neonatal diseases
Skip this Video
Download Presentation
Neonatal Diseases

Loading in 2 Seconds...

play fullscreen
1 / 98

Neonatal Diseases - PowerPoint PPT Presentation

  • Uploaded on

Neonatal Diseases. RC 290. Respiratory Distress Syndrome (RDS). Also known as Hyaline Membrane Disease (HMD). Occurrence. 1-2% of all births 10% of all premature births Greatest occurrence is in the premature and low birth weight infant. Etiology & Predisposing Factors. Prematurity

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about ' Neonatal Diseases' - cassandra-lara

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
respiratory distress syndrome rds

Respiratory Distress Syndrome(RDS)

Also known as Hyaline Membrane Disease


  • 1-2% of all births
  • 10% of all premature births
    • Greatest occurrence is in the premature and low birth weight infant
etiology predisposing factors
Etiology & Predisposing Factors
  • Prematurity
    • Immature lung architecture and surfactant deficiency
  • Fetal asphyxia & hypoxia
  • Maternal diabetes
    • Increased chance of premature birth
    • Possible periods of reflex hypoglycemia in the fetus causing impaired surfactant production

Surfactant deficiency

  • Decreased FRC
  • Atelectasis
  • Increased R-L shunt
  • Increased W.O.B.
  • Hypoxemia and eventually hypercapnia because of V/Q mismatch
pathophysiology cont
Pathophysiology (cont.)

Atelectasis keeps PVR high

  • Increased PAP
  • Lung hypoperfusion
  • R-L shunting may re-occur across the Ductus Arteriosus and the Foramen Ovale
hypoxia hypoxemia results in anaerobic metabolism and lactic acidosis

Hypoxia/hypoxemia results in anaerobic metabolism and lactic acidosis

This damages the alveolar-capillary membrane causing formation of hyaline membranes. Hyaline membranes perpetuate all of the problems in the lung

the cycle continues until surfactant levels are adequate to stabilize the lung
The cycle continues until surfactant levels are adequate to stabilize the lung
  • Symptoms usually appear 2-6 hours after birth
    • Why not immediately?
  • Disease peaks at 48-72 hours
  • Recovery usually occurs 5-7 days after birth
clinical findings physical
Tachypnea (60 BPM or >)


Nasal flaring

Expiratory grunting

Helps generate autoPEEP

Decreased breath sounds with crackles

Cyanosis on room air



Clinical findings: Physical
clinical findings lab
Clinical Findings: Lab
  • ABGs: initially respiratory alkalosis and hypoxemia that progresses to profound hypoxemia and combined acidosis
  • Increased Bilirubin
  • Hypoglycemia
  • Possibly decreased hematocrit
time constant is decreased since elastic resistance is so high

Time constant is decreased since elastic resistance is so high

Increased elastic resistance means decreased compliance!

rds treatment primarily supportive until lung stabilizes
RDS Treatment: Primarily supportive until lung stabilizes
  • NTE, maintain perfusion, maintain ventilation and oxygenation
  • O2 therapy, CPAP or mechanical ventilation
    • May require inverse I:E ratios if oxygenation can not be achieved with normal I:E ratio
  • Surfactant instillation!!!
    • May cause a sudden drop in elastic resistance!
prognosis complications

Prognosis is good once infant makes it past the peak (48-72 hours)

Complications possible are:

  • Intracranial Bleed
  • BPD (Bronchopulmonary Dysplasia)
  • PDA (Patent Ductus Arteriosus)
transient tachypnea of the newborn ttn

Transient Tachypnea of the Newborn (TTN)

Also known as Type II RDS or Retained Lung Fluid

occurrence similar to rds

Occurrence: Similar to RDS

More common in term infants!

etiology predisposing factors1
Etiology & Predisposing Factors
  • C-section
    • These infants do not have the fluid expelled from their airways as occurs in vaginal delivery
  • Maternal Diabetes
    • Increased chance of C-section due to LGA
  • Cord Compression
  • Anesthesia
ttn pathophysiology
TTN Pathophysiology

Primary problem = retained lung fluid

  • Fluid not expelled from airways because of C-section
  • Poor absorption of remaining fluid by pulmonary capillaries and lymphatics
  • If retained fluid is in interstitial spaces, compliance and TC are decreased
  • If retained fluid is in airways,airway resistance and TC are increased
  • TTN can be restrictive , obstructive, or both!
  • Fluid usually clears by itself after 24-48 hours after birth
clinical signs
Clinical Signs
  • Tachypnea (usually rate is greater than seen in RDS)
  • Minimal (if any) nasal flaring or expiratory grunting
  • ABG’s: mild hypoxemia. PaCO2 depends on whether problem is restrictive or obstructive
ttn cxr
  • Coarse peri-hilar streaks
  • Prominent lung vasculature
  • Flattened diaphragms if fluid is causing obstruction/air-trapping
ttn treatment like rds it is primarily supportive
TTN Treatment: Like RDS, it is primarily supportive
  • Monitoring and O2 therapy
  • Possibly CPAP or mechanical ventilation
prognosis complications1
  • Prognosis is very good
  • Main complication is pneumonia
    • Often initial diagnosis
patent ductus arteriosus pda

Patent Ductus Arteriosus-PDA_

Failure of the D.A. to close at birth or a re-opening of the D.A. after birth. Allows shunting between the pulmonary artery and the aorta

  • 1 per 2000 term babies
  • 30-50% of RDS babies
etiology predisposing factors2
Etiology & Predisposing Factors
  • Prematurity
    • D.A. not as sensitive to increasing PaO2
  • Hypoxia
    • Decreasing PaO2 allows it to re-open for up to three weeks after birth
  • Thus, a PDA can occur in a premature infant who is NOT hypoxic or in a term baby who is hypoxic
    • Worst case is a premature infant who is hypoxic!
  • D.A. fails to close or it re-opens
  • Then shunting occurs between the pulmonary artery and the aorta
  • The direction of the shunt depends on which vessel has the higher pressure
    • A PDA can cause L-R shunting or R-L shunting!
  • Clinically, most PDA’s refer to a L-R shunt
clinical signs1
Clinical Signs
  • Tachypnea, bounding pulses, hyperactive pre-cordium
  • Decreased breath sounds and possibly some crackles
  • Possible murmur over left sternal border
    • Murmur is loudest when D.A. just starts opening or when it is almost closed
clinical signs cont
Clinical Signs (cont.)
  • ABGs – hypoxemia with respiratory acidosis
  • If R-L shunting, the PaO2 in the upper extremities, ie pre-ductal, will be greater than the PaO2 in the umbilical artery, ie post-ductal!
  • TC – decreased if L-R shunting causes pulmonary edema; increased if fluid spills into airways and increases airway resistance
  • CXR – if L-R shunt, butterfly pattern of pulmonary edema with possible cardiomegaly
pda treatment
PDA Treatment
  • Basic – NTE, O2, may require CMV if not already on the ventilator
  • Medical
    • L-R shunt that fails to close: Indomethacin (Indocin)
    • R-L shunt: Priscoline (Tolazoline) to decrease PVR; also nitric oxide
  • Surgical –if medical treatment fails, the PDA may be surgically ligated
prognosis complications2

Good prognosis when baby responds to medical treatment

May develop :

  • Shock
  • CHF
  • Necrotizing Enterocolitis (NEC)
meconium aspiration syndrome mas

Meconium Aspiration Syndrome-MAS-

Syndrome of respiratory distress that occurs when meconium is aspirated prior to or during birth

  • 10-20% of ALL births show meconium staining
    • 10-50% of stained babies may be symptomatic
  • More common in term and post-term babies
etiology predisposing factors3
Etiology & Predisposing Factors
  • Intra-uterine hypoxic or asphyxic episode
  • Post-term
  • Cord compression
pathophysiology check valve effect
Pathophysiology: Check Valve Effect

Causes gas trapping (obstruction)

If complete obstruction, then eventually atelectasis occurs

Irritating to airways, so edema and bronchospasm

Good culture ground for bacteria, so pneumonia possible

pathophysiology cont1
Pathophysiology (cont.)
  • V/Q mismatch leads to hypoxia and acidosis which increases PVR
  • TC increases because it increases airway resistance
  • Meconium is usually absorbed in 24-48 hours; there are still many possible complications
clinical signs2
Respiratory depression or distress at birth



Meconium stained body

Possible cyanosis on room air

Moist crackles

ABGs – hypoxemia with combined acidosis

CXR – coarse, patchy infiltrates with areas of atelectasis and areas of hyperinflation

May see flattened diaphragms if obstruction is severe

Clinical Signs
m a s treatment
Amnioinfusion – artificial amniotic fluid infused into uterus to dilute meconium

Proper resuscitation at birth(clear meconium from trachea before stimulating respiration)

Oro-gastric tube



NaHCO3 if severe metabolic acidosis

Broad spectrum antibiotics

Bronchial hygiene

May need mechanical ventilation

Slow rates and wide I:E ratios because of increased TC

Low level of PEEP may help prevent check valve effect

May need HFO

M.A.S. Treatment
prognosis complications3
Prognosis & Complications

Good prognosis if there are no complications



Pulmonary baro/volutrauma

Persistent Pulmonary Hypertension (PPHN)

persistent pulmonary hypertension pphn

Persistent Pulmonary Hypertension-PPHN-

Also known as Persistent Fetal Circulation


results in r l shunting across the d a and the foramen ovale

Failure to make the transition from fetal to neonatal circulation or a reversion back to the condition where pulmonary artery pressure exceeds aortic pressure

Results in R-L shunting across the D.A. and the Foramen Ovale

  • Usually term and post-term babies
  • Females more often than males
  • Symptoms may take 12-24 hours after birth to develop
etiology predisposing factors4
Etiology & Predisposing Factors
  • M.A.S – most common
  • Hypoxia and /or acidosis, eg RDS
  • Any condition that causes PVR to increase
  • Primary problem is pulmonary artery hypertension
    • Infants arterial walls are thicker and they are more prone to vasospasm
  • If pulmonary artery pressure gets high enough, blood will shunt R-L across the D.A. and Foramen Ovale
    • Remember, conditions that drive up PAP usually make the D.A. open
  • Lung is hypoperfused resulting in refractory hypoxemia and hypercapnia
clinical signs3
Clinical Signs
  • Refractory hypoxemia and cyanosis
  • Shock and tachypnea
  • Murmur possible
  • Pre-ductal PaO2 > post-ductal PaO2
    • Hypoxemia with combined acidosis
  • CXR usually OK when compared to infants condition
pphn treatment
PPHN Treatment
  • NTE and O2
  • Nitric Oxide
    • Often in conjunction with HFO
  • Priscoline, Indocin may also be used
  • If completely unresponsive to therapy ECMO may be tried
prognosis complications4
Prognosis & Complications

Prognosis depends on how well infant responds to treatment


  • Shock
  • Intracranial bleed
  • Internal bleeding
    • Especially a problem if Priscoline is used
wilson mikity syndrome pulmonary dysmaturity

Wilson – Mikity Syndrome-Pulmonary Dysmaturity-

Respiratory distress that develops after the first week of life and presents with definite CXR changes

  • Usually in <36 weeks gestational age and birth weight <1500 grams
  • After first week of life
    • No prior symptoms
etiology predisposing factors5
Etiology & Predisposing Factors
  • Exact etiology unknown
  • Appears to be due to immature lung and airways trying to function
  • Not due to O2 toxicity or mechanical ventilation!
  • Immature alveoli and T-B tree causes V/Q mismatch
  • Areas of atelectasis and hyperinflation develop
pathology cont
Pathology (cont.)

3 Stages

  • Stage 1
    • 1-5 weeks after birth
    • Diffuse areas of atelectasis and hyperinflation
  • Stage 2
    • 1-5 months after birth
    • Cystic (hyperinflated) areas coalesce and cause flattening of the diaphragms
  • Stage 3
    • 5-24 months after birth
    • Cystic areas start to clear up
clinical signs4
Clinical Signs
  • Tachypnea
  • Cyanosis on room air
  • Some retractions and/or nasal flaring
  • Decreased breath sounds with crackles
  • ABGs – respiratory acidosis with hypoxemia
  • CXR consistent with the stage of the disease
wilson mikity treatment
Wilson – Mikity Treatment
  • Is purely supportive-there is no medicinal or surgical treatment
  • O2 and NTE
    • Some cases require mechanical ventilation
  • Maintain fluids/electrolytes and caloric intake
  • Watch for infection
prognosis complications5
Prognosis & Complications

Prognosis good if infant survives stage 2


  • PDA
  • Cor Pulmonale
  • CNS damage
bronchopulmonary dysplasia bpd

Bronchopulmonary Dysplasia-BPD-

A result of RDS and/or its treatment that results in areas of fibrosis, atelectasis, and hyperinflation

etiology predisposing factors6
Etiology & Predisposing Factors
  • RDS and prematurity
  • Triad of O2, ET tube, and mechanical ventilation
pathology 4 stages
Stage 1

Acute phase of RDS

Stage 2

4-10 days after the onset of RDS

Areas of atelectasis and hyperinflation

Stage 3

2-3 weeks after RDS

Hyperinflated areas start to coalesce

Fibrosis starts to develop

Stage 4

1 month after the onset of RDS

Diaphragms start to flatten

Interstitial fibrosis evident on CXR

PPHN may start to develop

O2 dependency develops

Pathology: 4 Stages
clinical signs5
Clinical Signs
  • Tachypnea
  • Persistent retractions
  • A-B spells
  • Cyanosis on room air
  • Decreased breath sounds with crackles
  • ABGs – respiratory acidosis (may be compensated) with hypoxemia
  • CXR – consistent with stage of disease
bpd stage 4 cxr
BPD: Stage 4 CXR

Interstitial fibrosis and flattened diaphragms

bpd treatment
BPD Treatment
  • Prevention is best! Use the least amount of intervention for the least amount of time!
  • Supportive care
    • O2, NTE, bronchial hygiene, maintain fluids/electrolytes
    • Diuretics if needed to prevent fluid overload and heart failure
  • Possibly vitamin E
prognosis complications6
Prognosis & Complications

Good if infant survives to age 2

    • 50% mortality if PPHN develops


  • PHTN
  • Cor Pulmonale
  • Respiratory Infections
  • CNS damage
diaphragmatic hernia

Diaphragmatic Hernia

Congenital malformation of the diaphragm that allows abdominal viscera into the thorax

  • 1 per 2200 births
etiology predisposing factors7
Etiology & Predisposing Factors
  • Exact unknown but may be related to vitamin A deficiency
  • Usually occurs during the 8-10th week of gestation
  • 80% occur on the left at the Foramen of Bochdalek
  • Abdominal viscera enters thorax and compresses developing lung
  • As baby attempts to breathe after birth, the stomach and bowel fill with air and cause further compression of the lung
    • Severe restriction!
clinical signs6
Clinical Signs
  • Cyanosis
  • Severe respiratory distress with retractions and nasal flaring
  • Bowel sounds in chest
  • Uneven chest expansion
  • Decreased breath sounds on affected side
  • ABGs – profound hypoxemia with combined acidosis
  • CXR – loops of bowel in chest with shift of thoracic structures towards unaffected side, eg dextrocardia
diaphragmatic hernia treatment
Diaphragmatic Hernia Treatment
  • Immediate ET tube and NG tube
    • No BVM – it will make things worse!
  • Surgical repair
  • Post operative ECMO and/or HFO
    • May need NO with HFO
prognosis complications7
Prognosis & Complications

50% mortality


  • Pneumothorax
  • PDA
  • Hypoplastic lung
4 main types
4 Main Types
  • Pneumothorax
  • Pneumomediastinum
  • Pneumopericardium
  • PIE (Pulmonary Interstitial Emphysema)
    • Gas from ruptured alveoli dissects along perivascular and interstitial spaces
    • Causes airway compression (obstruction) and alveolar compression (restriction)
    • May lead to pneumothorax, pneumomediastinum, or pneumopericardium


1-2% of all births

(not all are symptomatic)

etiology predisposing factors8
Etiology & Predisposing Factors
  • Positive pressure ventilation
  • Increased airway resistance/airway obstruction
  • RDS
clinical signs7
Sudden cyanosis (except with PIE)

Respiratory distress

Mediastinal shift

Sudden hypotension (except with PIE)

Crepitus (if sub-Q emphysema develops)

Unequal chest expansion

Decreased breath sounds and hyperressonance

ABGs – hypoxemia with respiratory acidosis


Clinical Signs

Small Pneumothorax


Big Pneumothorax

cxr pneumomediastinum
CXR: Pneumomediastinum

Note how air does NOT outline the apex of the heart

cxr pneumopericardium
CXR: Pneumopericardium

Note how air completely outlines the heart

air leak syndrome treatment
Air Leak Syndrome Treatment
  • Prevention! Use the least amount of intervention for the shortest time possible!
  • Chest tube for pneumothorax
  • HFO may help prevent and/or resolve PIE
prognosis and complications
Prognosis and Complications
  • Good as long as shock and/or cardiac tamponade does NOT occur
  • PIE puts infant at risk for BPD
necrotizing enterocolitis nec

Necrotizing Enterocolitis-NEC-

Necrosis of the intestinal mucosa

  • 20% of all premature births
  • Males = Females
  • Most common in low birth weight babies who experience perinatal distress
etiology predisposing factors9
Etiology & Predisposing Factors

Exact cause unknown but seen with the following:

  • Intestinal ischemia
  • Bacterial colonization
  • Early formula feeding
  • Intestinal ischemia due to hypoperfusion, eg shock, or vascular occlusion, eg, clot from umbilical artery catheter
  • Bacterial colonization after ischemia starts necrosis
  • Early formula feeding may provide substrate needed for further bacterial growth and further necrosis
clinical signs8
Clinical Signs
  • Abdominal distention
  • Poor feeding
  • Blood in fecal material
  • Lethargy
  • Hypotension
  • Apnea
  • Decreased urine output
  • Bile stained emesis
  • CXR – bubbles in intestinal wall
nec treatment
NEC Treatment
  • NPO and NG suction
  • IV hydration and hyperalimentation
  • Broad spectrum antibiotics
    • Ampicillin, Gentamycin
  • Minimum pressure on abdomen
    • No diapers or prone positioning
  • Monitor for/treat sepsis
  • Necrotic bowel may need surgical resection
prognosis complications8
Prognosis & Complications
  • Mortality is 20-75%
    • Best prognosis if infant does NOT require any surgery
  • Main complication is sepsis
  • Infants who have bowel resection may develop malabsorption syndrome
tetralogy of fallot
Tetralogy of Fallot
  • VSD
  • Over-riding aorta
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy
  • Significant cyanosis because of R-L shunt
complete transposition of the great vessels
Complete Transposition of the Great Vessels
  • Pulmonary artery arises from left ventricle and Aorta arises from right ventricle
  • R-L shunt through PDA, ASD, or VSD needs to be present for infant to survive until corrective surgery
    • Balloon septostomy during cardiac catheterization
truncus arteriosus
Truncus Arteriosus
  • Aorta and pulmonary artery are the same vessel
  • Large VSD
  • Requires MAJOR surgical repair
  • Mortality is 40-50%