55274777 respiratory-distress-in-newborn

PRESENTER: JOY W. KAMAU

FACILITATOR:DR. SONGOK

RESPIRATORY DISTRESS SYNDROME

• Distinguish between respiratory distress and RDS

• Definition of RDS• Incidence and risk factors• Pathogenesis• presentation• Diagnosis• Treatment• Complications• Prognosis

OUTLINE

Respiratory distress is a symptom complex arising from disease processes that cause failure to maintain adequate gaseous exchange

• Tachypnea (>60bpm)

• Grunting, Flaring, Retractions/ recessions (GFR)

• Cynosis

• Reduced air entry

Obstruction of the airway Lung parenchymal disease

1- Choanal atresia 2- Congenital stridor 3- Tracheal or bronchial stenosis

1- Meconium aspiration 2- Respiratory distress syndrome 3- Pneumonia 4- Transient tachypnea of the newborn

(retained lung fluid) 5- Pneumothorax 6- Atelectasis 7- Congenital lobar emphysema

Non-pulmonary causes Miscellaneous

1- Heart failure 2- Intracranial lesions 3- Metabolic acidosis

1- Disorders of the diaphragm e.g. (diaphragmatic hernia)

2- Pulmonary haemorrhage 3- Pulmonary hypoplasia

CAUSES OF RESPIRATORY DISTRESS

  0   1  2

 Cyanosis  None  In room air  In 40% FIO2

 Retractions None  Mild  Severe

 Grunting  None  Audible with stethoscope

 Audible without stethoscope

 Air entry Clear  Decreased or delayed  Barely audible

 Respiratory rate

 Under 60   60-80  Over 80 or apnea

 Score:  > 4 = Clinical respiratory distress; monitor arterial blood gases > 8 = Impending respiratory failure

DOWNE’s SCORING OF RESPIRATORY DISTRESS

• (RDS) is a condition of increasing respiratory distress, commencing at, or shortly after, birth and increasing in severity until progressive resolution occurs among the survivors, usually around 2nd to 7th day

• Maybe primary or secondary

• Incidence and severity is inversely proportional to gestational age• <28wks- 60-80%• 28-32wks- 25-50%• 32-36wks- 15-30%• >37 wks- 5%• rare at term

RISK FACTORS• Neonates younger than 33-38 weeks• Weight less than 2500g• Maternal diabetes• Cesarean delivery without preceding labor• Precipitous labor• Fetal asphyxia• Second of twins• Cold stress• Previous history of RDS in sibling• Males• whites

DECREASED RISK

• Use of antenatal steroids

• Pregnancy-induced or chronic maternal hypertension

• Prolonged rupture of membranes

• Maternal narcotic addiction

• Chronic intrauterine stress

• IUGR or SGA

• Thyroid hormones

• Tocolytic agents

ETIOLOGY AND PATHOPHYSIOLOGY.

• Surfactant deficiency is the 1O cause of RDS. • Low levels of surfactant cause high surface tension • High surface tension makes it hard to expand the

alveoli.• Tendency of affected lungs to become atelectatic at

end-expiration when alveolar pressures are too low to maintain alveoli in expansion

• Leads to failure to attain an adequate lung inflation and therefore reduced gaseous exchange

Pulmonary Surfactant decreases surface tension

PATHOPHYSIOLOGY

Structure of lung surfactant

major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins (surfactant proteins SP-A, -B, -C, -D), cholesterol

• With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells .

• Wk 20: start of surfactant production and storage. Does not reach lung surface until later

• Wk 28-32: maximal production of surfactant and appears in amniotic fluid

• Wk 34-35; mature levels of surfactant in lungs• The amounts produced or released may be

insufficient to meet postnatal demands because of immaturity.

• Surfactant inactivating states eg maternal DM may lead to surfactant of lower quality/ immature

• Rare genetic disorders may cause fatal respiratory distress syndrome eg.

• Abnormalities in surfactant protein B and C genes

• gene responsible for transporting surfactant across membranes (ABC transporter 3 [ABCA3]) are associated with severe and often lethal familial respiratory disease

Prematurity, BA, hypoxemia, hypotension, iatrogenic lung injury, cold stress

Low surfactant, high ST

Difficulty expanding alveoli with increased recoil

Hyaline membrane

Proteinaceous outflow & edema

Small alveolar units

atelectasis

Decreased lung compliance

Exhaustion

V-Q mismatch

Greater work of breathing

Chest wall:• Hyper- compliant• Indrawing• Low resistance to

lung recoil

atelectasis Decreased lung compliance

Hypercapnia, acidosis

Right- left shunt

High P.V. resistance

Pulmonary vasoconstriction

More hypoxia, worsening lung injury

apnoea

pathologyInflammation so accumulation of neutrophils in the lungAtelectasis and hyaline membraneDecrease fluid absorption and lung edema; liver-like lungHemorraghe & interstitial emhysema esp if ventilated

CLINICAL COURSE• Signs of RDS in minutes to hours after birth

• Tachypnea, prominent (often audible) Grunting, Flaring, Retractions, (GFR) and Cyanosis relatively unresponsive to oxygen

• Breath sounds normal or harsh bronchial

• Crepitations esp over posterior lung bases

• Natural course is worsening cyanosis and dyspnea

• If inadequately treated, hypotension, fatigue, cyanosis, and pallor increase

• grunting decreases or disappears as the condition worsens

• Apnea as infants tire: OMINOUS needs immediate intervention

• mixed respiratory-metabolic acidosis, edema, ileus, and oliguria (end-organ damage and complications)

• Respiratory failure may occur

• Usually illness peaks in 3 days, then gradual improvement

• Improvement is often heralded by spontaneous diuresis and the ability to oxygenate the infant at lower inspired oxygen levels or lower ventilator pressures

• Death may occur esp from day2-3

MORTALITY

• Death is rare on the 1st day, • usually occurs between days 2 and 7

• causes are: – alveolar air leaks (interstitial emphysema,

pneumothorax),– pulmonary hemorrhage– Intracranial hemorrhage

• Late mortality from bronchopulmonary dysplasia

Is a Clinical diagnosis: respiratory distress occurring soon after birth. Pay attention to risk factors! Pulse Oximetry: aim for SPO2 >85%. ROUTINE!

Full blood count and Cultures to check for sepsis: rem culture only positive 40-50% of the time!! gastic aspirates/ buffy smears for GBS

Chest radiograph: air bronchogram, reticular/ ground-glass appearance after 6-12 hrs to full opacity later on.

Blood gases: hypoxia, hypercapnia, acidosis. Signs of RESP FAILURE determine mgmt eg CPAP vs ventilation etc

Electrolytes, glucose, renal and liver function

Echocardiogram: diagnosing PDA, determine the direction and degree of shunting, making the diagnosis of pulmonary hypertension and excluding structural cyanotic heart disease

Supportive mgmt: Oxygen at the minimum FiO2 to maintain arterial O2 at 60-

80mmhg equivalent to 85-95% SPO2. Thermoregulation: baby in humidified (60-80%)incubator. Aim

for core temp of 36.50 CIVF (10% dextrose; avoid fluid overload so dont go above

140ml/kg!)Adequate caloric intakeBroad spectrum antibiotics in all infants with RDS after taking

samples for septic screen (Xpen-Genta)Correct electrolyte imbalancesPrevent and correct anemiaMay need NaHCo3 in severe acidosis (3-5mEq but based on pH

ie the lower the ph, the higher the dose)Vitamin A 5,000 IU 3times/ wk for 4wks; reduces BPD Endotracheal Surfactant (100mg/kg)CPAP/ Mechanical ventilation if O2 is not working

Treatment of RDS

Surfactant Laboratory Container Concentration Recommended dose

Curosurf Farmalab-Chiesi 1.5 & 3 ml 80 mg/ml 100 to 200 mg/kgPorcine

Survanta Abbott 4ml & 8 ml 25 mg/ml 100 mg/kgBovine

Alveofact Boeringer 1.2 ml 40 mg/ml 100 mg/kgBovine

Exosurf Wellcome 13.5 mg/ml(DPPC) 5 ml/kgSynthetic

Prophylaxis of infants >1350g but with pulmonary immaturityPropylaxis of infants <1350g at risk of RDSRescue therapy of infants with RDS

PREVENTION OF RDS

Avoid neonatal hypothermiaGood control of maternal Diabetes mellitus in pregnancyActive mgmt of labour to avoid birth asphyxiaPrenatal corticosteroids 48hrs before deliveryAvoid unnecessary CS/ induction Single dose surfactant to at risk, premature infants at birthPrenatal assessment of fetal lung maturity

Lecithin –sphingomyelin ratio <1.5 prior to delivery suggests prematurity. If >2.0, has PPV of 95-100%

Absence of phospatidylglycerol means immaturity: if present, has PPV of 96-100%

Surfactant albumin ratio >0.47 has PPV of 95%Lamellar body counts >30-40000 has PPV of 97%

COMLICATIONS

acute

Apnea

Air leak

infection

ICH

PDA & foramen ovale

End-organ hypoxic injury

Results from slow absorption oflung fluid

Term born by LSCS/IDM /maternal asthma

Mild respiratory distress

Peaks at about 36 hours of life

Resolve spontaneously

Transient Tachypnea of the Newborn

Pneumonia & Sepsis have various manifestations including typical signs of distress as well as temperature instability

Common pathogen- Group B Streptococcus, Staph aureus, Streptococcus aureus, Streptococcus Pneumoniae,Gm neg rods

Risk factors- prolonged rupture of membranes, prematurity,& maternal fever

CXR- bilateral infiltrates suggesting in utero infection.

NEONATAL PNEUMONIA

Incidence- 1.5- 2 % in term or post term infants.

Meconium is locally irritative, obstructive & medium for for bacterial culture

Meconium aspiration causes significant respiratory distress. Hypoxia occurs because aspiration occurs in utero.

CXR- Patchy atelectasis or consolidation.

MECONIUM ASPIRATION SYNDROME

Apnea of prematurity

> 50% of infants <1500g requireintervention for apneaTreatments• Stimulation• CPAP• Intubation• Medication:

CaffeineMethylxanthinesTheophyllineDoxapram

• Oxygen

pneumothorax

Spontaneous -1-2%

MAS ,hypoplastic lung,aggressive resuscitation,CPAP,ventilation

Tension pneumothorax-immidiate drainage

Prognosis

• Bad prognosis