Premature infant. Pediatric care for the premature children + Most frequent diseases of premature infants Flashcards

1
Q

what are the terminology of prematurity ?

A

extremely preterm = below 28 weeks

very preterm = 28 weeks and less than 32 weeks

moderate preterm = less than 34wks - 32 weeks

late preterm = 34 weeks to less than 37 weeks

—— less than 37 weeks = preterm——-

early term = 37 weeks to less than 39 weeks

term =39-less than 41 weeks

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2
Q

preterm babies are usually not SGA correct ?

A

yes

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3
Q

there are morphological characteristics which can helps determine the age of the baby such as?

A

ballard score
nippes become visible in the 31 gestational week - if visible we know the baby has passed its 31st gestational week

position go the testis in the inguinal canal and scrotum

neurological development

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4
Q

what are the aetiology of preterm labour ?

A

50 percent remain unknown

maternal factors = pr eclampsia 
mother's age lower than 16 or higher than 40 
smoking 
vibration 
alcohol 
drugs 
stress 

anemia , diabetes , hyperthyroidism

uterine anomlais- tumors , cervical insuffieicny , vaginal infections and infection of the cervix

prom- usually infections , placenta previa , twin pregnancy ,

fetus - IUGR ,
multiple fetus
polyhydroaminos - uterine stretch pathway

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5
Q

how can we diagnose PROM ?

A

good test for this is cervical and vaginal fibronectin - substance of basement membrane protein produced but the membrane - when fetal membranes are disrupted - fibronectin is secreted into the vaginal and cervix

A positive fetal fibronectin test at 22 to 24 weeks
predicts more than
half of the
spontaneous preterm
births that occur before 28 weeks.
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6
Q

what re the characteristic features of preterm babies ?

A

small

head bigger to body

translucent skin with visiblee blood vessels

fine lanugo hair

soft pliable ear cartilage

soft bones

closed eyes

listless and inactive

extended extremities

partially developed REFLEX ACTIVITIES- lack of suction reflex

INABILITY TO MAINTAIN BODYTEMP = less body fat

inability to excrete urine

female - prominent clitorious

ABNORMAL BREATHING PATTERNS - shallow and irregular pauses

lower muscle tone

problems feeding - difficulty sucking or coordinated swallowing

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7
Q

what are preterm babies dangerously susceptible to ?

A

no surfactant produced so respiratory distress = hyaline membrane disease or respiratory distress syndrome

immature respiratory centre so cannot breath periodically = apnea

metabolic acidosis

more susceptible to hypoglycaemia

hyperbilirubinemia

heart failure = patent ductus arteriosus

INFECTIONS -sepsis and necrotic enterocolitis

intraventricular haemorrhages

fluid and electrolyte imbalance

RETINOPATHY of prematurity

anemia

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8
Q

what are the long term problems for preterm babies ?

A
bronchopulmonary dysplasia 
delayed growth and development 
mental or physical disability or delay 
increased risk for intellectual disability 
cerebral palsy 
vision and hearing loss = retinopathy
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9
Q

what are the standard care given to preterm babies

A

baby should be dried and effectively covered and warm

electie intubation for extremely low birth weight babies = less tan 1000g

exogenous surfactant given
corticosteroids for lung development through endotracheal tube

ventilator - continuous positive airway pressure

less than 30 weeks old - IV fluid and nasogastric

30-34 = nasogastric / breast feeding

more than 34 = breast feeding or katori

10 percent of daily calories should be derived for protein
40 percent - carbs
5 percent fats

2.5-3.5 mew/kg/per day

vit a recommended for preterm promoting epithelial repair and minimise fibrosis

vit D - prevents rickets

vitamin K 0.5mg should be given intramuscularly
factors 2 , 7 , 9 ,1 administers
prevent haemolytic disease of the new born

immunisation and put in sterile conditions
antibiotics given if there are signs of infection

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10
Q

for a preterm baby it is put in a system of neonatal intensive care unit which measure what ?

A
there is overhead warmer 
they eyes are sealed closed  closed 
there is a ventilator 
a feeding tube = feeding method 
oxygen saturation monitor 
Iv pump 
IV pump with umbilical artery catheter = feeding method 
PICC line - central line = feeding method 
ECG and blood pressure monitor / HR 
temperature monitor 
bilirubin lights 
incubator
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11
Q

what is kangaroo care

A

placing a premature baby in an upright position on the mothers bare chest allowing tummy to tummy contact and planning the premature baby in between the mother’s breast

and baby head is tubers so the ear is above the parents heart

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12
Q

kangaroo care has been shown to help prmature newborn with ?

A

body temp

allow easy access to breast feeding

increase weight gain - allows the baby total into deep sleep = allows the baby to conserve energy

increased intimacy and attachment

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13
Q

what are the symptoms for necrotising enetrocoitis

A

poor feeding
blood in stool
vomiting bile
failure to thrive

later on
abdominal discolouration , peritonitis
intestinal perforation
systemic hypotension

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14
Q

what is necrotising enterocolitis ?

A

where a portion of the bowel dies it is thought to involve the combination of poor blood flow and infection of the intestines

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15
Q

how can we prevent necrotising enetroclitis

A

use breast milk

probiotics

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16
Q

when is the typical onset of enterocolitis ?

A

after 4 weeks of life

generally inversely proportional to the gestational age of the baby birth

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17
Q

how is the diagnosis of necrotising enterocolitis ?

A

radiography

transillumination of the abdomen

Bells stages of disease
stage 1 = mild symptoms such as apnea , lethal , bradycardia , temp instability
abdominal distension , increased gastric residual bloody stools
no radiological signs

stage 2
mild to moderate symptoms
additional intestinal signs : absent bowel sound and abdominal tenderness

radiologic - pneumatosis intestinal or portal venous gas

lab =metabolic acidosi , thrmbocytopenia

stage 3
hypotension
peritonitis and striking abdominal distension
radiology = pneumoperitoneum

lab test = metabolic and resp acidosis
DIC

US = bowel gas , sentinel loop

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18
Q

what is the treatment for necrotising colitis ?

A
bowel rest by stopping oral  feeding, 
gastric decompression with nasogastric tube suction , fluid repletion to correct electrolyte abnormalities
parenteral nutrition always 
antibiotic therapy 
mechanical ventilation 

supine and left lateral decubitus abdominal X-rays should be performed every six hours

As an infant recovers from NEC, feeds are gradually introduced. “Trophic feeds” or low-volume feeds (<20 ml/kg/day) are usually initiated firs

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19
Q

Where the disease is not halted through medical treatment alone, or when the bowel perforates what is the course of action in NE

A

emergency surgery to resect the dead bowel is generally required, although abdominal drains may be placed in very unstable infants as a temporizing measure

In the case of an infant whose bowel is left in discontinuity, the surgical creation of a mucous fistula or connection to the distal bowel may be helpful as this allows for re-feeding of ostomy output to the distal bowel. This re-feeding process is believed to improve bowel adaptation and aid in advancement of feeds.

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20
Q

some children may suffer what whenextensive portions of the bowel had to be removed in NE ?

A

short bowel syndrome = malabsorption disorder

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21
Q

a patent ductus arteriousus creates what type of shunt ?

and what are the signs and symptoms ?

diagnosis ?

A

left to right shunt

signs and symptoms depends on the size of the shunt

pulse can be bounding , systolic murmur audible ,
apnea , bradycardia , increased oxygen requirement

echocardiography - doppler through ultrasound

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22
Q

what are the main problems in the left to right shunt in PDA?

A

HYPERperfusion in lung circulation = pulmonary haemorrhages

HYPOperfusion of system circulation to gut and brain = NEC

heart failure - increase volume load on left side of heart = bounding pulses , hyperactive pericardium , murmur , cardiomegaly

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23
Q

patent ductus arteriosuus closes physiologically in premature babies?

A

yes however they are more delayed especially if there is respiratory distress syndrome

normally the physiological closure is within 24 hours and the anatomical closure several weeks later

= arterial hypoxemia and reduced response to oxygen prevents the fast closure of ductus arteriosusu in children

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24
Q

what can treat this closure of ductus arteriosus?

A

echocardiography done when there is congestive heart failure with all the symptoms that persists heart failure to ratio between left atrium and aortic root diameter ratio normal is 0.86 if it is more than 1 or 1.1 early treatment started with indomethacin

inhibitors of prostaglandin such as ASA (cogulative effects and bilirubin displacement ) or indomethacin (renal function :( ) closure of persistant ductus arteriosus

surgical ligation

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25
Q

what re the signs for respiratory distress syndrome ?

A

increased resp rate - tachypnea - more than 60 breaths per min

chest wall recession - sternal and subcostal undraping

tachycardia

expiratory grunting = to create positive pressure

nasal flaring

cyanosis

prolonged periods of apnea

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26
Q

is respiratory disease is treated or not the acute symptoms lasts how many days ?

A

2-3 days
first day child worsens
second day - baby remarkably stable
resolution on the third day

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27
Q

what can be differential diagnosis to respiratory distress syndrome ?

A

acute respiratory distress syndrome - widespread inflammation of the lungs

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28
Q

how can we diagnose respiratory distress syndrome ?

A

bell shaped chest

chest x ray - decreased lung volume , absence of thymus - after 6 hrs

in pregnancy over 30 weeks fetal lung maturity checked by amniocentesis
L/S ratio and PG - phosphatidylglycerol
less than 2:1 and absence of PG means there is no lung maturity

surfactant an albumin ratio
less than 35 indicates immature lungs
greater than 55 inidicates mature surfactant production

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29
Q

what is the treatment for respiratory distress syndrome ?

A

CPAP- continuous positive airway pressure

intravenous fluid to stabilise the blood sugar and blood blood pressure

if the baby shows signs of worstenng - endotracheal tubing
or put in mechanical ventilation
CPAP

exogenous pulmonary surfactant given through the breathing tube

extracorporeal membrane oxygenation = cannot be placed until over 2KG
because small blood vessels for cannulation giving higher vascular resistance

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30
Q

in severe RDS what is the problem ?

A

bronchopulmonary dysplasia

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31
Q

there are four grades of intraventricular haemorrhages what are they ?

A

grade 1 - germinal matrix bleeding where there are tender vessels
grade 2 - bleeding occurs inside the ventricles

grade 1 and two are small amounts bleeding

grade 3 and 4
grade 3 - the blood presses the brain tissue the ventricles are enlarged with he blood
grade 4 the bleeding is directly involved with the brain tissue - intraparenchymal haemorrhage
most severe being uniltarel hemorrhagic infraction = resulting in hemiplegia = paralysis of one side of the body

here blood clots can form and reduce the drainage of cerebrospinal fluid giving hydrocephalus

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32
Q

what are the symptoms in intraventricular haemorrhages

A

apnea

change in blood pressure and heart rates

decreased muscle tone

decreased reflexes

excessive sleep

seizures and abnormal movements

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33
Q

how is the diagnosis done of intraventricula hemorrhegae ?

A

all babies born before 30 weeks should have ultrasoundd of the head

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34
Q

what is the treatment for intravenetricular haemorrhages ?

A

no way to stop the bleeding

give diuretics
streptokinase therapy

most recently combo of drainage , irrigation and fibrinolytic therapy = DRIFT therapy

blood transfusion given to maintain blood pressure

if fluid builds ip to point that there is cancer - a spinal tap done to relive the pressure

surgery needed to place a tube shunt to drain the fluid from the brain

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35
Q

what is the prognosis of intravenetricular haemorrhages ?

A

less tan half the baby with low grade intraventricular haemorrhages have long term problems

severe problems leads to developmental delays and problems controlling movement and one third with severe bleeding die

36
Q

how can we prevent intraventricular hemorrhegs ?

A

give corticosteroids to pregnant women - develop lungs - reduce RDS risk - therefore reduce IVH risk

umbilical cords are not clamped right away have less risk for IVH

37
Q

most intravenetricular haemorrhages occurs when after birth and what increases its chances

A

after 72 hours

extracorporeal membrane oxygenation

congenital cytomegalovirus

38
Q

surfactant is produced by which type of pneumocystis ? and what triggers its release

A

type 2 = premature infants pneumocystis not fully mature

cortisol = adrenal gland not fully functional

39
Q

where does the term hyaline membrane disease come from in respiratory distress syndrome ?

A

proteinaceous exudate from hypoxemia

40
Q

what are the complications for respiratory distress syndrome ?

A

pneumothorax
intracerebral hemorrhage
bronchopulmonary dysplasia from artificial ventilation

41
Q

what is pneumothorax ?

and what are the types of pneumothorax ?

A

A pneumothorax occurs when some of the tiny air sacs (alveoli) in a baby’s lung become overinflated and burst. This causes air to leak into the space between the lung and chest wall (pleural space)

spontaneous = resolves without tretammnet , no respiratory distress syndrome either

loculated - sealed off , resolved without treatment

tension positive pressure - creates a ball/valve mechanism

42
Q

what causes pneumothorax in premature infants ?

A

respiratory distress syndrome in premature babies

and when the baby needs a ventilator the extra positive pressure can burst the alveoli for these air scare not able to expand easily due to the decrease of surfactant

meconium aspiration syndrome

pneumonia

= all needing mechanical ventilation
resuscitation

43
Q

what are the symptoms in pneumothorax ?

A
hype resonance on the affected side 
irritability 
cyanosis 
tachycardia 
tachypnea 
flair of nostrils 
grunting in breathing 
restlessness 
chest and admonimal muscle retraction aid in breathing
44
Q

what is the diagnosis for pneumothorax ?

A

transillumination - pockets of air will show up as lighter areas

chest X ray = lungs are wide because no air in it = elapsed alveoli from respiratory distress
pleura is black

45
Q

what is the treatment for pneumothorax ?

A

oxygen mask given

tension pneumothorax (As air builds up in the chest, it can push the heart toward the other side of the chest. This puts pressure on both the lung that hasn’t collapsed and the heart.) chest drain decompression by needle catheter and then insert a chest tube

46
Q

how can we prevent pneumothorax

A

mechanical ventilation is always at the lowest possible

47
Q

what is hypothermia bad for neonates ?

A

hypoglycaemia
failure to thrive
mortality increases

48
Q

why’re preterm babies especially vulnerable to hypothermia ?

A

large surface area compares to mass = convection heat loss then heat generated

skin is thin and heat permeable

they have
little subcutaneous fat for insulation

organs are not fully functional to produce heat metabolically

Poorly developed metabolic mechanism for responding to thermal stress (e.g. no
shivering)

Greater body water content

49
Q

what are the ways there can be heat loss in neonates

A

Evaporation: when amniotic fluid evaporates from the skin. from skin and breathing or sensible (sweating).

  • Conduction: when the newborn is placed naked on a cooler surface, such as table, scale, cold bed. The transfer of heat between two solid objects that are touching
  • Convection: when the newborn is exposed to cool surrounding air or to a draft from open doors, windows or fans, the transfer of heat from the newborn to air or liquid
  • Radiation: when the newborn is near cool objects, walls, tables, cabinets, without actually being in contact with them. The transfer of heat between solid surfaces that are not touching.
50
Q

how do babies produce heat ?

A

metabolic process
muscle activity - restlessness and crying
flexed position yo decrease surface area
peripheral vasoconstriction
non shivering thermogenesis - metabolism of brown fat produce heat thermal receptors – hypothalamus – synthetic nervossystem and NE release to brown fat found in kidney , adrenal gland , head , neck , heart

51
Q

consequence of hypothermia in children

A

cold — activation of non shivering thermanogensis — metabolism of brown fat — increased o2 consumption – increased resp rate — pulmonary vasoconstriction – tissue hypoxia – peripheral vasoconstriction — anaerobic metabolism – metabolic acidosis

metabolism of brown fat – increased glucose use – hypoglycaemia

52
Q

how many degrees is hypothermia ?

A

ewborn’s axillary temperature drops below 36.3°C

53
Q

what are the signs and symptoms for hypothermia ?

A

Acrocyanosis and cool, mottled, or pale skin
• Hypoglycemia
• Bradycardia
• Tachypnea, restlessness,

shallow and irregular respirations

apnea,

metabolic acidosis

Decreased activity, lethargy, hypotonia

Feeble cry, poor feeding

54
Q

how do we manage hypothermia ?

A

arm chain” is a set of interlinked procedures to be performed at birth and during the next few hours and days after birth in order to minimize heat loss in all newborns

warm delivery room 
immediate drying 
skin to skin contact 
brest feeding - within one hour 
appropriate clothing and blanket 
keep mother and newborn together for 24 hours a day in warm room 
warm transportation
55
Q

how is the severity of hypothermia measured inneonats ?

A

mild = 35–36.3 degrees

moderate = 32 -34.9 degrees

severe below 32

56
Q

for mild hypothermia what is done to treat it ?

A

skin to skin contact in warm room
place cap on newborn head
cover mother and newborn in warm blankets

57
Q

what is the treatment for moderate hypothermia ?

A

radiant heater

warm incubator

58
Q

what is the treatment for severe hypothermia

A

warm incubator

59
Q

how can we deliver nutrition whenpretm infants cannot swallow

A

nasogastric tube - and mothers breast milk

breast milk needs to ne supplemented with phosphate and protein calories and calcium

60
Q

when is parenteral nutrition needed

A

typically when the birth weight is below 1kg

61
Q

why s breast milk the most advisable for nutrition

A

passive immunity through IgA

cows milk based formula = NE

cannulation - septicaemia increase

62
Q

when taking care of preterm babies iron what needs to be considered

A

iron is transferred to the fetus in the last trimester and therefore can have low iron stress

this can also be in addition to inadequate erythropoietin repose

iron supplements are given

63
Q

why do preterm infant have increased risk for infection

A

because IgG is the only antibody transferee through placenta and also mostly in the last trimester = increased infection in pretty

in addition PROM is caused due to cervical inflammation which can spread o the premature newborn

can be nosocomial - hospital derived since they are exposed to catheters and mechanical ventilation and long hospital stays

64
Q

intraventricular haemorrhage is also caused by ?

A

perinatal asphyxia

65
Q

retinopathy of prematurity is also called retrolental fibroplasia and terry syndrome has what pathophysiology

A

disorganised growth of genital blood vessels which may result in scarring and retinal detachment

By the fourth month of pregnancy, the fetal retina has begun to develop vascularization. Such formation of blood vessels appears to be very sensitive to the amount of oxygen supplied, either naturally or artificially.

the blood vessels grow from the retina outwards and this process is complete few weeks before full term of delivery the blood vessels conintue to grow normally ROP does not occur however continue to grow abnormally with fibrovascular proliferation ROP occurs and cause haemorrhages

when the blood and abnormal vessels are reabsorbed it may give rise to multiple bad like membranes which can pull up the rentina and eventually lead to blindness

66
Q

what are the risk factors of retinopathy of prematurity ?

A

in preterm babies(esp below 32 weeks) relieving neonatal intensive care in which oxygen therapy is used FOR THE lungs

the direct growth of the blood vessels is related to relatively low areas of oxygen

VERY low birth weight = 35 percent
less than 1500g

infection

67
Q

people with ROP have what complications ?

A

strabismus , glaucoma , cataracts and shortsightedness myopia in later life

68
Q

what is the cause of bronchopulmonary dysplasia in neonates ?

A
treated with long term oxygen 
or supplemented oxygen 
mechanical ventilation 
RDS 
abnormal lung development 
antenatal infection 

which is needed in low birth weight and preterm infants

69
Q

what re the signs and symptoms of BPD ?

A

feeding problems - oral tactile hypersensitivity after prolonged intubation

hypoxemia

hypercapnia

crackles wheezing

hyperinflation

70
Q

what s the pathophysiology of BPD

what is the definition of BPD ?

A

BPD is a chronic respiratory disease

oxygen conc more than 40 percent is toxin to the neonatal lung

prolonged high oxygen delivery causes necrotising bronchitis and alveolar septa injury with inflammation and scarring this is due to the generation of superoxides and hydrogen peroxides and oxygen radicals which disrupt the membrane lipids

resulting in hypoxemia

BPD is oxygen dependance at 36 weeks post conceptual age accompanied by clinical and radiographic findings due to failure RDS resolving

71
Q

how do you diagnose BPD ?

A

chest x ray show widespread opacification and sometimes cystic changes by phases

lung opacification
then cysts
then areas of overdistenton and atelectasis
then spongelike appearance

and in histopathopoligy BPD reveal interstitial edema , atlesctasisi , mucosal metaplsao , interstitial fibrosis an necrotising obliterative bronchitis

for neonates treated with more than 21% oxygen for at least 28 days

for gestational age less than 32 weeks :

mild = breathing room air at 36 weeks 
moderate = need 30 percent of oxygen at 36 weeks 
severe = need more than 30 percent oxygen or positive air pressure CPAP at 36 week 

for gestational age 32 weeks or older

mild = breathing room air at postnatal age of 56 or at discharge

moderate = need less that 30 percent oxygen 56 days postnatally or at discharge

severe need 30 percent or more oxygen with or without CPAP 56 days postnatal age

72
Q

what is the clinical management of BPD ?

A

to reduce oxygen toxicity and barotrauma ventilator settings are reduced to lower the partial pressure of pa02 to 50 mmhg and higher paco2 = 50 to 75mmhg)

dexamethasone therapy reduce inflammation and improve pulmonary function

steriods given to babies less than 8 days old can prevent
however risk of neurodevelopment sequels such as cerebral palsy outweighs the benefits
= low dose may be given

oxygen therapy - CPAP or high flow nasal cannula therapy

73
Q

what are other common problems that premature infants also low birth weight baby developmentalp ?

A

low birth weight babies develop cerebral palsy but more common is learning disabilities

learning difficulties risk is at greatest off born before 26 gestational week

fine motor skills difficulties
concentration
behavioural problems

74
Q

to try and prevent retrolental fibroplasia what Pa02 do we give premature babies

A

keep it 50-80mmhg

75
Q

what are the clinical managmnet of BPD ?

A
oxygen dependance 
hypercapnia 
compensatory metabolic alkalosis 
pulmonary hypertension 
failure to thrive
76
Q

what s the complication of BPD ?

A

right sided heart failure

77
Q

when having mechanical ventilation with BPD what is a common occurrence with these positive air pressure which can worsen BPD ?

A

barotrauma

78
Q

what are the complications of BPD?

A
hyperinflation 
reactive airways 
developmental delay 
higher risk or severe respiratory syncytial virus pneumonia 
higher risk for asthma
79
Q

what is pulmonary dysmaturity or wilson mikety syndrome ?

A

affecting premature infants or SMALL for gestational age of less than 1.5kg

and occurs 1-5 weeks after birth

chronic lung disease that closely related to bronchopulmonay dysplasia

alveoli that have failed to grow and multiple not due to RDS

80
Q

what is the symptoms of wilson mikety syndrome

A

cyanosis , dyspnea , wheezing , hyperinflation , corpulmonale , failure to thrive

81
Q

what is the diagnosis of wilson mikety syndrome

A

chest x ray

lung cysts - interstitial emphysema
diffuse infiltrats
hyper inflated lungs
flattened diaphragm

82
Q

what is the treatment for wilson mikety syndrome

A

give oxygen therapy

diuretics

83
Q

what is pneumopericardum ?

A

air enters the pericardial cavity
LIFE THREATENING
recognised in preterm neonates associates with severe lung pathology after vigorous lung resuscitation or in the presence of assisted ventilation

84
Q

why is pneumopericardium life threatening ?

A

lead to cardiac tamponade and death

85
Q

what are the signs and symptoms of pneumopericardium ?

A

dyspnea
cyanosis = heart is an ineffectual pump
chest pain
pluses paradoxes

becks triad when cardiac tamponade
muffled heart sounds
hypotension , rased jugular venous pressure

86
Q

how do we diagnose pneumopericardium ?

A

halo around the heat

When air and fluid mix together in the pericardial sac, a tinkling sound superimposed over a succussion splash is heard. This is known as a “Bruit de Moulin”,

Air between the anterior parietal pericardium and the thoracic cage may also give rise to the “Hamman’s Sign” – which is a crunching sound typically heard on auscultation of the chest, but may sometimes be heard even with the unaided ear.