1: Newborn male infant evaluation and care Flashcards

1
Q

Tobacco

A
  • Maternal tobacco use during pregnancy increases the risk for low birth weight in the fetus.
  • There are no characteristic facial abnormalities associated with maternal tobacco use during pregnancy.
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2
Q

Alcohol

A
  • There is no “safe” amount of alcohol that can be consumed during pregnancy to ensure that fetal alcohol syndrome does not occur.
  • FAS is a distinct pattern of facial abnormalities, growth deficiency, and evidence of CNS dysfunction.
  • Victims of FAS may exhibit cognitive disability and learning problems (i.e., difficulties with memory, attention, and judgment) as well as neurobehavioral deficits such as poor motor skills and impaired hand-eye coordination.
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3
Q

Marijuana

A

distinctive effects havent been identified

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4
Q

Heroin and other opiate medications

A
  • Maternal heroin use is assoc w/ inc r/o fetal growth restriction, placental abruption, fetal death, preterm labor and intrauterine passage of meconium.
  • All infants born to women who use opioids during pregnancy should be monitored for symptoms of neonatal abstinence syndrome (i.e. uncoordinated sucking reflexes leading to poor feeding, irritability, and high- pitched cry) and treated if indicated.
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5
Q

Cocaine and Other Stimulants

A
  • cause vasoconstriction leading to placental insufficiency and low birth weight
  • National Institute on Drug Abuse notes that “exposure to cocaine during fetal development may lead to subtle, yet significant, later deficits in some children, including deficits in some aspects of cognitive performance, information processing, and attention to tasks abilities that are important for success in school.”
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6
Q

SGA

A

Newborns who are noted to be smaller than expected for their gestational age are considered small for gestational age (SGA).

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7
Q

Although they are not synonymous, SGA is often used interchangeably with

A

-Fetal growth restriction-Intrauterine growth retardation (noted d/r pregnancy) and/or -Intrauterine growth restriction (IUGR);

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8
Q

Etiologies of SGA at Birth (1/4)-Maternal Factors

A
  • Both young and advanced maternal age
  • Maternal prepregnancy short stature and thinness
  • Poor maternal weight gain during the latter third of pregnancy
  • Nulliparity
  • Failure to obtain normal medical care during pregnancy
  • Cigarette smoking, cocaine use, other substance abuse
  • Lower socioeconomic status-African-American ethnicity (in the U.S.)-Uterine and placental abnormalities (see below)
  • Polyhydramnios
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9
Q

Etiologies of SGA at Birth (2/4)-Fetal factors

A

-Chromosomal abnormalities (e.g., trisomies) and syndromes -Metabolic disorders-Congenital infections (e.g., “TORCH” infections: Toxoplasmosis, “Others”, Rubella, Cytomegalovirus, and Herpes simplex type 2. Examples of “Others” include HIV, Hepatitis B, Human parvovirus, Syphilis and Zika. )-Structural abnormalities

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10
Q

Etiologies of SGA at Birth (3/4)-medications and other exposures

A

-Amphetamines-Antimetabolites (e.g., aminopterin, busulfan, methotrexate) -Bromides-Cocaine-Ethanol-Heroin and other narcotics (e.g., morphine, methadone)-Hydantoin-Isotretinoin-Metal (e.g., mercury, lead)-Phencyclidine-Polychlorinated biphenyls (PCBs)-Propranolol-Steroids-Tobacco (carbon monoxide, nicotine, thiocyanate) -Toluene-Trimethadione-Warfarin

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11
Q

Etiologies of SGA at Birth (4/4)-Uterine and placental abnormalities

A

-Avascular villi-Decidual or spiral artery arteritis-Infectious villitis (as with congenital or TORCH* infections)-Multiple gestation (limited endometrial surface area, vascular anastomoses) -Multiple infarctions-Partial molar pregnancy-Placenta previa and abruption-Single umbilical artery-Umbilical thrombosis-Abnormal umbilical vascular insertions-Syncytial knots-Tumors, including chorioangioma and hemangiomas

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12
Q

Maternal GBS Facts (1/2)

A

-GBS infection is a major cause of neonatal bacterial sepsis.-The incidence of early onset GBS disease is 0.6/1000 live births.-30% of pregnant women have vaginal or rectal colonization of GBS.

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13
Q

Maternal GBS Facts (2/2)

A

-Sans antibacterial ppx 1-2% of infants born to colonized women develop invasive disease (sepsis, pna and meningitis).-RF for early onset GBS dz include prolonged rupture of membranes, prematurity, intrapartum fever and previous delivery of infant who developed GBS dz.

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14
Q

The management of babies born to mothers who are colonized with Group B streptococcus depends on a number of factors (5)

A

-Clinical appearance-Evidence of maternal chorioamnionitis-Receipt of GBS prophylactic antibiotics by mother during labor -Duration of membrane rupture greater than 18 hours-Gestational age less than 37 weeks

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15
Q

NBN management of GBS: Any infant who is ill appearing

A

undergo a full diagnostic evaluation (CBC, blood culture, chest x-ray and lumbar puncture) and receive IV antibiotics.

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16
Q

NBN management of GBS: Well appearing infants

A

undergo a limited laboratory evaluation (CBC and blood culture) or simply be closely monitored over the first few days of life

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17
Q

Components of Apgar score include

A

-Appearance (skin color)-Pulse (heart rate)-Grimace (reflex irritability)-Activity (muscle tone)-Respiration

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18
Q

The change in Apgar score between 1 and 5 min

A

may be a useful indicator of response to resuscitation.

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19
Q

a score below 7 at 5 min should prompt

A

continued resuscitation, with re-assessment every 5 min, up to 20 min, until a score of 7 is achieved.

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20
Q

Ballard assessment tool

A

uses signs of physical and neuromuscular maturity to estimate gestational age.

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21
Q

Small for gestational age (SGA)

A

Weight below the 10th percentile for gestational age

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22
Q

Term

A

Born at > 37 weeks’ gestation

23
Q

Symmetric IUGR

A

growth pattern in which head, length, and weight are decreased proportionately. Congenital infections may adversely affect brain growth and often result in symmetrical IUGR.

24
Q

Asymmetric IUGR

A

-greater dec in the size of the length and/or weight without affecting head circumference (“head-sparing phenomenon”).-Poor delivery of nutrition to the fetus (example maternal smoking) often results in asymmetric IUGR

25
Q

Risks for SGA NBN (1/3): hypoglycemia

A

Etiology:-Decreased glycogen stores-Heat loss -Possible hypoxia-Decreased gluconeogenesiss/s: Commonly asymptomatic, though may exhibit poor feeding and listlessness

26
Q

Risks for SGA NBN (2/3): hypothermia

A

Etiology:-Cold stress-Hypoxia-Hypoglycemia-Increased surface area-Decreased subcutaneous insulations/s: Commonly asymptomatic, though may exhibit poor feeding and listlessness

27
Q

Risks for SGA NBN (3/3): Polycythemia

A

Etiology: -Chronic hypoxia-Maternal-fetal transfusions/s: -“Ruddy” or red color to skin-Respiratory distress -Poor feeding -Hypoglycemia

28
Q

Discharge teaching should include the following

A

-Reasons to seek immediate medical care, including fever, signs of poor feeding, worsening jaundice-Expectations for nml feeding, stooling, UOP-Safety issues (including placing the newborn on his back to sleep, proper infant auto restraint, avoiding cigarette smoke exposure.)-Plan for physician outpatient followup in 48-72 hrs -Social Services f/u plan-24 hr emergency contact info

29
Q

In addition to remembering the ABCs (or airway-breathing-circulation), keep in mind some of the special features of newborn resuscitation

A

-Use universal precautions-WARM & DRY the infant and remove any wet linens immediately. Infants have a large surface area relative to their body weight and can thus experience significant hypothermia from evaporation.-STIMULATE the infant to elicit a vigorous cry. This helps clear the lungs and mobilize secretions.-SUCTION amniotic fluid from the infant’s nose and mouth. This helps clear the upper airway.-INITIATE FURTHER resuscitation if required. This may include using blow-by oxygen, positive pressure (bag- valve mask) ventilation with oxygen, chest compressions, and medications.

30
Q

Demonstration of Primitive Reflexes (1/6): Rooting

A

Newborn turns his head toward your finger when you touch his cheek.

31
Q

Demonstration of Primitive Reflexes (2/6): Sucking

A

Newborn sucks on your finger when you touch the roof of his mouth.

32
Q

Demonstration of Primitive Reflexes (3/6): Startle (Moro)

A

Support NBN’s head w/ 1 hand and butt w/ the other. W/ the head in a midline position, the hand supporting it is quickly dropped to a position approx 10 cm below its original supporting position, and the head is caught in its new position. In response, the newborn will flex his thighs and knees, fan and then clench his fingers, with arms first thrown outward and then brought together as though embracing something.

33
Q

Demonstration of Primitive Reflexes (4/6): Palmar and Plantar Grasps

A

-Newborn grasps your finger when you stroke it against the palm of his hand or plantar surface of his foot.

34
Q

Demonstration of Primitive Reflexes (5/6): Asymmetrical Tonic Neck Response

A

Turning the newborn’s head to one side causes gradual extension of arm toward direction of infant’s gaze with contralateral arm flexion–like a fencer.

35
Q

Demonstration of Primitive Reflexes (6/6): Stepping Response

A

Newborn’s legs make a stepping motion when you hold him vertically above the table and stroke the dorsum of his foot against the table edge.

36
Q

Red Reflex Examination in Neonates: How?

A

turn off the room lights and stand at least a foot away from the child’s face with the illuminated ophthalmoscope

37
Q

Infants with more darkly pigmented skin

A

light golden colored or silver-tinged “red reflex.”

38
Q

An absent red reflex (no reflection noted) may be caused by

A

-A cataract-An opacified cornea (such as in mucopolysaccharidosis)-Inflammation of the anterior chamber-Developmental anomalies of the eye-Retinoblastoma, a potentially lethal malignancy (careful examination of the eye of an infant with retinoblastoma often identifies a white, irregular mass within the globe).

39
Q

Treating Neonates to Prevent Hemorrhagic Disease of the Newborn

A

intramuscular administration of Vitamin K at birth

40
Q

Type of VKDB-early (0-24h after birth)

A

-Severe-Mainly found in infants whose mothers used medications (e.g antiepileptic drugs or isoniazid) that interfere with how the body uses vitamin K

41
Q

Type of VKDB-classical (1-7d after birth)

A

-Bruising-Bleeding from the umbilical cord

42
Q

Type of VKDB-late (2-12 weeks after birth is typical, but can occur up to 6 months of age in previously healthy infants)

A

-30-60% of infants have bleeding within the brain-Tends to occur in breastfed only babies who have not received the vitamin K shot-Warning bleeds are rare

43
Q

Infants weighing more than 2000 grams born to mothers positive for hepatitis B surface antigen (HBsAg):

A

-Should receive hep B vaccine + hep B immune globulin (HBIG) within 12h of delivery.-Additionally, these infants should receive routine series of the vaccine beginning at age 1 mo. -Vertical transmission can be prevented in 85-95% of cases using these interventions.-At 9-18 mo, child should be tested for anti-HBs (Ab to Hep B surface antigen) and HBsAg, and, if found to have inadequate antibody protection, should be re-immunized.

44
Q

Infants born to mothers not tested for HBsAg:

A

-Should receive hep B vaccine within 12h of delivery.Administration of HBIG can be delayed until the maternal HBsAg is known, and is effective if given within 7 days following delivery if the patient is greater than 2 kg at birth.

45
Q

identifying and teating N gonorrhea why is it important

A

because ophthalmia neonatorum can result in perforation of the globe of the eye and blindness.

46
Q

Chlamydia trachomatis conjunctivitis in newborns

A

more common than gonococcal, but chlamydia typically occurs at 7-14 days after birth, and neonatal prophylaxis does little to prevent chlamydia conjunctivitis

47
Q

Routine NBN Meds (1/3): Vit K

A

NBN routinely receive an intramuscular injection of vit K to prevent hemorrhagic disease of the newborn (also referred to as vitamin K deficiency bleeding/VKDB). The efficacy of oral Vitamin K is unknown.

48
Q

Routine NBN Meds (2/3): Hep B vaccine

A

consider:-maternal Hepatitis B status (HBsAg positive, status unknown or HBsAg negative) -weight of NBN (>/< 2000g) ….when deciding the timing of the first dose of Hep B vaccine and whether or not Hep B Ig is needed to dec risk for vertical transmission

49
Q

Routine NBN Meds (3/3): Erythromycin (also tetracycline or silver nitrate)

A

One of these antibiotics is administered topically to prevent gonococcal conjunctivitis.

50
Q

Look for the following prenatal screening lab tests in the maternal record:

A

-Maternal blood type, Rh and antibody screen -Rubella IgG-Hepatitis B Surface Antigen (HBSAg)-HIV antibody-RPR or VDRL-Urinalysis-Urine nucleic acid amplification testing (NAAT) for chlamydia and gonococcus -Urine or vaginal culture for group B streptococcus-Hepatitis C antibody (in women with a history of IV drug use)-TB skin test (e.g. Mantoux) or TB blood test (e.g. Quantiferon) (in women w/ HIV or who live w/ someone w/ active TB)

51
Q

A 33-year-old G1P0 female with a history of medically controlled seizures gives birth vaginally to a boy with IUGR at 38 weeks’ gestation. The newborn is noted to have dysmorphic cranial features and his head circumference is 28.5 cm (< 5th percentile). What is another associated abnormality you might expect to see in this newborn?

A

The mother was on an anticonvulsant for her seizures. Taking anticonvulsants during pregnancy may lead to cardiac defects, dysmorphic craniofacial features, hypoplastic nails and distal phalanges, IUGR, and microcephaly. Mental retardation may be seen. A rare neonatal side effect is methemoglobinuria.

52
Q

A 19-year-old female in her 38th week of pregnancy goes into active labor. Shortly after birth her baby is noted to have a high-pitched cry, tremulousness, hypertonicity, and feeding difficulties. The baby is otherwise developmentally normal and the remainder of the physical exam also is normal. What is the drug the baby’s mother likely used during her pregnancy?

A

Heroin is the correct choice. Opiate use during pregnancy may result in several different symptoms, including CNS findings (irritability, hyperactivity, hypertonicity, incessant high-pitched cry, tremors, seizures), GI symptoms (vomiting, diarrhea, weight loss, poor feeding, incessant hunger, excessive salivation), and respiratory findings (including nasal stuffiness, sneezing, and yawning).

53
Q

A mother brings her 20-day-old male infant to your clinic for the child’s first visit. You learn that the infant was born at home to a 28-year-old G1P1, and the infant has not yet received newborn screening. During your history, you learn that the infant has been vomiting 2 to 3 times per day, and the mother reports that her son seems fussier than her friends’ infants. On exam, you note an eczematous rash and a musty odor to the infant’s skin and urine. Which enzyme deficiency would you expect the infant to display?

A

This infant likely has phenylketonuria (PKU), an autosomal recessive disorder of amino acid metabolism caused by a deficiency in the enzyme phenylalanine hydroxylase. Affected infants are normally detected by newborn screening, but can present with vomiting, hypotonia, musty odor, developmental delay, and decreased pigmentation of the hair and eyes. The best developmental outcomes occur if a phenylalanine-restricted diet is initiated in infancy.