DR.

GERALDINE RAMIREZ RT3 – 2nd SEMESTER

LECTURE – WEEK 5
PNEUMONIA/ SEPSIS
It occurs frequently in newborns

3 types:
 Congenital Pneumonia
 Intrapartum Pneumonia
 Postnatal Pneumonia

Congenital Pneumonia
An inflammatory condition of the lungs affecting
primarily the microscopic air sacs known as alveoli

Causes:
 Most often seen with chorioamnionitis,
prematurity and meconium aspiration
 Prematurity
 Prolonged rupture of membranes CLINICAL ASSESSMENT
 Maternal temp > 38C  Gray, pale color
 Foul smelling amniotic fluid  Lethargy
 Rupture of membranes before the onset of labor  Temperature instability
 Non-reassuring fetal well-being test results  Skin rash-petechia
 Fetal tachycardia  Tachycardia
 Meconium in the amniotic fluid  Glucose issues Hypoperfusion
 Maternal hx of STDs  Oliguria
 Recurrent maternal UTI PROM> 18 hours
before delivery RESPIRATORY ASSESSMENT
 Tachypnea Apnea, irregular breathing pattern
ETIOLOGY  Grunting
 Congenital pneumonia may be infectious or  Retractions
noninfectious  Nasal flaring
 Group B Streptococcus (GBS)  Colorful secretions Rales, rhonchi
 Nontypable Haemophilus influenzae  Cyanosis
 Other gram-negative bacilli
 Listeria monocytogenes RADIOLOGICAL INVESTIGATION
 Enterococci When considering pneumonia, devote particular
 Staphylococcus aureus attention to the following:
 Noninfectious pneumonia are a class of diffuse  Costophrenic angles
lung diseases. They include: diffuse alveolar  Pleural spaces and surfaces
damage, organising pneumonia, nonspecific  Diaphragmatic margins
interstitial pneumonia, lymphocytic interstitial  Cardiothymic silhouette
pneumonia, desquamative interstitial  Pulmonary vasculature
pneumonia aspiration  Right major fissure
 Transmission of congenital pneumonia usually  Air bronchograms overlying the cardiac shadow
occurs via 1 of 3 routes:
 Lung expansion
 Hematogenous
 Patterns of aeration
 Ascending
 Aspiration
Pneumothorax
PATHOPYSIOLOGY Refers to the presence of air in the pleural space
Causes:
 May occur spontaneously or due to trauma to
the lungs or the chest wall
 Spontaneous pneumothorax occurs due to the
rupture of pleural blebs

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DR. GERALDINE RAMIREZ RT3 – 2nd SEMESTER
LECTURE – WEEK 5
 Iatrogenic injury occurs while performing any
thoracic, cardiac, or any chest wall surgeries
 Trauma may be due to gunshot injuries, stab
injuries, blunt trauma over the chest wall

Pneumothorax and other Air Leaks

History
o What happened in the delivery room?
o Was positive pressure given?
o Large amount of negative pressure generated
with the 1st breath?

Respiratory Assessment
Tension Pneumothorax
 Tachypnea
 The communication between the lung and pleural
 Nasal flaring
cavity is small and valvular
 Grunting
 It allows air entry during inspiration but prevents
 Retractions it from escaping during expiration
 BS absent or decreased  Therefore, pleural pressure is more than the
atmospheric pressure
Clinical Assessment
 Cyanotic
 pale, gray
 Heart Rate
o Tachycardia
o Bradycardia
o PEA
 Perfusion
o Capillary Refill (CRT)
o Blood Pressure if monitoring Arterial
o Line, narrowing pulse pressure •
Deformities of Chest Wall
o Asymmetry of chest
CHEST X-Ray speaks for itself!!

TYPES
Simple/ Closed pneumothorax
1. The opening in the lung is very small, hence, it heals
rapidly
2.There is no continuous communication between the
lung and the pleural cavity
3. The mean pleural pressure is less than the
atmospheric pressure

Open/Sucking pneumothorax
 The ruptured site remains open and there is a
communication between the pleural cavity and the
bronchus forming the broncho-pleural fistula
RADIOLOGICAL FINDINGS
 Pleural pressure is equal to the atmospheric Chest X-ray :
pressure  Hyper translucency between the lung & thoracic
cage.
 Due to broncho-pleural fistula, infection in the  Razor sharp border of the collapsed lung.
pleural space is common and hence leads to  Shifting of mediastinum on the opposite side of
pyopneumothorax injury.

Chest CT scan:

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DR. GERALDINE RAMIREZ RT3 – 2nd SEMESTER
LECTURE – WEEK 5
 Intrapleural gas along with loculated
pneumothoraces.
 Pleural effusion, pneumothorax.

Chest Ultrasound:
 Smooth horizontal echogenic lines are seen above
and below the pleural lines.
 Absence of lung sliding and B-lines

CLINICAL FEATURES
Closed pneumothorax
 Reduced chest expansion
 Hyper-resonant note on percussion.
 Reduced air entry. Pneumothorax
 Mediastinal shift to opposite side.  Right lateral decubitus view of pneumothorax
 Decreased Tactile Vocal Fremitus (TVF).
 Decreased Vocal Resonance.

Open pneumothorax :
 Crackpot sound on percussion.
 Amphoric breath sounds.
 Voice and cough sounds may be heard with
metallic echo.

Tension pneumothorax :
 Displacement of the mediastinum with
respiration. Pneumopericardium
 Dyspnoea
 Cyanosis.
 Tachycardia.
 Increased respiratory rate.
 Decreased blood pressure.
 Respiratory failure

SURGICAL MANAGEMENT

 Supplemental oxygen:
It is administered to facilitate resorption of
pleural air.
 Aspiration:
It is done during thoracocentesis to aspirate the
air in pleural cavity.
 Tube thoracostomy:
Chest tube is connected to a water seal device
with or without suction and is kept until the
pneumothorax resolves.
 Thoracoscopy:
Video - Assisted Thoracoscopy (VATS) is done
to perform mechanical pleurodesis.

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DR. GERALDINE RAMIREZ RT3 – 2nd SEMESTER
LECTURE – WEEK 5
 Lactic Acid
Congenital Abnormalities of the  Chest X-ray
Lung and Thorax Congenital Heart Disease - Heart shape and size
(CHD) - PBF
 Congenital Diaphragmatic Hernia (CDH)  Echocardiogram
 Congenital Cystic Adenomatoid - best test - diagnosis
 Malformation  Cardiac cath for possible intervention
 Tracheal Abnormalities
 Esophageal Atresia
 Pulmonary Hypoplasia Congenital Diaphragmatic Hernia Congenital
Cystic Adenomatoid Malformation
Congenital Heart Disease
 Defect present at birth- often picked up on early  Ideally diagnosed in utero
ultrasound  Develops during pseudoglandular stage, but
Increased risks: CCAM can form up to 35 weeks
o Parents have CHD  Normally compromised at delivery
o Siblings have CHD  requiring immediate intubation
o Maternal diabetes  CDH more commonly found on left side
 Exposure to German measles, toxoplasmosis,
or if mother HIV+ Congenital Diaphragmatic Hernia
 Alcohol use during pregnancy A diaphragmatic hernia is defined as a communication
 Cocaine use during pregnancy between the abdominal and thoracic cavities with or
TWO TYPES OF CHD: without abdominal contents in thorax
 Acyanotic-blood returning to right side of
heart passes through lungs-usually defect in Types
heart wall, or obstructed valve or artery  Anatomically:
o Pink baby  Hiatal (esophageal hiatus)
o Saturations within normal limits  Paraesophageal
o Low sats  Retrosternal (Morgagni)
 Cyanotic- have a mixing of oxygenated blood  Posterolateral (Bochdalek)
with venous blood – shunting ductus, PFO,
ASD, VSD ETIOLOGY
o Blue baby
 Congenital
 Traumatic
RESPIRATORY ASSESSMENT
 Respirations EPIDEMIOLOGY
- Normal
Incidence:
- Tachypnea
 1/2000-1/5000 live births
 Saturations depend upon defect:
 M:F-1:2
- Acyanotic lesions sats are more normal
- Cyanotic lesions acceptable sats are low  Left side more common (85%)
- 70% is acceptable; ideally on 21% FiO2  Sporadic
 Familial (Autosomal recessive, multifactorial)
CLINICAL ASSESSMENT  Associated anomalies
 HR  CNS lesions
- Slow, fast, variable  Omphalocele
- Murmur  Esophageal atresia
 BP  Cardiovascular lesion
- Check in all 4 extremities  Part of trisomy 21, trisomy 13, trisomy 18
 PULSES
 CRT
 COLOR
- Acyanotic
- Cyanotic
LABS AND TEST
 ABGS- dependent upon defect

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DR. GERALDINE RAMIREZ RT3 – 2nd SEMESTER
LECTURE – WEEK 5

INITIAL MANAGEMENT
RESPIRATORY ASSESSMENT  Aggressive respiratory support (rapid
 Tachypneic endotracheal intubation, sedation
 Retractions  NG tube insertion and urinary catheterization
 Nasal flaring needed
 Grunting  Pre- and postductal oxygenation and arterial
 Breath Sounds pressure have to be monitored continuously by
o Decreased on the affected side umbilical arterial catheter placement
o May hear bowel sounds in chest with  Prolonged Bag and mask contraindicated
125
CLINICAL ASSESSMENT GOAL
Scaphoid Abdomen  Pre ductal SaO2>= 85%
o classic sign  PIP<25 cm of water
Color  Permissive hypercapnia PaCO2 (45-60 mm Hg)
o cyanotic
Heart Rate TREATMENT
o fast, slow or normal  Ventilatory Strategies
o shifting of apex beat to contralateral  Conventional mechanical ventilation
o side of hernia  HFOV
o increased chest wall diameter
 ECMO
o delayed presentation
Goal:
o often right
o regurgitation  Oxygenation without barotrauma
o vomiting due to intestinal obstruction  PIP=<25cmH2O
o incarceration of intestine  Rate 30-60 bpm
DIAGNOSIS
 Nitric Oxide
 Perfusion
- depends upon the severity  Selective pulmonary vasodilator
 X-Ray- best diagnostic tool  ECMO
o bowel, stomach, liver in chest  Lower limit of weight required>= 2000
 ABGS  Can be venoarterial and venovenous
o acidosis, hypoxemia and hypercarbia SURGICAL REPAIR
o prenatal usg at 16-24 week of gestation  Mostly after 48 hrs after stabilization and
o polyhydramnios, chest mass, resolution of pulmonary hypertension
mediastinal shift, gastric bubble in  Delayed in newborn on HFOV • Most common
thoracic cavity approach: subcostal approach Laparoscopic
o after delivery: cxr with a nasogastric and thoracoscopic repair Native tissue vs
tube patch(GORE-TEX, porous
o barium study Relative indicators for stability
o echocardiography  Requirement of conventional ventilation
o amniocentesis  Only
 Low PIP
Left Congenital Diaphragmatic Hernia
 FiO2<50%

Recent advances in treatment

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DR. GERALDINE RAMIREZ RT3 – 2nd SEMESTER
LECTURE – WEEK 5
 Liquid ventilation: Tracheal installation of
perfluorocarbon (PFC) to replace as a carriage
for oxygen and carbon dioxide
 Fetal surgery: Human tracheal occlusion
(fetoscopic endoluminal tracheal occlusion)

COMPLICATION
 GERD (50%)
 Intestinal Obstruction (20%)
 Recurrent diaphragmatic hernia (5-20%)
 Delayed growth in 1st 2 years of life
 Neurocognitive defect (more common in
infants requiring ECMO)
 Pectus excavatum
 Scoliosis

PROGNOSIS
 Overall survival of CDH 67%
 Spontaneous fetal demise: 7-10%

POOR PROGNOSIS
 Associated major anomalies
 Symptoms before 24 hrs of age
 Severe pulmonary hypoplasia
 Need for ECMO

PERSISTENT FETAL CIRCULATION

 Also known as Persistent Pulmonary
Hypertension of the Newborn
 Abbreviated as PFC, PPH, PPHNB

Persistent Pulmonary Hypertension (PPHN)

 Pulmonary hypertension resulting in severe
hypoxemia secondary to R>L shunt thru PFO
and/or PDA
 Usually affecting term or near-term infants
May be extremely difficult to manage

 Continuance of fetal circulation postpartum

 R to L shunting through PDA
 R to L shunting through FO
 Severe hypoxemia

1. High arterial PO₂

Constriction of ductus arteriosus → it closes, becoming
the ligamentum arteriosum.

Right ventricle output now flows entirely into the

pulmonary circulation.

Pulmonary vascular resistance becomes lower than

systemic vascular resistance→Shunt through ductus
arteriosus reverses & becomes left to right.

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DR. GERALDINE RAMIREZ
LECTURE – WEEK 5
2. Increased volume of pulmonary blood flow returning
to left atrium→ Increases left atrial volume and
pressure→ Closure of foramen ovale (functionally)
→Becomes Fossa Ovalis.
CLOSURE OF:
Foramen ovale :
 Functional Closure: 3rd month of life.
 Anatomical closure of septum primum &
septum secundum by 1 year of age.
RT3 – 2nd SEMESTER
 Foetal:
1. Birth asphyxia-prolonged hypoxemia leads to release
of humoral factors which cause vasoconstriction and
remodelling of pulmonary vasculature
(abnormal muscularization of arterial wall with >>
medial thickness) →decreased cross sectional area of
the vessels >> PVR.
2.Parenchymal lung diseases like pneumonia,
surfactant deficiency, meconium aspiration-reversible
due to vasospasm.

Ductus arteriosus: 3.Pulmonary developmental abnormalities like

 Functional Closure: By 10-15 hr in a normal CDH,Potter syndrome (parenchymal hypoplasia)
neonate. Alveolar capillary dysplasia (malalignment of
pulmonary veins and arteries).
 Anatomic closure: May take several weeks.
 In a full-term neonate, oxygen is the most
4. Congenital heart disease (left and right sided
important factor controlling ductal closure. obstructive lesions) myocardial dysfunction,
 When the PO, in the blood passing through the myocarditis, intrauterine constriction of DA.
ductus reaches about 50 mm Hg, the ductal wall
constricts 5.Infections-viral/bacterial pneumonias, sepsis cause
3. Removal of the placenta from the circulation → Also vasospasm by release of thromboxanes by suppressing
results in closure of the ductus venosus. endogenous NO production and by direct endotoxin
mediated myocardial depression
The left ventricle is now coupled to the high-resistance
systemic circulation→ its wall thickness begins to 6 Genetic predisposition - low levels of NO metabolites,
increase. arginine diminished endothelial NOS expression
• In contrast, the right ventricle is now coupled to the 7. Mechanical factors like low cardiac output,
low-resistance pulmonary circulation →its wall hyperviscosity, polycythemia.
thickness decreases slightly.
PPHN
Persistent Pulmonary Hypertension of  History
the Newborn (PPHN)
 Meconium
 Disruption of normal transition of fetal
 Asphyxia
circulation to neonatal circulation
 Stress
 "Persistent fetal circulation"
 Pneumonia/Sepsis
 Suprasystemic resistance in the pulmonary
 Primary Pulmonary Hypertension -
vasculature
Dysfunction in pulmonary endothelial
PVR > SVR
vasodilating mechanism
 CDH/CCAM
 Leading to perpetuation of R->L shunt through
foramen ovale and/or ductus arteriosus
RESPIRATORY ASSESSMENT
 Resulting in diminished pulmonary perfusion
and systemic hypoxemia. o -Tachypnea
 Incidence is 1-2/1000 live births. o -Retractions
o -Grunting
 More common among full term and post term
o -Nasal flaring
neonates
o Infants tend to be term
 In preterm neonates, RDS may be complicated
o Non responsive hypoxemia
by PPHN
o Right sided PaO2 (preductal) 15 torr
higher than left
RISK FACTORS
o PPHN
 Maternal: o Hyperoxia test (100% hood)
o fever, anemia,pulmonary disease,UTI, o PaO2> 100 is lung disease
DM,drugs like o PaO2 = 50 to 100 is either lung or heart
aspirin/NSAID's/SSRI's, o Hyperoxia test (100% hood)
smoking(antenatally)

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DR. GERALDINE RAMIREZ RT3 – 2nd SEMESTER
LECTURE – WEEK 5
o PaO2 > 100 is lung disease  Requires immediate intervention to reverse
o PaO2 = 50 to 100 is either lung or heart hypoxemia, improve pulmonary and systemic
o disease perfusion, preserve end organ function
o PaO2 <50 is fixed right to left shunt  Supplemental oxygen (postductal SaO2 is
>90% and < 98%)
BREATH SOUNDS  Intubation, mechanical ventilation (persisting
-Depend on cause hypoxemia, hypercapnea, acido is)
Pre and Post-ductal saturations to monitor  In the absence of pulmonary disease
shunting- best indicator if ECHO not available mechanical ventilation with rapid,low pressure
 If fixed R to L shunt is suspected Obtain pre and and short inspiratory time
post ductal Pa02  PPHN + parenchymal lung disease -> High
 Difference < 15 torr, no ductal shunting frequency oscillatory ventilation/High
 Difference > 15 torr, ductal shunting frequency jet ventilation (MAS,air leak)
 disease PaO2 <50 is fixed right to left shunt
Sildenafil
CLINICAL ASSESSMENT  PDE-5 inhibitor
Color  Inhibits metabolism of NO
o Blue/gray  >> available NO
X-Ray  Dose: 0.4mg/kg/dose IV over 3hrs followed by
o Depends on cause a continuous infusion of 1.6mg/kg/24hrs for up
o Usually with decreased blood flow, minimal to 7 days
lung markings

DIAGNOSIS
 Presents within 18 hours of birth
 Respiratory distress
 Marked cyanosis
 Differential cyanosis between regions perfused
by preductal and postductal vasculature
Lab
o Dependent on cause
o Many present with abnormal
Platelets/PT/ Fibrinogen
ABG
o Respiratory and metabolic acidosis

 Prominent precordial impulse

 Loud,single or narrowly split $2
 Systolic murmur
 A gradient of 10% or more in oxygen saturation
between preductal and postductal areas
 ECMO
 CXR appears normal or shows associated  Extra Corporeal Membrane Oxygenation
 parenchymal lung disease  Used when conventional therapy and INO
 ECG shows RV strain or hypertrophy treatment fails
 ECHO shows hemodynamic shunting, helps to  Criteria to start ECMO: oxygenation index of
evaluate ventricular function,tricuspid >30 in 2 ABG's taken 30 minutes apart &
insufficiency and to exclude congenital heart alveolar-arterial oxygen difference > 600
disease  Intravascular volume support Dobutamine and
 Color doppler shows presence of vasopressors
 intracardiac/ductal shunting  Correct hypoglycemia, hypocalcemia (to
provide adequate substrates to the
MANAGEMENT myocardium)
 Case fatality rate of 30-60%  Neutral/alkalotic pH reduces PVR (by sodium
bicarbonate boluses)

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DR. GERALDINE RAMIREZ RT3 – 2nd SEMESTER
LECTURE – WEEK 5
 Sedation and analgesia with fentanyl/morphine
(prevents release of catecholamines which
activate
 pulmonary adrenergic receptors) Muscle
relaxants like pancuronium
 Correct polycythemia, hyperviscosity (partial
exchange transfusion with normal saline to
maintain HCT between 50-55%)
 Other therapies: Magnesium sulfate,
adenosine, tolazoline, calcium channel
blockers, inhaled prostacyclin, inhaled ethyl
nitrite

PROGNOSIS
 Neurodevelopmental sequelae in 15-20%
 Hyperventilation reduces cerebral perfusion,
leads to sensorineural hearing loss
 Prolonged ventilation leads to development of
chronic lung disease 20% risk of
rehospitalization within 1 year of discharge

Bronchopulmonary Dysplasia
 Abbreviated as BPD
 Obstructive disease
 Definition-02 usage, 28 days post partum
 Causitive factors:
o 02
o Airway Pressure
o Time of exposure

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