Neonatal Diseases

Presentation Transcript

Neonatal Diseases RC 290

Respiratory Distress Syndrome (RDS) Also known as Hyaline Membrane Disease (HMD)

Occurrence 1-2% of all births 10% of every untimely birth Greatest event is in the untimely and low birth weight newborn child

Etiology & Predisposing Factors Prematurity Immature lung engineering and surfactant lack Fetal asphyxia & hypoxia Maternal diabetes Increased shot of untimely birth Possible times of reflex hypoglycemia in the embryo creating hindered surfactant generation

Pathophysiology Surfactant inadequacy Decreased FRC Atelectasis Increased R-L shunt Increased W.O.B. Hypoxemia and in the long run hypercapnia due to V/Q jumble

Pathophysiology ( cont .) Atelectasis keeps PVR high Increased PAP Lung hypoperfusion R-L shunting may re-happen over the Ductus Arteriosus and the Foramen Ovale

Hypoxia/hypoxemia brings about anaerobic digestion system and lactic acidosis This harms the alveolar-slender film creating arrangement of hyaline layers. Hyaline films propagate the greater part of the issues in the lung

The cycle proceeds until surfactant levels are sufficient to balance out the lung Symptoms generally show up 2-6 hours after birth Why not instantly? Ailment crests at 48-72 hours Recovery more often than not happens 5-7 days after birth

Tachypnea (60 BPM or >) Retractions Nasal flaring Expiratory snorting Helps create autoPEEP Decreased breath sounds with crackles Cyanosis on room air Hypothermia Hypotension Clinical discoveries: Physical

Clinical Findings: Lab ABGs: at first respiratory alkalosis and hypoxemia that advances to significant hypoxemia and consolidated acidosis Increased Bilirubin Hypoglycemia Possibly diminished hematocrit

CXR: Normal

RDS CXR: Ground Glass Effect

RDS CXR: Air Bronchograms & Hilar Densities

Time steady is diminished since versatile resistance is so high Increased flexible resistance implies diminished consistence!

RDS Treatment: Primarily strong until lung settles NTE, look after perfusion, keep up ventilation and oxygenation O2 treatment, CPAP or mechanical ventilation May require opposite I:E proportions if oxygenation can not be accomplished with ordinary I:E proportion Surfactant instillation!!! May bring about a sudden drop in flexible resistance!

Prognosis/Complications Prognosis is great once baby makes it past the pinnacle (48-72 hours) Complications conceivable are: Intracranial Bleed BPD (Bronchopulmonary Dysplasia) PDA (Patent Ductus Arteriosus)

Transient Tachypnea of the Newborn (TTN) Also known as Type II RDS or Retained Lung Fluid

Occurrence: Similar to RDS More basic in term babies!

Etiology & Predisposing Factors C-segment These babies don't have the liquid removed from their aviation routes as happens in vaginal conveyance Maternal Diabetes Increased possibility of C-segment because of LGA Cord Compression Anesthesia

TTN Pathophysiology Primary issue = held lung liquid Fluid not ousted from aviation routes due to C-area Poor ingestion of staying liquid by aspiratory vessels and lymphatics If held liquid is in interstitial spaces, consistence and TC are diminished If held liquid is in airways,airway resistance and TC are expanded TTN can be prohibitive , obstructive, or both! Liquid ordinarily clears without anyone else following 24-48 hours after birth

Clinical Signs Tachypnea (as a rule rate is more prominent than seen in RDS) Minimal (assuming any) nasal flaring or expiratory snorting ABG's: mellow hypoxemia. PaCO2 relies on upon whether issue is prohibitive or obstructive

TTN CXR Coarse peri-hilar streaks Prominent lung vasculature Flattened stomachs if liquid is creating hindrance/air-catching

TTN Treatment: Like RDS, it is essentially steady Monitoring and O2 treatment Possibly CPAP or mechanical ventilation

Prognosis/Complications Prognosis is great Main intricacy is pneumonia Often beginning conclusion

Lab Time!

Patent Ductus Arteriosus - PDA_ Failure of the D.A. to close during childbirth or a re-opening of the D.A. after birth. Permits shunting between the aspiratory conduit and the aorta

Occurrence 1 for every 2000 term babies 30-half of RDS children

Etiology & Predisposing Factors Prematurity D.A. not as touchy to expanding PaO2 Hypoxia Decreasing PaO2 permits it to re-open for up to three weeks after birth Thus, a PDA can happen in an untimely newborn child who is NOT hypoxic or in a term infant who is hypoxic Worst case is an untimely baby who is hypoxic!

Pathophysiology D.A. neglects to close or it re-opens Then shunting happens between the aspiratory course and the aorta The bearing of the shunt relies on upon which vessel has the higher weight A PDA can bring about L-R shunting or R-L shunting! Clinically, most PDA's allude to a L-R shunt

Clinical Signs Tachypnea, bouncing heartbeats, hyperactive pre-cordium Decreased breath sounds and potentially a few crackles Possible mumble over left sternal outskirt Murmur is loudest when D.A. just begins opening or when it is practically shut

Clinical Signs ( cont .) ABGs – hypoxemia with respiratory acidosis If R-L shunting, the PaO2 in the furthest points, ie pre-ductal, will be more prominent than the PaO2 in the umbilical conduit, ie post-ductal! TC – diminished if L-R shunting causes aspiratory edema; expanded if liquid spills into aviation routes and builds aviation route resistance CXR – if L-R shunt, butterfly example of aspiratory edema with conceivable cardiomegaly

PDA Treatment Basic – NTE, O2, may require CMV if not as of now on the ventilator Medical L-R shunt that neglects to close: Indomethacin (Indocin) R-L shunt: Priscoline (Tolazoline) to diminish PVR; likewise nitric oxide Surgical –if therapeutic treatment comes up short, the PDA might be surgically ligated

Prognosis/Complications Good anticipation when child reacts to restorative treatment May create : Shock CHF Necrotizing Enterocolitis (NEC)

Meconium Aspiration Syndrome - MAS-Syndrome of respiratory misery that happens when meconium is suctioned preceding or amid birth

Occurrence 10-20% of ALL births demonstrate meconium recoloring 10-half of recolored infants might be symptomatic More basic in term and post-term babies

Etiology & Predisposing Factors Intra-uterine hypoxic or asphyxic scene Post-term Cord pressure

Pathophysiology: Check Valve Effect Causes gas catching (hindrance) If finish obstacle, then in the long run atelectasis happens Irritating to aviation routes, so edema and bronchospasm Good culture ground for microscopic organisms, so pneumonia conceivable

Pathophysiology ( cont .) V/Q crisscross prompts to hypoxia and acidosis which increments PVR TC increments since it builds aviation route resistance Meconium is normally caught up in 24-48 hours; there are still numerous conceivable intricacies

Respiratory sadness or trouble during childbirth Hyperinflation Pallor Meconium recolored body Possible cyanosis on room air Moist crackles ABGs – hypoxemia with joined acidosis CXR – coarse, inconsistent penetrates with zones of atelectasis and territories of hyperinflation May see smoothed stomachs if deterrent is extreme Clinical Signs

Amnioinfusion – manufactured amniotic liquid imbued into uterus to weaken meconium Proper revival at birth(clear meconium from trachea before empowering breath) Oro-gastric tube NTE O2 NaHCO3 if serious metabolic acidosis Broad range anti-toxins Bronchial cleanliness May require mechanical ventilation Slow rates and wide I:E proportions in light of expanded TC Low level of PEEP may help forestall check valve impact May require HFO M.A.S. Treatment

Prognosis & Complications Good forecast if there are no inconveniences Complications: Pneumonia Pulmonary baro/volutrauma Persistent Pulmonary Hypertension (PPHN)

Persistent Pulmonary Hypertension - PPHN-Also known as Persistent Fetal Circulation - PFC-

Failure to make the move from fetal to neonatal course or an inversion back to the condition where aspiratory vein weight surpasses aortic weight Results in R-L shunting over the D.A. what's more, the Foramen Ovale

Occurrence Usually term and post-term babies Females more frequently than guys Symptoms may take 12-24 hours after birth to create

Etiology & Predisposing Factors M.A.S – most basic Hypoxia and/or acidosis, eg RDS Any condition that causes PVR to increment

Pathophysiology Primary issue is aspiratory supply route hypertension Infants blood vessel dividers are thicker and they are more inclined to vasospasm If pneumonic course weight gets sufficiently high, blood will shunt R-L over the D.A. furthermore, Foramen Ovale Remember, conditions that drive up PAP typically make the D.A. open Lung is hypoperfused bringing about hard-headed hypoxemia and hypercapnia

Clinical Signs Refractory hypoxemia and cyanosis Shock and tachypnea Murmur conceivable Pre-ductal PaO2 > post-ductal PaO2 Hypoxemia with joined acidosis CXR typically OK when contrasted with newborn children condition

PPHN Treatment NTE and O2 Nitric Oxide Often in conjunction with HFO Priscoline, Indocin may likewise be utilized If totally inert to treatment ECMO might be attempted

Prognosis & Complications Prognosis relies on upon how well baby reacts to treatment Complications Shock Intracranial drain Internal draining Especially an issue if Priscoline is utilized

Wilson – Mikity Syndrome - Pulmonary Dysmaturity - Respiratory trouble that creates after the primary week of life and presents with positive CXR changes

Occurrence Usually in <36 weeks gestational age and birth weight <1500 gra