Full Term Newborn Disease Flashcards
1
Q
What is the most common underlying diagnosis of persistent pulmonary hypertension of the newborn?
A
Meconium Aspiration Syndrome
2
Q
A change from fetal circulation to adult circulation requires what to occur?
A
A drop in PVR and a significant increase in SVR.
3
Q
What change in the blood gas, sensed by chemoreceptors in the aorta and carotid artery, causes a chemical message to be sent to the brain stem to increase ventilation?
A
A drop in PaO2.
4
Q
Which of the following describes cardiomegaly in infants?
A
A heart silhouette occupying >60% of the thoracic diameter.
5
Q
Which of the following are considered proper management of persistent pulmonary hypertension of the newborn?
A
Decrease pulmonary vascular resistance and Minimize ventilator-induced lung injury.
6
Q
What is the most frequently used pulmonary vasodilator for neonates?
A
Inhaled nitric oxide.
7
Q
Complications of extracorporeal life support include which of the following?
A
IVH, Cardia dysrhythmias, Infection, and Bleeding.
8
Q
What are the advantages of using venovenous ECMO support?
A
Spares the carotid artery and Potential emboli remain on the venous side of the patient.
9
Q
What factors show an increased risk for meconium aspiration syndrome?
A
Maternal, hypertension, and Fetal distress.
10
Q
Which of the following is NOT an indication for intubation and ventilation in neonates with meconium aspiration syndrome?
A
Respiratory alkalosis.
11
Q
What is Persistent Pulmonary Hypertension of the Newborn (PPHN)?
A
A syndrome with severe hypoxemia and high pulmonary artery pressures that occurs when the pulmonary vascular resistance (PVR), normally high in utero, fails to decrease at birth.
12
Q
When does PPHN usually present?
A
At birth or shortly after.
13
Q
What is PPHN characterized by?
A
By a failure to establish adequate pulmonary and systemic oxygenation.
14
Q
What happens if PPHN goes without treatment?
A
It can cause severe cardiac dysfunction, multiorgan dysfunction, and death.
15
Q
Where is a PDA located and what issue does it cause?
A
It is in the aorta and pulmonary artery and causes a lack of O2 to get to the rest of the body because it is not being picked up by the lungs.
16
Q
What happens if normal pulmonary vasculature is impeded?
A
It can result in sustained high pulmonary artery pressure.
17
Q
What is the result of persistent PPHN?
A
Hypoxemia and cyanosis.
18
Q
What is preductal SPO2?
A
Oxygen saturation is taken from an area where arterial blood supply comes prior to ductus arteriosus. Primarily the right hand.
19
Q
What is post ductal SPO2?
A
Oxygen saturation taken from an area where arterial blood supply comes after ductus arteriosus which is typically placed on the lower limbs.
20
Q
When is PPHN suspected?
A
When the preductal SPO2 and the post ductal SPO2 shows greater than a 10% difference.
21
Q
What does the ABG show in PPHN?
A
When PaO2 has a 15mm difference between pre and post ductal.
22
Q
What is the oxygen index equation (OI)?
A
Paw x FIO2 x 100/PaO2.
23
Q
What happens when there is a higher OI number?
A
It worsens the patient’s ability to oxygenate despite high levels of support.
24
Q
What is an Oxygen Index greater than 20 an indication for?
A
Inhaled Nitric Oxide (iNO).
25
What is an Oxygen Index greater than 40 an indication for?
Extracorporeal Membrane Oxygenation (ECMO).
26
What is the management and treatment for PPHN?
O2 therapy (maintain PaO2 90-120), conventional mechanical ventilation (CMV), HFOV when CMV pressures or rates are too high, pulmonary vasodilators such as iNO maintain HCT at 35% to 45%, and ECMO for pts who are unresponsive to above therapeutic measures w an OI \>40.
27
What is nitric oxide?
It Is a substance produced by nearly every cell and organ in the human body.
28
What are the functions of nitric oxide?
Vasodilation, platelet inhibition, immune regulation, enzyme regulation and neurotransmission.
29
What is nitric oxides main use in the medical environment?
For smooth muscle relaxation of the pulmonary vascular bed.
30
What does inhaled nitric oxide do?
Selectively dilates the pulmonary vasculature adjacent to open lung units.
31
What is general usage for iNO?
A failure of ventilation to restore normal PVR.
32
Why do we want vasodilation
Because everything is constricted.
33
iNO only works where?
It only works where the blood flow goes it has a short 1/2 life and only works w open alveoli.
34
What is the recommended starting dose for nitric oxide?
20 ppm
35
Half life of iNO
\<5 sec
36
What does iNO combine with?
Hb and methemoglobinemia and nitrate.
37
What is a positive response to iNO therapy?
It is evident by an increase in oxygenation (SpO2 and PaO2) as well as a decrease in the preductal and postductal SpO2 gradient.
38
What are the 2 most common side effects of iNO?
Rebound hypoxemia and methemoglobinemia.
39
How do you prevent rebound hypoxemia?
iNO weaning is done in increments which avoids abrupt discontinuation of iNO.
40
What problems cause a need for iNO?
Swallowed meconium, severe resp distress, or something that has caused.
41
What will not benefit from iNO?
Atelectatic or fluid-filled lungs due to no uptake of gas.
42
When will iNO have improved outcomes?
If more reaches capillary endothelium by opening collapsed alveoli which will increase the degree of vasodilation.
43
What is the responsiveness to iNO enhanced by?
The use of PEEP and high-frequency ventilation.
44
What shows responsiveness after using iNO?
Increase of 20% O2 saturation.
45
iNO should not exceed by how much?
80 ppm
46
Where is iNO bled into the vent circuit?
Before the humidifier.
47
How do you analyze iNO and NO2 concentrations?
Gas is read at the sample line placed prior to the patient-circuit interface.
48
What happens when nitric oxide is combined with oxygen
It produces NO2 which is toxic.
49
What factors influence NO2?
Oxygen concentration, NO concentration and the time they are in contact.
50
Who is at highest risk of NO2?
Those that are receiving high O2 concentrations and low ventilator flow rates.
51
What is extracorporeal membrane oxygenation (ECMO)?
A technique used to support the heart and/or lungs externally when the native heart and/or lungs are no longer able to provide adequate support.
52
What is the lung goal when using ECMO?
To prevent nitrogenic damage caused by high mean airway pressure.
53
What is the heart goal when using ECMO?
To prevent the use of high doses of toxic medications to keep the heart functioning.
54
What is the patient criteria for using ECMO?
OI greater than 40, no major cardiac defects, reversible lung disease, gestation age greater than 33 weeks, mechanical ventilation less than 14 days, no major intraventricular hemorrhage, and no significant coagulopathy or bleeding complications.
55
What are the 2 types of ECMO support?
Venovenous that take blood out of right atrium and put back there and venoarterial which take blood out of right atrium and put back into the aorta.
56
What can be done with the ventilator once ECMO has been initiated and the patient is stabilized?
Ventilator settings can be reduced.
57
What kind of vent settings is appropriate when ECMO is providing respiratory support?
PIP 20, PEEP 10, RR 10, and FiO2 30%-40%.
58
What does ECMO stand for?
Extracorporeal life support (ECLS).
59
What is the purpose of ECMO?
What is the purpose of ECMO?
60
What is the major pathophysiologic condition that ECMO treats?
Persistent pulmonary hypertension of the newborn (PPHN).
61
What neonatal conditions can hypoxic states result from?
Meconium aspiration syndrome, diaphragmatic hernia, sepsis, and RDS.
62
What does ECMO interrupt?
The cycle of PPHN minimizes the need for excessive ventilation, while the underlying condition is resolved.
63
What factors show an increased risk for meconium aspiration syndrome?
It usually is associated with perinatal depression and asphyxia. Periods of stress and fetal hypoxemia will cause the fetus to take deep, gasping inspirations that can force the contents of the nasopharynx to pass the glottis into the airway
64
What is meconium aspiration syndrome?
Respiratory distress occurring soon after delivery in a meconium-stained infant. It involves aspiration of meconium into the central airways of the lung.
65
Who are mostly affected by MAS (meconium aspiration syndrome)?
Term and post-term infants.
66
What are the factors associated with increased risk of MAS?
Post-term pregnancy (greater than 42 weeks), preeclampsia or eclampsia, maternal hypertension, maternal diabetes, intrauterine growth retardation, abnormal biophysical profile, oligohydramnios, maternal heavy smoking, abnormal fetal HR, the presence of fetal distress, low 5 min Apgar Ethnicity, and home birth.
67
Meconium is the byproduct of what?
Metabolic waste of gestation.
68
What is meconium like?
Sticky, viscous, consistency like tar, odorless and almost sterile.
69
What happens when amniotic fluid is stained with meconium?
Gasping or deep irregular respirations can result in aspiration.
70
What does meconium inhibit?
Surfactant function and is directly toxic to the pulmonary epithelium.
71
What are the 3 levels of meconium airway obstruction?
Partial obstruction, ball valve obstruction, and total obstruction.
72
What is partial obstruction?
It allows some air passage into and out of the alveoli.
73
What is the ball valve obstruction?
It allows air in the alveoli during inspiration but closes during expiration. causes air trapping At rest, the airway lumen is partially obstructed. With inspiration, negative intrathoracic pressure opens the airway and relieves the obstruction. Gas enters and expands the alveoli. With expiration, intrathoracic pressure changes to a positive force, which narrows the airway and causes total occlusion. Gas cannot be expelled and is trapped within the alveoli. It is difficult to provide ventilation to infants with severe MAS. These infants often retain CO2 and need increased ventilator support. Because of high airway resistance, the lungs have a long time constant. High ventilator rates and pressures increase the risk for air trapping and volutrauma. .
74
What is total obstruction?
It will not allow air in during inhalation or exhalation and leads to atelectasis and hypoventilation.
75
What are symptoms of meconium aspiration?
Abnormal respiratory rate may manifest as tachypnea, but w fatigue may deteriorate to apnea. Increase resp effort, grunting, nasal flaring and retractions. Cyanosis, Increased AP diameter of the chest if the newborn has air trapping. Asymmetry of the chest is also common if air leaks develop.
76
What is the management and treatment of Meconium Aspiration Syndrome (MAS)?
Supplemental O2 via nasal cannula to MV, HFOV, and ECMO. If the infant’s condition worsens, CPAP or mechanical ventilation may be indicated. CPAP is indicated if the primary problem is hypoxemia. By distending the small airways, CPAP can sometimes overcome the ball-valve obstruction and improve both oxygenation and ventilation.
77
MAS Symptons before birth
• Before birth, thick meconium, fetal tachycardia, and absent fetal cardiac accelerations during labor are evidence that the fetus is at high risk for MAS.
78
MAS Auscultation
auscultation may reveal diminished or unequal breath sounds, rales, rhonchi or wheezing
79
MEC and Surfactant
Can interfere with surfactant and lead to RDS
80
Hypoxemia and MEC
• Hypoxemia associated with MAS can lead to the development of hypoxia induced vasoconstriction and vasospasm o Vasospasm can cause pulmonary hypertension and right to left shunt
81
MAS can result in the growth of what
• MAS can result in chemical pneumonitis as it promotes the growth of bacteria
82
MAS Chest X-ray
• The chest radiograph usually shows irregular pulmonary densities, which represent areas of atelectasis, and hyperlucent areas, which represent hyperinflation secondary to air trapping • May show partial airway obstruction and air trapping o Can result in pneumothorax • CXR can also show o Atelectasis o Consolidation
83
3 Primary Problems in MAS
o Obstruction occurs because of plugging of the airways with particulate meconium. This obstruction often is of the ball- valve type, which allows gas entry but prevents gas exit. Ball- valve obstruction causes air trapping and can lead to volutrauma o The lung tissue injury caused by MAS is chemical pneumonitis. Additionally, there are various chemical effects, inflammatory responses, cytokine and chemokine activations, complement activation, and phospholipase A2 activation. o Persistent pulmonary hypertension with intracardiac and extra- cardiac right-to-left shunting frequently complicates MAS
84
What is PPHN
• Persistent pulmonary hypertension of the newborn (PPHN) is a complex syndrome with many causes • The common denominator in PPHN is a return to fetal circulatory pathways, usually because of elevated PVR.
85
PVR as the baby goes from fetal circulation to after birth
o When the baby tries to go from using the placenta as gas exchange to using their lungs and there will be a return to fetal circulation pathways after birth PVR from the pulmonary artery is high and systemic resistance is low which is the opposite of what is normally seen in adults • This is because there is low oxygen in the lungs making the blood vessels constrict, which is the opposite from what happens to the blood vessels in the systemic circulation where when you have low oxygen, they will dilate o If the PVR does not decrease then the right to left shunt through the ductus arteriosus an foramen ovale will not close and PPHN can occur • This condition results in further right-to-left shunting, severe hypoxemia, and metabolic and respiratory acidosis.
86
Fetal circulation
• PVR is high, and systemic vascular resistance (SVR) is low. This condition produces a PVR/ SVR ratio greater than 1. • A fetus has two anatomic shunts that are not present in older infants, children, or adults: the foramen ovale and ductus arteriosus. • With a PVR/SVR ratio greater than 1 and the anatomic shunts, blood flow bypasses the lung either at the atrial level (foramen ovale) or at the pulmonary artery (ductus arteriosus). • Intrauterine total pulmonary blood flow and systemic arterial O2 saturation (SaO2) are low. • In the transition to extrauterine life, PVR decreases owing to gas filling the lungs and increasing PaO2 in the pulmonary venous circulation. • SVR increases with the removal of the pla- centa from the circulation, and this makes the PVR/SVR ratio less than 1. If PVR does not decrease to allow the PVR/SVR ratio to become less than 1, the infant has PPHN.
87
Three types of PPHN
Vascular Spasm Increase Muscle Wall Thickness DEcreased Cross section Area
88
PPHN-Vascular Spasm
Acute event that can be triggered by any different conditions Ex. Hypoxemia, hypoglycemia, hypotension, and pain
89
PPHN-Increased Muscle Wall Thickness
• Chronic condition develops in utero, in response to several different causative factors such as, chronic fetal hypoxia increased pulmonary blood flow (e.g. intrauterine closure of ductus arteriosus), and pulmonary venous obstruction (e.g. total anomalous pulmonary venous return with obstructed below diaphragm return)
90
PPHN-Decreased Cross Sectional Area of Pulmonary Vessels
Related to hypoplasia of lungs. CDH, Oligohydramnios syndrome
91
PRIMARY PUMONARY VASOCONSTRICTION
• Chronic intrauterine hypoxia • Pulmonary hypoplasia • Anatomic malformation • Intrauterine close of ductus arteriosus • Altered smooth muscle development • Idiopathic cause • Stress upon the mom placing the mom in a hypoxic state
92
SECONDARY PULMONARY VASOCONSTRICTION
• Perinatal asphyxia • CDH-Congenital Diaphrmatic Hernia • Respiratory Disress Syndrom (RDS) • Pneumonia • Hypoglycemia • Hypothermia • Hypotension • Sepsis • CHD (congenital heart defect) o A lot of times the different diagnosis of PPHN is CHD
93
Clinical Manifestation of PPHN
• Suspected when oxygen saturation are rapidly changing despite adequate ventilation and changes to FiO2 o Refractory Hypoxemia is hypoxemia that is not improving when we are applying oxygen to a patient • In infants with a significant shunt through the ductus arteriosus, there usually is a substantial gradient (\>5%) between preductal and postductal O2 saturation. o This gradient can be found easily if two pulse oximeters are placed on the infant, one on the right arm and the other on either leg. • Tachypnea, mild to moderate respiratory distress with cyanosis and refractory hypoxemia within first 12 hours of life • An audible murmur may be present due to aortic regurgitation • Grunting, intercostal retractions and nasal flaring present
94
How can we tell if there is a R-L shunt?
1. Hyperoxia Test
2. Pre and Post Ductal SpO2 Testing
3. Pre and Post Ductal ABG
95
R to L Shunt
Hyperoxia Test
This is to check if the cyanosis is pulmonary or cardiac (R-L Shunt) in origin
Increase FiO2 100% for 10 min and then draw and ABG, and if PaO2 has not increased you can assume there is a shunt
If PaO2 is \<100mmHg then there is a R-L shunt and it is cardiac in nature
96
R to L Shunt
Pre and Post Ductal SpO2 Testing
This is the standard of what we do right now
Place SPO2 monitors on the right arm (preductal) and either leg (postductal)
If SPO2 difference is \>5% a R-L shunt is present
97
R to L Shunt
Pre and Post Ductal ABG Testing
ABG from right radial (preductal) and from UAC (postductal)
greater than 20 mmHg difference – shunting is present
98
PPHN Differential Diagnosis
* Parenchymal Lung Disease
* Congenital Heart Disease
99
PPHN Lab Findings
Arterial blood gases show an increase in A-a gradient with marked acidosis and severe hypoxemia
Low volume murmur on ECHO
Chest x-ray- only aid diagnosis if cause of PPHN is respiratory in origin
Any lung disease noted is usually out of proportion to the degree of oxygen required
100
PPHN Management
**PRIMARY GOAL: Decrease PVR**
O2 to promote pulmonary vasodilation
Surfactant if cause is related to RDS
Intubation and Ventilation (may require HFOV)- ventilate to normal PaCO2 and pH
iNO to treat PA Vasoconstriction (this is the big use for nitric oxide)
Sedation and Analgesia
ECMO
Restrict handling/suctioning
Want to minimize any kind of external stimuli and will team up with the nurse so that everyone can get there assessment done at once instead of repeated stumli
101
Transient Tachypnea of the Newborn Cause
* During most births, approximately two-thirds of this fluid is expelled by thoracic squeeze in the birth canal; the rest is reabsorbed through the lymphatic vessels during initial breathing. These mechanisms are impaired in infants born by cesarean section or infants with incomplete development of the lymphatic vessels (preterm or small-for-gestational-age infants).
* The residual lung fluid causes an increase in airway resistance and an overall decrease in lung compliance.
* Because compliance is low, the infant must generate more negative pleural pressure to breathe. This process can result in hyperinflation of some areas and air trapping in others.
102
TTNB Risk Factors
* Most infants with TTN are born at term without any specific predisposing factors in common
103
TTNB Pathophysiology
* Disrupted lung fluid clearance
* Decreased compliance due to excessive fetal lung fluid
* Decreased inspiratory effort leads to delayed pulmonary absorption of fetal lung fluid
* Increased alveolar-arterial oxygen gradient
104
TTNB Clinical Manifestations
## Footnote
##
* Onset usually within the first hour post delivery
* Presents with tachypnea up to 150bpm
* Cyanosis
* Grunting
* Retractions
* Nasal flaring
* ABG may reveal mild to moderate hypoxemia, hypercapnia, and respiratory acidosis
* During the first few hours of life, infants with TTN breathe rapidly.
105
TTNB Chest X-Ray
* The chest radiographic findings, which may initially be indistinguishable from pneumonia, are hyperinflation, which is secondary to air trapping, and perihilar streaking.
* The perihilar streaking probably represents lymphatic engorgement.
* Pleural effusions may be evident in the costophrenic angles and interlobar fissures.
106
TTNB Management
* Maintain adequate oxygenation and ventilation
* Supplemental oxygen
* CPAP when higher FIO2 is required
* PPV if required
* Because the retention of lung fluid may be gravity-dependent, frequent changes in the infant’s position may help speed lung fluid clearance.
* Because TTN and neonatal pneumonia have similar clinical signs, intravenous administration of antibiotics should be considered for at least 3 days after appropriate culture samples are obtained.
* Clearing of the lungs evident on a chest radiograph and with clinical improvement usually occurs within 24 to 48 hours.
* A few infants with TTN eventually have persistent pulmonary hypertension.
107
What is Transient Tachypnea of the Newborn (TTN)?
A condition of term or near-term infants characterized by mild respiratory distress during the first few hours of life.
108
What is TTN caused by?
Failure to clear fetal lung fluid prior to delivery.
109
What are the main risk factors of TTN?
Delivery via C-section, macrosomia (birth weight above the 90th percentile), maternal asthma, maternal diabetes, and male gender.
110
What are the clinical manifestation of TTN?
Respiratory distress within 6 hours of birth, RR \>60, grunting, nasal flaring, and retractions.
111
What is the management and treatment of TTN?
O2 therapy: O2 hood or nasal cannula connected to an air oxygen blender to maintain O2 sat 90-96, CPAP 4-6 to resolve moderate respiratory distress, withholding of enteral feeds, administration of intravenous fluids, administration of antibiotics, and of thermoregulation (keep warm).
