RESPIRATORY DISTRESS IN THE NEWBORN

Objectives
Identification of Respiratory Distress in the Newborn

Development of the lungs

Overview of Hyaline Membrane Disease Differential Diagnoses:

1) Transient Tachypnoea of the Newborn 2) Pneumonia

Respiratory Distress in the Newborn

Respiratory distress that becomes manifested by

tachypnoea, intercostal retractions, reduced air exchange, cyanosis, expiratory grunting, and nasal flaring is a nonspecific response to serious illness Not all of the disorders producing neonatal respiratory distress are primary diseases of the lungs

Respiratory Distress in the Newborn

The differential diagnosis of respiratory distress

includes:

1) pulmonary, 2) cardiac, 3)hematologic, 4) infectious, 5) anatomic, and 6) metabolic disorders These may involve the lungs directly or indirectly

Respiratory Distress in the Newborn

Surfactant deficiency causes respiratory distress

syndrome (RDS), resulting in cyanosis and tachypnea; Infection produces pneumonia, shown by interstitial or lobar infiltrates; Meconium aspiration results in a chemical pneumonitis with hypoxia and pulmonary hypertension; Hydrops fetalis causes anemia and hypoalbuminemia with high-output heart failure and pulmonary edema; and Congenital or acquired pulmonary hypoplasia causes pulmonary hypertension and pulmonary insufficiency

Aetiology of Respiratory Distress

It is clinically useful to differentiate the common

causes of respiratory distress according to gestational age

PRETERM INFANT
Respiratory

distress syndrome (RDS)* Erythroblastosis fetalis Nonimmune hydrops Pulmonary hemorrhage

Aetiology of Respiratory Distress

FULL-TERM INFANT
Primary

pulmonary hypertension of the neonate* Meconium aspiration pneumonia* Polycythemia Amniotic fluid aspiration

Aetiology of Respiratory Distress

PRETERM AND FULL-TERM INFANT
Bacterial

sepsis (GBS)* Transient tachypnea* Spontaneous pneumothorax Congenital anomalies (e.g., congenital lobar emphysema, cystic adenomatoid malformation, diaphragmatic hernia) Congenital heart disease Pulmonary hypoplasia Viral infection (e.g., herpes simplex, CMV) Inborn metabolic errors

IDENTIFICATION OF RESPIRATORY DISTRESS IN THE NEWBORN

Identification of Respiratory Distress in the Newborn (Signs)

Newborn infants with respiratory problems develop the

following signs of respiratory distress: Tachypnoea (>60 breaths/min in newborn) Laboured breathing with chest wall recession (particularly sternal and subcostal indrawing) Nasal flaring Expiratory grunting Cyanosis if severe

Respiratory distress in neonates can develop at any time from birth up to 28 days. Signs and symptoms may be apparent immediately upon delivery or develop minutes or hours afterward.

Normal Respiratory Rates

Silverman Respiratory Scale

Substernal Recession

Intercostal Recessions

Sternal Recession

Nasal Flaring

Cyanosis

Cyanosis
Cyanosis becomes evident when there is 5g

unsaturated heamoglobin It follows that anaemia may interfere with the perception of cyanosis Jaundice may also interfere with the perception of cyanosis It is therefore imperative that arterial blood gas analysis be performed in all infants with significant respiratory distress, whether or not cyanosis is perceived

Important Points to note in the Newborns Hx

Gestational Age Antepartum infection Duration of rupture, color of amniotic fluid, maternal

temperature/tachycardia ( to detect meconium aspiration + chorioamnionitis) Onset and duration of respiratory symptom

DEVELOPMENT OF THE LUNG

Introduction
The lungs as breathing organs are unnecessary for intrauterine

existence. Nevertheless, they must be developed to such an extent that they are immediately ready to function following birth. This explains why the entire development extends from the embryonic period through the fetal period up to birth (and even afterwards). During intrauterine life, the lungs are an important source of amniotic fluid.

Milestones of prenatal lung development

Embryonic phase
The embryonic phase of lung development begins with the

formation of a groove in the ventral lower pharynx, the sulcus laryngotrachealis After a couple of days - from the lower part - a bud forms, the true lung primordium In the further subdivision into the two main bronchi the smaller bud on the left is directed more laterally than the somewhat larger one on the right that - parallel to the esophagus - is directed more caudally. Thus the asymmetry of the main bronchi, as they present in adults, is already established.

Embryonic phase (contd)

The subsequent divisions of the endodermal branches also

take place unequally in that on the right three further buds form and, on the left, only two, corresponding to the later pulmonary lobes. In the next division step, which occurs at the end of the embryonic period, the segments of the individual pulmonary lobes arise. At the end of the embryonic period the first segments appear in the five (three right and two left) lobes of the lungs. With their distended ends the lungs resemble an exocrine gland.

Development of the lungs up to the end of the embryonic period

Embryonic phase (contd)

At this time the pulmonary vessels have formed

themselves. The pulmonary circulation system is formed out of the 6th pharyngeal arch artery. These develop somewhat differently than the other 4 aortic arches in that first a vessel plexus forms around the lung anlage, originating from the aortic sac. The true 6th aortic arch is only then formed after vessels also from the dorsal aorta - grow into this plexus and thus a connection between the truncus pulmonalis and dorsal aorta has arisen.

Pseudoglandular phase
At this stage the lungs resemble the development of a tubulo-

acinous gland.
According to the classical view, the entire air-conducting

bronchial tree up to the terminal bronchioli are set down in this phase (16 generations).
With the end of the pseudoglandular phase, 20 generations are

partially present in the lungs, which means that at this point in

time the respiratory ducts have already been formed.

Pseudoglandular phase
The primordial system of passages, the air-conducting

bronchial tree, is initially coated by cubic epithelium. These are the precursor cells of the ciliated epithelium and of the secretory cells. In humans, the first ciliated epithelial cells can be found in the 13th week of pregnancy. In the respiratory part the first typically lung-specific cells, connected to the terminal bronchioli, appear: the type II pneumocytes (alveolar cells). The developing broncho-pulmonary epithelium begins to produce amniotic fluid, which is also found in the lungs up to the time of birth.

Pseudoglandular phase
The differentiation of the lungs takes place in

a centrifugal direction. In the central, air-conducting portions of the lungs the epithelium begins to differentiate into cilia-carrying cells and goblet cells. After the 10th week cartilage and smooth muscle cells as well as bronchial glands can be found in the wall of the bronchi. The peripheral sections partially retain - until far beyond the pseudoglandular phase - cubic epithelium that is still little differentiated. This is important for a further proliferation of the bronchial tree into the surrounding mesenchymal tissue.

Canalicular phase
In the classical description of lung development, in this phase

the canaliculi branch out of the terminal bronchioli. The canaliculi compose the proper respiratory part of the lungs, the pulmonary parenchyma. All of the air spaces that derive from a terminal bronchiolus form an acinus. Each one comprises respiratory bronchioli and the alveolar ducts and later the alveolar sacculi. The chief characteristic of this canalicular phase is the alteration of the epithelium and the surrounding mesenchyma.

Canalicular phase
Along the acinus, which develops from the terminal

bronchiolus, an invasion of capillaries into the mesenchyma occurs. The capillaries surround the acini and thus form the foundation for the later exchange of gases. The lumen of the tubules becomes wider and a part of the epithelial cells get to be flatter. From the cubic type II pneumocytes develop the flattened type I pneumocytes. A sufficient differentiation of the type II pneumocytes into the type I pneumocytes and the proliferation of the capillaries into the mesenchyma marks an important step towards the fetus being able to survive outside the uterus after roughly the 24th week of pregnancy.

Canalicular phase
At the end of this canalicular phase which is the

beginning of the saccular phase(25 weeks) - a large part of the amniotic fluid is produced by the lung epithelium. From this time on, the maturity of the lungs can be measured clinically based on the activity of the type II pneumocytes, which begin to produce the surfactant. The ratio of lecithin to sphingomyelin in the amniotic fluid, which increases with fetal age is determined. In this stage developmental damage already affects the gas-exchange components and result in structural alterations of the later pulmonary parenchyma.

Saccular phase
From the last trimester whole clusters of sacs form on

the terminal bronchioli, which represent the last subdivision of the passages that supply air. In the saccular phase the last generation of air spaces in the respiratory part of the bronchial tree is born. At the end of each respiratory tract passage smoothwalled sacculi form, coated with type I and type II pneumocytes. The septa between the sacculi are still thick and contain two networks of capillaries that come from the neighboring sacculi.

Saccular phase
The interstitial space is rich with cells and the proportion of

collagen and elastic fibers is still small. This matrix, though, plays an important role for the growth and differentiation of the epithelium that lies above it. At the end of this phase the interstitial fibroblasts begin with the production of extracellular material in the interductal and intersaccular space. At birth, i.e., at the end of the saccular phase, all generations of the conducting and respiratory branches have been generated. The sacculi are thin, smooth-walled sacks and correspond to the later alveolar sacculi.

Alveolar phase
The alveolar phase begins in the last few weeks of the

pregnancy, new sacculi and, from them, the first alveoli form.
Thus, at birth, 1/3 of the roughly 300 million alveoli should be

fully developed.
The alveoli, though, are only present in their beginning forms. Between them lies the parenchyma, composed of a double

layer of capillaries, that forms the primary septa between the

alveolar sacculi.

Alveolar phase
Already before birth these alveolar sacculi get to be

increasingly complex structurally. Thereby, a large number of small protrusions form along the primary septa. Soon, these become larger and subdivide the sacculi into smaller subunits, the alveoli, which are delimited by secondary septa. Ultrastructural investigations show that overall where such alveoli appear, they are surrounded by elastic fibers that form the interstitial septa between two capillary nets. In the first 6 months, their number increases massively. This "alveolarization" and therewith the formation of secondary septa should - to a limited extent still continue up to the first year and a half of life.

Classification in the adult lung

In the adult lung one distinguishes

between conducting and respiratory zones.

In the conducting zone, all branches of the bronchial tree,

the walls of which contain cartilage tissue and

seromucous glands, are bronchi.
As soon as cartilage and glands are no longer

present, bronchioli are involved.

Classification in the adult lung

According to their function the respiratory tract passages

are divided into conducting and respiratory zones:

Conducting zone = 16 generations Segmental bronchi are continued by several generations of Intersegmental bronchi (up to ca. 1 mm diameter). After these follow the Bronchioli (< 1mm diameter) that after several divisions go over into Terminal bronchioli (ca. 0.4 mm diameter). They subdivide numerous times and represent the end stretch of the purely conductive respiratory tract. The measurements come from histological findings.

Classification in the adult lung

Respiratory zone = 7 generations

Out of the terminal bronchioli several generation of

Respiratory bronchioli (= 3 generations) proceed. From

them follow several generations of Alveolar ducts (= 3 generations) that in Alveolar sacculi (last generation = 23rd generation) end

HYALINE MEMBRANE DISEASE

Hyaline Membrane Disease

Also known as Respiratory Distress Syndrome Definition An acute illness, usually of pre-term infants, developing within 4-6 hrs. of birth, characterized by tachypnoea(> 60bpm) and other signs of respiratory distress such as intercostal retractions, expiratory grunting and cyanosis in room air.

Recap of Surfactant Production

Produced by type 2 pneumocytes of the alveoli beginning at

approximate the 24-26th week of gestation. Composed of lecithin and phosphatidylglycerol Has 4 main proteins i.e. A, B, C & D By 34-36 weeks gestation sufficient quantities are made to prevent atelectasis during extra-uterine life. Glucose/glycerol precursor converted into phospholipids and surfactant proteins which are packaged into small lamellar bodies in the golgi apparatus. Small lamellar bodies coalesce into mature lamellar bodies which are released via exocytosis

Function of Surfactant
Prevention of atelectasis

Reduces surface tension at low lung volumes when

concentrated at the end of expiration Increases lung recoil by increasing surface tension on expansion of the alveoli and decreasing concentration of surfactant. NB- a lecithin: sphingomyelin ratio of 2:1 indicates pulmonary maturity.

Pathophysiology
Absence of surfactant leads to poor pulmonary

compliance Atelectasis Decreased gas exchange Hypoxia Acidosis Debris from damaged cells in addition to exudative necrosis and leaked protein give a hyaline membrane appearance on microscopy and ground glass appearance on CXR. NB 4 hours of breathing are necessary for formation of hyaline membranes.

Hyaline Membrane Disease

EPIDEMIOLOGY:
US incidence of 14% in LBW babies Incidence at 35-36 wks gestation ~ 5%

Incidence at 29-30 wks gestation ~65%

Approx 20% of neonatal deaths Risk factors also include race, sex and maternal

antenatal morbidity and method of delivery. Approx. 20% of neonates with RDS will have sequelae of chronic lung disease

Hyaline Membrane Disease

PRESENTATION AND DIAGNOSIS:
Signs of respiratory distress starting within 8hrs of life

ABG hypoxaemia, hypercapnia, acidosis

RFTs hypocalcaemia, hyperkalaemia RBG hypoglycaemia CXR bell shaped thorax, hypoaeration, bilateral diffuse

reticulogranular opacities, peripheral air bronchograms LAB FINDINGS - Low PaO2 level, High PaCO2, Falling pH, Respiratory acidosis initially, followed by respiratory and metabolic acidosis later.

Hyaline Membrane Disease

PROGRESSION OF SYNDROME
Symptoms progressively worsen and peak within 72hrs

there may be development of oedema, apnoea etc. Resolution usually begins with diuresis and a fall in pulmonary vascular resistance. Resolution typically begins circa the 4th day of the syndrome CXR findings may show progressive opacification and obscuration of the cardiac borders.

Severe respiratory distress syndrome (RDS). Reticulogranular opacities are present throughout both lungs, with prominent air bronchograms and total obscuration of the cardiac silhouette. Cystic areas in the right lung may represent dilated alveoli or early pulmonary interstitial emphysema (PIE).

SEVERE RESPIRATORY DISTRESS This X ray shows the white out pattern

Hyaline Membrane Disease

MANAGEMENT
Prevention antenatally Resuscitation and ventilation

Surfactant replacement therapy

Hyaline Membrane Disease

PREVENTATIVE MEASURES
Prevention of pre-term labour via use of tocolytics,

antibiotics in cases of infection & cervical cerclage. Use of antenatal corticosteroids

Hyaline Membrane Disease

Antenatal Corticosteroids
Betamethasone or Dexamethasone used Decrease the risk of RDS in the neonate and

increase the effect of surfactant replacement therapy postnatally Betamethasone 12mg IM q24h 2 Dexamethasone 6mg IM q12h 4 Of maximal benefit 48 hours to 7 days prior to preterm delivery.

Hyaline Membrane Disease

RESUSCITATION
Includes prevention of hypothermia and hypoxia All neonates born less than 29 weeks gestation should

be intubated in order to receive prophylactic exogenous surfactant. Neonates >999g can be ventilated with air or oxygen. Drugs used include: 1. Adrenaline 2. Sodium bicarbonate 3. Naloxone 4. Glucose 5. Albumin

Hyaline Membrane Disease

Ventilation CPAP: Indicated at birth in high risk infants and post surfactant replacement therapy who are still high risk for RDS. Infants with worsening respiratory distress Post-extubation Start at levels of 3-4cm H2O and increase to 6-8 cm H2O If failure occurs switch to mechanical ventilation.

Hyaline Membrane Disease

Mechanical Ventilation
Pressure controlled ventilation typically used. Indicated in high risk infants Those with desaturation

Persistence of apnoea or bradycardia

Cardiorespiratory collapse Ensure PIP is not excessively high Rates > 60bpm decrease risk for pneumothoraces Selective sedation may be given if the infants respiratory

efforts do not coincide with the mechanical ventilation rate

Hyaline Membrane Disease

SURFACTANT THERAPY
Can be given prophylactically or as a rescue dose Usually given intra-tracheally When given prophylactically, high risk infants are

intubated at birth and surfactant given prior to the onset of respiratory symptoms Prophylactic surfactant is associated with better outcomes than rescue administration Early use of rescue doses are associated with a better outcome than delayed administration Surfactant therapy is potentiated by the use of antenatal corticosteroids.

Hyaline Membrane Disease

What is to be achieved with management:
Parameter PaO2 Ideal Level 60-70mmHg (90% SPO2)

pH

>7.25

Respiratory Rate

30-50 bpm

DDx: Transient Tachypnoea of the Newborn

Definition
Transient tachypnea of the newborn (TTN) is a

parenchymal lung disorder characterized by pulmonary edema resulting from delayed resorption and clearance of fetal alveolar fluid. It is also called Rapid breathing of the newborn, neonatal wet lung syndrome or Type II respiratory distress syndrome.
Avery, ME, Gatewood, OB, Brumley, G. Transient tachypnea of newborn. Possible delayed resorption of fluid at birth. Am J Dis Child 1966; 111:380.

Transient Tachypnoea of the Newborn

Transient tachypnoea of the newborn is the most

common cause of neonatal respiratory distress, in neonates . It is a benign, self-limited condition, there are increasing data to suggest that TTN increases a newborn's risk for developing a wheezing syndrome early in life.

Transient Tachypnoea of the Newborn- Clinical Presentation

The clinical presentation includes tachypnoea

immediately after birth or within two hours, with other predictable signs of respiratory distress. Symptoms can last from a few hours to two five days. Respiratory Distress Do you remember some signs of respiratory distress????

Clinical Presentation
The clinical presentation of respiratory distress in the

newborn includes: apnea, cyanosis(severe cases of TTN), expiratory grunting, inspiratory stridor, nasal flaring, poor feeding, tachypnea (more than 60 breaths per minute).
subcostal, or supracostal spaces.

There may also be retractions in the intercostal,

Epidemiology
Respiratory distress occurs in approximately

7 % of neonates TTN: Most common cause of neonatal respiratory distress Constituting more than 40 percent of cases

aafp.org

Etiology

Slow or decreased absorption of fetal lung fluid, including

fluid accumulation in the interstitial space resulting in

decreased pulmonary compliance decreased tidal volume increased dead space

Disruption of sodium transport by lung epithelia has been

postulated recently as reason for ineffective transepithelial alveolar fluid movement.

http://www.5mcc.com/5mcc/ub/view/Select-5-Minute-Pediatric-Consult/14152/0.4/transient_tachypnea_of_the_newborn__ttn_

Etiology
Causes of Tachypnoea in a Newborn
Transient tachypnoea of newborn

Respiratory infections (pneumonia)

Aspiration syndromes (meconium, blood, or amniotic fluid) Congenital malformations (congenital diaphragmatic hernia, cystic adenomatoid malformations) and Central nervous system irritation (subarachnoid hemorrhage) or disease (hypoxic-ischemic encephalopathy)

Hyaline membrane disease (respiratory distress syndrome)

Edema, pulmonary (left-to-right shunts with failure, anomalous venous drainage) Air leaks (pneumothorax) and Acidosis (metabolic)

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

The birth of a child is preceded by several changes to prepare for the transition from intra-uterine to extra-uterine life.

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

Five major events that establish the lungs as the organ of gas exchange at birth include:
(1) clearance of fetal lung fluid (2) establishment of spontaneous breathing (3) decrease in pulmonary vascular resistance (4) release of surfactant (5) cessation of the right-to-left shunting of venous blood returning to the heart

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

During fetal life..

Fluid is secreted into the alveoli to maintain

normal growth and function Fetal lung volume approximates the functional residual capacity that would be established once air breathing is initiated. Clearance of lung fluid can be affected by several factors, and its impairment culminates in tachypnoea

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

Mechanism of Fetal and Neonatal Lung Fluid Transport

Before birth: Active secretion of chloride ions from alveolar cells into the alveolar space Na+ and H2O accompany ClAround the time of birth:
Type II cell apical epithelial sodium channels (ENaC) become

activated by adrenergic stimulation

Basolateral Na+/K+ ATPase helps move Na+ into the interstitium Cl - and water passively along with it through the paracellular and

intracellular pathways

Most interstitial lung liquid moves into the pulmonary circulation;

some drains via the lung lymphatics

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

Mechanism of Fetal and Neonatal Lung Fluid Transport

Copyright 2008 American Academy of Pediatrics, Guglani, L. et al. Pediatrics in Review 2008;29:e59-e65

Risk Factors
Cesarean delivery

Maternal asthma
Macrosomia Male sex

Maternal diabetes

Risk Factors

Copyright 2008 American Academy of Pediatrics, Guglani, L. et al. Pediatrics in Review 2008;29:e59-e65

Diagnosis
Based on clinical and radiologic findings

Presentation
Within a few hours of birth : Tachypnoea Retractions Grunting Respiratory rates: > 60 breaths/min, usually 80 - 100 breaths/min, and sometimes higher..

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

INVESTIGATIONS
Tests: Pulse oximetry: Oxygen saturation should be maintained >96%. Arterial blood gas: Metabolic acidosis with base deficit suggests asphyxia. CBC: Decreased or increased WBC count and increased immature forms (e.g., bands) suggest infection. Blood culture: Positive results indicate infection.

Imaging:
Chest radiograph: Transient tachypnoea of the newborn indicated by prominent central pulmonary vascular markings (central perihilar streaking), fluid lines in the fissures, hyperaeration, flat diaphragms, cardiomegaly and, occasionally, pleural fluid

cc.com/5mcc/ub/view/Select-5-Minute-Pediatric-Consult/14152/all/transient_tachypnea_of_the_newborn__ttn_

Radiographic Features

Prominent perihilar vascular markings

(due to engorged periarterial lymphatics, edema of the interlobar septae, and fluid in the fissures) Some degree of hyperinflation Fluid may be seen at the costophrenic angles, with widening of intercostal spaces Diffuse parenchymal infiltrates, a wet silhouette around the heart, or intralobar fluid accumulation

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

Radiographs of two babies who have transient tachypnea of the newborn of differing severity

Copyright 2008 American Academy of Pediatrics, Guglani, L. et al. Pediatrics in Review 2008;29:e59-e65

Picture 1- Neonate at age 6 hours. Overaeration and streaky, bilateral, pulmonary interstitial opacities and prominent perihilar interstitial markings are seen along with mild cardiomegaly.

Picture 2- Same patient as in Picture 1 at age 2 days. Cardiomegaly has disappeared. Pulmonary parenchymal abnormalities are diminishing, but perihilar, streaky markings persist.

Same patient as in Pictures 1 and 2 at age 4 days. Normal heart size and clear lungs are seen.

Transitional Delay
Since many babies experience tachypnoea for a period

of time after birth, shorter periods of tachypnoea sometimes are referred to as "transitional delay."
May be part of the spectrum of retained fetal lung fluid

syndromes, with TTN being more severe than typical transitional delay

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

Transitional Delay
Minimum number of hours of tachypnoea for a diagnosis

of TTN) is arbitrary but could range from 2 to 12 hours.

Six hours may be a practical choice for the cutoff

between "transitional delay" and TTN because by this time, the baby may not be able to take feedings orally, requiring other arrangements.

Pediatrics in Review. 2008;29:e59-e65, 2008 American Academy of Pediatrics

Treatment
Emergency care:

Initially, nothing by mouth until respiratory status stabilized and diagnosis clarified Oxygenmay help reduce respiratory distress if patient hypoxic Continuous positive airway pressure or mechanical ventilation if indicated Antibiotics if pneumonia or sepsis suspected Furosemide (diuretic) has not been shown to improve transient tachypnea of the newborn. IV fluids if NPO Monitoring of respiratory status using continuous pulse oximetry and respiratory and heart rate monitoring Typically 25 days

Supportive care:

Duration of therapy:

Complications
Hypoxia

Respiratory fatigue
Pneumothorax Respiratory or metabolic acidosis

Complications
Occasionally, air leaks (eg, a small pneumothorax or

pneumomediastinum) may be seen in infants who have increased work of breathing

Infants delivered by elective cesarean section prior to 39

weeks gestation may develop pulmonary hypertension and may require extracorporeal membrane oxygenation (ECMO)
newborn is a risk factor for future wheezing syndromes in childhood and may not be as transient as previously thought.
http://emedicine.medscape.com/article/976914-followup

Several reports suggest that transient tachypnoea of the

Prognosis
Self-resolving disorder with excellent prognosis

References
Avery, ME, Gatewood, OB, Brumley, G. Transient

tachypnea of newborn. Possible delayed resorption of fluid at birth. Am J Dis Child 1966; 111:380. Kumar A, Bhat BV. Epidemiology of respiratory distress of newborns. Indian J Pediatr. 1996;63:938. Liem, JJ, Huq, SI, Ekuma, O, et al. Transient tachypnea of the newborn may be an early clinical manifestation of wheezing symptoms. J Pediatr 2007; 151:29.

DDx: Pneumonia

Neonatal Pneumonia

Definition
An inflammatory pulmonary process that may

originate in the lung or be a focal complication of a contiguous or systemic inflammatory process

Pathogenesis
Consider direct and indirect injury Direct injury by the invading agent usually results from

synthesis and secretion of microbial enzymes, proteins, toxic lipids and toxins.

Indirect injury is mediated by secreted molecules such as

endotoxin, leukocidin and toxic shock syndrome toxin-1 which may alter vasomotor tone and integrity, change characteristics of tissue perfusate and interfere with the delivery of oxygen and nutrients.

On a molecular level

Release of toxic substances from granules

Migration of phagocytes

Initiation of cascades

Injury to host tissues, alter endothelial and epithelial integrity, vasomotor tone, intravascular haemostasis

On a macroscopic level
Increase in airway smooth muscle tone and

resistance Increase in mucous secretion Presence of inflammatory cells and debris in the secretions.
The materials may further increase airway resistance

and obstruct the airways, partially or totally causing airtrapping and atelectasis.

The end result

Alveolar diffusion barriers may increase

Intrapulmonary shunts worsen

V/Q mismatch may further impair gas exchange. Increase work of the myocardium to overcome the

alterations in the pulmonary vasculature resistance that accompany the changes of pneumonia.

Etiologic Factors: Bacterial and Viral

May be acquired:

1) transplacentally 2) through birth canal 3) after delivery

Etiologic Factors: Most common Bacterial Agent?

Group B streptococcus

Affects 1-4 in 1000 live births

<3/7 in term and near term infants

Etiologic Factors: Other common bacterial agents

Escherichia coli (especially in very low birth weight infants i.e.

<1500g).

Klebsiella spp. Listeria spp . Staphylococcus. Pseudomonas (later onset disease).

Chlamydia trachomatis (pneumonia as late as 3-4/52 after birth).

Nontypable H. Influenzae.

Etiologic Factors: Most common viral agents

Prenatally and postnatally acquired CMV Postnatally acquired influenza, RSV and adenovirus

Classification of Neonatal Pneumonia

Pneumonia that becomes clinically evident within 24

hours of birth may originate at 3 different times.

1) true congenital pneumonia - pneumonia is already established at birth. (2) intrapartum pneumonia- pneumonia is acquired during passage through the birth canal.

(3) postnatal pneumonia.-infection occurs after the birth process.

Congenital Pneumonia
True congenital pneumonia is already established at

birth. It may become established long before birth or relatively shortly before birth. Transmission of congenital pneumonia usually occurs via 1 of 3 routes:
Hematogenous Ascending Aspiration

Haematogenous spread
If the mother has a bloodstream infection, the

microorganism can readily cross the few cell layers that separate the maternal from the fetal circulation at the villous pools of the placenta.
Consider transient bacteremia following daily

activities such as brushing teeth and other potential disruptions of colonized mucoepithelial surfaces. (without significant maternal illness).

Aspiration
Aspiration of infected or inflamed amniotic fluid.

Common features with ascending infection.

Infection of the amniotic fluid often involves

ascending pathogens from the birth canal but may result from haematogenous seeding or direct introduction during pelvic examination, amniocentesis.

Intrapartum
Intrapartum pneumonia is acquired during passage

through the birth canal.

transmission, or

It may be acquired via hematogenous or ascending

Aspiration of infected or contaminated maternal fluids,

mechanical or ischemic disruption of a mucosal surface

that has been freshly colonized with a maternal organism of appropriate invasive potential and virulence.

Postpartum
Postnatal Pneumonia occurs via the colonization of a

mucoepithelial surface with an appropriate pathogen from a maternal or environmental source

The frequent use of broad-spectrum antibiotics in many

obstetrical services and neonatal intensive care units (NICUs) often results in predisposition of an infant to colonization by resistant organisms of unusual pathogenicity

Enteral feedings may result in aspiration events of significant

inflammatory potential. Indwelling feeding tubes may further predispose infants to gastroesophageal reflux and other aspiration events.

Presentation
Fever and difficulty breathing are the commonest

presenting symptoms usually preceded by an upper respiratory tract infection. Cough Lethargy Poor feeding An unwell child Localised chest, abdominal, or neck pain is a feature of pleural irritation and suggests bacterial infection.

Physical findings
Pulmonary

Extrapulmonary
Local

Pulmonary
Persistent tachypnea (RR> 60/min)

Expiratory grunting
Accessory respiratory muscle recruitment (e.g. Nasal

flaring, subcostal, intercostal and sternal recessions). Cyanosis of central tissues (such as trunk, consistent with severe derangement of gaseous exchange from severe pulmonary dysfunction

Pulmonary
Asymmetry of breath sounds and chest excursions

End inspiratory respiratory coarse crackles over the

affected area.

Extrapulmonary
Temperature instability

Rash
Jaundice at birth Tachycardia

Glucose intolerance
Abdominal distension Oliguria

Localized
Conjuctivitis

Vesicles or other skin lesions

Unusual nasal secretions

On Examination
Respiratory distress is noticed soon after birth or

during first 24 hours.

The newborn may die from pneumonia without

manifesting distress
The classic signs of consolidation with dullness on

percussion, decreased breath sounds and bronchial breathing over the affected area are usually absent.

Predisposing factors to pneumonia

Preterm labour Preterm rupture of membranes Prolonged active labour with cervical dilatation

Maternal pyrexia (>38C)

Foul smelling amniotic fluid Previous infant with neonatal infection Meconium in the amniotic fluid

Predisposing factors to pneumonia

Fetal tachycardia Recurrent maternal UTI

Uterine tenderness

Investigations: Important studies to be considered

Blood cultures Serologic tests CSF cultures

Complete blood count with white cell differential

Nasopharyngeal culture Tracheal aspirate Chest X ray

Chest X-Ray

Features of CXR
May vary from :

1) streak density to, 2) diffuse opacification to, 3) granular appearance

Management
Most cases can be managed at home but indication

for admission include: oxygen saturations< 93 percent. Severe tachypnea and difficulty breathing Grunting Apnoea Not feeding or family unable to provide appropiate care.

Management
General Supportive care should include analgesia for

pain and oxygen for hypoxia.

Fluids should be given if necessary, ensuring that an

excessive volume is not given because of potential inappropriate ADH secretion.

Physiotherapy has no role.

Management
Initial antibiotic treatment includes penicillin

(usually ampicillin) and an aminoglycoside (such as gentamicin). This would comprise broad spectrum antibiotics treatment.
Indicated for early onset pneumonia.

Management
Later onset pneumonia should include coverage for

staphylococcus.
When the causative organisms are identified, narrow

spectrum antibiotics are used and continued for a minimum of 10 days.

DDx: Meconium Aspiration Syndrome

Introduction
Meconium is the first stool of an infant,

composed of materials ingested during the time the infant spends in the uterus ( bile, amniotic fluid, lanugo, mucus, desquamated cells) Normally stored in the intestines until after birth but can be expelled prior to birth in the amniotic fluid or during labor and delivery where it is seen as a sign of foetal distress.

Signs and Symptoms

Meconium stained amniotic fluid (green-yellow

appearance) Staining of infants skin, umbilical cord, nailbed After birth Rapid/ Labored breathing, cyanosis, Low APGAR score, tachypnea, hypoxia, hypercapnia, acidosis Abnormal lung sounds

Diagnosis
Foetal Cardiotocography (CTG) tachycardia,

bradycardia or absence of fetal accelerations respiratory distress at birth or shortly after birth Infantile Chest X ray showing 1) diffuse or local linear or patchy infiltrates, 2) consolidation or atelectasis, and 3) hyperaeration with or without air leaks

Pathophysiology
Meconium passage occurs by three distinct

mechanisms: (1) as a physiologic maturational event (2) as a response to acute hypoxic events (3) as a response to chronic intrauterine hypoxia

Pathophysiology
If an infant aspirates meconium before, during, or

after birth: the material may block the airways efficiency of gas exchange in the lungs is lowered resultant hypoxemia Pathophysiology inflaming airways (pneumonitis) and possibly leading to chemical pneumonia. Persistent pulmonary hypertension of the newborn (PPHN) Surfactant Dysfunction Meconium aspiration pneumonia

Pathophysiology
The pH of meconium is approximately 7.10 to

7.20. Aspiration of meconium may cause airway irritation. The enzymes and bile salts of meconium may cause a release of cytokines, which can result in diffuse toxic pneumonitis.

Treatment
Endotracheal suction

Assisted ventilation
Surfactant therapy- Lucinactant (Surfaxin) Inhaled Nitric Oxide

If severe hypoxia persists Extracorporeal Membrane Oxygenation (ECMO) may be beneficial .

Prognosis
Perinatal deaths are related to perinatal depression

(asphyxia),airway obstruction, and development of PPHN. Pulmonary sequelae Nearly 50% of all affected infants develop reactive airway diseases during the first 6 months after birth. Mild airway obstruction or exercise-induced asthma often present in the children at 6 to 8 years of age

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