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Peds Patho Exam 3 > Neonatal > Flashcards

Neonatal Flashcards

1
Q

Lung Development: weeks 4-16 (5)

A
  1. 4-8: embryonic
  2. 5-16: pseudoglandular
  3. formation of major airways
  4. formation of bronachial tree and portions of respiratory parenchyma
  5. birth of acinus
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2
Q

Lung Development: weeks 16-24 (4)

A
  1. canalicular
  2. last generation of lung periphery is formed
  3. epithelial differentiation
  4. air-blood barrier formed
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3
Q

Lung development: weeks 24-36 (3)

A
  1. saccular
  2. expansion of air spaces
  3. surfactant detectable in amniotic fluid
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4
Q

Surfactant (3)

A
  1. Lines alveoli on top of the water layer, lowering the surface tension and allowing alveoli to expand
  2. Insufficient surfactant: collapsed alveolus and inadequate oxygen exchange
  3. Sufficient surfactant: expanded alveolus and adequate oxygen exchange
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5
Q

Bronchopulmonary dysplasia (BPD) definition

A

Persistent oxygen dependency up to 28 days of life

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6
Q

Classic BPD (3)

A

Is a neonatal form of chronic pulmonary disorder that follows primary course of respiratory failure in the first few days of life (IATROGENIC)

  1. Premature infants and had ineffective surfactant and required intervention from us (mechanical ventilation and oxygen)
  2. Forcing in pressure to keep alveoli open → in interim putting in a lot of pressure that caused damage to lung tissue
  3. Cytokines got involved and there was a lot of inflammation and they developed scaring and areas in lung tissue of atelectasis and over inflammation
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7
Q

New BPD (3)

A
  1. In extremely low birthweight infants
  2. Little initial ventilatory support or oxygen need
  3. Potential Intrauterine exposures
    * Preventing BPD is still a challenge
    * There is some intrauterine exposure that leads to alveolar hyperplasia
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8
Q

BPD Severity (5)

A
  1. Mild BPD- weaned from any supplemental oxygen (at 36 weeks)
  2. Moderate BPD- continue to need up to 30% oxygen
  3. Severe BPD- requirements exceed 30% and/or include continuous positive airway pressure or mechanical ventilation
  4. The severity of BPD-related pulmonary dysfunction is early childhood is more accurately predicted by an oxygen dependence at 36 weeks in infants < 32 weeks gestational age
  5. Classified according to the type of respiratory support required to maintain a normal arterial oxygen saturation (89%)
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9
Q

BPD Incidence (3)

A
  1. The most influence important of which is lung maturity
  2. BPD increases with decreasing birthweight/gestational age
  3. Affects ~30% of infants with birthweight < 1000 grams
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10
Q

BPD Pathophysiology (5)

A

A primary lung injury is not always evident at birth

  1. Transition period, not enough surfactant require oxygen
  2. Intervene at this time so they don’t get tired, maintain at steady level in terms of respiratory status and perfusion
    * For their gut and brain; protective mechanism
  3. Secondary development of persistent lung injury is associated with an abnormal repair process and leads to structural changes leads to……..
  4. Arrested alveolarization → no longer recruit like they should leads to….
  5. Pulmonary vascular dysgenesis
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11
Q

BPD and Inflammation (2)

A
  1. Central to the development of BPD. An exaggerated inflammatory response – alveolar influx of numerous pro-inflammatory cytokines as well as macrophages and leukocytes occurs in the first few days of life in those infants in whom BPD subsequently develops.
  2. Exaggerated inflammatory process, intervene and develop tissue damage and sets off cascade of inflammatory response
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12
Q

BPD and Mechanical Ventilation

A

Volutrauma/barotrauma is one of the key risk factors for the development of BPD.
Minimizing the use of conventional mechanical ventilation (CMV) by the use of early NCPAP, noninvasive ventilatory support and early use of methylxanthines (caffeine) ~ fewer days of CMV and lesser use of postnatal steroids

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13
Q

BPD and Oxygen Exposure (4)

A
  1. Classic BPD- before the age of exogenous surfactant was always associated with prolonged exposure to oxygen (Fio2 >60%).
  2. Hyperoxia can have major effects on lung tissue – proliferation of alveolar type II cells and fibroblasts, alterations in the surfactant system, increased inflammatory cells and cytokines, and decreased alveolarization.
  3. Today – exposure to prolonged high oxygen is limited ~ a New BPD (NBPD) is observed
  4. NBPD- association with oxygen and persistent CMV in the first 2 weeks is not a dominant factor. Changing goals of Spo2 in the 85-93% range rather than > 95% has led to decrease in need for supplemental oxygen at 36 weeks.
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14
Q

BPD Pathogenesis and Risk Factors (8)

A
  1. Prematurity: Lung is most susceptible to damage in saccular stage of development (23-32 wks GA).
  2. Fetal growth restriction: Increases vulnerability of lungs.
  3. Mechanical ventilation: Large tidal volumes over-distend airways and airspaces.
  4. Oxygen toxicity: High concentrations of inspired O2 cause overproduction of cytotoxic reactive O2 metabolites.
  5. Infection (postnatal): Sepsis increases risk of BPD.
  6. Genetics: Underlying factors still not known.
  7. Late surfactant deficiency: Transient surfactant dysfunction or deficiency increases risk of BPD.
  8. Patent ductus arteriosus: Seems to increase risk, but not a direct correlation because closing ductus does not decrease risk of BPD.
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15
Q

BPD Major Risk Factors (5)

A
  1. Prematurity
  2. White race
  3. Male sex
  4. Ureaplasma – tracheal colonization
  5. Increased survival rates of the ELBW infant
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16
Q

BPD Other Risk Factors (5)

A
  1. RDS
  2. Sepsis
  3. Oxygen therapy
  4. Vitamin A deficiency
    * Plays a role in tissue healing and these babies lack vitamin A
    * Do not supplement but something to look at for future
  5. Symptomatic PDA
    * Flooding lungs, tissue damage
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17
Q

BPD Labs (5)

A
  1. Used to rule out differential diagnosis – sepsis, PDA
  2. Arterial blood gas levels (reveal carbon dioxide retention)
  3. Electrolytes (elevated serum bicarbonate, hyponatremia, hypokalemia, elevated urea nitrogen and creatinine)
  4. CBC (neutropenia or elevated WBC – sepsis)
  5. Urinalysis (elevated RBCs – nephrocalcinosis – prolonged diuretics)
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18
Q

BPD Imaging

A

Chest radiograph- Most frequently appears as diffuse haziness and lung hyperinflation. Streaky interstitial markings, patchy atelectasis intermingled with cystic areas and overall hyperinflation.

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19
Q

Necrotizing Enterocolitis Definition

A

Ischemic and inflammatory necrosis of the bowel primarily affecting neonates after the initiation of enteral feeding

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20
Q

NEC Incidence (3)

A
  1. NEC is predominately a disorder of preterm infants 6-10% weighing <1500 grams
  2. Highest incidence in the most premature infants
  3. Can also occur in term infants, may have a preexisting medical condition
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21
Q

NEC Patho (4)

A
  1. Initiate mucosal damage via a final common pathway involving activation of an inflammatory cascade
  2. Mucosal damage results in invasion of the bowel walls by gas producing bacteria à resulting in gas accumulation (pneumatosis intestinalis) seen on X-ray
  3. Sequence of events may progress to transmural necrosis or gangrene of the bowel wall à perforation and peritonitis.
  4. This is really a multifactorial theory. Several risk factors including prematurity, formula feeding, ischemia, and bacterial colonization interact.
22
Q

NEC Risk Factors (8)

A

a. Prematurity
b. Microbial colonization
c. Enteral feedings
d. Circulatory instability
e. Maternal cigarette smoking
f. CHD
g. Polycythemia
h. Blood transfusion

23
Q

NEC Clinical Presentations (7)

A
  1. Term infants usually have an underlying illness predisposing them to NEC and diagnosed in 1st week of life
  2. Premature infants – most between 14 – 20 days of age or 30-32 weeks postmenstrual age.
  3. Early clinical presentation may include feeding intolerance, increased gastric residuals, bloody stools.
  4. Specific Abdominal signs - Abdominal distention, tenderness, abdominal skin discoloration, emesis, bilious drainage from NGT
  5. Nonspecific signs – signs of sepsis (apnea, bradycardia, temperature instability, hyper or hypoglycemia, hypotension)
  6. Clinical course is variable – 30% mild presentation that responds to medical treatment
  7. ~7% have fulminant course with rapid progression to septic shock –> metabolic acidosis –> death.
24
Q

NEC Diagnosis (3)

A
  1. NEC is a tentative diagnosis in any infant presenting with the triad of feeding intolerance, abdominal distention, and grossly bloody stools
    * CLASSIC TRIAD*
    * Don’t always have to have grossly bloody stools
  2. Be Aware – the earliest signs may be identical to those of neonatal sepsis
  3. Labs – CBC, CRP, Blood culture, Stool culture, Electrolyte panel
25
Q

NEC Imaging: Flat Plate (2)

A
  1. Supportive findings – abnormal gas pattern, ileus, fixed loop, area suspicious for pneumatosis
  2. Confirmatory findings – Pneumatosis intestinalis, intrehepatic portal venous gas
26
Q

NEC Imaging: lateral decubitus (2)

A
  1. Presence of free air is indicative of intestinal perforation. Serial films every 6-8 hours for those at risk of perforation
  2. Left side down – right side up —- air will rise above the liver if perforation
27
Q

Normal Eye Development (4)

A
  1. Eye first noticeable ~ 22 days
  2. Optic grooves developing neural tube
  3. By the end of the 6th week eyes are formed
  4. Lids are fused shut until ~26 weeks gestation
28
Q

Retinopathy Definitions (5)

A
  1. A disorder of the developing retinal vasculature resulting from interruption of the normal progression of newly forming retinal vessels.
  2. Vasoconstriction and obliteration of the advancing capillary bed are followed in succession by neovascularization extending into the vitreous, retinal edema, retinal hemorrhages, fibrosis and eventual detachment of the retina
  3. In most the process is reversed before fibrosis occurs
  4. Advance stages may lead to blindness
  5. Occurs chiefly in premature infants, so it is called retinopathy of prematurity
29
Q

Two Phases of ROP

A
  1. Early vasoconstriction and obliteration of the capillary network
  2. Vasoproliferation
30
Q

Early vasoconstriction and obliteration of the capillary network (2)

A
  1. Seems to occur in response to high oxygen concentrations
  2. Low levels of IGF1 in preterm infants – this may contribute to the lack of retinal blood vessel formation in early ROP
31
Q

Vasoproliferation (2)

A
  1. Follows the period of high oxygen exposure/insult in response to angiogenic factors –VEGF- released by the hypoxic retina.
  2. Theory supported – Phelps and Rosenbaum studied kittens – made them hyperoxic and recovered in room air or 13% oxygen – those in hypoxic environment had worse ROP – suggests retinal hypoxia plays a role in ROP (VEGF is a known product of the hypoxic retina)
32
Q

ROP Risk Factors (5)

A
  1. Extreme prematurity is known to be the significant risk factor
  2. Oxygen alone and ROP association in not so clear
  3. Transient hyperoxemia - ?
  4. Apnea, sepsis, IVH, anemia?
  5. ? Possibly erythropoietin (angiogenic) has been implicated?
33
Q

Clinical Presentation of ROP by stages (5)

A
  1. Stage I – thin demarcation line develops between the vascularized region of the retina and the avascular zone
  2. Stage II- This line develops into a RIDGE protruding in to the vitreous
  3. Stage III-Extra-retinal fibrovascular proliferation occurs with the ridge-
  4. Stage IV-Fibrosis and scarring occurs as the vascularization extends into the vitreous- traction occurs on the retina- partial retinal detachment
  5. Stage V – complete retinal detachment
34
Q

Retina Zones (2)

A
  1. Zone I close to the posterior pole is severe –
  2. Zone III least severe in the peripheral retina (regresses spontaneously)
    i. Zones are area in the eyes*
    ii. Zone 1 we are talking about central area of eye
    iii. Zone 3 = peripheral retina
    iv. Baby with stage 3 zone 1 = worst case scenario = outcome is potential loss of central vision
35
Q

Intracranial Hemorrhage Terminology (3)

A
  1. An ICH can occur in term and preterm infants.
  2. In term infants ICH tends to be subdural, subarachnoid, or subtentorial and is most often related to birth trauma.
    * Forceps, vacuum
  3. In preterm infants the most common ICH is bleeding from the subependymal germinal matrix and may result in IVH.
36
Q

Germinal Matrix (4)

A
  1. Located between the caudate nucleus and the ependymal lining of the lateral ventricle and is normally NOT seen on cranial ultrasound.
  2. The germinal matrix is the site of proliferating neuronal and glial precursors in the developing brain - which is located above the caudate nucleus - in the floor of the lateral ventricle, and caudothalamic groove.
  3. From the GM cells migrate peripherally to form the brain
  4. The germinal matrix contains a rich network of fragile thin-walled blood vessels – and is predisposed to hemorrhage.
37
Q

GM Bleed

A

GM bleed is most frequent before 35 weeks gestation and is typically seen in very low birth-weight (<1500g) premature infants because they lack the ability for auto regulation of cerebral blood flow.

38
Q

IVH Overview (8)

A
  1. IVH is the most common intracranial hemorrhage in preterm infants.
  2. It is bleeding from the subependymal germinal matrix.
  3. IVH is the most common CNS complication of a preterm birth.
  4. IVH is associated with the immaturity of the germinal matrix of the lateral ventricles.
  5. Acidosis, birth asphyxia, shock, blood pressure fluctuations and hypoxia are common related problems
  6. Bleeding can be confined to the GM or it may rupture into either lateral ventricle and become a unilateral or bilateral IVH
  7. By 36 weeks the GM has involuted in most infants.
    i. Do not need anymore
    ii. Population of babies under 36 weeks are more at risk
  8. Following IVH further insult by venous thromboses may result in thalamic infarction.
39
Q

IVH Incidence (3)

A
  1. Overall occurrence of IVH in preterm infants <1500g ~13-15%
  2. Vary by gestation
  3. Greatest risk of GM/IVH in preterm infants BW <750g
40
Q

IVH Patho (5)

A
  1. GM is a weakly supported and highly vascularized area
  2. The blood vessels in this area are immature and prone to hypoxic-ischemic injury
  3. The vessels are irregular and rupture easily during times of sick preterm infants lives when they a sudden rise or fall in systemic blood pressure – this causes the cerebral blood flow to increase with rupture of the vessels.
  4. Close proximity to the lateral ventricles allows for rupture through the GM subependymal layer and entrance of blood into the lateral vents
    i. If expands or becomes larger going to spread into the lateral ventricles and progresses from there and extend into the tissue
    ii. Then see hydrocephalus and neurological sequelae
  5. This occurs ~80% of the time
41
Q

Intracranial Hemorrhage Consequences (4)

A
  1. GM destruction can lead to impairment of myelination and brain growth
  2. Leads to reduction in cerebral perfusion in the first 2 weeks of hemorrhage
    * A bleed happens and overtime is resolves, what it leaves behind is what we worry about
  3. Posthemorrhagic hydrocephalus (PHH) common in infants with highest grade of IVH
  4. Periventricular leukomalacia (PVL) a frequent accompaniment of IVH but not directly caused by IVH
42
Q

Intracranial Hemorrhage Risk Factors (7)

A
  1. Prematurity
  2. RDS – closely related clinical circumstance to GM/IVH
  3. Birth asphyxia
  4. Hypotension/shock
  5. Acidosis
  6. Procedures – tracheal suctioning, repositioning and mydriatrics.
  7. ? Fetal inflammatory responses – chorioamnionitis – cytokine response – these have vasoactive properties and cause exaggerated blood pressure changes – neonatal sepsis- hypotension and shock – GM/IVH.
43
Q

Intracranial Hemorrhage Clinical Manifestations (3)

A
  1. Varied
  2. Apnea, Lethargy, change in activity pattern, mimic sepsis, drop in hematocrit, bulging fontanel – need neuroimaging to confirm
  3. Vague symptoms – look for clinically then go to neuro imaging
44
Q

Intracranial Hemorrhage Diagnosis (7)

A
  1. Cranial Ultrasound – procedure of choice
  2. Portable, no sedation, less expensive
  3. Screening with US should be done on all preterm infants from day 1 to discharge with final US at 36 weeks or before discharge
  4. Typically btw days 1-7
  5. 50% of all GM /IVH may occur on day 1
  6. 90% occur by day 4
  7. 20-40% of those that occurred by day 4 will progress
45
Q

IVH (2)

A
  1. Severity and a means to follow for comparison

2. Both are grades/classes from I-IV

46
Q

IVH Prognosis (1 short and 4 long term)

A

Short term outcome: Depends on birthweight, gestational age and complications of prematurity

Long term outcome:

  1. Depend primarily on the extent of parenchymal injury and added effects of the short term complications
  2. Lower IQ, learning problems, motor deficits, hearing, behavioral problems
  3. Bilateral IVH has been proven to correlate with CP as opposed to unilateral IVH
  4. PVL has a higher incidence of CP outcomes
47
Q

Periventricular Leukomalacia Overview (6)

A
  1. PVL is an ischemic brain injury followed by necrosis of periventricular white matter adjacent to the lateral ventricles.
  2. Usually nonhemorrhagic event resulting from hypotension, apnea, or HIEvents known to decrease CBF
  3. PVL is symmetrical in distribution (bilateral) IVH is usually unilateral.
  4. Periventricular leukomalacia (PVL) is the most common ischemic brain injury in premature infants.
  5. The ischemia occurs in the border zone at the end of arterial vascular distributions next to lateral ventricle
  6. Prematurity is the greatest risk factor for PVL
48
Q

PVL Anatomical Risks (3)

A
  1. Distal arterial perfusion of the watershed zones
  2. Immature vessel autoregulation
  3. Predispose preterm brain to ischemia
49
Q

PVL Cellular Risks (3)

A
  1. Cytokines
  2. Reactive oxygen species
  3. Target the pre-myelinating oligodendrocytes – interfering with myelination of white matter
50
Q

PVL Pathophysiology (6)

A
  1. Together these factors (anatomical and cellular)
  2. Underdevelopment of the white matter in the periventricular area àPeriventricular leukomalacia
  3. PVL occurs because of ischemia induced injury to the oligodendrocytes in the periventricular area of the developing brain
  4. Cytokine-induced damage may occur from maternal or fetal infections
  5. A white matter lesion develops:
    * Hypotension à ischemia à lesion
    * Premature infants have impaired cerebrovascular blood flow autoregulation à increases susceptibility to PVL
    * Decreased blood flow affects the white matter at the borders of the lateral ventricles
  6. Looks like swiss cheese brain
51
Q

PVL Prognosis (6)

A
  1. High risk for development of neurodevelopmental deficits
  2. PVL – associated with spastic diplegia (mild)
  3. Severe PVL – quadriplegic
  4. High incidence of intellectual impairment and visual disturbances
    * Nystagmus
    * Strabismus
    * Blindness
  5. Based on patho – areas of lack of white matter going to see deficits*
  6. Grades of PVL; mild to severe
52
Q

Plus Disease

A

ASSOCIATED WITH ICROP

May occur when vessels posterior to the ridge become dilated and tortuous

Peds Patho Exam 3 (7 decks)

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