations Otitis Media w/ effusion collection of fluid in the middle ear behind the tympanic membrane w/c is not infected w/ bacteria. Behavioral: Difficulty hearing or responding as expected to sounds Examinations :

Otitis Media
2 Inflammation of the middle ear, accompanied by infection 2 Most common childhood illness 2 Peak incidence is in the first 2 years of life particularly from 6-12 months of age. Occurrence Common, frequent among boys Children who attend child care centers in those w/ allergies Children exposed to tobacco smoke Those who used pacifiers for several hours daily Common during cold months Cleft lip & palate Down syndrome Etiology Cause: 1. Unknown 2. Eustachian tube dysfunction

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 2 Tympanic membrane is retracted or neutral immobile or partly mobile tympanic membrane 2 Yellow or gray tympanic membrane 2 Opaque or thickened tympanic membrane w/ visibility of landmarks reduced. Clinical Therapy 1. Symptomatic treatment & pain relief 2. Careful observation of hearing acuity over several months. 3. Speech assessments if loss of hearing acuity occurs 4. Developmental assessment Diagnostics 1. Otoscopic examination 2. Special gradient acoustic reflectometry (SGAR) 3. Flat tympanogram 4. Audiologic test Treatment acute otitis media  Tx. w/ antibiotic therapy for 10 days in children under 6 years  For children 6 years & over, 5-7 days  Tx. Is delayed for 48-72 hours after dx. In children 6 mos. To 2 years w/ non-severe illness.  Choice of antibiotic depends on the probable organism, ease of administration, cost, previous effectiveness & any history of allergies  First line therapy -Amoxicilin dose 80-90 mg/kg/day  Second line amoxicilin w/ Cefuroxime 30 mg/kg/day Cefdinir 14 mg/kg/day Cefprodoxine 10 mg/kg/day Omeffusion Evaluated periodically to be sure there is not an additional AOM that needs treatment. OME generally improve w/in 3 mos. Follow up w/ audiologic test Myringotomy Tympanostomy tubes Recommended for children w/ bilateral middle ear effusion & hearing deficiency of greater than 20 decibels for over 3 mos. Nursing Management 1. Assess the tympanic membrane for color, transparency, mobility, presence of landmarks & light reflex. 2. Ask parents whether the child has had a fever, been fussy or have been pulling on the ears or any sings of impaired hearing. Nursing Diagnoses 1. Risk for imbalanced body temperature 2. Fatigue 3. Sensory/ perceptual alteration auditory

Myelodysplasia/ Spina Bifida

Also called meningomyelocele Malformation of the spinal cord & spinal canal Defect in one or more vertebrae through w/c spinal cord contents can protrude Malformation can occur anywhere along the vertebral column Sac like protrusion on the infants back Causes: Unknown Environmental factors Genetic factors Maternal health condition Clinical Manifestations Thoracic or Lumbar 1-2 level paralysis of the legs, weakness & sensory loss in the trunk & lower body region. Lumbar 3 level can flex hips & extends knees, the ankles & toes are paralyzed Lumbar 4-5 level can flex hips & extend the knees, weak or absent ankle extension, toe flexion & hip extension Sacral level mild weakness in ankles & toes, bladder & bowel functions may be affected Sensory loss is more pronounced on the back of the legs Sensory loss around the anus, genitalia & feet Renal damage result of neurologic impairment & urinary retention Interruption of the Spinal cord at the site of the Spinal Defect:

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 1. Loss of motor & sensory fxn of the abdomen & lower extremities dependent on defect level 2. Scoliosis or kyphosis 3. Incontinence of urine or urinary retention 4. Incontinence of feces or constipation 5. Sensory loss around genitalia Muscle imbalance Hip abnormalities Foot deformities Chiari II Malformation hydrocephalus Infants: Difficulty swallowing Apnea, respiratory difficulty Sustained backward arching of the head Older Children: Choking, hoarseness, vocal cord paralysis Disordered breathing during sleep Stiffness or spasticity of arms & hands Brain & spinal cord abnormalities Learning problems Problems w/ perceptual motor skills Memory & organization problems Problems w/ numerical reasoning Diagnostics Radiographic imaging UTZ CT scan MRI Treatment Surgery Braces Assistive devices Bladder intervention Nursing Management 1. Cover the sac w/ sterile saline dressing to protect its integrity & monitor for leakage of CSF 2. Positioning 3. Assess bowel & bladder involvement 4. Frequently assess v/s 5. Feed infant w/ the head turned to one side until surgery has been performed 6. Comfort the infant before surgery Post op: 1. Monitor v/s 2. Watch out for symptoms of infection 3. If ventriculoperitoneal shunt was placed Watch out for hydrocephalus IICP Infection 1. Inspect the surgical site for CSF leakage 2. Positioning 3. Begin gentle range of motion exercises 4. Support the parents

Meningitis
f Is an inflammatory response of the meninges characterized by an increased number of blood cells & protein in the cerebrospinal fluid. Classification: Viral Meningitis is caused by various viruses, such as the coxsackie viruses, mumps virus, & the virus of lymphocytic choriomeningitis. Bacterial Meningitis greatest risk are NB & infants. This is the common cause of meningitis among adults. Signs & Symptoms 1. Irritable or lethargic 2. Fever 3. General malaise 4. Headache 5. Photophobia 6. Gastrointestinal distress 7. Upper respiratory symptoms 8. Maculopapular rash Meningeal Irritations: 1. Stiff neck 2. Back pain 3. Positive Kernig sign 4. Positive Brudzinski sign Diagnostics: 1. Laboratory work Blood analysis Urine analysis 2. Lumbar puncture Cerebrospinal fluid analysis 3. Polymerase chain reaction testing Treatment: Same as bacterial meningitis Treatments are supportive of symptoms Nursing Management:

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 1. 2. 3. 4. 5. Supportive care Keep the room dark & quiet Give fluids Proper positioning Explain medical &nursing procedures in terms the family & child can understand. 6. Keep parents informed about the child s condition & progress. 7. Discharge planning & teaching for home care. 8. Explain to the parents the recovery may take several weeks. 6. Muscle or joint pain 7. Headache 8. Photophobia 9. Esotopia 10. Nuchal rigidity 11. Opisthotonic position 12. Positive Kernig s & Brudzinski s sign Symptoms can progress to: 1. Seizures 2. Apnea 3. Cerebral edema 4. Subdural effusion 5. Hydrocephalus 6. Disseminated intravascular coagulation 7. Shock 8. IICP Diagnostics 1. Blood cultures 2. CBC 3. Serum electrolytes & osmolality, clotting factors 4. Lumbar puncture 5. Gram stain & culture 6. CT scan Treatment 1. Antibiotics administered intravenously for 7-21 days depending on the organism & the child s clinical response. Ex. Ampicillin, aminoglycosides, cefotaxime, ceftriaxone, penicillin G. 2. Cortocosteriods given to children over 6 weeks of age to reduce the risk for severe neurologic squalae such as sensorineural hearing loss. 3. NPO - Infants & children receive nothing by mouth IV fluids are initially restricted to 2/3 maintenance as careful monitoring for IICP & syndrome of inappropriate antidiuretic hormone. If the child is in shock aggressive fluid resuscitation is performed t maintain the cerebral perfusion pressure. Complications 1. Hydrocephalus 2. Subdural effusion

Bacterial Meningitis
greatest risk are NB & infants. It is more virulent than viral meningitis & it is sometimes fatal. Etiology g It occurs secondary to other infections such as: otitis media, sinusitis, pharyngitis, pneumonia, septic arthritis, brain trauma or a neurological procedure. Bacteremia spreads the infectious agent to the CNS & an inflammatory response follows. The brain now becomes hyperemic & edematous. Infection can also spread to the ventricles. Three Organisms that cause most cases in children between 2 months 12 years of age: 1. Haemophilus influenzae type B 2. Neisseria meningitidis 3. Streptococcus pneumoniae Symptoms in Young Infant 1. Fever 2. Change in feeding pattern 3. Vomiting or diarrhea 4. Anterior fontanel may be bulging or flat 5. Infant may be alert, restless or lethargic or irritable Symptoms in Older Children 1. Febrile 2. Can have confusion 3. Delirium or impaired consciousness 4. Irritable, lethargic or confused 5. Vomiting

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 3. Developmental delay 4. Learning problems 5. Behavior problems 6. Meningococcal septicemia Nursing Management 1. Assess physiologic status, v/s & LOC 2. Measure head circumference 3. Be alert for potential signs of change in the child s condition & response to treatment. 4. Monitor the child s ability to control secretions & to drink sufficient fluids 5. Assess sensory deficits 6. Identify parent s concerns about this potentially life threatening condition. Nursing Diagnoses Risk for aspiration Risk for deficient fluid volume Anticipatory grieving Care giver role strain Anxiety Metabolic disturbances Fatigue Idiopathic or not provoked by unknown stimuli. Genetic factors Acquired seizures may be caused by underlying pathologic conditions: Trauma Infection Hypoglycemia Endocrine dysfunction Toxins Tumors or lesions Partial/Focal Seizure G Caused by abnormal electrical activity in one hemisphere or a specific area of the cerebral cortex, most often the temporal, frontal or parietal lobes. G Generalized seizures are the result of defuse electrical activity that begins in both hemisphere of the brain, simultaneous & spreads throughout the cortex into the brain stem. G Movement & spasms displayed by the child are bilateral & symmetric. Febrile Seizures t Are generalized seizure that usually occur in children as the result of rapid temperature rise above 390C/ 1020F in association w/ an acute illness. t No evidence of intracranial infection or other defined caused. t Usually seen between 3 months & 5 years w/ a peak incidence between 17-24 months of age. Clinical Manifestations Type of Seizure & Cause: Complex partial seizure: Partial/Focal seizure Onset; 3 years of age to adolescence Consciousness is impaired immediately or gradually after a simple partial onset Lasts 30 sec. up to 5 minutes. Post seizure amnesia or confusion May have abnormal motor activity Aura frequently present, unusual taste or odor

Seizure
Are periods of abnormal electrical discharges in the brain that causes involuntary movement & behavior & sensory alterations. Epilepsy g Is a chronic disorder characterized by recurrent unprovoked seizures secondary to a CNS disorder. g Infants are susceptible to developing epilepsy in the first year of life & incidence decreases w/ age. g The median age for the development of epilepsy is 5-6 years. Etiology: Seizures are the result of abnormal excessive concurrent electrical discharges from the cortical neuronal network of cells on the surface of the brain. Chemical changes w/in the neurons create an electrical negativity the enables the transfer of information between neurons. These cells can be triggered by either environmental or physiologic stimuli such as: Emotional stress Infection

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Feelings of anxiety, fear or dj vu Abdominal pain Staring into space, mental confusion Automatisms Simple partial seizure Onset; any age No loss of consciousness Lasts less than 30 sec. No post seizure confusion No aura Motor response may involve one extremity Sensory responses involve paresthesia Jacksonian march tonic contractions of either fingers of one hand, toes of one foot, or one side of face become clonic or tonic-clonic movements; marches up to adjacent muscles of either affected extremity or same side of the body. Generalized seizure Tonic-clonic seizures (grand mal seizure) Onset: any age before 6 months of age, strong familial incidence. Abrupt onset seizure, 1-2 min., loss of consciousness post seizure confusion May or may not have aura Body becomes stiff & rigid followed by rhythmic jerking. Drooling & foaming Eyes roll upward & deviate to one side w/ pupils dilated. Abdominal or chest wall rigidity w/ leg, head & neck extended, arms flexed or contracted. Cry or grunt Urinary or bowel incontinence Characterized by: 1. Sleepiness 2. Difficulty in arousal 3. Hypertension 4. Diaphoresis 5. Headache 6. Nausea 7. Vomiting 8. Poor coordination 9. Decreased muscle tone 10. Confusion 11. Amnesia 12. Slurred speech 13. Visual disturbances 14. Combativeness Absence seizure (petit mal or lapse seizure) Onset: age 3-12 years w/ remission in adolescence More prevalent in females May go on to develop other generalized seizure Hyperventilation or flashing lights may trigger a seizure. Brief loss of consciousness, usually lasts 5-10 sec. rarely exceeds 30 sec. No post seizure confusion Frequent attacks 50-100 per day No aura Child may continue simple movements such as: walking, looking Staring; usually w/ glazed eye appearance Rolling of eyes, eye blinking, ptosis or fluttering of eyelids Amnesia Myoclonic seizure Progressive or degenerative encephalopathy like: Tay Sachs disease. Onset; as early as 2 years but more prevalent in school age child or adolescent. No loss of consciousness No postictal period Attacks occur most often upon falling asleep or awakening quick involuntary muscle jerks. Infantile spasms (myoclonic epilepsy of infancy) Onset; begin at age 3 mos. Resolve by 2 years Positive hx. of gestational difficulties May occur w/ altered consciousness Occurs in clusters 5-150 per day Episodes of absent flexor, extensor or mixed jerks occurring in flurries Eye rolling Crying, pallor or cyanosis Regression in development Irritability Seizure activity increases in intensity & severity over time. Akinetic or Atonic seizures (drop attacks) Onset; first seen at 2 years, disappear by 6 years. Momentary loss of consciousness Falls to ground w/ sudden loss of postural tone. Quickly regains consciousness

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Diagnostics 5 Thorough hx. 5 Complete neurological examinations 5 Lab works 5 ECG 5 CT scan 5 MRI 5 Angiography Treatment Anticonvulsants Antipyretics Surgery Emergency med:  Diazepam First line med: carbamazepine, ethosuximide, phenobarbital, phenytoin, primidone, valproic acid Second line med: clonazepam, gabapentin, lamotrigine, tiagabine, topiramate Nursing Management 1. Assess & monitor the child s physiologic status. 2. Postictal period: monitor the child s v/s, perform neurologic checks & keep environment safe 3. Maintain patent airway 4. Protect child from injury 5. Assess the family s adaptation to the seizure disorder including how well the family is coping. Nursing Diagnoses 1. Ineffective breathing pattern 2. Ineffective airway clearance 3. Risk for trauma 4. Chronic low self esteem 5. Anxiety 6. Ineffective therapeutic regimen management 7. Readiness for enhanced family processes Etiology Unknown Genetic transmission, immune responses Neurotransmitters such as dopamine, serotonin Clinical Manifestations 1. Apparent by the time a child is 3 years of age. 2. Impairment in the ff. three areas: (1)Social reciprocity (2)Communication (3)Behavior 1. Stereotypy 2. Extreme aversion to touch, loud noises & bright lights 3. Emotional lability is common 4. Speech & language difficulties or delays are common. 5. Rituals 6. Disturbances in rate or sequence of development 7. Cognitively impaired but can demonstrate a wide range of intellectual ability & functioning Diagnostics Diagnostic & Statistical Manual of Mental Disorder IV Edition. Neuro-imaging DNA analysis Electroencephalogram Nursing Management 1. Stabilize environmental stimuli 2. Provide supportive care 3. Enhance communication 4. Provide anticipatory guidance Nursing Diagnoses 1. Impaired verbal communication 2. Impaired social interaction 3. Disturbed thought process 4. Risk for injury 5. Risk for caregiver role strain 6. Disabled family coping: compromised Attention Deficit Disorder is a variation in central nervous system processing characterized by developmentally inappropriate behaviors involving inattention.

Autism
Pervasive developmental disorder Begins in early childhood characterized by impaired social interactions & communication w/ restricted interest, activities & behavior.

Attention Deficit Hyperactivity Disorder

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. hyperactivity & impulsivity accompanying inattention; common among boys four times than girls. Affects from 4% - 12% of all school age children. Etiology 1. Exposure to high levels of lead in childhood 2. Prenatal exposure to alcohol 3. Genetic factors 4. Other contributing factors 5. Daily TV exposure at ages 1-3 years is associated w/ attention problems at 7 years. Clinical Manifestation 1. Decreased attention span 2. Impulsiveness, increased motor activities 3. Various developmental learning disabilities 4. Difficulty completing tasks, fidgets constantly 5. Frequently loud & interrupts others 6. Sleep disturbance. 7. Difficulty developing & maintaining social relationships. 8. Shunned or teased by other children. 9. Girls w/ ADHD shows less aggression & impulsiveness Clinical Therapy 1. Obtain an accurate diagnosis by a pediatric mental health specialist 2. Combination of approaches: Environmental changes Behavioral therapy Pharmacotherapy Methylphenidate (Ritalin, Concerta) Dextroamphetamine (Dexedrine, Adderall) 3. Chiropractic manipulation, biofeedback visual & auditory therapy 4. Dietary interventions Elimination of dietary components, such as highly processed foods, sugar, aspartame & yeast 3. Supplements such as iron, magnesium, zinc & vitamin B6, herbs such as Pycnogenal, melatonin & ginkgo biloba. Nursing Management 1. Have the parents describe: Birth history The child s behavior Childs attention span in detail Child s activity level & impulsiveness Distractibility Attention deficit in activities of daily living Way of reacting Extent of impulsiveness when the child is receiving medication. Administer medication Watch out for side effects: Anorexia Insomnia Tachycardia 2. Minimize environmental distractions: 3. Implement behavioral management plans 4. Provide emotional support 5. Promote self esteem Nursing Diagnoses 1. Impaired verbal communication 2. Impaired social interaction 3. Chronic low self esteem 4. Risk for injury 5. Risk for caregiver role strain

Burns
Any injury to tissues of the body caused by hot objects or flames, electricity, chemicals, radiation or gases w/c the extent of the injury is determined by the nature of the agent, length of time exposed, part of the body involved & depth of burn It is the third leading cause of injury & deaths in children between 1 & 14 years of age. Four Main Types of Burns 1. Thermal burns most common in children results from flames, scalds, grease or contact w/ hot objects, stove curling iron. 2. Chemical burns occurs when children touch or ingest caustic agents. 3. Electrical burns caused by direct or alternating current in electrical wires, appliances, high voltage wires. 4. Radiation burns results from exposure to radioactive substances or sunlight Etiology Infants thermal burns are common Toddlers thermal, electrical, chemical

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Preschool thermal, scalding hot appliances School-age thermal , play w/ matches fireworks, electrical appliances, climb high voltage, chemical common combustion experiments Clinical Manifestations Depth Classification of Burns  Partial thickness the injured tissue can regenerate & heal  Full thickness injured tissue can not regenerate, AKA third degree burns Superficial Partial Thickness (First Degree) Damages only the outer layer of skin Burn is painful & red Heals in a few days Erythema, blanches on pressure No bullae, peeling after a few days d/t premature cell death Partial Thickness (Second Degree)  Involves epidermis & upper layers of dermis may have sparing of sweat glands & sebaceous glands  Heals in 10-14 days Full Thickness (Third Degree)  Involves all of epidermis & dermis  May involve underlying tissue  Nerve endings usually destroyed  Requires skin grafting  Skin may appear brown, black, deep cherry red white to gray, waxy or translucent & usually no pain  Injured area appear sunken Assessment of Burns Severity 1. Depth of the burn injury 2. BSA 3. Circumferential burns Initial Treatment 1. Ensure the child s airway 2. Remove jewelry & clothing 3. Moist soaks or ice 4. Tetanus vaccine Goals of Treatment 1. Decrease burn fluid losses 2. Prevent infection 3. Control pain 4. Promote nutrition 5. Salvage all viable tissue Special Consideration 1. Assess for increase in cyanosis, deep tissue pain & capillary refill time & decrease pulse distal to a circumferential burn. 2. Ensure airway patency 3. Special splinting & physical therapy 4. Frequent dressing changes are required Wound Management Goals 1. To speed wound debridement 2. To maintain moist wound conditions & adequate circulation 3. To conserve body heat & fluids 4. Protect from infection 5. Control scarring & prevent scar contracture  The entire body is bathed  Sedation  Intact blisters  Antibacterial agents  Cover the burned area  Hydrotherapy  Skin grafting  Autografting  Trans-cyte  Pressure garments  Cosmetic surgery Nursing Management 1. Emergency assessment 2. Obtain information about the burn 3. Take burn history 4. Thorough physical assessment 5. Monitor v/s, pain control, daily weight measurement 6. Monitor circulatory & respiratory status 7. Head to toe assessment at the beginning of every shift 8. Systemic specific assessment 9. Watch out for signs of infection 10. Strict I & O monitoring 11. Assess child s concern on appearance & the stress of hospitalization 12. Prevent complication 13. Wound care 14. Provide emotional support

Poisoning
The condition or physical state produced by the ingestion of, injection of, inhalation of, or exposure to a poisonous substance.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. common cause of death & injury in children between 1-4 y/o Young children are at risk for poisoning because they characteristically explore their environment Clinical Manifestations Type: Corrosives 1. Severe burning pain in the mouth, throat or stomach 2. Swelling of mucus membranes 3. Edema of lips tongue & pharynx 4. Violent vomiting, drooling, inability to clear secretions 5. Signs of shock 6. Anxiety 7. Agitation Clinical Therapy Do not induce vomiting Dilute toxin w/ water to prevent further damage Give activated charcoal Hydrocarbons 1. Gagging, choking 2. Coughing 3. n/v 4. Alteration in sensorium 5. Weakness 6. Respiratory symptoms of pulmonary involvement Clinical Therapy Do not induce vomiting Use gastric lavage if severe central nervous system & respiratory impairment are present Provide supportive care Decontaminate skin by removing clothing & cleansing skin Acetaminophen 1. n/v 2. Sweating 3. Pallor 4. Hepatic involvement Clinical Therapy Induce vomiting or perform gastric lavage Administer charcoal Salicylate 1. n/v 2. Dehydration 3. Diaphoresis 4. Hyperpnea 5. Hyperpyrexia 6. Bleeding tendencies 7. Oliguria 8. Tinnitus 9. Convulsions 10. Coma Clinical Therapy Depends on the amount ingested Induce vomiting Administer intravenous sodium bicarbonate fluids, vitamin K Mercury 1. Tremors 2. Memory loss 3. Insomia 4. Weight loss 5. Diarrhea 6. Anorexia 7. Gingivitis Clinical Therapy Induce vomiting Administer intravenous fluids & sodium bicarbonate Desferoxamine chelation therapy Moderate toxicity 16-69 ug/dL 1. Arthralgia 2. General fatigue 3. Difficulty concentrating 4. Muscular exhaustability 5. Tremor 6. Headache 7. Diffuse abdominal pain 8. Vomiting 9. Weight loss 10. Constipation 11. Anemia Severe toxicity >70 ug/dL 1. Paresis 2. Encephalophaty 3. Lead line 4. Colic Clinical Therapy Blood lead level Pb B below 10 ug/dL Pb - B between 20-69 ug/dL Pb B above 25 ug/dL

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Pb- B level greater than 70 ug/dL Chelation Therapy The use of ethylenediamenitetraacetic acid (EDTA) to remove toxic metals & substances from the body. Involves the administration of an agent that binds with lead, increasing its rate of excretion from the body. Calcium disodium EDTA (CaNa2 EDTA) Demecaprol (BAL) D- penicillamine or succimer (DMSA) Management  Focuses on stabilizing the child s condition  Identifying the toxic agents/substance  Reversing any undesirable effects  Eliminating the substance from the child s body Perpetrator is the parent or another person legally responsible who: 1. Inflicts or allows another to inflict physical or emotional pain or injury. 2. Creates or allows another to create a significant risk of serious physical or emotional pain or injury 3. Commits or allows another to commit an act of sexual abuse, as defined by law against the child. Abuse involves an act of commission, that is actively doing something to a child physically, emotionally or sexually. Neglect involves an act of omission, such as not providing adequate nutrition, emotional contact or necessary physical care. Physical Abuse the deliberate maltreatment of another individual that inflicts pain or injury & may result in permanent or temporary disfigurement or even death. Physical Neglect deliberately withholding of or failure to provide the necessary & available resources to the child. Emotional Abuse involves shaming, ridiculing, embarrassing, insulting the child Verbal Abuse is a common method of emotional abuse, yelling obscenities at the child, calling the child names, threatening to put the child away. Emotional Neglect is characterized by the care takers emotional unavailability to the child. Sexual Abuse is the exploitation of a child for the sexual gratification of an adult.

Common forms of Sexual Abuse

Oral/genital contact Fondling & caressing the genitals Anal intercourse Rape Sodomy Prostitution Forcing viewing of or participation in pornography Etiology Most common abusers is the child s parent, guardian, boyfriend of the child s mother. Risk factors associated w/ abusive behavior in adults include the following:  Psychopathology  Poor parenting experience  Marital stressors & problem w/ partners  Environmental stressors  Social isolation  Inappropriate expectations for the developmental level of the child. Clinical Manifestation Child Abuse: 1. Multiple bruises in various stages of healing 2. Scald burns w/ clear lines of demarcation 3. Rope, belt. Cord marks seen at mouth, buttocks, back legs & arms 4. Burn scars in various stages of healing 5. Multiple fractures 6. Shortness of breath & distress upon being moved 7. Sedation from overmedication 8. Exacerbation of chronic illness Physical Neglect: 1. Undernourishment 2. Unclean clothes & body 3. Poor dental health 4. Inappropriate clothes for the season Emotional Abuse, Emotional Neglect & Verbal Abuse: 1. Fear 2. Poor physical growth 3. Failure to meet appropriate developmental milestones 4. Difficulty relating to adults

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 5. Impaired communication skills 6. Behavioral manifestations Clinical Therapy 1. Careful history taking 2. Thorough physical examination 3. X-ray, CT scan, MRI 4. Urinalysis 5. Genitourinary examination Nursing Management 1. Comprehensive hx & physical examination w/ documentation of findings 2. Consultation w/ social services agencies in the community. 3. Use of therapeutic communication techniques 4. Trusting relationship 5. Health hx sequence should include: 1. Parental concerns 2. General family hx 3. Specific child hx 6. Obtain details how injuries occurred 7. Compare notes/reports obtained from each family member for lack of consistency & details 8. Interview parent & child separately as well as together 9. Assess the child s general appearance 10. Be alert for the signs of shaken child syndrome 11. Document the findings, lab, specimen other items 12. Record physical findings as observed 13. Take photographs to document the location, nature & extent of injuries 14. Prevent further injury 15. provide supportive care Nursing Diagnoses  Pain  Impaired skin integrity  Delayed growth & development  Imbalanced Nutrition  Impaired health maintenance  Fear  Risk for injury  Risk for directed violence  Defensive coping  Chronic low self esteem  Disabled family coping Sexual Abuse Anxiety Rape trauma syndrome Ineffective role performance Disturbed personal identity

Cerebral Palsy
Is a disorder of movement & posture that results from a non progressive abnormality of the immature brain occurring in the prenatal, peri-natal or post natal period. A motor function disorder caused by a permanent, non-progressive brain defect or lesion present at birth or shortly thereafter. Etiology Caused by congenital, hypoxic, ischemic or infectious intrauterine insults to the CNS. Prematurity is most often related to CP caused by injury to the white matter of the brain by conditions such as intraventricular hemorrhage. Intapartum asphyxia Neonatal sepsis & hyperbilirubenemia CNS infection & head trauma, acquired brain injury & subsequent motor disfunction Clinical Manifestations 1. Hypotonia 2. Hypertonia 3. Athetosis 4. Ataxia 5. Hemiplegia 6. Diplegia 7. Quadriplegia Cerebral Palsy by Type of Insult Spastic - cerebral cortex or pyramidal tract injuryPersistent hypertonia, rigidity Exaggerated deep tendon reflexes Persistent primitive reflexes Dyskinetic extrapyramidal basal ganglia injury Impairment of voluntary muscle control Bizarre twisting movements Tremors, difficulty w/ fine & purposeful motor movements Exaggerated posturing Rigid muscle tone when awake & normal or decreased muscle ton when asleep Consistent muscle tone that may change hour to hour or day to day Ataxic - cerebellar, extrapyramidal injury

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Abnormalities of voluntary movement involving balance & position of the trunk & limbs Difficulty controlling hand & arm movements during reaching Increased or decreased muscle tone Hypotonia in infancy Muscle instability & wide based unsteady gait Mixed injuries to multiple areas No dominant motor pattern Unique compensatory movements & posture to maintain control over specific neuromotor deficits Clinical Therapy 1. Ultrasonography 2. Neuromotor tests 3. Referrals to physical, occupational, speech therapy, special education 4. Surgical interventions 5. Physical therapy 6. Medications to control seizures Nursing Management 1. Assess child at each health care visit for developmental delays. 2. Provide adequate nutrition 3. Maintain skin integrity 4. Promote physical mobility 5. Promote safety 6. Promote growth & development 7. Foster parental knowledge 8. Provide emotional support Nursing Diagnoses 1. Risk for constipation 2. Impaired tissue integrity 3. Impaired verbal communication 4. Impaired home maintenance management 5. Chronic pain 6. Delayed growth & development Common Health Problems in Preschooler Leukemia  It is characterized by a proliferation of abnormal white blood cells in the body.  Is among the most commonly diagnosed pediatric malignancies in children under 14 years of age.  A cancer of the blood forming organs. Types Acute Lymphoblastic Leukemia Most common type of childhood leukemia Accounts for 25% of all childhood cancer & 75% of leukemia s in children. Peak age at onset is 2 to 4 years Common in whites & boys Acute Nonlymphocytic Leukemia Refers to all leukemia from myeloid cells 17% of childhood leukemia s are ANLL Most common in children younger than 2 years of age & in adolescents. Common in males than females & in Asian/Pacific Islanders, Hispanic, whites. Etiology & Pathophysiology  Exposure to infectious agents  Genetic factors  Children with immune deficiency status such as: Ataxia-telangiectasia Congenital hypogammaglobulinemia  Exposure to ionizing radiation when in utero & chemical agents such as treatment w/ chemotherapy.  Stems cells in the bone marrow produce immature WBC that cannot function normally.  Cells proliferate rapidly by cloning instead of normal mitosis, causing the bone marrow to fill w/ abnormal WBC s.  The abnormal cells then spills out into the circulatory system where they steadily replace the normally functioning WBC s 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Clinical Manifestation Fever Pallor Overt signs of bleeding Lethargy Malaise Anorexia Large joint or bone pain Hepatospleenomegaly Lymphadenopathy h/a Vomiting Papilledema Sixth cranial nerve palsy

Cardinal Signs of Bone Marrow Failure

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Petechiae Frank bleeding Joint pain Common sites of Infiltration 1. Testicles 2. Spinal cord 3. Bone marrow Clinical Therapy Blood count & bone marrow aspiration Rapid flow cytometric assay DNA analysis Radiation therapy & chemotherapy Additional radiation & chemotherapy for relapse Bone marrow transplantation for relapse of ALL Four Phases of Chemotherapy 1. Induction Maximum cell death occurs during induction phase 2. Consolidation L-asparaginase Doxorubicin 3. Delayed intensification Uses additional drugs Target the leukemic cells that have survived 4. Maintenance of remission Aimed at destroying the remaining leukemic cells Treatment for Acute Lymphoblastic Leukemia Induction Phase Prednisone Vincristine L-asparaginase Daunorubin CNS prophylaxis intrathecal methotrexate Consolidation Phase L-asparaginase Daunorubin Delayed intensification Vincristine Ara-C Cyclophosphamide Maintenance phase 6-mercaptopurine or 6thioguanine Methotrexate Treatment for Acute Nonlymphocytic Leukemia Induction Phase Daunorubin Doxorubicin Mitoxantrone Cytarabine Consolidation Phase Etoposide Teniposide Nursing Management 1. Thorough physical assessment 2. Perform assessment q 8 or more often depending on the chemotherapy regimen. 3. Once chemotherapy has begun: Monitor renal functioning Monitor dietary intake Ask parents in any behavioral changes 4. Pain assessment & evaluation 5. Evaluation of level of knowledge & coping skills of child & family. For Physical Care on Chemotherapy 1. Have rest periods each day 2. Avoid exposure to people w/ illnesses 3. Drink generous amounts of water 4. Eat a healthy diet, frequent small & nutritious meals to obtain enough nutrients 5. Take medicines prescribed to decrease nausea. 6. Maintain good oral hygiene 7. Avoid sun exposure & check skin every day. 8. Allow time to eat nutritious food to promote bowel elimination. 9. Promote bowel elimination through regular dietary & toileting practices. 10. Report any signs of infection, changes in condition or other concerns. Emotional Care 1. Be prepared for loss of hair 2. Continue contact w/ friends via phone, internet 3. Relaxation techniques

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 4. Talk w/ clergy, teacher, parents, friends, supportive people about the experience. 5. Keep a journal to record feelings & experiences. Nursing Diagnoses 1. Imbalanced nutrition; less than body requirements 2. Risk for infection 3. Risk for injury 4. Activity intolerance 5. Pain 6. Disturbed sleep pattern 7. Anxiety 4. Glomerular damage on the remaining kidney. Wilm s Tumor Staging System Stage I Tumor is limited to the kidneys & completely excised. Surface of renal capsule is intact Tumor not ruptured before or during removal No residual Stage II Extend beyond the kidneys Regional extension of the tumor is present Penetration outer surface of the renal capsule Vessels outside the kidney are infiltrated or contain tumor thrombus. Stage III f Residual nonhematogenous tumor is confined to the abdomen f Diffuse peritoneal contamination tumor extends beyond the surgical margins either microscopically or grossly f Tumor not resectable because of local infiltration into vital structures. Stage IV Hematogenous metastasis Stage V  Bilateral renal involvement is present at diagnosis  Stage each side according to the above criteria on the basis of extent of disease before biopsy. Nursing Management Thorough baseline assessment Do not palpate the abdomen Monitor BP carefully Nursing Diagnoses Risk for infection Impaired urinary elimination Ineffective cardiopulmonary tissue perfusion Risk for care giver role strain Risk for impaired home maintenance

Wilm s Tumor (Nephroblastoma)

Intra-renal tumor A common tumor of childhood & accounts for 6% of all childhood tumors Occurs most frequently between 2 & 5 years of age Can also occur in adolescents & adults. Etiology & Pathophysiology Associated w/ several congenital anomalies  Aniridia  Hemihypertrophy  Genitourinary anomalies  Genetic link  Beckwith-Weidemann syndrome Wilm s tumor grows very quickly Clinical Manifestation 1. Asymptomatic 2. Firm, lobulated mass located to one side of the midline in the abdomen 3. Hypertension 4. Hematuria Clinical Therapy Treatment: 1. Surgery 2. Chemotherapy & radiation Long Term Complications of Treatment 1. Liver damage 2. Portal HPN 3. Mild cirrhosis

Asthma
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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Also called bronchial asthma Chronic inflammatory disorder of the airway w/ airway obstruction that can be partially or completely reversed & increased airway responsiveness to stimuli. It is the most common chronic illness. Etiology & Pathophysiology Multi factorial  Environmental exposures  Viral illnesses  Allergens  Genetic predisposition 2. Methylxanthines theophyline, aminophyline 3. Mast cell inhibitors cromolyn sodium, nedocrimil 4. Corticosteriods beclomethasone, budesonide, fluticasone, triamcinalone 5. Leukotriene modifiers Montelukast, zafirlukast Other 1. Hyposensitization (allergy shots) Nursing Management 1. Assess child s current respiratory status. Assess child s breathing Inspect chest for retractions Auscultate quality of breath sounds Assess child s color Heart rate Cough or stridor O2 saturation Head to toe assessment 2. Maintain airway patency 3. Meet fluid need 4. Promote rest & stress reduction 5. Support family participation Nursing Diagnosis 1. Ineffective airway clearance 2. Impaired gas exchange 3. Risk for deficient fluid volume 4. Anxiety/fear 5. Ineffective therapeutic regimen management

 React excessively in response to a stimulus & cause airway obstruction  Stimulus or trigger initiates asthmatic episodes w/c could be inflammatory or non inflammatory.  Triggers increase the frequency & severity of smooth muscle contraction & airway responsiveness is enhanced through inflammatory mechanisms. Clinical Manifestations Asthma in Children by Severity of Acute Exacerbations: Clinical Therapy Diagnosis of asthma has four key elements: 1. Symptoms of episode air flow obstruction 2. Partial reversibility of broncho spasm w/ bronchodilator treatment 3. Exclusion of alternative diagnosis 4. Confirmation by spirometry of measurement of forced expiratory flow variability. Skin testing Medical management Rescue medication 1. Beta2-agonists albuterol, metaproterenol, tubutaline, levabuterol 2. Corticosteriods methylprednisolone, prednisone, prednisolone 3. Anticholinergic - ipratropium Controller medication 1. Beta2 agonists

Urinary Tract Infection

May be bacterial, viral or fungal Incidence among NB & young infants associated w/ structural defects. Incidence in older children attributed to the shorter urethra Cystitis lower UTI involves the urethra or bladder. Pyelonephritis upper UTI involves the urether renal pelvis & renal parenchyma. Etiology

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 1. Caused by Escherichia coli, staphylococcus, klebsiella, proteus, pseudomonas, enterobacter, enterococcus 2. Urinary stasis 3. Incomplete emptying of the bladder 4. Infrequent voiding 5. Irritated perineum 6. Constipation 7. Masturbation 8. Sexual abuse 9. Vesicourethral reflux Risk of Kidney damage increases in the ff. instances: 1. UTI in infant less than 1y/o 2. Delay in diagnosis & effective antibacterial treatment for an upper UTI 3. Anatomic obstruction or nerve supply interruption 4. Recurrent episodes of upper UTI Lower UTI Clinical Manifestation 1. Frequency 2. Dysuria 3. Urgency 4. Enuresis 5. Strong smelling urine 6. Cloudy urine 7. Hematuria 8. Abdominal pain 9. Fever Clinical Therapy 5-7 days course of Trimethropin & Sulfamethoxazole or Antibiotic matching organism sensitivity Encourage oral fluids Analgesics Upper UTI Clinical Manifestation 1. High fever 2. Chills 3. Abdominal pain 4. Flank pain 5. Costovertebral angle tenderness 6. Persistent vomiting 7. Moderate to severe dehydration Clinical Therapy Rehydration Antipyretics IV antibiotics initially then transitioned to oral antibiotics matching organism sensitivity for a total of 7-10 days Nursing Management 1. History of urinary symptoms 2. Assess infant for toxic appearance 3. Measure child s weight, height & plot on growth curve 4. Take BP 5. Palpate abdomen, subprapubic & costovertebral areas for masses, tenderness & distention 6. Observe urinary stream if possible 7. Perform u/a including specific gravity 8. Health teachings:  Teach proper perineal hygiene  Encourage to increase fluid intake  Avoid holding urine for long period  Caution against tight underwear  Encourage child to void frequently  Discourage bubble baths, bath oils, hot tubs  Instruct sexually active adolescent girls to void before & after sexual intercourse. Nursing Diagnosis 1. Impaired urinary elimination 2. Risk for disproportionate growth 3. Urinary retention 4. Ineffective therapeutic regimen management 5. Risk for fluid volume deficit

Health Problems Most Common in School Aged Children

Diabetes Mellitus
The most common metabolic disease in children. It is a disorder of carbohydrate, protein, & fat metabolism that is primarily a result of a deficiency or complete lack of insulin secretion by the beta cells of the pancreas or resistance to insulin. Two Main Types of Diabetes Mellitus

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. Type I Diabetes Mellitus Most children have immune-mediated formerly called insulin dependent DM or juvenile DM. Includes patients w/ diabetes caused by an autoimmune process dependent on insulin to prevent ketosis. The onset in children is sudden Peak incidence occurs in children 5-7 y/o & again at puberty but it may be present at any age. Etiology & Pathophysiology Caused by genetic component Environmental influences Autoimmune response that damages the pancreatic cells Familial tendencies Insulin helps transport glucose into the cells so that the body can use it as energy source. Environmental factors lead an autoimmune destruction of the beta cells in the islet of Langerhans. Lack of insulin results in arise in blood glucose level & a decrease in the glucose level inside the cells. If glucose is unavailable to the cells for metabolism free fatty acids provide an alternate source of energy. The liver metabolizes fatty acids at an increased rate producing acetyl coenzyme A by products ketone bodies accumulate in the body. Clinical Manifestations 1. Polyuria 2. Polydipsia 3. Recent weight loss 4. Short duration of symptoms 5. Ketoacidosis 6. Ketosis 7. Initial period decreased insulin requirement , then need insulin for survival 8. Unexplained fatigue, lethargy, h/a, stomachaches, occasional enuresis Clinical Therapy 1. Blood glucose monitoring Fasting plasma glucose 126 mg/dl or 7 mmol/L Two hour plasma glucose 200 mg/dl or 11.1 mmol/L Plasma glucose concentration 200 mg/dl or 11.1 mmol/L

2. Lab test Test for antibodies, insulin autoantibodies & islet cell cytoplasmic auto-antibodies 3. Insulin Basal bolus therapy Conventional Insulin therapy 4. Dietary management 5. Exercise Basal Bolus therapy  Lower blood glucose levels, stabilize glucose levels & eliminate ketones  Insulin are adjusted according to frequent serum glucose monitoring at least four times a day.  It can be administered by an insulin pump; continuous subcutaneous insulin infusion CSII or by multiple daily injections MDI.  Basal insulin is administered once a day (Lantus, Glargine ) or twice a day (Humulin or Ultralente).  Bolus of rapid acting insulin is administered w/ each meal & snack based on the carbohydrates consumed. Basal Bolus therapy for Type I DM includes: 1. Monitoring blood glucose four to eight times a day & once a week at midnight & 3 am. 2. Consistent carbohydrate counting 3. Anticipating exercise in the routine Conventional Insulin therapy  Consists of daily administration of a combination of a short acting (regular) intermediate acting (NPH or Lente) long acting (Ultralente) insulin before breakfast & before the evening meal.  Rapid acting insulin is administered w/ each meal to carbohydrate intake Advantages of Rapid Acting Insulin (Lispro): 1. Decrease number of nocturnal hypoglycemic episodes.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 2. Meal coverage for toddlers who have unpredictable food consumption. 3. Flexibility for adolescent concerned about weight gain who do not want to eat a mid morning snack. Insulin Action: Subcutaneous Route Nursing Management 1. Assess the child s physiologic status 2. Monitor blood gases, glucose & electrolyte 3. Assess dietary & caloric intake 4. Assess the ability of the child or family to manage care. 5. Developmental assessment 6. Provide education 7. Oral health 8. Disease prevention strategies 9. Injury prevention strategies Nursing Diagnosis 1. Risk for deficient fluid volume 2. Ineffective breathing pattern 3. Ineffective denial Type II Diabetes Mellitus Is a disease associated w/ insulin resistance Alteration of insulin receptor that signals the presence of insulin in the anterior of cells. It may be connected w/ insulin secretory defect in the pancreas The single most important risk factor for type 2 DM is obesity Onset peak age puberty Risk Factors  Low physical exercise  Diet high in fat  Minority race  Polycystic ovary syndrome Etiology & Pathophysiology Caused by a complex metabolic disorder in w/c the child has insulin resistance & insulin fails to transfer glucose into the cells. w/ increased weight the visceral fat produces cytokine hormone that desensitizes the insulin receptor. Pancreatic cells produce more insulin in an attempt to facilitate glucose transfer & over come the insulin resistance The islet of Langerhans beta cells fail in their ability to hypersecrete insulin w/c leads to impaired glucose tolerance & overt diabetes develops. Clinical Manifestations 1. Obese 2. Acanthosis nigricans 3. Long duration of symptoms 4. Polyuria, polydipsia 5. Glycosuria w/o ketonuria in 33% of cases on initial presentation 6. Ketoacidosis on initial presentation in 5% to 25% of cases. 7. Lipid disorders 8. Hypertension 9. Androgen mediated problems 10. Excessive weight gain Clinical Therapy 1. Diet w/ decrease calories & low-fat foods. 2. Decrease sedentary activity time or increase routine physical activity. 3. Blood glucose monitoring 4. Oral medication to improve insulin sensitivity. Nursing Management Assess BMI Family history of DM Over weight child is a reason to begin screening for the condition Monitor blood glucose levels & blood pressure Assess the child s diet activity pattern Consider evaluating the siblings for diabetes. Nursing Diagnosis 1. Imbalanced nutrition 2. Activity intolerance 3. Fatigue 4. Ineffective therapeutic regimen management 5. Situational low self esteem

Rheumatic Fever
A systemic inflammatory disease that may develop as a delayed reaction to an inadequately treated infection of the upper respiratory tract by group A beta hemolytic streptococci This disorder causes changes in the heart, joints, brain & skin tissues.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. The onset is sudden Often occurring 1-5 symptom free weeks after recovery from a sore throat or scarlet fever. Early Symptoms 1. Fever 2. Joint pain 3. Nose bleeds 4. Abdominal pain 5. Vomiting Major Manifestations 1. Migratory polyarthritis 2. Aschoff s bodies 3. Endocarditis or carditis 4. Subcutaneous palpable nodules near the joints 5. Erythema marginatum 6. Spiking fever 7. Sydenham chorea/ St. Vitus dance Clinical Therapy  Laboratory testing of Antistreptolysin O (ASLO) titer of 320 Todd units.  Antibiotics penicillin, sulfadiazine, erythromycin  Aspirin  Echocardiogram  Steroids  Long term antibiotic prophylaxis Nursing Management 1. Throat culture 2. Emphasize the importance of giving all doses of the antibiotic prescribed when the culture is positive. 3. In severe cases child must be hospitalized; nursing care focuses on assessing the child s condition promoting recovery & ensuring adherence w/ the treatment regimen. 4. During the acute inflammatory phase: 5. Administration of prescribed medication as ordered 6. Handle joints carefully 7. Provide quiet activities 8. Encourage visits, telephone calls from family & friends 9. For child w/ chorea provide emotional support 10. During recovery phase: Activities should be limited Provide rest periods Reassure that the child s parents about the effects of choria will eventually subside Discharge Daily low dose of antibiotics Monthly long acting antibiotic injection is given. Importance of prescribed medication is understood by parents Stress the importance of telling future health care providers about the history of the rheumatic fever to prevent ineffective endocarditis during invasive procedures. Make sure parents understands that the child s future sore throats may be streptococcal & throat culture should be taken even when the child is taking antibiotics. Importance of the follow up care, prevent new infections & monitor heart function.

Juvenile Rheumatoid Arthritis

Is a chronic autoimmune inflammatory disease characterized by joint inflammation resulting in decreased mobility, swelling & pain that occurs slightly more often in girls than in boys. Most common type of arthritis in children & adolescents & occurs between 2-5 or between 9-12 y/o. Characterized by: 1. Pain 2. Impaired mobility 3. Interference w/ normal growth & development Etiology & Pathophysiology: 1. Cause is unknown 2. Autoimmune basis Three Types of Juvenile Rheumatoid Arthritis: 1. Pauciarticular arthritis primarily affects the knees, ankles & elbows & occur more frequently in females.

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 2. Systemic arthritis affects both male & female, manifested by a high fever, polyarthritis & rheumatoid, it also affects internal organs & joints. 3. Polyarticular arthritis involves many joints of the hands & fingers; affects the hips, knees, feet, ankles & neck. Clinical Manifestations 1. Fever 2. Rash 3. Lympadenophaty 4. Spleenomegaly 5. Hepatomegaly 6. Could be restricted to a few joint or be systemic 7. Limp 8. Slow rate of growth or uneven growth 9. Pain 10. Stiffness 11. Loss of motion 12. Swelling Clinical Therapy  History & assessment findings Onset before the age of 16 & persisting for at least 6 weeks w/ no other identifiable cause  Laboratory test Rheumatoid factor human leukocyte antigen (HLA) B27, antinuclear antibodies (ANA)  Medical management  Physical therapy  Surgery maintain & improve joint function in children w/ joint contractures  Medical Management Salicylates (Aspirin) Non-steroidal anti-inflammatory drugs, (Tolmetin sodium, Narpoxen, Diclofenac, Ibruprofen) Sulfazaline & methotrexate Nursing Management  Careful history  Assess joint for swelling & deformities, fever, nodules under the skin, growth delays & enlarged lymphnode.  Promote improved mobility To maintain joint function, strengthen muscles, increase tone, maintain body alignment. Prevent deformities such as contractures ROM exercises Encourage to perform ADL Warm compress to soothe involved muscles Adherence to prescribed medication  Encourage adequate nutrition Nursing Diagnosis 1. Activity intolerance 2. Impaired physical mobility 3. Anxiety 4. Pain 5. Disturbed body image Scabies A highly contagious infestation caused by the mite sarcoptis scabiei. It is spread by skin to skin contact Children of both sexes can be affected Prevalence in children under 2 years of age. Etiology & Pathophysiology Skin to skin contact Female mite burrows into the outer layer of the epidermis (stratus corneum) to lay her eggs Larvae hatch in approximately 2-4 days & proceed toward the surface of the skin. The cycle is repeated 14-17 days late Hypersensitivity to the ova & mite feces causes irritation intense pruritus approximately 1 month after infestation. Clinical Manifestation 1. Rash w/ various type of lesions 2. Severe pruritus that worsens at night 3. Lesions may appear as linear, threadlike, grayish burrows 1-10 cm in length, which may end in a pin point vesicle. Clinical Therapy  Confirmed diagnosis by examination under the microscope of scrapings from a burrow.  Treatment  Application of scabicide, 5% permethrin lotion, over the entire body from the chin down,

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. proceeded by warm soap & water bath.  Precipitated sulfur in petrolatum for 3 successive nights is used to treat scabies in infant under 2 months.  Second treatment is used 1 week later  All members of the household should be treated, even if they have no symptoms  If itching persist for 1-2 weeks after treatment ; oral antihistamine (Benadryl, Atarax). Nursing Management 1. Advice & educate parents about the transmission by close contact. 2. Changed clothing, bedding, pillow cases daily, wash w/ hot water & iron before use 3. Non-washable toys & other items should be sealed in plastic bags for 5-7 days 4. Family members not infected should avoid touching the child until after treatment is completed. 5. Inform parent s about signs of secondary infections & itching & nodules persist for weeks after effective treatment 6. Encourage use of emollients 7. Educate the child & parents about its spread, treatment measures to prevent recurrence. of hair accessories, brushes hats, towels & bedding.  Female louse lays her eggs (nits) on the hair shaft close to the scalp  Incubation period of eggs to hatch is 8-10 days. Clinical Manifestation 1. Intense pruritus & complaints of dandruff that sticks to the hair 2. Secondary effects of scratching include: Inflammation Pustules Bacterial infection Clinical Therapy Treatment involves pediculocide shampoo  Pyrethrum w/ an enzyme lice egg remover ovicidal rinse, Permethrin (Nix).  Permethrin cream  Fluconazole  Malathion Nursing Management 1. Careful assessment 2. Thorough interventions & education treatment should be complete before returning to day care or school. 3. Teach the child not to share clothing, head wear & combs 4. Follow prescribed specification of pesticides as directed 5. Avoid the eyes & mouth of the child during use 6. Use a fine toothed comb & tweezers to remove the nits. 7. Comb 1 inch section from the scalp outward & pin these out of the way when done. 8. Put the child under a bright light & use distractions such as video to keep child entertained during the procedure 9. Cut off the hair shorter to remove the nits. 10. Bedding, clothing should be changed daily, wash w/ hot water & detergent & dried in hot drier for 20 min. 11. None essential bedding & clothing can be stored tightly sealed bag for 2-3 weeks & then washed.

Pediculosis Capitis
It is an infestation of the hair & scalp of blood sucking lice. Infestation occurs among children of all socioeconomic levels. Infestation of the skin & body w/ lice Infestation of the eyelids & eyelashes w/ lice

Pediculosis corporis

Pediculosis palpebrarum

Pthirus pubis
Formerly called pediculosis pubis. Infestation of the pubic hair region w/ lice. Etiology  Head lice live & reproduce only on humans & are transmitted by direct hair to hair contact or indirect contact such as sharing

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This legal document is a private property of Mr. Marius Clifford Billedo and any unauthorized reproduction is strictly prohibited without prior consent to the owner and the publisher. 12. Hair accessories, brushes should be discarded or soaked in hot soapy water for 10 min. 13. Vacuum furniture & carpets & treat them w/ a hot iron when possible; use insecticides in the home to kill the lice w/ w/c young children & pets come in contact is not recommended. 14. Seal toys & other personal item that cannot be washed or dry put in a clean plastic bag for 2 weeks.  Bullous impetigo, vesicles stimulated by a toxin enlarge into bullae w/ straw-colored fluid & then rupture.  A thin honey colored crust forms when the bullae rupture  When the crust is removed a moist erythematous lesion w/ a collar of skin around the erosions is seen. Commonly occurs in moist skin folds. Clinical Therapy Diagnosed by gram stain & bacterial culture Removal of the crusts & application of topical antibiotic Crust are soaked in warm water & gently scrubbed off w/ an antiseptic soap. Topical bactericidal ointment:  Bacitracin, Mupirocin applied for 57 days  Dicloxacillin, Erythromycin Oral antibiotic may be used for bullous impetigo Recurrent impetigo Nursing Management 1. Advise parents to follow treatment as prescribed. 2. Observe all close contacts & family members for lesions. 3. Infected child should not share towels or toiletries w/ others & that all linens & clothing used by child should be washed separately w/ detergent in hot water. 4. Fingernails should be kept short & clean to prevent spreading infection by scratching. 5. Sanitize toys & surfaces; importance of regular cleaning the home.

Impetigo
 Is a highly contagious, superficial (epidermal) bacterial infection caused by streptococci, staphylococci or both.  The most common sites are the face, around the mouth the hands, neck & extremities.  It is the most common skin bacterial skin condition in children. Etiology & Pathophysiology  Minor skin abrasions, lesions, insect bites, burns & dermatitis provide the portal for the infectious agent commonly present in the environment.  Group A beta hemolytic streptococcus  Staphylococcus aureus  Common in children who are in close physical contact w/ others; child care settings, poor hygiene  Impetigo lesions begin as a vesicle or pustule surrounded by edema & redness  Progress to exudate & crusting stage  Initially serous vesicular fluid becomes cloudy & the vesicle rupture, leaving a honey colored crust covering an ulcerated base.  Common sites include the :  Intriginous areas  Skin folds neck, axillae or diaper rash  Rash my spread to the face & extremities by self innoculation.

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