2.1.1 Acute Lung Injury Flashcards

1
Q

What is another name for neonatal respiratory distress syndrome?

A

Hyaline membrane dz

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2
Q

What is the most common cause of respiratory distress in premature infants?

A

Neonatal respiratory distress syndrome

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3
Q

What two factors attribute to neonatal respiratory distress syndrome?

A

Immature lung tissue and lack of surfactant

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4
Q

What is a histological characteristic of neonatal RDS?

A

hyaline membrane in peripheral airspaces

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5
Q

What are the different gestation ages and their corresponding rate of neonatal RDS?

A

<28 wks: 60% of infants born

28-34 wks: 30% of infants born

34 wks and beyond: under 5%

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6
Q

What type of cells produce surfactant?

A

Type II pneumocytes

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7
Q

How does surfactant affect the surface tension and pressure required to maintain alveoli patency?

A

Surfactant reduces surface tension at the air-liquid barrier; less pressure to keep alveoli patent and aerated

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8
Q

What is the composition of surfactant?

A

Lecithin, phosphatidyl glyceral, hydrophobic glycoproteins (SP-B, SP-C)

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9
Q

Describe how sufficient surfactant in a newborn aids with respiration.

A

The first breath of life needs high inspiratory pressures to expand lungs; lungs retain 40% of the residual air volume after 1st breath; subsequent breaths require less inspiratory pressure (reduced surface tension)

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10
Q

Describe how a deficiency in surfactant leads to neonatal respiratory distress.

A

The first breath of life needs high inspiratory pressures to expand lungs; Lungs collapse with each additional breath, so each successive breath requires as much effort as the first. Stiff atelectatic lungs are further impeded by the soft thoracic wall that is pulled in as the diaphragm descends

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11
Q

Describe the pathophysiological progression of neonatal RDS starting with prematurity and finishing with hyaline membrane.

A
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12
Q

What changes occur b/t 22 and 32 wks of gestation that allow for better respiratory outcomes for a neonate?

A

Lungs continue to develop and divide. The epithelium transitions from cuboidal to squamous. The alveoli become more closely apposed to surrounding capillaries.

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13
Q

A congested, atelectatic lung (prior to first breath) has the gross appearance of what organ? Does it sink or float?

A

Liver; sink

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14
Q

What are the arrows pointing at?

A

Hyaline membranes that come as a result of neonatal RDS

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15
Q

What are 2 factors that increase surfactant production? Decrease surfactant production?

A

Increase: Glucocorticoids, Labor

Decrease: Insulin (infants of diabetic mothers), congenital surfactant deficiency (SFTBC genes)

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16
Q

What are some of the ways to manage neonates at risk of and/or experiencing neonatal RDS?

A

Assess maturity using amniotic fluid phospholipids

Delay labor

Induce lung maturity w/ corticosteriods

Surfactant replacement therapy

Oxygenation/ventilation

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17
Q

What length of survival indicates an excellent chance of recovery in NRDS?

A

3-4 days

18
Q

What are the three types of complications associated with neonatal RDS?

A

Air leaks

Complications of oxygen therapy

Complications of prematurity

19
Q

What are two possible complications of oxygen therapy?

A

Bronchopulmonary dysplasia

Retrolental fibroplasia (retinopathy of prematurity)

20
Q

What are the two phases of retrolental fibroplasia?

A

Phase I: hyperoxic phase of therapy

  • Reduced VEGF
  • Endothelial apoptosis

Phase II: w/ hypoxic room air ventilation

  • VEGF levels recover
  • Retinal vessel proliferation
21
Q

What are some of the complications/factors that contribute to the respiratory issues associated with bronchopulmonary dysplasia?

A
  1. Abnormality in alveolar septation (reduced surface area)
  2. Dysregulation of pulmonary vasculature development
  3. Superimposed effects of hyperoxemia, hyperventilation, prematurity, inflammatory mediators
22
Q

A majority of infants gradually improve from bronchopulmonary dysplasia. What is the typical timeline for this gradual improvement?

A

2-4 months

23
Q

What are some other causes of respiratory disress in the neonate?

A

excessive maternal sedation

fetal head injury

blood or amniotic fluid aspiration

nuchal cord

transient tachypnea of the newborn

meconium aspiration syndrome

infection

persisten fetal circulation (persistent pulmonary HTN)

pulmonary hypoplasia

24
Q

What is pulmonary edema?

A

Increase in interstitial fluid which then accumulates within alveolar spaces

25
Q

What are the three causes of pulmonary edema?

A
  1. Hemodynamic disturbances (cardiogenic)
  2. Alveolar wall injury (microvascular or epithelial injury)
  3. Undetermined origin (head injury, high altitude)
26
Q

What are two hemodynamic changes that would lead to pulmonary edema?

A

Increased hydrostatic pressure, decreased plasma colloid pressure

(both result in an increase in filtration force)

27
Q

What are the three most common causes of hemodynamic pulmonary edema (in order of most common to least common) and some examples?

A
  1. Increased hydrostatic pressure (L-sided HF, volume overload, pulmonary vein obstruction)
  2. Decreased oncotic pressure (low protein states, renal disease, liver disease, protein-losing enteropathies)
  3. Lymphatic obstruction
28
Q

What is this an image of?

A

Congestion of alveolar capillaries and fluid-filled alveoli

29
Q

What are the brown-tinged cells?

A

Hemosiderin-laden macrophages - “heart failure cells”

30
Q

What does this patient have, doc?

A

Pulmonary edema

31
Q

What are some potential sources of microvascular injury that results in pulmonary edema?

A

Infection: pneumonia, septicemia

Inhaled gases

Liquid aspiration

Drugs and chemicals

Shock, trauma

Radiation

Transfusion related

32
Q

Widespread pulmonary edema as a result of alveolar injury can lead to what condition?

A

Acute Respiratory Distress Syndrome (ARDS)

33
Q

What is the histological manifestation of acute lung injury?

A

diffuse alveolar damage (DAD)

34
Q

What is name for noncardiogenic pulmonary edema?

A

Acute Lung Injury, abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates in the absence of cardiac failure

35
Q

What are the clinical manifestations of ARDS?

A

rapid onset (days to wks) of severe life-threatening respiratory insufficiency, cyanosis, severe arterial hypoxemia refactory to oxygen therapy, diffuse alveolar infiltrates

36
Q

What are some of the causes of ARDS?

A

Infections, Gastric aspiration, Sepsis, Trauma, inhalants, chemicals/drugs, shock, metabolic, hypersensitivity reactions

37
Q

What is the pathogenesis of ARDS?

A
38
Q

What are the three stages of difuse alveolar damage?

A

Edema, Destruction stage (hyaline membranes), Organizing Stage (pneumocyte hyperplasia, fibrosis)

39
Q

What are some of the processes involved in resolution of ARDS/DAD?

A

resorption of the exudate and dead cell removal, fibrogenic cytokines, epithelial cell repopulation, endothelial repopulation

40
Q

What do these histo slides illustrate?

A

Fibrosis - honeycomb lung

41
Q

What is acute interstitial pneumonia?

A

ALI/DAD of unknown etiology, rare, mean age of 59, acute respiratory failure following upper respiratory tract infection-like illness