55274777 respiratory-distress-in-newborn
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Transcript of 55274777 respiratory-distress-in-newborn
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PRESENTER: JOY W. KAMAU
FACILITATOR:DR. SONGOK
RESPIRATORY DISTRESS SYNDROME
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• Distinguish between respiratory distress and RDS
• Definition of RDS• Incidence and risk factors• Pathogenesis• presentation• Diagnosis• Treatment• Complications• Prognosis
OUTLINE
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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
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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
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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
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• (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
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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
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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
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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
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Pulmonary Surfactant decreases surface tension
PATHOPHYSIOLOGY
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Structure of lung surfactant
major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins (surfactant proteins SP-A, -B, -C, -D), cholesterol
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• 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
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• 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
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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
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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
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pathologyInflammation so accumulation of neutrophils in the lungAtelectasis and hyaline membraneDecrease fluid absorption and lung edema; liver-like lungHemorraghe & interstitial emhysema esp if ventilated
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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
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• 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)
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• 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
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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
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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
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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
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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
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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%
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COMLICATIONS
acute
Apnea
Air leak
infection
ICH
PDA & foramen ovale
End-organ hypoxic injury
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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
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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
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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
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Apnea of prematurity
> 50% of infants <1500g requireintervention for apneaTreatments• Stimulation• CPAP• Intubation• Medication:
CaffeineMethylxanthinesTheophyllineDoxapram
• Oxygen
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pneumothorax
Spontaneous -1-2%
MAS ,hypoplastic lung,aggressive resuscitation,CPAP,ventilation
Tension pneumothorax-immidiate drainage
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Prognosis
• Bad prognosis