Respiratory Distress Of The Newborn

PEDIATRICS 2 Respiratory Diseases of the Newborn Dr. Alabastro 2nd Shifting September 8, 2008 S.M.V. DEVELOPMENT OF THE LUNG



Early Embryonic Development (3-7 weeks AOG) Major conducting airways formed Pseudoglandular Stage (7-16 weeks AOG) Bronchial tree and acinar tubes develop Canalicular Stage (16-24 weeks AOG) Vascularization of mesenchyme Saccular Stage (24-38 weeks AOG) Alveoli develop Alveolar Stage (36 weeks AOG) - Remodeling ofcapillary bed → Increased surface area → Type I epithelial cells → Start of increase of Type II epithelial cells

APNEA VS PERIODIC BREATHING

RESPIRATORY SYSTEM

 

Fetal breathing detected as early as 11th week AOG Placenta is the medium of gas exchange in utero



Lungs – medium of gas exchange at birth; lined by type I epithelial cells



Surfactant synthesized by type II alveolar cells – present in lungs by 20 weeks, in amniotic fluid by 28-32 weeks Premature infants are prone to hyaline membrane disease



MECHANISM OF RESPIRATION

     

 

Thoracic cage compressed during vaginal delivery Ejection of tracheal fluid (most removed by pulmonary circulation, the rest by lymphatics) Passive inspiration of air or recoil of chest wall Blood into pulmonary capillaries (open with lung expansion) Established respiration when umbilical cord is clamped In CS, mechanism is absent since there is no initial chest compression; tracheal fluid: 1/3 goes to lymphatics, 2/3 goes to circulation Fetal circulation = parallel type Neonatal circulation = series type

FACTORS CONTRIBUTING TO FIRST BREATH





Physical stimuli: gravity, light, decrease skin temperature/cold temperature, simple physical stimuli Chemoreceptors - Fall in pO2 and pH to stimulate breath

-

Rise in pCO2 due to placental interruption Redistribution of CO because of closure of the shunts

Lowering of body temperature

Apnea cessation of breathing for more than 20 sec. associated with bradycardia, cyanosis, pallor Periodic Breathing cessation of breathing for less than 20 sec. with no bradycardia, cyanosis, pallor TYPES: Central Apnea – problem in the brain; cessation of airflow and respiratory effort (CNS control of respiration) - Obstructive Apnea – problem I the lungs; cessation of airflow with continuous respiratory effort (disturbances in O2 delivery by perfusion, ventilation defects, hyaline membrabe disease) Mixed – central and obstructive ETIOLOGY: 1. Hours after birth a. Oversedation b. Dysphyxia c. Seizures d. Hypermagnesemia e. Hyaline membrane disease 2. < 1 week a. Post-extubation b. Atelectasis c. PDA d. PV-IVH e. Apnea of prematurity 3. > 1 week a. Post-hemorrhage b. Hydrocephalus with increase ICP 4. 6-10 weeks a. Anemia of prematuriy 5. Variable a. Sepsis b. NEC c. Meningitis d. Aspiration e. GER f. Cardiac pneumothorax g. Colds h. Stress MANAGEMENT: 1. Laboratory exam according to presumed etiology – ex. Infection → CBC, culture 2. Apnea of prematurity is a diagnosis of exclusion 3. Management based on cause – ex. Sepsis → treat infection

MARY YVETTE ALLAIN TINA RALPH SHERYL BART HEINRICH PIPOY KC JAM CECILLE DENESSE VINCE HOOPS CES XTIAN LAINEY RIZ KIX EZRA GOLDIE BUFF MONA AM MAAN ADI KC PENG KARLA ALPHE AARON KYTH ANNE EISA KRING CANDY ISAY MARCO JOSHUA FARS RAIN JASSIE MIKA SHAR ERIKA MAQUI VIKI JOAN PREI KATE BAM AMS HANNAH MEMAY PAU RACHE ESTHER JOEL GLENN TONI

PEDIATRICS 2 Respiratory Diseases of the Newborn Page 2 of 3

4.

5. 6. 7. 8.

Tactile/proprioceptive stimulation intermittent) Increase O2 as necessary

(mild

and

Nasal or ETT continued positive airway pressure (CPAP) – mixed/ obstructive Mechanical ventilation (prolonged & recurrent) Methylxanthine – loading dose: 5 mg/kg; maintenance: 1-2 mg/kg/dose q 6-8 hrs IV/PO

IMPORTANT DATA 1. OB history  LMP or gestation (usually in premature but also seen in postterm or term in CS); increase stress - decrease surfactant



CYANOSIS

CAUSES: 1. Respiratory: upper and lower airways 2. Cardiac: abnormal connections, obstructed pulmonary blood flow 3. CNS: asphyxia (result of poor APGAR score); Intracranial: HPN/hemorrhage 4. Hematologic: methemoglobinemia 5. Metabolic: hypoglycemia 6. Others: polycythemia, blood loss RESPIRATORY DISTRESS

CAUSES: 1. Respiratory causes a. Upper respiratory obstruction (Choanal atresia) b. Pulmonary disease (RDS/MAS) 2. Non-respiratory causes a. Congenital heart disease/failure b. Intracranial lesions c. Neuromuscular disorder d. Metabolic disturbance e. Infection RESPIRATORY DISTRESS SYNDROME Absence or deficiency of surfactant  Extreme prematurity  Transient stress  Impairment of release mechanism  Death of cells responsible for surfactant (type II cells) Decreased pulmonary blood flow with resulting ischemia Pulmonary atelectasis and interstitial edema Diminished surfactant Intrapartum asphyxia C-section Prematurity Familial predisposition Acidosis Progressive Atelectasis Hypoventilation - increase pCO2, decrease pO2, decrease pH apnea hypothermia neonatal asphyxia transient tachypnea Hypotension “shock” hypovolemia

2.

Lecithin:sphingomyelin ratio – should be 2 for surfactant to be enough (lecithin must be more than sphingomyelin)  Increase risk factors for infection o Maternal factors o Amnionitis o PROM > 12 hours  Increase risk factor for stress: preeclampsia Group B streptococcal pneumonia/sepsis

CLINICAL COURSE/MANIFESTATIONS 1. Tachypnea within minutes after birth 2. grunting, intercostals & subcostal retractions, nasal flaring, duskiness (lighter than cyanosis) 3. Normal or decrease breath sounds, basal fine rales 4. Progressive, worsening of cyanosis & dyspnea relatively unresponsive on O2 5. If untreated, worsens but grunting decreases; apnea and irregular respiration 6. Gradual improvement from 3-5 days 7. Complications: 2-7 days (air leaks & hemorrhage) DIAGNOSIS 1. Clinical course 2. Chest X-ray: fine granularity 3. Blood gas analysis 4. Septic work up 5. CBC 6. 2-D echo DIFFERENTIALS 1. Pneumonia 2. Transient tachypnea – disappears in 3 days, responds to O2 3. PPHPN – complication of hyaline membrane disease 4. Cyanotic heart disease 5. Aspiration syndrome 6. Spontaneous pneumonia 7. Pleural effusion 8. Diaphragmatic contraction 9. Congenital anomalies (2D-echo) TREATMENT 1. Maintain blood gases paO2= 55-70 mmHg pCO2= 45-55 mmHg pH=7.25-7.45 2. Hypoxia and respiratory acidosis Warm humidifier O2 CPAP by nasal prong assisted ventilation 3. Metabolic acidosis: Na bicarbonate 4. Hypotension: dopamine, colloid fluid, fluids and electrolytes

PEDIATRICS 2 Respiratory Diseases of the Newborn Page 3 of 3

5. 6.

7.

Hypothermia: 36.5-37°C Antibiotics Exogenous surfactant: endotracheal intubation in 1st 24 hours q 6-12 hrs for 2-4 doses

MANAGEMENT OF COMPLICATIONS 1. PDA: Indomethacin 0.2 mg/kg 12-24 hrs 3 doses/surgical; avoid CHF (diuresis, fluid restriction) 2. Pulmonary hemorrhage: coagulation profile, transfusion, racemic epinephrine 3. PPHPN: volume, fluids & electrolytes, correct acidosis, vasopressor 4. Chronic lung disease: continued mechanical ventilation, nutrition, fluid restriction; treatment of infection, furosemide; bronchodilators; dexamethasone MECONIUM ASPIRATION SYNDROME







In utero, passage of meconium with subsequent gasping respiration due to asphyxia, causing the aspiration of meconium-stained amniotic fluid May result in mechanical aspiration, chemical inflammation, bacterial infection, persistent fetal circulation, severe hypoxia and acidosis Medium for bacterial proliferation

HISTORY DATA  Antepartum & intrapartum events that may cause fetal distress or intrauterine asphyxia  Meconium in amniotic fluid  Gestational age of fetus  Usually seen in post-term infants FINAL COMPLICATIONS 1. Atelectasis 2. PPHPN 3. Air leaks 4. Hypercapnea, hypoxia CLINICAL MANIFESTATION 1. General appearance: depressed activity, meconium-stained (greenish with smell), postmature 2. Signs of respiratory distress: tachypnea, retractions, flaring, grunting, increase AP diameter of chest, cyanosis 3. Degree of respiratory distress: may appear normal at birth; moderate/severe: evident at birth 4. May improve after 72 hours if mild LABORATORY EXAMS 1. Chest X-ray: hyperinflated lung fields, flat diaphragm, coarse irregular pulmonary densities with area of atelectasis & consolidation; “snowstorm pattern” 2. ABG: hypoxia, acidosis, abnormal O2, decrease pO2, increase pCO2 3. Tracheal aspirate, CS

4.

Septic work up: blood culture, urine, feces, secretions

MANAGEMENT 1. Prevent aspiration 2. Suction: direct laryngoscopy, oropharynx, nares, trachea 3. Respiratory support: ABG analysis 4. Chest X-ray (AP, Lateral), CS, CBC 5. Start antibiotics 6. Management of complications: atelectasis, air leaks, PPHPN 7. If unresponsive: surfactant, NO, Extracorporeal membrane oxygenation (ECMO) Complete obstruction → atelectasis Incomplete/ partial obstruction → air trapping → air leaks Continuous compromise → PPHPN