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Final Review > Perinatal Diseases > Flashcards

Perinatal Diseases Flashcards

1
Q
A
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2
Q

Retinopathy of Prematurity

Crucial Factors

A

Birth weight

Gestational age

Number of days O2 administered

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3
Q

Retinopathy of Prematurity (ROP)

(Retrolental Fibroplasia)

A
  • Abnormal eye condition
  • Occurs in premature/low birth weight infants that receive supplemental O2
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4
Q

Retinopathy of Prematurity (ROP)
Pathophysiology

A

•Excessive fiO2

retinal vasoconstriction

necrosis of blood vessels

new vessels form and increase in number

hemmhorage of delicate new vessels cause scarring

scarring can lead to retinal detachment and blindness

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5
Q

Other Factors Associated with ROP:

A

Hypercapnia, hypocapnia, IVH, Infection, Lactic Acidosis, mineral deficiencies,

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6
Q

Retinopathy of Prematurity (ROP)

Clinical Manifestations

(Retrolental Fibroplasia)

A

Poor eye tone, loss of tracking.

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7
Q

Retinopathy of Prematurity (ROP)

Laboratory Findings:

(Retrolental Fibroplasia)

A

Ultrasounds will identify retinal damage.

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8
Q

Retinopathy of Prematurity (ROP)

Modes of Treatment

(Retrolental Fibroplasia)

A

Prevention

Decrease FiO2’s as low as possible

Cryotherapy and laser therapy can be performed based on severity

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9
Q

Retinopathy of Prematurity (ROP)

Prognosis

(Retrolental Fibroplasia)

A

Varying degrees of sight loss and potential blindness

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10
Q

IVH - Intraventricular Hemorrhage:

A
  • Very common in low birth weight babies (premature infants)
  • Incidence ranges from 20% –80%
  • About 40% of IVH are associated with development of hydrocephalus
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11
Q

IVH - Intraventricular Hemorrhage:
Risk Factors

A

Prematurity

Birth asphyxia

Hypoxia,

Hypercapnia,

acidosis,

RDS,

pneumothorax,

changes in hemodynamic status,

rapid blood volume expansion,

PDA

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12
Q

IVH - Intraventricular Hemorrhage:
Pathophysiology

A
  • Bleeding starts in the germinal matrix (a highly vascular network that matures and gets smaller with gestational age)
  • Immature vasculature in premature infants
  • blood fills the ventricles
  • compression of brain parenchyma
  • Any factor that increases or decreases cerebral blood flow will cause rupture
  • Patient condition will deteriorate depending on size of bleed.
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13
Q

Intraventricular Hemorrhage

Clinical Manifestations

A
  • subtle to catastrophic
  • Range from asymptomatic to bulging fontanels, sudden drop in hematocrit, apnea, hypotension, hypotonia, bradycardia, acidosis, seizures, and loss of consciousness.
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14
Q

Intraventricular Hemorrhage

Diagnosis

A
  • Head Circumference-Will be done daily to see if there is swelling
  • Ultrasound
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15
Q

Intraventricular Hemorrhage

Management

A
  • best treatment is prevention
  • Supportive treatment – maintain CPP, suppress seizures, manage respiratory status
  • Ventricular drains and serial lumbar punctures can drain excess CSF
  • Complications are more severe with the higher grade bleeds – can range from developmental delay to overt vegetation or death.
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16
Q

Congenital Diaphragmatic Hernia

A
  • CDH is a severe disease that manifest as severe respiratory distress
  • Characterized by abnormal opening due to closing failure or membrane hypoplasia that leaves an opening between the peritoneal and pleural spaces
  • So the abdominal content will move up and take over
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17
Q

What are the 2 types of congenital diaphragmatic hernia

A
  • Bochdalek Hernia
    • Lateral and posterior defect
    • Usually will occur in the left hemidiaphragm
    • Most common
      • Occurs 90% of the time
  • Morgagni Hernia
    • Medial and anterior
    • Occurs on both sides
    • Liver will prevent some up the upwards movement
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18
Q

Congenital Diaphragmatic Hernia

Pathophysiology

A
  • Lung Hypoplasia
    • Decrease Alveolar Count
    • Decreased pulmonary vasculature
  • Pulmonary hypertension
  • Unusual anatomy of inferior vena cava
  • Left lung does not have enough space to develop properly
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19
Q

Congenital Diaphragmatic Hernia

Chest X Ray

A

Loop and air in the thoracic cavity

Mediastinum will be pushed to the right

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20
Q

Congenital Diaphragmatic Hernia

Clinical Manifestations

A
  • Significant respiratory distress at birth with severe hypoxia and acidosis
  • Scaphoid Abdomen
    • Depressed Triagular shape
  • Heart displaced to the oppsoite side of hernia
  • Barrel Chest
  • Increased PVR with a persistent shunt
    • Worsening right to left shunt
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21
Q

Congenital Diaphragmatic Hernia

Diagnosis

A

In utero with an ultrasound

CXR

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22
Q

Congenital Diaphragmatic Hernia

Management

A
  • Immediate intubation and mechanical ventilation
    • We have to intubate immediately as BMV will push air into the intestines
  • Paralysis
  • OG/NG
  • HVOV
    • Low volume, low pressure, and high frequency
    • This is the 1st line of defense
  • Inhaled iNO for the pulmonary hypertension
  • ECMO
    • Not routinely use and Edmonton and Vancouver are the only centres in Canada with pediatric ECMO
  • Surgery
    • Can help, but it will not reverse the hypoplastic lung
    • Remember that these problem tend to occur along with other problems so surgery may not be an option right away
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23
Q

Congenital Diaphragmatic Hernia

Prognosis

A

50% mortality

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24
Q

Periventricular Leukomalacia (PVL)

A

Area of infarct due to hypoxic ischemic encephalopathy.

The most common ischemia brain injury in premature babies, but is also seen in term infants

Often occurs concomitantly with IVH

Caused by asphyxia either in utero, during labour, or in the postnatal phase.

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25
Q

Periventricular Leukomalacia (PVL)

Pathophysiology

A

Occurs in the white matter adjacent to the lateral ventricles

Injury occurs in response to hypotension, ischemia, and necrosis due to asphyxia.

Can also results from increased fluid or hemorrhagecompressing arterioles in the white matter.

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26
Q

Periventricular Leukomalacia (PVL)

Clinical Manifestation

A
  • Decreased tone
  • Apneas and bradycardias
  • Irritability
  • Seizures
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27
Q

Periventricular Leukomalacia (PVL)

Lab Findings

A

•Densities or cysts on cranial US.

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28
Q

Periventricular Leukomalacia (PVL)

Management

A
  • No treatment is currently available.
  • Increased risk of developing Cerebral Palsy, developmental delays and Epilepsy
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29
Q

Hyperbilirubinemia

A

Bilirubin is created when hemoglobin breaks down

After birth, the babe needs to be fed early to establish normal GI flora to initiate the babe’s mechanism of breaking down the biliinto the conjugated form. If this is not possible or there are other problems, the biliwill not be broken down and will start building up unconjugated bili.

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30
Q

Neonatal Jaundice

A
  • Occurs in 50% of normal births
  • Can occur due to delayed feeding, hemolytic disease, liver/gut defects.
  • Kernicterus is severe hyperbilirubinemia that toxifies the baby and leads to CNS impairment, seizures, motor dysfunction.
  • Treatment for Jaundice:
    • Phototherapy (blue light) helps to form conjugated bilirubin to allow excretion, and exchange transfusion.
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31
Q

Necrotizing Enterocolitis (NEC)

A

Usually occurs in premature infants

Inflammatory destructive bowel disease

Characterized by necrosis of the colon and ileum caused by intestinal ischemia

Necrosis will cause abdominal distension, sepsis, hypoxemia, respiratory failure, intestinal perforation

Gangrene can also occur

Related to asphyxia in utero

Mortality depends on severity of disease and increases with low birth weight

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32
Q

Omphalocele

A
  • A protrusion of variable amounts of abdominal organs from an opening below the umbilicus Gastroschisis.
  • Protrusion of the abdominal organs from an opening beside the umbilicus, R side.
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33
Q

Trisomies

A
  • Chromosomal disorders with variable defects
  • Trisomy 21 is Down’s Syndrome – maternally derived extra chromosome 21.
34
Q

Spina Bifida

A
  • Variable degrees of failure of the vertebral column to close fully.
  • Can be fully exposed or partially.

Can include meninges, spinal cord, or both.

35
Q

Tracheoesophageal Fistula

A

Defect with atresia of the upper esophagus with communication to the trachea

Results from a utero malformation

The reflux of saliva and gastic acid into the trachea results in aspiration pneumonitis

Crying of the infant often results in the distension of the stomach with air and the elevation of the diaphragm contributing to respiratory distress

36
Q

Types of TR Fistula

A
  1. Esophageal atresia with a distal TF (most common)
  2. Isolated esophageal atresia with a long gap of missing esophagus between proximal and distal esophageal pounches
  3. TEF without esophageal atresia
  4. Esophageal atresia with proximal fistula
  5. Esophageal atresia with both proximal and distal TEFs
37
Q

Tracheoesophageal Fistula

Clinical Manifestation

A
  • Excessive oral secretions
    • Bubbling and frothing at the mouth
  • Drooling may be associated with chocking or gasping
  • Sporadic and/or continuous respiratory distress with cyanosis-Especially during feeding
  • Repeated regurgitation
  • Distended abdomen with bagging
  • Babies with this will have infection problems
38
Q

Tracheoesophageal Fistula

Diagnosis

A

Inability to pass to the stomach

Chest and abdominal x-ray

39
Q

Tracheoesophageal Fistula

Management

A

Intubation and ventilation

Distended abdomen (aerophagia)

Keep HOB upright at 30

Frequent oral suctioning

Broad spectrum antibiotics

Surgical repairs

40
Q

Tracheoesophageal Fistula

Prognosis

A

90% survival with surgical repair

41
Q

Pierre-Robin Syndrome

A
  • Congenital anomaly that presents itself with a small mandible and oropharynx that causes the tongue to occlude the airway
  • Defect characterized by (all will result in obstruction)
    • Mandibular hypoplasia
    • Posterior/downward placement of tongue
    • Micrognathia
    • Cleft palate
42
Q

Pierre-Robin Syndrome

Clinical Manifestation

A

Symptoms vary with degree of severity of obstruction from mild to severe respiratory distress

Respiratory distress is not relieved through crying

Very difficult to BMV and intubate

43
Q

Pierre-Robin Syndrome

Management

A
  • Prone position
    • Allows the tongue to fall forward and open airway
  • Nasotracheal Intubation
  • Temporary insertion of OPA and NPA
  • A nasotracheal tube can help maintain a patent airway
  • Trach and surgical repair
44
Q

Pierre-Robin Syndrome

Prognosis

A

Good prognosis may or may not require surgical repair

45
Q

Choanal Atersia

A
  • A blockage or absence of the posterior nares due to congenital malformation
    • Can be membranous or bony in origin
  • Obstruction can be unilateral or bilateral
  • Occurs twice as often in females
  • Occurs in 1/700 births
46
Q

Choanal Atersia

Clinical Manifestation

A

·Respiratory distress with cycle of distress and cyanosis with momentary relief of obstruction

·Clinical improvements when the neonates cries

·Significant respiratory distress at birth because babies are naturally nose breathers which is why when in respiratory distress they open their mouths to cry

47
Q

Choanal Atresia

Diagnosis

A

The inability to pass a catheter through the nares into the oropharynx

48
Q

Choanal Atresia

Management

A

Stimulation so infant breathes through mouth

Oral airway

Intubation

49
Q

Choanal Atresia

Prognosis

A

Good with reconstruction

50
Q

Tracheomalacia

A

Flaccidity of supporting tracheal cartilage

Widening of posterior membranous wall

Reduced A-P airway caliber

Can occur from high pressure ventilation or a difficult intubation suction

51
Q

Tracheal Stenosis

A

Typical around a vascular ring

Narrowing of eth trachea due to a birth defect

Can also be caused by a traumatic/chronic intubation

Hardening and narrowing

52
Q

Vascular Ring

A

A vascular ring is a congenital abnormality

There can be a vascular ring are the trachea and esophagus

53
Q

Tracheomalacia/Tracheal Stenosis

Pathophysiology

A

Both result in a decreased radius on inspiration

Recurring pneumonia

Hyperinflation

54
Q

Tracheomalacia/Tracheal Stenosis

Clinical Manifestations

A

Chronic wheezing which worsens with increased WOB

Hypoxemia

Hyperinflation

55
Q

Tracheomalacia/Tracheal Stenosis

Lab Findings

A

Viewed with a flexible bronchoscopy

56
Q

Tracheomalacia/Tracheal Stenosis

Management

A

Observation

Balloon dilation (stenosis)

Tracheal resection

Tracheostomy tube

CPAP

57
Q

Tracheomalacia/Tracheal Stenosis

Prognosis

A

Good with surgical care

58
Q

Choanal Atersia

Clinical Manifestation

A

·Respiratory distress with cycle of distress and cyanosis with momentary relief of obstruction

·Clinical improvements when the neonates cries

·Significant respiratory distress at birth because babies are naturally nose breathers which is why when in respiratory distress they open their mouths to cry

59
Q

Tracheomalacia/Tracheal Stenosis

Prognosis

A

Good with surgical care

60
Q

Tracheomalacia/Tracheal Stenosis

Management

A

Observation

Balloon dilation (stenosis)

Tracheal resection

Tracheostomy tube

CPAP

61
Q

Tracheomalacia/Tracheal Stenosis

Lab Findings

A

Viewed with a flexible bronchoscopy

62
Q

Tracheomalacia/Tracheal Stenosis

Clinical Manifestations

A

Chronic wheezing which worsens with increased WOB

Hypoxemia

Hyperinflation

63
Q

Tracheomalacia/Tracheal Stenosis

Pathophysiology

A

Both result in a decreased radius on inspiration

Recurring pneumonia

Hyperinflation

64
Q

Vascular Ring

A

A vascular ring is a congenital abnormality

There can be a vascular ring are the trachea and esophagus

65
Q

Tracheal Stenosis

A

Typical around a vascular ring

Narrowing of eth trachea due to a birth defect

Can also be caused by a traumatic/chronic intubation

Hardening and narrowing

66
Q

Tracheomalacia

A

Flaccidity of supporting tracheal cartilage

Widening of posterior membranous wall

Reduced A-P airway caliber

Can occur from high pressure ventilation or a difficult intubation suction

67
Q

Choanal Atresia

Prognosis

A

Good with reconstruction

68
Q

Choanal Atresia

Management

A

Stimulation so infant breathes through mouth

Oral airway

Intubation

69
Q

Choanal Atresia

Diagnosis

A

The inability to pass a catheter through the nares into the oropharynx

70
Q

Choanal Atersia

A
  • A blockage or absence of the posterior nares due to congenital malformation
    • Can be membranous or bony in origin
  • Obstruction can be unilateral or bilateral
  • Occurs twice as often in females
  • Occurs in 1/700 births
71
Q

Pierre-Robin Syndrome

Prognosis

A

Good prognosis may or may not require surgical repair

72
Q

Pierre-Robin Syndrome

Management

A
  • Prone position
    • Allows the tongue to fall forward and open airway
  • Nasotracheal Intubation
  • Temporary insertion of OPA and NPA
  • A nasotracheal tube can help maintain a patent airway
  • Trach and surgical repair
73
Q

Pierre-Robin Syndrome

Clinical Manifestation

A

Symptoms vary with degree of severity of obstruction from mild to severe respiratory distress

Respiratory distress is not relieved through crying

Very difficult to BMV and intubate

74
Q

Pierre-Robin Syndrome

A
  • Congenital anomaly that presents itself with a small mandible and oropharynx that causes the tongue to occlude the airway
  • Defect characterized by (all will result in obstruction)
    • Mandibular hypoplasia
    • Posterior/downward placement of tongue
    • Micrognathia
    • Cleft palate
75
Q

Tracheoesophageal Fistula

Prognosis

A

90% survival with surgical repair

76
Q

Tracheoesophageal Fistula

Management

A

Intubation and ventilation

Distended abdomen (aerophagia)

Keep HOB upright at 30

Frequent oral suctioning

Broad spectrum antibiotics

Surgical repairs

77
Q

Tracheoesophageal Fistula

Diagnosis

A

Inability to pass to the stomach

Chest and abdominal x-ray

78
Q

Tracheoesophageal Fistula

Clinical Manifestation

A
  • Excessive oral secretions
    • Bubbling and frothing at the mouth
  • Drooling may be associated with chocking or gasping
  • Sporadic and/or continuous respiratory distress with cyanosis-Especially during feeding
  • Repeated regurgitation
  • Distended abdomen with bagging
  • Babies with this will have infection problems
79
Q

Types of TR Fistula

A
  1. Esophageal atresia with a distal TF (most common)
  2. Isolated esophageal atresia with a long gap of missing esophagus between proximal and distal esophageal pounches
  3. TEF without esophageal atresia
  4. Esophageal atresia with proximal fistula
  5. Esophageal atresia with both proximal and distal TEFs
80
Q

Tracheoesophageal Fistula

A

Defect with atresia of the upper esophagus with communication to the trachea

Results from a utero malformation

The reflux of saliva and gastic acid into the trachea results in aspiration pneumonitis

Crying of the infant often results in the distension of the stomach with air and the elevation of the diaphragm contributing to respiratory distress

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