Neonatology Flashcards
1
Q
• Suspect transient tachypnea of the newborn (TTN) if:
A
o Late pre-term or term infant after caesarean delivery without labor
o Chest radiograph showing bilateral perihilar linear streaking secondary to engorged vessels
2
Q
• Suspect respiratory distress syndrome (RDS) if:
A
o Preterm infant (with greater risk in decreasing gestational age)
o Infant born to a diabetic mother
o Chest radiography showing diffuse, granular, ground-glass appearance with air bronchograms and low lung volume
3
Q
• Suspect persistent pulmonary hypertension if:
A
o Infant with history of bacterial infection, poor intrauterine growth, and non-reassuring fetal heart rate patterns
o Chest radiography can show clear lung fields with decreased pulmonary vascularity
4
Q
o Management for suspected persistent pulmonary hypertension should include the following:
A
- Echocardiogram to differentiate between primary cardiac disease and Primary Pulmonary Hypertension
- Oxygen initially administered at high concentrations to reverse pulmonary vasoconstriction
- Circulatory support with fluids and vasopressors to reduce right-to-left shunting
- In severe cases, using vasodilators such as nitric oxide can reduce pulmonary vascular resistance
5
Q
• Suspect early-onset pneumonia if:
A
o Lethargy, apnea, tachycardia, poor perfusion
o Chest radiograph findings of bilateral alveolar densities with air bronchograms
6
Q
• Requirements for the transition from fetal to neonatal life
A
o Replacement of alveolar fluid with air
o Onset of regular breathing
o Increase in pulmonary blood flow
• Secondary to increased systemic vascular resistance and decreased pulmonary vascular resistance
7
Q
Definition and causes of central cyanosis
A
o Results when the deoxygenated hemoglobin in the blood exceeds 5 gm/dL. Causes include:
• Alveolar hyperventilation
• Ventilation-perfusion mismatch
• Right to left shunt
• Diffusion impairment
• Abnormal hemoglobin with decreased oxygen affinity
8
Q
Definition and causes of peripheral cyanosis
A
o Systemic arterial oxygen tension is normal, but increased oxygen extraction causes a wide systemic arteriovenous oxygen difference, resulting in increased deoxygenated blood on the venous side.
9
Q
• The primary life threatening causes of cyanosis in children include:
A
o Respiratory dysfunction • Decreased inspired oxygen • Upper airway obstruction • Impairment of chest wall or lung expansion • Intrinsic lung disease o Circulatory dysfunction • Congenital heart disease • Pulmonary edema • Pulmonary hypertension • Pulmonary embolism • Pulmonary hemorrhage • Shock o Methemoglobinemia
10
Q
what is considered post-term?
A
GA >42 weeks
11
Q
what are the most common complications of patients born post-term?
A
• Macrosomia:
o Most common presentation
o Fetal weight and head circumference continue to increase
o Increased risk of birth injury due to their large size
• Fetal growth restriction:
o Can also occur due to a poorly functioning placenta that cannot provide adequate nutrition
o Will present as a long, thin, small for gestational age infant with dry, peeling skin
12
Q
• Perinatal mortality is thought to increase in post-term infants due to the following reasons:
A
o Feto-placental insufficiency
o Asphyxia (with and without meconium)
o Intrauterine infection
13
Q
• Neonatal complications in post-term infants include:
A
o Shoulder dystocia o Neurologic birth injury o Meconium aspiration o Persistent pulmonary hypertension o Perinatal asphyxia
14
Q
What is the optimal intervention to prevent post-term births?
A
Induction of labor at 41 weeks gestation
o When this is not possible, neonatal management consists of screening and treating the complications associated with prolonged pregnancy
15
Q
What is the definition of pre-term infant?
A
GA <37 weeks
16
Q
• Preterm infants are more likely to have the following complications:
A
- Hypothermia
- Hypoglycemia
- Respiratory distress
- Apnea
- Hyperbilirubinemia
- Feeding difficulties
17
Q
what’s the cause of hypothermia in pre-term babies?
A
- Occurs because they have less white adipose tissue for insulation and cannot generate heat as well from brown adipose tissue.
- They also have a larger surface area/weight ratio and lose heat more quickly.
18
Q
what’s the cause of hypoglycemia in pre-term babies?
A
• Because of an inadequate response to the loss of maternal glucose supply after birth.
19
Q
What is the cause of respiratory distress in pre-term babies?
A
- Because of lung immaturity (lung development of the terminal sacs occurs around 34-36 weeks).
- Infants may also miss the surfactant surge that occurs around 34 weeks.
20
Q
What is the cause of apnea in pre-term babies?
A
- Because of immature respiratory control.
- Apnea of prematurity is a disorder that reflects the transition of intermittent breathing in the placenta to continuous breathing postnatally.
21
Q
What is the cause of hyperbilirubinemia in pre-term babies?
A
- Because of the immature hepatic bilirubin conjugation pathways
- The risk for kernicterus is also increased because of the relative immaturity of the blood-brain barrier compared to term infants
22
Q
What is the cause of feeding difficulties in pre-term babies?
A
- Because of immature oro-buccal coordination and swallowing mechanisms.
- Breast-feeding is still the best feeding method but requires closer monitoring.
23
Q
What is hyperbilirubinemia?
A
• Hyperbilirubinemia is normally defined as an elevated total serum bilirubin (TB) > 5 mg/dL; however, in infants ≥ 35 weeks gestation a TB in the 95th percentile on the hour-specific Bhutani monogram is a more appropriate definition.
24
Q
What is physiologic Jaundice?
A
• Physiologic jaundice is a nonpathologic indirect hyperbilirubinemia that peaks between days 3 and 5, and is never present before 24 hours of age.
25
How common is physiologic jaundice? What causes it?
• Extremely common and occurs due to several physiological changes that take place at birth:
Increased production: a high neonatal hematocrit and shorter life span of fetal red cells leads to large red cell turnover, with higher levels of bilirubin production;
Decreased clearance: a latent deficiency of the enzyme uridine diphosphogluconurate glucuronosyltransferase (UGT1A1) that conjugates bilirubin to make it water-soluble;
An increase in enterohepatic circulation.
26
What is breast milk jaundice?
o Nonpathologic indirect hyperbilirubinemia that presents 3 to 5 days after birth and peaks within two weeks.
27
What is breast feeding jaundice?
o Pathologic indirect hyperbilirubinemia that typically occurs during the first week of life as lactation failure leads to inadequate intake with resultant unrepleted fluid loss and significant hypovolemia. (not to be confused with breast milk jaundice)
28
What causes of pathologic indirect hyperbilirubinemia?
- Isoimmune hemolytic anemias: ABO and Rh incompatibility
| - Breast feeding failure
29
What is significant about ABO and Rh incompatibility?
o Can lead to an indirect hyperbilirubinemia with a positive direct Coombs’ test
• A direct Coombs’ test is positive for the presence of maternal antibody on the surface of neonatal red blood cells.
30
What is ABO incompatibility?
o ABO incompatibility occurs when a type O mother with a fetus of a different blood type produces small amounts of weakly-reacting anti-AB IgG which cross the placenta and result in an isoimmune hemolytic anemia.
• It is the most common cause of pathologic unconjugated hyperbilirubinemia.
• Note that unlike Rh incompatibility, prior maternal antigen sensitization is not required for ABO incompatibility.
31
What is Rh incompatibility?
o Rh incompatibility occurs when a previously sensitized Rh-negative mother with an Rh-positive fetus produces anti-Rh IgG that cross the placenta and produce a robust isoimmune hemolytic process with a significant unconjugated hyperbilirubinemia.
32
What does the following suggest?: Indirect hyperbilirubinemia in a neonate with a negative Coombs’ test and central venous hematocrit ≥ 70%
Polycythemia
33
What does the following suggest?: Indirect hyperbilirubinemia in a neonate with a negative Coombs’ test, increased reticulocyte count, and normal smear
prenatal hemorrhage/blood loss.
34
What should be done first for a neonate with indirect hyperbilirubinemia and a negative Coomb's test?
Should be evaluated with hematocrit, reticulocyte count, and smear.
35
What does the following suggest?: Indirect Hyperbilirubinemia in a neonate with a negative Coombs’ test, increased reticulocyte count, and abnormal smear
- Non-immune hemolysis
- Inherited red cell membrane defects (e.g. spherocytosis)
- Red cell enzymatic defects (glucose-6-phosphate dehydrogenase, pyruvate kinase)
- Or Thalassemia/hemoglobinopathy.
36
What does the following suggest?: Indirect hyperbilirubinemia in a neonate with a negative Coombs’ test, normal reticulocyte count, and normal smear
- Peri-/postnatal extravascular blood loss
- Bacterial sepsis
- Or Drug reaction
37
What's important to know about Direct hyperbilirubinemia? What causes it?
```
• Direct hyperbilirubinemia is always pathologic in the neonate, and may be attributable to:
o Biliary atresia
o Hepatitis
o Infection
o Inborn errors of metabolism
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38
What is kernicterus?
• When the indirect fraction of bilirubin exceeds 25-30 mg/dL, unconjugated bilirubin begins to deposit in the basal ganglia, pons, cerebellum, and hippocampus, causing acute bilirubin encephalopathy. The resultant yellowing of these tissues is known as kernicterus.
39
What is the initial treatment for unconjugated hyperbilirubinemia?
• Phototherapy using blue fluorescent lights
40
What cases of unconjugated hyperbilirubinemia would require the sue of exchange transfusion?
- Severe unconjugated hyperbilirubinemia as indicated by nomogram
- Total serum bilirubin > 25 mg/dL
- Or clinical manifestations of acute bilirubin encephalopathy
41
Is phototherapy effective in treating conjugated hyperbilirubinemia?
o Phototherapy is not effective in the setting of conjugated hyperbilirubinemia, and will result in a bronzing of the skin.
42
What is the most common cause of respiratory failure in premature infants?
- Neonatal respiratory distress syndrome, also known as hyaline membrane disease or surfactant deficiency disorder.
- It is characterized by insufficient surfactant levels and progressive atelectasis.
43
How does Neonatal Respiratory Distress Syndrome occur?
- Infants with insufficient surfactant have poor lung compliance from alveolar surface tension, resulting in areas of alveolar collapse and atelectasis.
- Alveoli are perfused but not ventilated.
- Lack of ventilation results in hypoxia, hypercapnea, and acidosis. These combined cause pulmonary arterial vasoconstriction and right-to-left shunting through the lung, foramen ovale and ductus arteriosus.
- Decreased perfusion now causes ischemic injury to the lung, decreasing surfactant further and allowing a proteinaceous effusion to enter the alveolar spaces.
44
When are mature levels of surfactant reached?
35th week of gestation
45
What is surfactant?
o Surfactant is composed mostly of lecithin (phosphotidylcholine) and other phospholipids. It coats the alveoli, reducing surface tension to oppose the collapsing pressure during expiration.
46
What are some risk factors for Neonatal Respiratory Distress Syndrome?
• Prematurity is by far the most important risk factor for NRDS. Other risk factors include:
o Male sex of infant
o Maternal diabetes
o Multiple births (leading to rapid labor) or Cesarean delivery without a trial of labor.
• These infants do not experience the normal labor process, which triggers a surge of glucocorticoids. These glucocorticoids promote lung maturation.
o Intrauterine asphyxia
47
What are protective factors that decrease the risk of Neonatal Respiratory Distress Syndrome?
o Prenatal corticosteroid use
| o Maternal hypertension
48
How does Neonatal Respiratory Distress syndrome Present?
• Infants present with rapid, shallow respirations of >60 breaths per minute. These infants are often asymptomatic at birth, with symptoms developing over minutes to hours.
o Grunting, nasal flaring, cyanosis and intercostal retractions may also be noted at birth or may develop, with breath sounds ranging from normal to harsh/tubular or rales. If untreated, cyanosis and pallor will worsen and hypotension, apnea and signs of multiorgan failure may result.
49
Whats the course of Neonatal Respiratory Distress Syndrome?
• Signs and symptoms generally peak in the first 3 days of life, after which gradual improvement is shown by decreased need for ventilator support and increased urinary output.
50
How is Neonatal Respiratory Distress syndrome diagnosed?
• Neonatal respiratory distress syndrome is diagnosed based on clinical findings, arterial blood gas, and chest x-ray.
- ABGs will show hypoxemia, hypercapnea and acidosis.
- Chest x-rays may be normal immediately after birth, but within a short time they will show a characteristic (but not pathognomonic) ground-glass granularity of the lung parenchyma.
51
How is lung fetal lung maturity assessed prenatally?
The ratio of lecithin to sphingomyelin of >2:1 in amniotic fluid is indicative of fetal lung maturity. If the ratio is less than 2:1, prophylactically treat mother with glucocorticoids.
52
How is Neonatal Respiratory Distress Syndrome managed?
o Prenatally, corticosteroids are used to prevent NRDS
• Prenatal corticosteroids are the mainstay of prevention for all women expected to deliver at less than 34 weeks. Pretreatment reduces incidence, severity and complications of NRDS. Avoidance of unnecessary or poorly timed c-sections also decreases the risk for NRDS
o Immediately after birth, treat respiratory distress with neonatal resuscitation.
o Pharmacotherapy includes artificial surfactant as soon as possible after birth. Ampicillin/gentamicin should be started until blood culture results return.
o Continuous positive airway pressure (CPAP) or intubation with mechanical ventilation is the backbone of respiratory support. Continuous monitoring in neonatal intensive care is crucial.
53
What is the expected outcome in NRDS?
• With treatment, 90% of infants with NRDS survive.
54
What's this rash?
1. Characterized by multiple erythematous macules and papules that progress to pustules.
2. They appear in the first 24-48 hours and are distributed in the trunk and proximal extremities.
3. They usually resolve in 5-7 days.
• Erythema toxicum neonatorum (Benign)
55
What's this rash?
1. Characterized by small pustules that can rupture and form macules that can persist for weeks to months.
2. They are more common in full term black infants.
• Transient neonatal pustular melanosis (Benign)
56
What's this rash?
1. Characterized by inflammatory papules that appear at 3 weeks
2. They are usually limited to the face and can be treated with soap and water and clear within 4 months.
• Neonatal acne (Benign)
57
What's this rash?
1. Common finding in newborns caused by accumulation of sweat beneath the eccrine sweat ducts that are obstructed by keratin.
2. They can present as papules or pustules and develop during the first week of life and are usually resolved by placing the infant in a cooler environment.
• Miliaria (Benign)
58
What is the Harlequin color change?
When an infant is lying on his side and causes intense reddening of the dependent side and blanching of the non-dependent side. It is entirely benign and lasts for seconds to minutes.
59
What is this lesion?
1. The most common pigmented lesions in newborns.
2. It appears as blue-grey macules that are often located in the sacral-gluteal area and the shoulders.
3. They are seen in infants of African, Asian, and Native American descent and usually fade within a year.
• Congenital dermal melanocytosis (Mongolian spot; Benign)
60
What is the Bronze baby syndrome?
Gray-brown discoloration that develops in infants 1-7 days after initiation of phototherapy for hyperbilirubinemia and resolves within several weeks after discontinuation of therapy.
61
What is this lesion?
1. Presents as a single or multiple pink-red patches in infants.
2. They occur in 40-60% of infants and occur mostly on the eyelid or back of the neck and fade within 1-2 years.
• Nevus simplex (macular stain, stork bite; Benign)
62
What is this lesion?
1. Capillary malformations that present in 0.1% of all newborns.
2. They can occur anywhere in the body and present as pink or red unilateral patches that enlarge as the child grows and eventually form darkened nodular components in adults.
3. Pulsed dye laser therapy is the standard of care.
• Port wine stains
63
What is Sturge-Weber Syndrome?
Rare congenital vascular disorder characterized by facial capillary malformation that involves the V1/V2 dermatome.
They are associated with leptomeningeal vascular malformations. The malformations may be associated with specific ocular or neurologic abnormalities that include seizure and hemiparesis. MRI is the test of choice to show the CNS abnormalities.
64
What's this rash?
1. Characterized by erythema and greasy scales.
2. It occurs most commonly on the scalp but also on the face, ears and neck.
3. It has a self-limited course and resolves in weeks to months.
4. Initial treatment should be conservative with application of an emollient and frequent shampooing followed by gentle removal of the scales.
• Seborrheic Dermatitis (Benign)
65
What is this lesion?
1. Rare congenital lesion that is a hamartoma that combines epidermal, sebaceous, follicular, and apocrine gland abnormalities.
2. The lesion is solitary and well circumscribed and yellow-tan in color.
3. The recommended treatment is surgical excision since it may have a risk of malignancy.
• Nevus sebaceous of Jadassohn
66
Cranial asymmetry persisting after DOL 2-3, is suspicious for...?
Craniosynostosis (premature fusion of the sutures leading to an asymmetrical skull)
67
What is this lesion?
1. Soft areas of the skull in the parietal region that feel like a ping-pong ball when pressed.
2. They can be pathologic in syphilis and rickets but are usually normal in infants and disappear in weeks to months.
o Craniotabes
68
What is this called?
1. An area of edema over the presenting part of the head.
2. It’s commonly present at birth, crosses the cranial sutures, and resolves in a few days.
o Caput succedaneum
69
What are these called?
1. Subperiosteal collections of blood secondary to birth trauma that do not cross suture lines.
2. They take weeks or months to resolve
o Cephalohematomas
70
Infant with asymmetric facies. Name the diagnosis:
1. Usually seen in infants who are delivered with forceps 2. Caused by damage to a mandibular branch of the facial nerve
3. Present with drooping mouth on the affected side.
4. They resolve within a few days to weeks
o Facial palsies
71
Infant with asymmetric facies. Name the diagnosis:
1. Seen with congenital absence or hypoplasia of the muscles of the mouth.
2. There is asymmetry of the face upon crying and this will usually become less noticeable as the child gets older
o Asymmetric crying facies
72
What are Epstein's pearls?
Small, white, benign, lesions on the palate that are seen in most babies. They resolve in a few weeks
73
What is this lesion?
| 1. Most common lymphatic malformation in children and usually presents as a painless, soft mass superior to the clavicle
• Cystic hygroma
74
What is the milk line?
• Accessory nipples are seen in 1/40 newborns and are found along the milk line, a line that extends from the axilla to the pubis
75
What is Diastasis recti?
The separation of the left and right side of the rectus abdominis, is common in newborns and gradually disappears as the infant develops
76
What is a Persistent Urachus?
The complete failure of the urachal duct to close and results in a fistula forming between the bladder and the umbilicus that causes urine to sometimes drain from the umbilicus
77
What is a Meconium plug? What is Meconium Ileus?
• Meconium plug
Obstruction of the left colon and rectum due to a dense, dry meconium
• Meconium ileus
The occlusion of the distal ileum due to inssipated meconium. Both meconium plug and meconium ileus can point to a manifestation of cystic fibrosis
78
What is Hydrometrocolpos?
Caused by an imperforate hymen with retained vaginal products.
It can be seen as a small cyst between the labia at the time of birth or lower abdominal mass later on in childhood
79
Important aspects of the male neonatal genital exam
• The testes should be palpable in the scrotum and should be equal in size.
If cryptorchidism is present, they will usually descend by 12 months and if not they are predisposed to malignancy
• The penis should be stretched to assess for length; normal penile length is 2.5-3.5 cm
• The urethral meatus should be seen without any retraction of the foreskin and assessed for position
80
What is hypospadias?
* The meatus is on the ventral surface of the penis in varying locations along the shaft.
* It is not associated with urinary malformations
81
What is Epispadias?
• The meatus is located along the dorsal surface of the penis and are associated with exstrophy of the bladder (bladder protrusion form the abdominal wall)
82
Name this Brachial plexus injury?
1. Causes the upper arm to be adducted and internally rotated with the forearm extended.
2. Wrist and hand movements are preserved
• C5-C6 injury (Erb’s palsy)
83
Name this Brachial Plexus injury?
| 1. Presents with isolated hand paralysis and Horner’s syndrome
* C8-T1 injury (Klumpke’s palsy)
| * C7-T1 injury causes flail arm and Horner’s syndrome
84
What are some complications related to the development and treatment of NRDS?
o Persistent patent ductus arteriosus
• Pulmonary vasoconstriction due to hypoxia in areas of atelectasis leads to increased pulmonary vascular resistance, which promotes right-to-left shunting and can lead to a persistent patent ductus arteriosus.
o Bronchopulmonary dysplasia
• Bronchopulmonary dysplasia (abnormal maturation of the lung tissue) occurs following barotrauma from mechanical ventilation.
o Retinopathy of prematurity
• Cycles of hypoxia and hyperoxia induce VEGF and lead to abnormal proliferation of blood vessels in the retina, leading to retinopathy of prematurity.
85
What is retinopathy of prematurity?
* Retinopathy of prematurity is a serious vasoproliferative disorder of the eye that typically affects extremely low birth weight premature infants.
* Retinal vascularization begins around 16 weeks’ gestation, growing circumferentially from the center outward until term when it becomes fully mature. Premature birth halts normal retinal vascular maturation.
86
What causes retinopathy or prematurity?
• Premature infants with respiratory failure are exposed to cycles of hypoxemia and hyperoxemia during mechanical ventilation.
o Periods of hypoxemia cause upregulation of retinal vascular endothelial growth factor (VEGF) and vessel proliferation.
o Periods of hyperoxemia cause oxygen toxicity and free radical damage to the vessels, which causes VEGF to be downregulated. This ultimately causes blood vessels to constrict and become obliterated.
87
What is the incidence of retinopathy of prematurity?
• The incidence of retinopathy of prematurity is reported to be between 50-70% in infants weighing less than 1250g.
88
How is retinopathy of prematurity diagnosed?
• Diagnosis must be made by an ophthalmologist who is experienced in evaluating infants with retinopathy of prematurity.
o The ophthalmologic evaluation is performed with pupil dilation so that the peripheral retina may be examined, which is the most common location retinopathy of prematurity is seen.
89
When should infants be screened for retinopathy of prematurity?
* Screening should be performed on infants weighing less than 1500g or a gestational age of 31 weeks or less.
* Retinopathy of prematurity may lead to life-long blindness.
90
What is Transient tachypnea of the newborn (TTN)?
* Transient tachypnea of the newborn (TTN) is a benign disorder that presents during the newborn period and is characterized by pulmonary edema from lack of resorption of alveolar fluid
* TTN occurs in about 6/1000 births
* TTN is a benign, self-limited condition that can last up to 72 hours in severe cases
91
What is the pathophysiology of TTN?
• In late gestation the lung switches from actively secreting chloride (and thus, fluid) to actively reabsorbing sodium (and thus, fluid).
o This leads to increased expression of sodium channels
o In immature lungs, expression of sodium channels is reduced leading to the inability to switch from fluid secretion to fluid absorption
• In TTN, fluid fills the air spaces and moves into the interstitium where it pools in the tissues and interlobar fissures until it is eventually cleared by the lymphatics. The excess fluid causes reduced pulmonary compliance, which leads to tachypnea to compensate for the increased work of breathing.
92
What are risk factors for developing TTN?
• Risk factors for TTN include cesarean delivery, infants born to diabetic mothers, and maternal asthma
93
What are the clinical characteristics of TTN?
• The onset of TTN is from the time of birth to within two hours of delivery
• Clinical features include:
o Tachypnea (respiratory rate > 60)
o Nasal flaring
o Expiratory grunting
o Mild subcostal and intercostal retractions
94
How is TTN diagnosed?
```
• TTN is a clinical diagnosis but does have radiographic findings that help support the diagnosis
• Radiographic findings include:
o Increased lung volumes
o Flat diaphragm
o Fluid in the interlobar fissures
o Prominent vascular markings
```
95
How is TTN managed?
• Management is supportive and includes:
o Supplemental oxygen via hood or nasal canula
o Neutral thermal environment
o Nutrition (if respiratory rate is greater than 80, tube feeding may be necessary)
