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Neonate > Exam 2 pt2 > Flashcards

Exam 2 pt2 Flashcards

1
Q

The presence of bacteria in the bloodstream
-This can be a transient, self-limited phenomenon, cleared by immune system without event but can also progress to sepsis

A

bacteremia

*can seed other sites such as bone, lung, and meninges

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2
Q

Bacteremia coupled with inadequate perfusion and end-organ involvement
Meaning, decreased blood flow
Causing damage to important organs

A

sepsis

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3
Q

Sepsis which occurs in a neonate within the first 3 days of life

A

early-onset sepsis (EOS)

*Vertical transmission

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4
Q

Sepsis which occurs after the first 3 days until 2 to 3 months of life (definitions vary)

A

Late-onset (LOS)

*Horizontal transmission

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5
Q

sx:

  • Temperature may be elevated or depressed. Recall that normal range is 36.5 to 37.5
  • Tachypnea; ie, respiratory rate > 60/min
  • Other signs of respiratory distress (retractions)
  • Poor color (cyanosis, poor perfuson= mallor)
  • Decreased responsiveness/lethargy
  • Poor feeding
  • Irritability or sleepiness
A

sepsis

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6
Q

Babies have a limited repertoire. Symptoms of ___ may be indistinguishable from non-infectious illness.

A

sepsis

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7
Q

mortality rate of EOS

A

15%

*Higher mortality in pre-term babies and Lower in full-term

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8
Q

what type of sepsis is even more likely to be complicated by meningitis with its attendant morbidity

A

late onset sepsis

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9
Q

Which bacterial organisms are involved with sepsis

A
  1. Group B Strep
  2. E. coli- actually #1 in preterm babies
  3. Other strep species, most commonly Pneumococcus
  4. Enterococcus (Group D strep)
  5. Staph (usually iatrogenic)
  6. Listeria
  7. Klebsiella
    * These organisms all come from vagina or its neighbor, the GI tract
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10
Q

How does transmission of sepsis occur?

A
  • During labor membranes rupture or become leaky
  • Organisms can ascend from the birth canal (vagina)
  • Fluid becomes infected, fetus inhales or swallows it and also becomes infected
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11
Q

if mom goes into labor early for no known reason think…

A

possible infection like sepsis (Premature babies are more vulnerable because of less adequate immune system)

*Very high risk for EOS
Also higher risk for mortality associated with sepsis
It may be that the premature labor was prompted by brewing infection

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12
Q

MAJOR RISK FACTORS of EOS

A

*Chorioamnionitis
Maternal Group B Strep carriage
Prolonged rupture of the membranes (18 hrs)
Prematurity

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13
Q

MINOR RISK FACTORS of EOS

A

Ethnicity (black women are at higher risk of GBS colonization)
Low socioeconomic status
Male sex
Low birth weight (>2500 grams)

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14
Q

Definition of Chorioamnionitis

A

Maternal temperature during labor > 38.o C or 1oo.4 F
And at least 2 other features
1. maternal leukocytosis- WBC > 15,000 in blood
2. maternal tachycardia- > 100 beats/min
3. fetal tachycardia- baseline > 160 beats/min
4. uterine tenderness (tenderness=elicited, pain=subjective)
5. foul smelling amniotic fluid

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15
Q

Gram positive bacteria

Carrier state in mother (in her normal flora)

A

GBS

*6-30% prevalence internationally

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16
Q

how is GBS transmitted

A
  • Not sexually transmitted
  • 50% vertical transmission
  • Late onset disease is horizontal transmission
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17
Q

____% of babies born to mothers with GBS will develop early onset sepsis

A

1%

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18
Q

___% reduction in GBS sepsis from 1990s

A

87%

*Currently- all moms are cultured for GBS at 36 weeks and treat when they go into labor

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19
Q

risk factors for GBS

A
  • Previous child who had early-onset GBS sepsis
  • GBS bactiuria during current pregnancy
  • Maternal fever/chorio
  • Preterm labor
  • We revert to these criteria now when GBS culture is not available
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20
Q

Definition of prolonged rupture

A

> 18 hrs

*The longer the membranes are ruptured, the higher the likelihood of ascending infection

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21
Q

definition of Prematurity

A

gestational age less than 37 yrs

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22
Q

sepsis workup includes

A
  • Blood culture is mandatory (1-2ml from 1 site)
  • Chest X-ray (almost always done)
  • Lumbar puncture, aka “spinal tap” (look for WBC in CSF)
  • Complete blood count (CBC)
  • C-reactive protein
  • Urine culture is NOT indicated in septic workup of a newborn in the first 3 days of life. It should be included in workup of late onset sepsis
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23
Q

blood culture of spesis characteristics

A

1-2ml

  • Almost all pathogens will grow within 48hrs
  • Positive blood culture is diagnostic of neonatal sepsis but negative culture does not rule it
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24
Q

When to include Spinal Tap for sepsis dx

A
  • positive blood culture (Best performed before starting antibiotics, can be delayed if baby is unstable)
  • sx referable to CNS (Neonates with symptoms of meningitis -TRUE lethargy, abnormal tone, excessive irritability, bulging fontanel, or septic shock)
  • being proactive before starting antibiotics
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25
Q

sx of meningitis

A

lethargy, abnormal tone, excessive irritability, bulging fontanel, or septic shock

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26
Q

important features of CBC to consider

A
  1. Total WBC count (but can be caused by stress too ie. labor)
  2. Differential
  3. Absolute neutrophil count
  4. Immature/total ratio (I/T)
  5. Immature leukocyte count
  6. Normal ranges are broad and depend upon timing **best time is at least 6 hours after birth

*can be a clue but not diagnostic

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27
Q

hematopoiesis

A

maturation and differentiation of WBC

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28
Q

the cell line most responsible for managing bacterial infections.

A

neutrophils

  • Mature cells of the granulocyte line
  • *Also known as polymorphonucleocytes or “polys”
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29
Q

Immature forms of neutrophils include:

A

Bands
Metamyelocytes
Myelocytes
Promyelocytes and myeloblasts are not in circulation so not on CBC

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30
Q

Hematopoiesis of neutrophils

A

myeloid stem cell–> myeloblast –> N. promyelocyte –> N. myelocyte–> N. Metamyelocytes —> N. Band—> Neutrophil

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31
Q
  • Generally make up about 60% of circulating white blood cells.
  • Their numbers can increase in times of stress, such as infection. Normal values for a newborn are 16,000 to 31,000!
A

neutrophil

*A low neutrophil count may be more ominous as it reflects an overwhelmed immune system.

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32
Q

how do u calculate absolute neutrophil count

A

the total percentage of all neutrophils x total white blood cell count

*NOTE: total neutrophil count = polys + bands+ myelocytes + metamyelocytes

WBC x % of all neutrophils
Ex. 15% poly + 5% bands = 20%
WBC x 20% = ANC

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33
Q

abnormal absoulte neutrophil count

A

less than 1750

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34
Q

First few hours of life, ANC is approximately ___ and what happens to the number

A

1800
*Rises to approximately 8000/cu.mm by 12hrs
Returns to 1800 by 3 days.

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35
Q

what is released in times of stress and to fight infection

A

immature neutrophils

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36
Q

how do u calculate Immature neutrophils

A

adding all immature forms of neutrophil line and dividing by total neutrophil count

*Upper limit of normal of 0.2

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37
Q

a protein synthesized by the liver in response to, and as part of, the inflammatory response

A

CRP

*Poor specificity- other perinatal conditions confound- asphyxia, fetal distress, MAS

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38
Q

normal CRP

A

less than 1.0

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39
Q

pattern of CRP release

A
  • Released 4-6hr after stress
  • Peaks at 24-48 hrs
  • Diminishes over time as inflammation resolves
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40
Q

The only truly specific laboratory test in the workup of neonatal sepsis is __

A

blood culture
*However, many times, we make a PRESUMPTIVE diagnosis of sepsis based upon “clues” of suggestive history and suggestive lab tests.

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41
Q

prophylaxis tx of GBS

A

penicillin-mother needs 2 doses of PCN prior to delivery
*Acceptable: at least one dose, at least 4 hours prior to delivery

*If mother is Penicillin-allergic, other antibiotics are used:
Clindamycin- sensitivities are checked during pregnancy
Vancomycin- very broad spectrum
*These probably work but there is not evidence for specific parameters

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42
Q

If adequate prophylaxis, eliminates risk of EOS GBS sepsis, can go home when?

If inadequate, needs how long of an observation period to watch for evidence of EOS?

A

If adequate prophylaxis, eliminates risk of EOS GBS sepsis, can go home in 24 hours

If inadequate, needs a 48 hours observation period to watch for evidence of EOS.

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43
Q

Mothers who have fever or signs of chorio are treated with

A

antibiotics during labor to prevent sepsis in newborn
(prophylaxis for mothers with chorio)

*baby must be observed for 48 hrs after birth

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44
Q

Treatment for Newborns with Sepsis

A

-need IV antibiotics (best choice is ampicllin and gentamicin)
-Duration
10 full days for sepsis
2 weeks if meningitis

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45
Q

AAP and CDC recommend babies born to mothers with diagnosis of chorio should have ___

A
  • sepsis workup

- i.v. antibiotics: Ampicillin and Gentamicin for 48 hours until cultures are negative

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46
Q

Current incidence of EOS is estimated __% and

Using current guidelines necessitates treating up to ___% of all newborns as if they are ill

A

0.05-0.12%

10%

*can use Kaiser spesis risk calculator to determine risk

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47
Q

by-product of RBC breakdown

A

bilirubin
*Bilirubin pigments are deposited in the skin and mucous membranes, causing the classic yellow or jaundiced appearance of the skin

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48
Q

when does jaundice occur

A

when an infant is hyperbilirubinemic

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49
Q

Jaundice first becomes visible____ and____ and progresses caudally to the ____

A

in the face
forehead
trunk and extremities

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50
Q

how to look for jaundice in a baby

A

Blanch the skin and look for an underlying yellow tone

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51
Q

average length of breastfeeding in the US and worldwide

and when are the biggest drop off in the US

A
  • US is 3-6 months (bc women have to get back to work) and 5 yrs worldwide
  • Biggest drop off is first leaving the hospital and the second is at 6 weeks when women go back to work
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52
Q

what % of women in CO exclusively b.f. at 3 months and 6 months and ever b.f

A

3 months- 50.3%**
6 months- 25.8%**
ever b.f- 81%

**meets US dept. of Heatlh goals

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53
Q

Breastfeeding initiation is less common in moms who:

A

Have lower education levels
Are single
Are teen

*mostly due to having to return to work, and these are the ones that would most benefit from b.f.

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54
Q

Five hospital maternity care practices that will help with successful breastfeeding:

A
  1. Infants are breastfed in the first hour after birth.
  2. Infants stay in the same room as their mothers.
  3. Infants are fed only breast milk and receive no supplementation (use human donor milk if need to supplement)
  4. No pacifier is used.
  5. Staff gives mothers a telephone number to call for help with breastfeeding.
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55
Q

provides Federal grants to States for supplemental foods, health care referrals, and nutrition education for low-income pregnant, breastfeeding, and non-breastfeeding postpartum women, and to infants and children up to age five who are found to be at nutritional risk.

A

WIC (women infants and children)

*have to choose bf or formula up front and can’t switch

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56
Q

Baby loses ___% of weight and then regains birth weight by day __

A

10%
10

*colostrum is less caloric

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57
Q

baby should have a yellow stool by day ___

A

5

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58
Q

what is the asymmetical latch

A

the babys nose should be pointed right at the nipple
-lower lip covers much more of the nipple and aerolar, babys tongue messages nipple to get milk out

*Nipple should not be latched (should Compress areolar and breast tissue)

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59
Q

___% of women in the United States elect to breastfeed and only about ___% are still breastfeeding at 6 months

A

75%

35%

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60
Q

indications for formula

A
  1. a substitute or supplement for human milk in infants whose mothers choose not to exclusively breastfeed
  2. For infants in whom breastfeeding is contraindicated
  3. As a supplement for breastfed infants whose intake of human milk is inadequate to support appropriate weight gain
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61
Q

Whey in breast milk is primarily ____, in cow’s milk it is ____

A

lactalbumin

lactoglobulin

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62
Q

use thawed room temp breast milk within ___hours

A

4-6 hrs

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63
Q

Use refrigerated breast milk within ___ hours (formula ___hrs).

A

48 hrs

24 hrs

*Do not freeze formula (breast milk can be frozen for 3-6 months)

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64
Q

Normal hematocrit in newborn is __-__%

A

45 - 60%

40-50 in an adult
*Newborns have a higher mean hematocrit than adults

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65
Q

pathology of jaundice

A
  • In utero, baby is relatively hypoxic
  • Hypoxia triggers production of erythropoietin, a hormone which stimulates red blood cell production
  • Jaundice occurs when this relatively large pool of RBCs are broken down, a process that can either be physiologic or pathologic in origin
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66
Q

As extra RBCs are broken down, bilirubin is released

A

physiological jaundice

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67
Q

Step 1:
RBC’s are destroyed in the _____.
-There, hemoglobin is separated into _____ and a ____

A

reticuloendothelial system

globin and a heme pyrrole ring

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68
Q

Step 2:

Heme is converted to ______

A

uncongugated bilirubin

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69
Q

Step 3:

Unconjugated bilirubin is released from the RES into the circulation where it is _____.

A

tightly but reversibly bound to albumin

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70
Q

Step 4:

The bilirubin-albumin complex is carried through the splenic vein to the _____

A

portal vein to the liver.

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71
Q

Step 5:

In the liver, the albumin- bilirubin complex is combined with glucuronic acid to make ______ or _____

A

a bile salt or conjugated bilirubin

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72
Q

Step 6:

Conjugated bili is pumped out of hepatocyte into ____

A

canalicular (bile duct) system

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73
Q

Step 7-10:

A
  1. Leaves liver through common bile duct
  2. Enters Duodenum
  3. Leaves body in
    stool
  4. Or is deconjugated and reabsorbed back into enterohepatic circulation
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74
Q
  • The fat soluble product of hemoglobin metabolism (must be secreted in stool)
  • Binds tightly and readily to albumin in serum; neither is changed by the union
A

Unconjugated bilirubin

*Known as “free bilirubin” regardless of whether it is bound to albumin or not

Unconjugated= indirect/prehepatic

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75
Q
  • Salts of glucuronic or sulfonic acids

- Water soluble

A

Conjugated bilirubin

*(essentially) Conjugated = Direct/post hepatic

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76
Q

Bilirubin is conjugated where

A

the Liver

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77
Q

Incorporated in to bile acids which act as a detergent to help in digestion of fats

A

conjugated bilirubin

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78
Q

In a normal newborn the direct bilirubin should be __ and ___ of the total bilirubin in the serum

A

less than 2mg/dl and less then 10% of the total bilirubin in the serum

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79
Q

Measures all bilirubin fractions in serum

A

total bili

*should be mostly unconjugated bili

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80
Q

measures 90% of conjugated bili.

A

direct bili

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81
Q

how to get value of indirect bili

A
  • Ordering “fractionated” bili will get you total and direct values
  • Indirect is a calculated value: Total – direct = indirect
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82
Q

causes of unconjugated hyperbilirubinemia

A
  • Hemolytic (physiological, pathologic, immune mediated, enzyme defects, pool of blood outside vascular system)
  • Prematurity
  • Associated w/ breastfeeding (breast milk jaundice, b.f jaundice)
  • Defects in Conjugation step (Crigler-Najjar, Gilberts, Asian descent)
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83
Q

-Normal hematocrit of term baby is 45- 60%
-begins to fall after delivery
-Nadir occurs at 2 months, with hematocrit as low as 28-30%
-Large # of RBCs destroyed in the process
-Hemolysis begins in utero, jaundice occurs
during the first 2 hours

A

Physiologic Hemolytic hyperbilirubemia

*peaks at 3-5 days (timing of 1st visit)

**UNCONJUGATED

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84
Q

-Occurs when a maternal antibody crosses
the placenta to attack fetal RBCs
-ABO most common, occurs in 20% of all births
-Begins in utero, therefore jaundice present during first few days of life

A

Pathologic Hemolytic hyperbilirubemia

-usually present 24-48 hrs of life

**UNCONJUGATED

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85
Q

___ antibody in ABO system

  • Works in the same way - if MOC is Rh- then she can make ____ antibodies
  • Rho-gam is ____ given at 28 weeks and after birth
A

D
anti-D antibodies

anti-D IgG

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86
Q

when mom is Rh- and baby is Rh+

A

Rh incompatibility

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87
Q
  • Breakdown of extravascular blood, eg. bruising or cephalohematoma
  • blood trapped between periostium and skull, caused by birth trauma
A

Hemolytic

UNCONJUGATED

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88
Q

Sex-linked disorder of cell membranes which makes them
vulnerable to hemolysis (More severe in males, Variable presentation in females)
-Usually occurs upon exposure to oxidants, especially medications or infections
-Protective against malaria
-Occurs in Mediterranean region, China, Africa
-Occurs in 10% of African Americans

A

Hemolytic: G-6PD Deficiency

*unconjugated

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89
Q

___% of premature infants become jaundiced

A

80%

*Premature infants conjugate more slowly bc their livers don’t fxn as well

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90
Q
  • Higher risk for BIND (bilirubin induced neurologic dysfunction) at lower levels of bilirubin.
  • Leaky blood-brain barriers
A

prematurity jaundice

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91
Q
  • Caused by inadequate oral intake
  • ncreases enterohepatic circulation
  • Essentially, dehydration
  • Occurs on days 2 to 5
  • baby’s hydration is the urgent problem
A

Breastfeeding jaundice

  • UNCONJUGATED
  • consider supplementation with pumped milk formula
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92
Q
  • Begins day 4
  • Can peak weeks 2 to 4
  • Persists up to 3 months
A

breastmilk jaundice

  • UNCONJUGATED
  • Totally benign– don’t interrupt nursing (Etiology unclear)
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93
Q
  • Defect in glucuronyl transferase (enzyme important in creating bile salts)
  • Typically, mild jaundice after puberty
  • Possibly related to breastmilk jaundice
  • Possibly related to increased jaundice in certain ethnic groups
  • Autosomal dominant
A

Gilbert’s

*UNCONJUGATED

**turns yellow when get stressed

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94
Q

Severe, often lethal form of hyperbili.

  • Clinically looks like kernicterus
  • Autosomal recessive
  • Occurs in one in one million live births
  • Virtual absence of glucuronyl transferase enzyme
  • Two Types (I, II)
A

Crigler-Najjar Syndrome

**UNCONJUGATED

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95
Q

requires lifelong PTX to avoid BIND and liver transplantation

A

Type I Crigler-Najjar Syndrome

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96
Q

treatable with Phenobarbital

A

Type II Crigler-Najjar Syndrome

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97
Q

Causes of Conjugated Hyperbilirubinemia

A

Hepatitis
Inborn Errors of Metabolism
Biliary atresia

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98
Q
  • Agents have a predilection for cannicular cells (cells of the ductal system)
  • Majority are “idiopathic”, self-limited without permanent damage
A

Infectious hepatitis
(Various infectious etiologies: Hep B, Rubella, CMV, Toxoplasmosis)

*CONJUGATEd

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99
Q
  • Inborn error of galactose metabolism caused by congenital enzyme deficiency
  • FTT,hepatosplenomegaly/cirrhosis, MR, cataracts
A

Galactosemia

  • CONJUGATED
  • Clinically, disease looks like hepatitis
100
Q

____ jaundice implies that conjugated bilirubin flow is obstructed

A

Cholestatic

101
Q

-Presents weeks 2 to 8 after birth
- Light stools***, dark urine, jaundice, weight loss and
irritability are hallmarks
-congenital absence of all or part of the biliary tree (ducts that drain bile from liver)

A

Biliary Atresia

  • *WORRY ABOUT THIS MOST
  • etiology is uncertained, may be viral

*CONJUGATED

102
Q

treatment of biliary atresia

A
  • Initially treated with Kasai procedure– intestine attached to liver
  • Ultimately need liver transplant
103
Q

History and physical questions to ask surrounding jaundice

A
  • Know MOC’s blood type and Rh
  • Any family history of hemolytic disease?
  • Any maternal history of infections during pregnancy? Hepatitis B status?
  • Prematurity?
  • Medications?
  • Baby’s diet history and stooling patterns
  • Physical findings consistent with intrauterine infections?
  • Hepato- or splenomegaly?
  • Hydration status
104
Q

Generally, in the first week of life, if there is no cause to suspect hepatitis, obtain a __

A

transcutaneous bilirubin level

*ALL babys are screened at 24 hrs of life

105
Q

indications for a bilirubin level

A
  1. baby appears jaundiced
  2. compelling risk factors for hyperbilirubinemia (ABO or rh “set-up;” ie. Risk for immune-mediated hemolysis, Family history to suggest genetic causes, History of, or signs which suggest viral infection, Prematurity, Asian)
106
Q

pros and cons of transcutaneous bilirubin monitoring

A

Pros:
inexpensive
good screening tool

cons:
require developing own guidelines

107
Q

In general–if the Tcb is in the __ we will draw a serum bilirubin

A

HIRZ (high intermediate risk zone)

*allow higher levels overtime

108
Q 
Interpreting Serum Values:
high risk zone:
high intermediate:
low intermediate:
low risk:
A

High risk zone: begin phototherapy
High intermediate: recheck 6-12 hrs +/- phototherapy
Low intermediate: recheck based on clinical progress
Low risk: no need to follow up

*get serum values for high and high-intermediate

109
Q

phototherapy: Blue light with wavelengths between 440 and 470 causes the outer ring of bilirubin to be turned 180 degrees.

how does this treatment help?

A

In this form it is less tightly bound to albumin, is more water soluble and can be eliminated from the body via the kidneys without conjugation

110
Q

Phototherapy is only effective in ____

A

unconjugated hyperbilirubinemia

*Use of PTX in conjugated hyperbili results in “bronze baby”, an unappealing discoloration of skin

111
Q
  • ________ is used to describe acute manifestations of BIND

- _____is used to describe chronic and permanent sequelae of BIND

A

Acute bilirubin encephalopathy or ABE

Kernicterus

112
Q
  • Form of brain damage associated with greatly elevated unconjugated bili
  • abnormalities of tone, high pitched cry, arching of back
A

Kernicterus

113
Q

Pathology: Bilirubin staining of basal ganglia and hippocampus
-Had occurred in babes with erythroblastosis fetalis and has become rare since the advent of rho-gam

A

Kernicterus

114
Q

protects skin from utero environment

helps baby regulate its temp and keep skin soft

A

vernix

115
Q

when normal: non-blanching lesions secondary to birth trauma or vigorous resuscitation

-bluebery muffin appearance

A

Petechiae

*When to be concerned
Mom has a hx of low platelets or infection risk


116
Q

downy hair present to varying degrees at birth



A

lanugo

*gets rubbed off in first 2-3 week of life

117
Q
  • Lace-like pattern of dusky erythema over trunk and extremities.
  • Normal in newborns who are cold - disappears on re-warming.
  • Can be a sign of poor perfusion in illness - look for other physical exam finding.
A

Mottling (cutis marmora

118
Q
  • Rare congenital vascular malformation.
  • Usually presents on one limb**
  • Associated with underlying muscular defects (50%).
  • Usually resolve with time - but should be followed for the risk of ulceration**
A

Cutis marmorata telangiectatica congenita (CMTC)

119
Q

Transient skin lesions

A

-Erythema Toxicum
-Milia
-Sebaceous Gland Hyperplasia
-Pustular Melanosis
-Normal Peeling
-Sucking Blisters


120
Q
  • White to yellow papule on a blotchy erythematous base.
  • Usually start on DOL 1 or 2.
  • Contain eosinophils - but etiology poorly understood.
  • Come and go over first 10 days of life.
  • Located everywhere except palms and soles.
  • Worse in areas of high friction and heat (such as back)
A

Erythema Toxicum

121
Q
  • Keratin filled epithelial cysts

- Often mistaken for neonatal acne which does not appear until 2 weeks of life

A

Milia

122
Q
  • More yellow than milia.
  • Caused by maternal androgen exposure.
  • Also spontaneously resolve
A

Sebaceous Gland Hyperplasia

123
Q
  • Fragile pustular rash that begins in-utero.
  • When pustules break they leave behind a white collarette with a central hyper-pigmented macule.
  • No inflammatory component.
  • Pustules usually removed during resuscitation or bath
A

Transient pustular melanosis

124
Q

do not use lotion for the first ____ of life because it will get into the blood stream

A

3 months

125
Q

immature thalmus

cause 1 side of body to be red

A

Harlequin Phenomenon

126
Q

____ represent an area of excess of one or more of the normal components of skin per unit areas.

Blood vessels, pigment cells, sebaceous glands, epidermis…

A

Birthmarks

127
Q

____ are blue-black macules commonly located over lumbosacral area

-Important to clearly record location of macules as they are easily confused for bruising.

A

Mongolian Spots

-Fade during first or second year of life. Most have disappeared by age 6-10.

128
Q

Light brown oval macules.
Single lesions occur.
Multiple lesions associated with neurofribromatosis.
Measure size and draw location.

A

Cafe Au Lait Spots

129
Q

Occurance: 99% present at birth- clinically subtle
Location: common on limbs, anywhere
Appearance: poorly circumscribed
Course: no change in size, grows with child, no involution
Vessel Type: predominately venous and capillary

A

Malformations

congenital vascular lesion

130
Q 
Occurance: 40% present at birth
Location: 40% present at birth
Appearance: well delineated
Course: rapid neonatal growth with slow involution
Vessel Type: predominately arterial
A

Hemangiomas

congenital vascular lesion

131
Q

Benign neoplasm resulting from rapid proliferation of endothelial cells.
Superficial (strawberry), deep or mixed.
Proliferate for 8-18 months then regress

A

hemangiomas

Regress by rule of 10:
50% gone by age 5, 90% gone by age 9 (10% per year).

132
Q

Indications for treatment of hemangiomas

A
  • Obstructed vision.
  • High-output heart failure.
  • Hemangiomas in diaper area because tend to ulcerate.
  • Facial lesions because they can disfigure even after they regress

**treatment is painful and not that helpfu

133
Q

Vascular Malformations

A
  • Nevus simplex (salmon patch or macular stain)
  • Port Wine statins
  • Cutis Marmorata
134
Q

Light red blanching macule on nape of neck (stork bite) or glabella/eyelids (angel kiss).
-Fade with time but always present - more pronounced when flushed

A

Nevus simplex

135
Q

-Flat dark pink to red macule found on face or limbs.
-Typically do not cross midline.
On face and involving an eye, may be associated with Sturge-Weber syndrome
-On legs can be associated with Klippel-Trenaunay-Weber syndrome

A

Port wine stain or Nevus Flameus (capillary)

136
Q

Hemangioma of face and meninges.

Associated with seizures

A

Sturge-Weber syndrome

137
Q

Port wine stain or Nevus Flameus on the legs
Associated with hemihypertrophy

*It is characterized by a triad of port wine stain, varicose veins and bony and soft tissue hypertrophy involving an extremity

A

Klippel-Trenaunay-Weber syndrome

138
Q

Light red blanching macule on nape of neck

A

stork bite

*nevus simplex

139
Q

Light red blanching macule on glabella/eyelids

A

angel kiss

*nevus simplex

140
Q

_____ must be considered if vesiculobullous or pustular lesions are found in a newborn

A

Infection

141
Q

viral infectious lesions and bacterial infectious lesions

A

Viral: Herpes Simplex, CMV, varicella zoster

Bacterial: Staphylococcus, bullous impetigo

142
Q
  • Slightly raised oval or linear area, yellow or orange.
  • Common on scalp, associated with alopecia.
  • Consist of hypertrophy of sebaceous glands (glands which produce acne later).
  • Malignant potential later in life - consider removal (basal cell carcinoma).
A

Sebaceious Gland Nevi

143
Q
  • Hamartomas arising from the embryonic ectoderm.
  • May be deeply or slightly pigmented.
  • Have either a unilateral or bilateral distribution, and often favor the extremities in what appears to be a dermatomal distribution.
  • Onset is usually at birth but may also occur in the second or third decade.
A

Epidermal Nevi

144
Q

Special Qualities of Newborn Skin

A

Thinner

Large Surface area-to-body ratio

145
Q

bathing a newborn

A
  • Sponge baths until cord separates.
  • Then bathe in water without soaps or bubbles no more than a couple times a week. Use soap only if baby very dirty or smelly.
  • Regular neck/skin fold cleanings with a burp cloth enough to keep an infant clean.
  • Water temp
146
Q

water temp when bathing a newborn

A

less than 120 degrees F

147
Q

how to prevent diaper rash

A
  • Change diaper with every feed.
  • Use mild wipes - without additives. (water and washcloth best!)
  • Allow area to fully dry before putting on new diaper.
  • Apply a thick layer of protective ointment or cream (such as one that contains zinc oxide or petroleum jelly)
148
Q

diaper rash
Has satellite lesions.
Most prominent in skin folds.

A

Candidal diaper rash

*caused by Candida albicans

149
Q

treatment of Candidal diaper rash

A

topical antifungal cream, eg, mycostatin

150
Q

Caused by chemical irritant.
20% of babies will develop by 2 yrs.
Most pronounced on convex areas, spares skin folds.

A

contact diaper rash

*tx by:
remove irritant, air dry, use petroleum barrier.

151
Q

Why not use cow’s milk?

A
  • Infants fed cow’s milk develop anemia
  • Higher concentrations of protein, sodium, potassium and chloride
  • Inadequate essential fatty acids, Vit E and zinc
152
Q

Powdered: one scoop of powder to___ oz of water = ___ cal/oz

A

2

20 cal/oz

153
Q

Formula should be fed ____

A

ad libitum, on demand

154
Q

Guidelines for intake:
Usually, for the first day, they will take __ml every 3 hrs

Rapidly increase to about __oz by day 3

Usual intake will be __ml/kg/day for first 3 months

A

Usually, for the first day, they will take 10-15ml Q 3 hours

Rapidly increase to about 1-1.5 oz Q 3-4 hours by 3 days

Usual intake will be 140-200 ml/kg/day for first 3 months

155
Q

For growth, baby needs a minimum of ____ cal/kg/day to thrive and grow
*Standard formula is 20cal/oz

A

100cal/kg/day

156
Q 
Goals for Growth:
Surpass birth weight by \_\_\_ 
0-3 months gain \_\_\_\_
3-6 months gain \_\_\_\_
6-12 months gain
A

Surpass birth weight by 2 weeks.
0-3 months gain 15-30 grams/day
3-6 months gain 15-20 grams/day
6-12 months gain 10-15 grams/day

157
Q

Vomiting or spitting up is common and does not require formula change unless:

A
  • there is inadequate growth
  • Due to weak sphincters

*Only change formula if blood in stool, weight loss, projective vomiting, extensive rash

158
Q

Stools tend to be ____ in color, occur ____ daily

A

pasty and brown

one to twice/day

159
Q

Constipation with slow weight gain may indicate _____

A

inadequate calories (volume or concentration – check history)

*constipation with good wt gain is common with formula!

160
Q

Begin complementary solids at ___

A

4-6 months

161
Q

____ formulas should be given to infants who have had a severe gastrointestinal reaction (abdominal pain with bloody diarrhea) to cow’s milk, since anywhere from 30% to 64% of babies will also have a similar reaction to soy

A

Hypoallergenic

162
Q

According to the AAP, the only formula-bed babies who should get soy formula are those with:

A
  • Parents who are strict vegans
  • A true diagnosis of lactose intolerance, which is actually rare in babies but more common among older kids and adults.
  • Congenital galactosemia (in which babies lack the enzyme that converts galactose, one of two sugars found in lactose, into glucose, a sugar the body is able to use).
163
Q

is the inability to digest the sugar lactose, found in cow’s milk and cow’s milk infant formulas

A

Lactose intolerance

*not the same as a “milk allergy”

milk allergy kid will not tolerate soy either

164
Q

If these children consume breast milk, cow’s milk, or other dairy products, galactose can build up in the system and damage the body’s cells and organs, leading to blindness, severe mental retardation, growth deficiency, and even death.)

A

Congenital galactosemia

165
Q

inflammation of mucosa resulting in GI discomfort and blood in stool

A

colitis

166
Q

it’s more common among infants (about 2% to 3% of babies), though most outgrow it. (80% by 4)

  • Diarrhea, vomiting, failure to thrive, colitis, eczema and respiratory symptoms
  • IgE mediated
A

milk allergy

*Skin prick test not accurate until 12 months.

167
Q

______ formulas have cow’s milk proteins that are broken down into small particles so they’re less allergenic than the whole proteins in regular formulas

A

Extensively hydrolyzed formulas

*Most infants who have a milk allergy can tolerate these formulas, but in some cases, they still provoke allergic reactions

168
Q

____ formulas, which contain protein in its simplest form (amino acids are the building blocks of proteins).

A

Amino acid-based infant formulas

169
Q

______ formulas also are on the market, but aren’t considered truly hypoallergenic and can still provoke a significant allergic reaction.

  • Use corn sugars rather than lactose sugars and partially digested proteins
  • **Marketed to treat colic
A

“Partially hydrolyzed” formulas

170
Q

The final common pathway of all of the pathology in this system is the ____ of passage of material along the tract because of:

A

obstruction

  1. atresia
  2. stenosis
  3. blockage
  4. dysmotility
171
Q

non-formation resulting in discontinuous lumen and complete obstruction

A

atresia

172
Q

contents of lumen harden to cause obstruction or external compression of tract occurs

A

blockage

173
Q

formation with restriction; i.e., limitation of diameter of lumen with partial obstruction

A

stenosis

174
Q

peristalsis, the rhythmic contraction of tract is abnormal leading to functional obstruction

A

dysmotility

175
Q

sx:
Presents with vomiting
Belly will be flat or scaphoid (concave

A

upper GI tract problem

  • From mouth to end of duodenum
  • Closer to mouth, sooner the emesis
176
Q

sx:
Presents with decreased or no stooling.
Belly will be distended

A

lower GI tract problem

*duodenum to anus

177
Q

“Air-fluid levels” reflect

A

decrease in peristalsis

178
Q

Radiology studies used to define location of a problem

A
  1. xray
  2. us
  3. contrast studies

*Air is present in the stomach immediately after birth.
By 24 hours of life air should appear in the rectum

179
Q

decreased swallowing, decreased GI motility, vomiting or gastric decompression

A

gassless abdomen

*Note: Resuscitation may increase the amount of bowel gas seen on x-ray

180
Q

perforation: contents of the bowl have gotten outside the bowel causing peritonitis –> pain w/ movement
get abdominal distension
abdominal tenderness
tympanic

A

acute abdomen

181
Q

Immediate interventions for GI problems

A
  1. Make baby N.P.O. – nothing by mouth until you have identified problem and have decided upon intervention
  2. Place nasogastric/oralgastric tube to decompress stomach of air and stomach contents
  3. Start I.V. to provide fluid maintenance
  4. Call surgeons
182
Q

The gastroesophageal sphincter in a newborn is present but does not have sufficient tone to prevent emesis. What goes down, easily returns.

A

wet burp or

the clincally significant version is known as gastroesophageal reflux

183
Q

Normal newborns all spit up for a variety of reasons:

A

“wet burp”, swallowed materials, overfeeding, stooling.

184
Q

sx:
-When mild, nuisance
-Pain of esophagitis
-Poor growth because of inadequate intake**
(Losing too much of feed, Refusal to eat b/o pain)
-Risk of aspiration and pneumonia

-commonly arch their back

A

Gastroesophageal reflux

GERD

185
Q

management for GERD

A
  • Feed small amounts frequently
  • Positioning during and after feeding (keep head above stomach)
  • Medications to prevent pain- H2 Blockers, PPIs
  • Motility agents (ex. Reglan)
  • Surgery
186
Q

In severe cases of gastroesphageal reflux, ______ may be warranted

A

fundoplication with gastrostomy feedings

187
Q

take fundus of the stomach and create an new sphincter

A

fundoplication

188
Q

Esophagus is discontinuous and there is communication between GI and respirtory tracts.

*most common malformation of the esophagus

A

esophageal atresia

189
Q

sx:

  • Drooling
  • Immediate vomiting after eating
  • Coughing
  • Abdomen may be distended or scaphoid
A

esophageal atresia

*usually present in the first few hours of life

190
Q

Occurs with tracheoesophageal fistula (TEF) in 85-90% of cases

_____ most common presentation

A

Proximal EA with distal TEF

191
Q

Malformation: Disordered elongation / separation of esophagus from trachea

  • 30-40% have associated anomalies (especially VACTERL)
  • May have history of polyhydramnios
A

esophageal atresia

192
Q

type of EA:
atresia only, 5-10%
belly will be concave

A

Type I

193
Q

type of EA:

  • Fistula only
  • presents later because esophagus is still intact, 5%
  • chronic cough, poor growing, repeated pneumonia
  • normal belly
A

Type II (H type)

194
Q

type of EA:
-Atresia plus lower fistula
belly is distended: fill up with air w/ each breath
85-95%

A

Type III B

195
Q

Type of EA:
rare
Atresia + upper fistula

A

Type III A

196
Q

type of EA:
rare
atresia + double fistula

A

Type III C

197
Q

Evaluation of Suspected Esophageal Atresia

A

Attempt to pass catheter from mouth to stomach

198
Q

xray:

Shows catheter in proximal esophagus with no air in stomach

A

EA

indicating no connection between distal esophagus and trachea

199
Q

VACTERL Association features:

A 
Vertebral anomalies	
Imperforate Anus
Cardiac defects (PDA,ASD,VSD)
Tracheoesophageal fistula
Renal anomalies
Limb anomalies (most often of radius)

*Present in 25- 30% of children with EA/TEF

200
Q 
sx:
Vomits a few minutes after each feeding
Seems hungry
Gets worse as days pass
Often presents with dehydration
Normal stool
No fever
No ill contacts 
-Increasing non-bilious emesis, after day 4, average 3 weeks
A

Pyloric Stenosis

*children 2 days to 2 months

201
Q

pyloric stenosis can result in ____

PE may show palpable firm mass in ____

A

Hypertrophy of muscular layer of pyloric channel

*PE may show palpable firm mass RUQ
“olive”

202
Q

treatment of pyloric stenosis

A

Very minor surgery

“Pyloromyotomy”- consists of incising the hypertrophic muscle from the outside to essentially loosen it up

203
Q

Bilious vomiting implies ___

A

obstruction distal to the ampulla

*Usual spitting up or feeding intolerance is not bilious; therefore, consider pathologic until proven otherwise

204
Q

sx:

  • vomiting (Vomiting begins soon after birth)
  • Abdominal distention may be present soon after birth, peaks at 24 to 48 hrs.
  • May pass meconium
A

Duodenal Obstruction

205
Q

Malformation:

Caused by incomplete re-canalization of gut during 8th to 10th week of fetal life

A

Duodenal Obstruction

206
Q

Less common

Caused by extrinsic compression of duodenum by a pancreas which encircles it

A

annular pancreas

207
Q

prenatal clues to duodenal obstruction

A
  1. polyhydramnios
  2. SGA
  3. Preterm (secondary to stress)
  4. Prenatal US (20 weeks) shows “double bubble”
208
Q

30% of babes with duodenal obstruction have ______, many have other anomalies as well

A

Down syndrome

*DS baby vomitting think duodenal obstruction

209
Q

If distal gas present, on abdominal film

A

duodenal stenosis rather than atresia

210
Q

50% of all atresias occur in ___-

A

jejunum or ileum

211
Q

midgut obstructions

A

atresia
stenosis
Malrotation/midgut volvulus

212
Q

Mesenteric attachments are posterior only
Midgut is free to move
Duodenum and proximal colon are fixed

A

Malrotation/midgut volvulus

213
Q 
Abnormal rotation (in \_\_\_\_\_\_ fashion) results in abnormal position, known as malrotation – as such, does not cause obstruction  BUT
May twist in either direction, causing a \_\_\_
A

clock-wise fashion

volvulus

214
Q

In addition to obstruction, malroatation with volvulus causes compromise of vascular system, resulting in:

A

resulting in necrosis, peritonitis, sepsis and shock

*THIS IS A SURGICAL EMERGENCY

215
Q

sx:

  • Apparently well child who presents with sudden onset of bilious vomiting
  • Initially intermittent
  • Abdominal distention (tenderness common)
  • Vascular compromise leads to acute abdomen – peritonitis, sepsis, shock, metabolic acidosis
A

Malrotation with Midgut Volvulus

*May occur at any time postnatally but 80% occur in neonatal period (first month)

216
Q

Clue to:

Associated with abdominal wall defects, intestinal atresias, congenital heart defect, situs inversus

A

Clue to presence of malrotation

217
Q

Abdominal X-ray shows dilated bowel with air fluid levels

A

Malrotation with Midgut Volvulus

218
Q

Upper GI shows abnormal ligament of Treitz

Barium enema show abnormal cecum position

A

Malrotation with Midgut Volvulus

219
Q

All bilious vomiting in the newborn is_____ until proven otherwise!

A

Volvulus

**this is a surgical emergency

220
Q

“Ladd Procedure” done to divide the peritoneal bands, unwind twisted portion and tack down the bowel to prevent it from happening again

A

tx in Malrotation with Midgut Volvulus

*done prior to volvulus is possible

221
Q

Large amount of intestinal loss results in _____

A

short bowel syndrome or death

*have removed a lot of internal surface area= poor absorption = failure to thrive

222
Q

distal bowel obstruction dx

A

meconium ileus
Hirschprung’s disease
Anal atresia

223
Q

sx:

A term newborn eats well for the first day, but then develops abdominal distention.

A

Typical presentation of lower tract obstruction

224
Q

presents with:

  • passage of little or no meconium in the newborn period
  • Abdominal distension
  • Air-fluid levels seen on x-ray, indicating decrease in peristalsis
A

lower tract obstruction

225
Q

sx:

  • Abdominal distention at or after birth
  • Viscous, inspissated meconium obstructs the mid-ileum
  • Simple obstruction (2/3) or complicated by volvulus, atresias, perforation, peritonitis
A

Meconium Ileus

*Associated with Cystic Fibrosis

226
Q

Diagnosis and treatment of Meconium Ileus by

A

gastrograffin enema

227
Q

Untreated, meconium ileus can cause ____

A

rupture of bowel, spilling intestinal contents into peritoneal space

*This results in peritonitis, infection of that space.

228
Q 
Presents as an acute abdomen: 
Rigidity
Tenderness
Fever
Shock
Death if untreated
A

Meconium Ileus with Perforation

229
Q

sx:

  • Constipation, delayed stooling, meconium plug
  • Abdominal distention
  • Congenital but rarely diagnosed in neonatal period- diagnosed by 4 months
  • Extreme cases: “Toxic megacolon”
A

Hirschprung’s Disease

  • 75- 80% male
  • Accounts for 25% of all congenital GI obstruct
230
Q

he appears constipated and strains excessively before passing stool. He has a stool only every 3-4 days. He sometimes vomits after meals. On exam his abdomen is mildly distended. He was noted to pass a hard rubbery plug of meconium with his first stool at 2 days of life.

A

Hirschprung’s Disease

*abnormal to have 1st stool on 2nd day of life

231
Q
  • Congenital absence of nervous plexuses of the colon
  • Always involves anus along with proximal segment of variable length
  • Peristalsis is abnormal in affected segment (skinny), causes functional obstruction with dilated bowel proximally
A

Hirschprung’s Disease

232
Q

The nervous plexus is missing in the ____, not permitting it to relax.

A

small section

233
Q
  • Abdominal films may show lack of gas in rectum

- Barium enema shows “transition zone”

A

Hirschprung’s Disease

234
Q
  • Suction rectal biopsy shows lack of ganglion cells

- Full thickness biopsies occasionally needed

A

Hirschprung’s Disease

235
Q

treatment of HD

A

NG decompression, IV fluids, antibiotics

236
Q

____ to promote stooling in HD

A

Initial enemas

237
Q

Laparoscopic or open “pull-through” of colon containing _____

A

ganglion cells to the anal verge

238
Q

sx:

  • PE shows no / abnormal anus
  • 75% have fistula to urethra, vagina, or perineum and may pass meconium
  • Associated with VACTERL, chromosomal, cardiac, and CNS anomalies
A

imperforate anus

239
Q

treatment of imperforated anus

A

surgially

longterm outcome good

240
Q

Although the causes of intestinal obstruction are______ rather than _____, it is often wise to begin antibiotics prophylactically

A

mechanical

infectious

241
Q

types of vental wall defects

A

Gastroschisis

Omphalocele

242
Q

sx:

  • Intestine present outside abdominal wall
  • Risks include motility problems, fluid loss, infection
  • Present at birth
A

ventral wall defects

243
Q

Immediate response for ventral wall defects

A
  1. Cover with saran wrap to prevent fluid losses
  2. NPO
  3. Start I.V.
  4. Start antibiotics
  5. Surgical intervention
244
Q
  • Malformation*
  • Failure of intestine to fully return to abdomen during fetal life
  • *Always associated with malrotation
A

omphalocele ventral wall defect

245
Q
  • Disruption**
  • Caused by vascular accident during fetal life
  • Dysmotility because has a thick peel on surface as result of contact with amniotic fluid
A

Gastroschisis ventral wall defect

246
Q

What is the conjunction step in the conjugation of bilirubin and where does it occur?

A
  • addition of glucuronic acid and requires glucuronyl transferase
  • occurs in the liver

Neonate (4 decks)

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