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Respiratory Distress in Newborn PowerPoint Presentation

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Description : Check out this medical titled "Respiratory distress in newborn” by Dr.mirzarahimi.

This medical is about respiratory distress in newborns, a serious condition that requires urgent medical attention. It is characterized by difficulty breathing, rapid breathing, grunting sounds, flaring of the nostrils, chest retractions, and bluish discoloration of the skin. Respiratory distress can occur immediately after birth or develop in the first few hours or days of life.

The potential causes of respiratory distress in newborns include Transient tachypnea of the newborn (TTN), Meconium aspiration syndrome (MAS), Respiratory distress syndrome (RDS), Pneumonia, and Congenital heart disease.

Treatment for respiratory distress in newborns may include oxygen therapy, mechanical ventilation, medications to help with breathing, and treatment for any underlying conditions. It is important to seek medical attention immediately if you notice any signs of respiratory distress in your newborn, as early treatment can improve outcomes.

Tags : Respiratory distress in newborn, Transient tachypnea of the newborn, Meconium aspiration syndrome, Respiratory distress syndrome, Pneumonia, Congenital heart disease, Neonatal-Perinatal Medicine, Neonatal-Perinatal Medicine

Published on : Jun 01, 2023 | Views : 2847 | Downloads : 8

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Slide 1-

Respiratory distress in newborn Dr.mirzarahimi
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Neonatal Respiratory Distress Signs and symptoms Tachypnea (RR > 60/min) Nasal flaring Retraction Grunting Delayed or decreased air entry +/- Cyanosis +/- Desaturation
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Neonatal Respiratory Distress Etiologies Pulmonary causes RDS Pneumonia TTN MAS Other aspiration syndrome Air leak syndrome Lung hemorrhage Lung hypoplasia Congenital malformations Systemic causes Infections Metabolic causes Temperature Anemia Polycythemia Congenital heart disease Pulmonary hypertension Neuromuscular disorder Anatomic causes Upper airway obstruction Airway malformation Space occupying lesion Rib cage anomalies Phrenic nerve injury diagnosis : Hx, Phx and L.F
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Neonatal Respiratory DistressAlgorithm Respiratory Distress (tachypnoea, retractions, grunt) Preterm Term < 6hrs old > 6hrs old < 6hrs old > 6hrs old HMD (RDS) Pneumonia Lung anomaly Pneumonia CHD Pul. Hemorrhage TTN MAS/PPHN Asphyxia Lung anomaly Air leak Pneumonia CHD
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Respiratory Distress Syndrome
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Introduction The most frequent cause of respiratory distress in premature infants. 60-80% of <28wk GA ; 15-30% of 32-36wk GA ; 5% of 37wk-term. Classic presentation of grunting, retractions, increasing O2 requirement, reticulogranular pattern and air bronchograms on CXR and onset < 6hrs age
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Pathogenesis Prematurity Prenatal asphyxia Reduced surfactant synthesis, storage, release Increased alveolar surface tension Progressive atelectasis Diffusion Uneven V/Q Hypoventilation gradient Hypoxemia CO2 retention Acidosis Pulmonary vasoconstriction Hypoperfusion Capillary endothelial damage Plasma leak Fibrin
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Pathology Gross : Lung firm, red, liverlike Microscopic : Diffuse atelectasis, pink membrane lining alveoli & alveolar ducts. Pulmonary arterioles with thick muscular coat, small lumen. Distended lymphatics Electron microscopic : Damage / loss of alveolar epithelial cells, disappearance of lamellar inclusion bodies, swelling of capillary endothelial cells
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Pathology (contd.) Biophysical : Deficient / absent surfactant Abnormal pressure volume curve Normal Vol RDS Pressure Severely reduced arterial bed with blockage near pulmonary arterioles
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Pathology (contd.) Biochemical : Diminished surface-active phospholipid (phosphatidylcholine) Diminished apoprotein content ( SP-A, B, C, D)
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Pathophysiology Reduced lung compliance (1/5th -1/10th) Poor lung perfusion ( 50-60% not perfused), decreased capillary blood flow R--> L shunting ( 30-60% ) Alveolar ventilation decreased Lung volume reduced Increased work of breathing Hypoxemia, hypercapnia, acidosis
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Physiologic abnormalities Lung compliance 10-20% of norm Atelectasis…areas not ventilated Areas not perfused Decrease alveolar ventilation Reduce lung volume
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Risk factor Prematurity Acidosis Hypoxia Hypercapnia Hypothermia C/S Asphyxia and stress Male Familial DM mother
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signs tachypnea retraction grunting Nasal flaring apneic episode cyanosis extremities puffy or swollen
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Chest X-ray Ground glass appearance Reticulogranular With air bronchograms
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Treatment Surfactant Prevention rescue Supportive Thermal Fluid and nutrition oxygen Mechanical ventilation
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complications Pneumothorax PDA Infection Line problems ROP Chronic lung disease
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Meconium aspiration
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M .A .S آسپيريشن مايع آمنيوتيك آغشته به مكونيوم ممكن است منجر به سندرم آسپيريشن مكونيوم گردد كه مربيديتي و مورتاليتي قابل ملاحظه اي دارد بنابراين مديريت زايمان با مايع آمنيوتيك آغشته به مكونيوم براي پيشگيري از آسپيراسيون اهميت زيادي دارد
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تركيب مكونيوم Cellular particle Bile pigment Lango Mocus Vernix Pancreatic secretion One gr meconium = one mg Billirubin
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Incidence دفع مكونيوم 8 تا 20 درصد كل زايمانها ( متوسط 12 %) مكونيوم آسپيريشن در 4 درصد مكونيومي ها دیده می شود وجود دارد. SGA و Post maturityعمدتا
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فيزيوپاتولوژي اگر چه فيزيوپاتولوژي كامل آن و علت دفع مكونيوم كاملا شناخته نشده اما اين پديده بندرت قبل از هفته 34 ديده مي شود بسياري از مكونيوم دفع كرده ها علامتي دال بر مشكل تنفسي يا دپرسيون نداشته اند و عده اي هم بعلت آسفيكسي مكونيوم دفع كرده اند
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علت دفع مكونيوم 1) پديده فيزيولوژيك : تكامل عصبي پاراسمپاتيك و برقراري پريستالتيسم روده اي در پاسخ به تكامل جنين (شيوع در ترم ها و نادر بودن در نوزادان نارس ) 2) هيپوكسي : مي تواند باعث افزايش پريستالتيسم روده ها و كاهش تو ن اسفنكترآنال شود (البته اكثر نوزادان با مايع آمنيوتيك مكونيال آپگار پايين و اسيدوز ندارند )
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Alarm of MAS 1- Thick meconium 2-Fetal tachycardia 3- lack of increase heart rate during intra partum monitoring 4-Low cord PH
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پاتوژنز
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MAS complication Partial obstruction o complete obstruction : Surfactant destruction Chemical pneumonitis &Bacterial pneumonia Asphyxia PPHN
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Clinical sign Classic sign: Post maturity nail, skin , umblical cord are heavily stained with a yellowish pigment Early sign (resp . Distress) : grunting & cyanosis & nasal flaring & retraction & marked tachypnea Characteristic sign : chest overinflation and Rale
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Radiography of M.A.S Coarse , nodular , irregular pulmonary densities with areas of diminished aeration or consolidation. Hyperinflation of the chest . Atelectasis Flattening of diaphragm Cardiomegally (manifestation of the underlying prenatal hypoxia)
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Chest.X.Ray
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Meconium Aspiration Syndrome
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Meconium Aspiration Syndrome
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ABG in M.A.S شواهدي از يك آلكالوز تنفسي هيپوكسي در مواقع شديد اسيدوز تنفسي و اسيدوز متابوليك شواهدي از شنت راست به چپ
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Management of M.A.S حضور مكونيوم در مايع آمنيوتيك دليل بردیسترس جنینی نيست وچنانچه ضربان قلب جنین و پی-اچ بند ناف طبيعي باشد پيش آگهي خوب است آميخته شدن مكونيوم با مايع آمنيوتيك باضافه ضربان قلب نا مناسب نويد دهنده يك آسفيكسي مي باشد
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Intra partum در اين گونه مواقع وقتي سر بيرون آمد در روي پرينه بايد ساكشن دهان وبيني و فارنكس با كاتتر نمره 12 يا 14 انجام شود (قبل از اينكه توراكس بيرون بيايد و نوزاد بخواهد تنفس كند ) اولين ارزيابي نوزاد متولد شده : vigorous or depress
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Criteria of vigorous 1) Heart rate greater than 100 beat /min 2) Good muscle tone 3) regular breathing
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Guidelines of the baby exposed to meconium Vigorous Immediate tracheal suction Meconium No meconium reintubate and suction PPV and suction again later Clear secretions and meconium initial resuscitation steps HR>100 HR<100 No Yes The American Academy of Pediatrics Neonatal Resuscitation Program Steering Committee management guidelines of the baby exposed to meconium:
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ET suction indication Only in non vigorous baby - depressed respirations - decreased muscle tone - heart rate < 100 beats per minute Pharyngeal suctioning of an infant before delivery of the shoulders. Removal of meconium from hypopharynx and larynx by large-bore catheter. Meconium aspirator attached to wall suction. Endotracheal intubation for removal of meconium in the lower airway.
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Management Prevention Monitor fetal status Amnioinfusion Suctioning +/- intubation and immediate suctioning Avoid harmful techniques Intervention Optimal thermal environment & minimal handling Respiratory care, Oxygen therapy & ECMO Keep stable V/S Surfactant therapy
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Steroid therapy for meconium aspiration syndrome in newborn infants The Cochrane Database of Systematic Reviews 2007 Issue 3, The Cochrane Library (ISSN 1464-780X Conclusions: At present, there is insufficient evidence to assess the effects of steroid therapy in the management of meconium aspiration syndrome (no significant reduction in mortality, duration of hospital stay, Duration of mechanical ventilation, incidence of air leak,increase in duration of oxygen therapy was seen with the use of steroids)
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Role of antibiotics in meconium aspiration syndrome Ann Trop Paediatr. 2007 Jun;27(2):107-13. Basu S, Kumar A, Bhatia BD. Division of Neonatology, Department of Paediatrics, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India. drsriparnabasu@rediffmail.com CONCLUSION: Routine antibiotic therapy is not necessary for managing MAS. No significant difference period of oxygen dependency (5.8 vs 5.9 days) day of starting feeds (4.0 vs 4.2) day of achievement of full feeds (9.4 vs 9.3) clearance of chest radiograph (11.7 vs 12.9 days) duration of hospital stay (13.7 vs 13.5 days)
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Surfactant for meconium aspiration syndrome in full term/near term infants Cochrane Database Syst Rev. 2007 Jul 18;(3):CD002054 El Shahed A, Dargaville P, Ohlsson A, Soll R. CONCLUSIONS: In infants with MAS, surfactant administration may reduce the severity of respiratory illness and decrease the number of infants with progressive respiratory failure requiring support with ECMO. The relative efficacy of surfactant therapy compared to, or in conjunction with, other approaches to treatment including inhaled nitric oxide, liquid ventilation, surfactant lavage and high frequency ventilation remains to be tested.
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PPHN prevention Avoid vasoconstriction Acidosis Hypoxia Metabolic disturbance - Hypocalcemia - Hypercalcemia - Hyperglycemia - Hypoglycemia Prevent right to left shunt
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Infections
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Infections Pneumonia & Sepsis have various manifestations including typical signs of distress as well as temperature instability. Common pathogen- Group B Streptococcus, Staph aureus, Streptococcus Pneumonia,Gm neg. rods
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Infections con.. Risk factors- prolonged rupture of membranes, prematurity,& maternal fever. CXR- bilateral infiltrates suggesting in utero infection.
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Congenital pneumonia Sepsis risk factors PROM Prematurity Maternal fever, discharge, abdominal pain, leukocytosis Colonization with GBS Same signs of RDS X-ray
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Transient Tachypnea of Newborn Most common cause of respiratory distress. Residual fluid in fetal lung tissues. Risk factors- maternal asthma, c- section, male sex, macrosomia, maternal diabetes
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TTN Tachypnea immediately after birth or within two hours, with other predictable signs of respiratory distress. Symptoms can last few hours to two days. Chest radiography shows diffuse parenchymal infiltrates, a “ wet silhouette” around heart, or intralobar fluid accumulation
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X-ray Fluid in the fissure
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Transient tachypnea of newborn Term Cesarian delivery Usually tachypnea without O2 requirment Resolve in 48-72 houres Lung fluid X-ray
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Other causes- Congenital malformations-Pulmonary hypoplasia, congenital emphysema, esophageal atresia & diaphragmatic hernia. Neurological causes- hydrocephalus & intracranial hemorrhage. Metabolic derangements-hypoglycemia, hypocalcemia, polycythemia.
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Congenital Heart disease Cyanotic Heart Disease- Tetralogy of fallot- ( VSD, Pulmonary stenosis, overriding aorta, RVH) Tricuspid atresia Transposition of great vessel Total anomalous pul. venous return Truncus arteriosus.
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Hyperoxia Test Obtain ABG–> Then place the patient on 100% O2 for 10 minutes then repeat ABG , If the cyanosis is pulmonary , the PaO2 should be increased by 30 mm of Hg. If the cause is cardiac , there will be minimal improvement in PaO2.