Respiratory Disorders In Neonates Respiratory Disorders In Neonates ASPHYXIA NEONATORUM Respiratory Distress Syndrome Transient tachypnea of the newborn Meconium Aspiration ASPHYXIA NEONATORUM ID: 919612
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Slide1
Dr .
Manahil Ghandour
Respiratory Disorders In Neonates
Slide2Respiratory Disorders In Neonates
ASPHYXIA NEONATORUMRespiratory Distress Syndrome
Transient tachypnea of the newborn
Meconium Aspiration
ASPHYXIA NEONATORUM
Slide4Asphyxia – Definition:
Inability of the newborn to establish spontaneous Breathing that result in the following biochemical changes:HypoxiaHyper capnia
Acidosis
Slide5WHEN DO YOU ANTICIPATE ASPHYXIA?
High risk pregnancies (maternal, fetal, placental)Complicated labor.
C/S
Slide6How Do You Assess Asphyxia?
2
1
0
SCORE
>100
< 100
Absent
H.Rate
Good Cry
Weak
Absent
R.Rate
N.colour
P.cyanosis
C.cyanosis
Colour
Cough or Sneeze
grimace
No response
Reflexes
Well flexed
Flexion of extremities
flaccid
Muscle Tone
Slide7Hypoxic Ischemic Encephalopathy (HIE)
( HIE )
Slide9Grade I HIE:
- Alternating periods of lethargy and
irritability
, hyper-alertness and jitteriness.
- Poor feeding.
- Exaggerated and/or a spontaneous Moro reflex.
- Increased heart rate and dilated pupil.
-
No seizure activity
.
- Symptoms resolved in 24 hours.
Slide10Grade II HIE:
- Lethargy.
- Poor feeding, depressed gag reflex.
-
Hypotonia
.
- Low heart rate and papillary constriction.
- 50-70% of infants display
seizures
, usually in the first 24 hours after birth.
Slide11Grade III HIE:
- Coma
.
- Flaccidity.
-
Absent reflexes
.
- Pupils fixed, slightly reactive.
-
Apnea
,
bradycardia
, hypotension.
-
Seizures are uncommon
.
Management of Hypoxic Ischemic Encephalopathy:
Slide13Management of Hypoxic Ischemic Encephalopathy:
-
Prevention is the best management.
-
Primary supportive measures.
- Treat seizures.
Slide14Respiratory Distress Syndrome
Slide15RDS
Respiratory distress syndrome (RDS) is the predominant clinical problem encountered in neonatal units. Incidence increases with lower gestational age. It is common in infants of less than 30 weeks gestation
Slide16RDS
RDS is caused by defective or delayed production of surfactant in structurally immature lungs. Surfactant (a mixture of phospholipids) is secreted into the pulmonary alveoli, reducing the surface tension of lung fluids, and thus contributing to the elasticity of pulmonary tissue , adequate lung expansion and to prevent atelectasis (lung collapse)
Slide17C/F Of RDS
The signs and symptoms of neonatal RDS are Tachypnoea (respiratory rate >60/minute); Nasal flaring Sternal and intercostal
recession
Central cyanosis;
Apnoea
;
Expiratory grunt
Slide18Diagnosis
Diagnosis is by history, blood gases showing impaired respiratory functionX-ray demonstrating the classic reticulogranular or ‘ground glass’ appearance and air
bronchograms
(radiolucent air-filled airways).
Slide19Prevention
prevent preterm delivery Steroids accelerate maturation of foetal lungs by stimulating type II pneumocytes to produce surfactant
Slide20Treatment
Surfactant
Slide21Complications and sequelae
pneumothorax, pulmonary interstitial emphysema, persistent pulmonary hypertension, necrotizing enterocolitis, intraventricular haemorrhage,patent ductus arteriosis
Slide22Transient tachypnea of the newborn (TTN)
Slide23(TTN)
(TTN) is a self-limited disease common in newborn. present within the first few hours of life withtachypnea, increased oxygen requirement, and ABGs that do not reflect carbon dioxide retention..
Slide24(TTN)
Slide25Meconium Aspiration
Slide26(MAS)
Meconium aspiration syndrome (MAS) occurs when a neonate inhales thick meconium. This is usually secondary to fetal hypoxia which causes increased peristalsis, relaxation of anal sphincters and reflex gasping.
Slide27(MAS)
Most meconium deliveries involve some meconium staining of the liquor but the babies are vigorous, needing no further intervention.
Slide28Significant aspiration of thick meconium, however, can induce 4 major pulmonary effects,
viz: Airway obstruction,
Surfactant
dysfunction,
Chemical
pneumonitis
and
Pulmonary hypertension
.
In the majority of cases, these changes begin to resolve after the first six hours of life, with consequent improvement in lung function.
Slide29Presentation of MAS
Obvious presence of meconium or dark green staining of the amniotic fluid.Green or blue staining of the skin at birth.Baby appears limp, with a low Apgar
score.
Breathing is rapid, or absent.
Signs of
postmaturity
(
eg
peeling skin) are present.
Fetal monitor may show
bradycardia
Slide30Investigations
Blood gas analysis showing low blood pH, increased pCO2, decreased pO2.A full blood count may be useful in excluding infectionChest X-ray shows patchy infiltrates, coarse streaking of both lungs, increased AP diameter and flattening of the diaphragm (due to hyperinflation).
Slide31Management
Suction - does not recommend routinely. However If the baby has depressed vital signs, laryngoscopy and suction under direct vision.Oxygen - depending on the degree of respiratory distress,
Antibiotics - these may be useful in ventilated baby.
Steroids - inhaled or systemic
Slide32Complications and prognosis
In mild cases, respiratory distress usually subsides in 2-4 days, although tachypnoea can persist for longer. Rarely, more prolonged respiratory damage can occur Cerebral hypoxia may lead to long-term neurological damage.
Slide33Prevention
More frequent diagnosis of abnormal fetal heart rate patterns Avoidance of post-mature delivery by elective Caesarean section have both been shown to reduce the incidence of meconium aspiration syndrome (MAS).
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