preterm infant’s major...
TRANSCRIPT
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Joanna Puskarz – Gąsowska
Department of Neonatology and
Neoanatal Intensive Care Unit
Preterm infant’s major
morbidities
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Preterm newborn
• 22-36 HBD
• 22-24 HBD extremely immature newborn
limit of neonatal possibilities
• Mortality 23 hbd- 85%
24 hbd- 45%
25 hbd- 21%
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Major morbidities
• Breath disorders
• Patent ductus artesiosus
• Intraventricular haemorrhagies
• Necrotizing enterocolitis
• Infections
• Retinopathy of prematurity
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Morphologic development of lungs
Stage Gestational week Morphologic changes
Embrional 4-6 Formation of infancy
airways
Paragrandular 7-16 Formation of junctive
airways
Tubular 17-28 Formation of respiratory
bunch
Saccular 29-35 Development of gases
exchange places
Alveolar 36 Development of alveoli
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Main causes of respiratory
disorders
• Transient tachypnea of newborn (TTN)
• Respiratory distress syndrome (RDS)
• Congenital pneumoniae
• Pulmonary hemorrhage
• Pneumothorax
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Another
• Congenital anomalies: choanal atresia,
laryngotracheal esophageal cleft, lung
hypoplasia, pulmonar sequestration,
congenital diaphragmatic hernia
• CNS: haemorrage, ischaemic- hypoxic
encephalopathy, apnea
• cardiovascular: congenital heart defects,
congestive heart failure, persistent pulmonary
hypertension of the newborn
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Another causes
• Sepsis
• Anaemia
• Hypothermia and hyperthermia
• Hypoglycaemia
• Hypovolemia
• Muscles disorders: myasthenia, muscular
dystrophy
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Symptoms of respiratory distress:
• Tachypnea >60’
• Intercostal diaphragmatic and sternal retraction
• Expiratory sounds
• Nasal flaring
• Cyanosis
• Tachycardia
• Apneas
• Abnormal breath sounds: stridor, wheezing,
rales
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Transient tachypnea on the
newborn (TTN)
• 5% psn term, 15% preterm
• Delayed resorption of lung fluid
• Risk factors: cc, birth asphyxia, fetal
polycythemia, infant of diabetic mother,
multiple gestation
• Resolve within 3-5 days
• X-ray- hyperexpansion of lung, fluid in minor
fissure, prominent pulmonary vascular
marking
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Zdjęcie ttn
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Respiratory distress syndrome
(RDS)
• 26-30 Hbd- 70%, 32-37 HBD- 20%,
>37 Hbd -5%
• Deficiency of surfactant
• SURFACTANT- lipoprotein – substance which
help to expand and prevent to collapse small
airspace
• Surfactant is produced by pneumocytes type II
since 24 Hbd,
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Criteria of diagnosis RDS
• Clinic: respiratory distress, cyanosis,
sat <85%, apneas, tachypnoe, unstable
temperature, hypotension, pulmonary edema,
peripheral edemas
• Laboratory: hypoxemia, hypercarbnia, acidosis
• Radiologic
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RDS I st- granular image of lungs
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RDS II st- bronchogram visible
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RDS III st- prominent pulmonary
vascular marking “milk glass”
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RDS IV st- with lungs, no heart
silhouette
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Surfaktant- indication
• 200 µg/kg intracheal
• Therapeutic- means R-ray or clinic symptoms
• Next dose – after 12 hours
• <26 HBD when FiO2 >0,3
• <28 when intubated ( but nCPAP first)
• 27-32 when FiO2 >0,4
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Persistant pulmonary hypertension
of the newborn PPHN
• High pulmonary circulation resistance and low
blood inflow – like in prenatal period
• Severe hypoxemia unproprate to X-ray- of
lung changes
• Cyanosis and asphyxia, high FiO2, high
parameters of mechanical ventilation
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PPHN- risk factors
• Birth asphyxia
• RDS
• MAS
• Congenital diaphragmatic haernia
• Congenital pneumoniae (GBS)
• Mitral valve atresia, left ventricle failure
• Myocarditis
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PPHN- diagnosis
• Pulmonary blood pressure higher than
systemic blood pressure
• Right-left flow through PDA and FO
• No congenital heart defects
• Severe asphyxia in spite of FiO2 1,0.
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PPHN- treatment
• Mechanical ventilation – conventional and
oscilatory
• Surfaktant ????
• iNO
• Catecholamines
• ECMO
• Mortality 20-40%
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Pneumothorax
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Interstitial emphysema
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Bronchopulmonary dysplasia
Fetal age <32 hbd > 32 hbd
Estimate moment 36 hbd or discharge >28 day of life <56 day of
life or discharge
Oxygen require >21 %
atleast 28 day of life
PLUS PLUS
Light BPD Breathing with air Breathing with air
Medium BPD FiO2 <0,3 FiO2 <0,3
Severe BPD FiO2 >0,3 or nCPAP FiO2 >0,3 or nCPAP
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Pathogenesis
• Oxygen toxicicty
• Mechanic trauma during MV barotrauma and
volumtrauma
• Inflammation
• Energetic deficiency
• Inhibition of proper process of lung
alveorisation
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Symptoms• Breathlessnes, oxygen therapy require
• Chronic hypercarbnia
• Retraction of stern, diaphragm, intercostal
muscles, tachypnoe
• Lots of mucofluid secretion in airways
• Acute episodes of bronchospasm
• Oedemas
• Recurrent pneumonias
• Abnormalities of calcium and phosphorus
• Psychomotor development retardation
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Treatment• Oxygen- therapy (PaO2 55-70 mmHg)
• High caloric diet (140-160 kcal/kg/d)
• Fluid restriction
• Diuretic drugs
• Steroid therapy
• Sildenafil
• Bronhodilatators, anti-inflammatory
• Blood transfusion (Ht >40%)
• Physical therapy
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Patent ductus artesiosus PDA
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PDA
• 45% in newborns with bw < 1500 g 100% in newborns with bw <1000 g
• Immaturity of endothelium of DA and inadequate response for vasoconstrictors
• Getting worse primary pathologic changes in immature lungs and extends time of mechanical ventilation
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PDA - concequences
1. Increasing of pulmonary blood flow
2. Decreasing of descending aorta blood flow.
3. Increasininf of resistence in MSA ant renal arteries
4. In diastole- there is back flow from abdominal organs – NEC,
renal insufficiency
5. In diastole backflow from brain circulation
6. Insreasing of LV preload – insufficiency of LV
7. Organs perfusion disorders
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Treatment
• In case of significant hemodynamic
importance
• Diagnose by echocardiography
• Pharmacological: indomethacin, iuprofen
• Surgical ligation
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Intravetricular hemorrhages IVH
24 hbd • 40 hbd
Gressens, P., Rogido, M., Paindaveine, B., and Sola, A. (2002).
The impact of neonatal intensive care practices on the developing brain. Journal of Pediatrics, 140(6), 646-653
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Classification of IVH –Papile,a
Io - subependymal hemorrhage
IIo - intraventricular hemorrhage without
lateral ventricular dilation
IIIo - intraventricular hemorrhage with
lateral ventricular dilation
PVHo – periventricular hemorrhage to cerebral
tissue- hemorrhagic infarct
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Classificaton intraventricular
hemorrhages Volpe’a
Io – to subependyma
IIo – intraventricular [10-50%]
IIIo - intraventricular >50%
IVo - intraventricular + hemorrhagic infarct
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IVH I
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IVH II
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IVH III
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IVH IV
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IVH IV
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Periventricular leukomalacia
necrosis of white matter caused by ischemia
Iº IIº
IIIºIVº
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Infantile cerebral palsy
Population morbidity: 8%
:
24 – 26 t.c. 30%
27 – 28 t.c. 24%
29 – 30 t.c. 4%
31 –32 t.c. 1%
in 61% there was tetraplegy
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NEC necrotizing enterocolitis
• 6-10 % preterm with bw <1500g
• Ischemic and inflammatory necrosis of the bowel primarily affecting premature neonates after initiation of enteral feeding
• Risk factors:
• prematurity
• enzymatic, hormonal, and immunological immaturity of intestines
• enteral feeding,
• bacterial colonization, (Klebsiella, E.coli, Enterobacter spp, Pseudomonas spp.)
• ischemia
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NEC
• Clinical signs
• Systemic: apneas, bradycardia, letargy, temperature instability, thrombocytopenia, respiratory and metabolic acidosis, hypotension, decrease urine output, respiratory failure
• GI: feeding intolerance, recurrent gastric residuals, abdominal distension, tenderness, absent bowel sounds, abdominal wall edema, indurations and discoloration
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Prominent abdominal distension
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Distension of bowels
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Pneumatosis inerstinalis
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Pneumoperitoneum
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Treatment
• Non-invasive: parenteral nutrition
• Gastric decompression
• Close monitoring of vital signs
• Respiratory and circulation support
• Strict fluid monitoring: intake and urine output, electrolytes
• Antibiotics
• Radiographic studies (even every 6-8 h)
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Surgical management
• Primary drain placement
• Laparotomy
resection of necrotic segment of bowels
enterostomy
Reanastomosis after 8-12weeks
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ROP- retionopathy of prematurity
• Disorder of the developing retinal vasculature
resulting from interruption of normal
progression of newly forming retinal vessels.
• Vasoconstriction and obliteration
• Neovascularisation
• Retinal edema
• Retinal haemorrhages
• Fibrosis an traction on, detachment of retina
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• 5,8% preterm and SGA
• 80% preterm with bw <750g
• Ophthalmologic examination 4weeks of life
next according to suggestion of
ophthalmologist
about 1 year of life
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Ethics problems
➢ Lethal congenital syndrome(trisomy of 13, 18)
➢ Congenital malformations with severe prognosis(hydrocephalus, spina bifida)
➢ Heart defects – poerative, but with high mortalityand risk of retardation (HLHS)
➢ Extremaly premature newborns 22-23 Hbd
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PRENATAL DIAGNOSTICS MAKES
DIRECTIONS FOR OBSTETRIC AN
NEONATAL ACTIVITIES
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GENETIC TESTINGS
are very important at time of birth!!!!
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PALIATIVE CARE
Blood tests Monitoring of vital
parameters
Special drugs
Mechanical ventilation
STOP !!!!!
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PREMATURITY IS
PROBLEMATIC AND
EXPENSIVE
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22 – 23 hbd-
LIMIT OF MEDICAL POSSIBILITIES
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What is the limit of resuscitation and saving
preterms ?
➢ 22 Hbd, 500 g BW, vital signs
➢ Physiological development of lungs :
23-24 Hbd ( WHO 1997)
➢ Epidemiology of survivers and development among
preterm newborns 23-24 tc (remember about
plasticity of immature brain)
➢ Wrong estimation or valuation of gestational age in
US ( Hbd- 4 days, BW 15%)
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Tys
Tyson et al.
2008 NEJM.
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General state and vital signs are most
important indication to resuscitation
favorable and adverse prognostic
factors
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Prognostic factors
• Favorable
– female
– HR>100/min
– Prenatal steroids
– Single
– BW > than expected
• Adverse
– male
– Trauma of tissue
– Lak of prenatal steroids
– HR<100/min
– Twins
– BW <500g
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CC
Type of delivery
PSN
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Ethic problem (Resuscitate or not)
How small is „to small” Parents will
Genaral state –
main indication to
start resuscitation
Resuscitation
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Ethic problems
ELBW newborn has all human rights
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We have to anserw
• If our treatment is’nt futile therapy?
• Do we should continue this therapy?
• Paliative care?
• Stop futile therapy is not euthanasia
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Thank YOU