55274777 respiratory-distress-in-newborn
TRANSCRIPT
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