Peds Perinatal Diseases (Part Ii)

Front 1

What is Intraventricular hemorrhage (IVH)?

Back 1

is bleeding inside or around the ventricles (between hemispheres by brainstem- causes swelling), the spaces in the brain containing the cerebral spinal fluid.

Risk factor for everything we do

Front 2

Intraventricular hemorrhage is most common in who?

Back 2

Premature babies

Especially in very low birth weight babies weighing less than 1,500 grams.

Infants 24-32 weeks gestation are at greatest risk.

Front 3

IVH Pathophysiology

Why does bleeding occur?

Who is more likely to have IVH?

Back 3

Bleeding can occur because blood vessels in a premature baby's brain are very fragile and immature and can easily rupture.

Babies with RDS or other complications of prematurity are more likely to have IVH.

The smaller and more premature the baby, the more likely IVH will occur.Nearly all IVH occurs within the first three days of life.

Front 4

Grade 1 of IVH

Back 4

bleeding occurs just in a small area of the ventricles.

(R and L side can have different grades)

Front 5

Grade 2 of IVH

Back 5

bleeding also occurs inside the ventricles.

Front 6

Grade 3 of IVH

Back 6

ventricles are enlarged by the blood.

Front 7

Grade 4 of IVH

Back 7

bleeding also occurs in the brain tissues around the ventricles.

(Severe- affects neurotransmission and thought process)

Front 8

Which grades of IVH are most common ?

Back 8

Grades 1 and 2 are the most common.

Occurring in about 75 percent of babies with IVH.

Often, there are no further complications.

Front 9

What grades of IVH are more serious?

Back 9

Grades 3 and 4 most serious

Hydrocephalus (too much cerebral spinal fluid in the brain) may develop after severe IVH.

Usually resulting in long-term brain injury to the baby.

*developmental delays and brain damage

Front 10

IVH Diagnoses

Back 10

A cranial (head) ultrasound is usually used to diagnose IVH.

Cranial ultrasound can view the inside of the baby's brain through the fontanelles, the spaces between the bones of the baby's head.

With the ultrasound, the amount of bleeding can be graded.

Front 11

IVH Treatment

Back 11

There is no specific treatment for IVH, so its best to prevent those factors that lead to its occurrence.

Front 12

How to lower the risk of IVH?

Back 12

Giving maternal corticosteroids before delivery has been shown to lower the risk of IVH in the baby.

Avoid wide swings in blood pressure, oxygenation, pH, low-dose indomethacin, will help to prevent the incidence and severity of IVH.

(Swings in PO2 causes swings in BP) this is also why we don't put a kid in trensdelenburg

Front 13

Perinatal Asphyxia

(Hypoxic-Ischemic Encephalopathy “HIE”) definition

Back 13

Perinatal asphyxia exists when an antepartum event, labor, or birth process diminishes the oxygen supply to the fetus, causing decreased fetal heart rate or newborn heart rate.

Front 14

What is the result of perinatal asphyxia ?

Back 14

The result is impairment of oxygen and carbon dioxide exchange and inadequate perfusion of the tissues and major organs.

Front 15

There are four clinical criteria, all of which must be present:

Back 15

Profound metabolic or mixed acidemia (pH < 7.00) on umbilical cord sample.

Persistence of an apgar score of 0 to 3 for more than five minutes.

Clinical evidence of neurological sequellae (deficit/drop) in the immediate neonatal period.

(Lack of reflexes)

Evidence of multi-organ system dysfunction in the immediate neonatal period.

Front 16

Disorders Associated with Perinatal Asphyxia

Back 16

Antepartum period:

Maternal diabetes, preeclampsia, fetal malformation, prematurity, post maturity, IUGR

Intrapartum period:

Breech presentation, meconium staining, Cephalo-pevlic disproportion, cord compression.

Other causes:

Uterine malformation, precipitous labor, abruptio placentae, maternal shock, cord prolapse, infection.

Postnatal period:

Severe pulmonary disease, congenital heart disease, large PDA, severe recurrent apneic spells, sepsis without cardiovascular collapse.

Front 17

Mild HIE

Back 17

hyper-alertness, uninhibited reflexes, sympathetic overactivity, duration <24 hours.

Front 18

Moderate HIE

Back 18

lethargy-stupor (sleepy/hard to arpuse), hypotonia (stiffer), suppressed primitive reflexes (rooting reflex), seizures.

Front 19

Severe HIE

Back 19

coma, flaccid tone, suppressed brain-stem function, seizures, increased intracranial pressure.

Front 20

Treatment of HIE

Back 20

Reverse hypoxia.

O2 Therapy

PPV

Alleviating tissue ischemia, if present.

Promoting adequate brain tissue oxygenation by maintaining or restoring cerebral perfusion in an attempt to relieve ischemia.

Sodium bicarbonate may be indicated with a severe, persistent metabolic acidosis.

Blood pressure should be maintained at levels that allow adequate perfusion to all body tissues.

Seizures if present, should be treated

Front 21

Intrauterine Pneumonia

Back 21

The mortality of intrauterine pneumonia is very high:

This is due to the fact that the fetus may have been very sick for quite some time before birth and no one knew.

6-15% of all neonatal deaths are due to pneumonia in the perinatal period

Front 22

Even if the OB/GYN knows that the fetus is infected, Intrauterine Pneumonia treatment is difficult due to?

Back 22

This is due to the ability of the placental barrier to keep the drugs out of the fetal circulation.

For example, penicillin is decreased by 50% and gentamicin level in the umbilicus are only 35% of the maternal blood levels

Front 23

Causes of intrauterine pneumonia

Back 23

Babies at risk for intrauterine pneumonia are infants of mothers who have premature rupture of the membranes [PROM].

The infective agents migrate into the uterus from the vagina, the urinary tract or the rectum.

Front 24

Bacterial Causes of intrauterine pneumonia

Back 24

Group B strep (GBS)

Staph A

E coli

Chlamydia

(More common than viral)

Front 25

Viral Causes of intrauterine pneumonia

Back 25

Cytomegaly virus (CMV)

Herpes virus

Haemophilus influenza

(Fever less than 100.4)

Front 26

Clinical signs of intrauterine pneumonia can be delayed for a few hours or days perhaps even longer.

Back 26

RDS at birth or within a few hours

Shock prominent

Early apnea

Pulmonary hemorrhage and infiltrates

Course infiltrates or collapse on CXR

Metabolic acidosis

Neutropnea

Hypotension

Streptococci seen on gram stain of gastric aspirate

Positive blood and gastric aspirate culture for streptococci

Front 27

Treatment of Intrauterine Pneumonia

Back 27

Supplementary O2 for hypoxia to keep PaO2 55-65

Intubation and ventilation if pH drops below 7.25 and CO2 rise to above 60 torr

Broad spectrum antibiotics by IV

CPT and suction to mobilize secretions, even if infant is not intubated.

Front 28

Pulmonary Interstitial Emphysema (PIE)

Back 28

Pulmonary interstitial emphysema (PIE) is an iatrogenic pulmonary condition of the premature infant with immature lungs.

PIE occurs almost exclusively with mechanical ventilation

(Iotragenic- we did it.

Result of barotrauma)

Front 29

What happens to the ventilatory pressure in PIE?

Back 29

The ventilatory pressure used to keep the alveolar ducts open also may cause rupture of the alveolar duct

Usually at the junction of the bronchiole and alveolar duct .

Gas escapes of into the pulmonary interstitium, lymphatics, and venous circulation.

Front 30

Pathophysiology of PIE

Back 30

Positive pressure ventilation may over distend the lungs that causing tearing the alveolar septa allowing gas that is under pressure to invade the interstitial tissue.

Once in the interstitium, the gas is picked up in the rich lymphatic network of the neonate and carried toward the pleural lymphatic and central bronchopleural lymphatics.

Front 31

How does the xray with PIE look?

Back 31

The interstitial air collecting appears as bubbly, cystic areas throughout the lung parenchyma on the x-ray.

Front 32

Infants who develop PIE already had what?

Back 32

Infants who develop PIE have already established pulmonary disease of prematurity with respiratory distress syndrome that is being treated with supplemental oxygen, endotracheal intubation, surfactant therapy, and positive pressure mechanical ventilation.

Front 33

PIE often occurs ____, being recognized in ______ region of the lung and quickly involving_______.

What happens to oxygen saturation and ventilatory requirements?

Back 33

PIE often occurs rapidly, being recognized in one region of the lung and quickly involving multiple lobes with fixed hyper expansion and worsening clinical condition.

Oxygen saturation of the blood falls, and ventilatory requirements increase.

Front 34

Treatment of PIE

Back 34

High frequency Ventilation

Avoid hand bagging during suctioning

Allow permissive hypercapnia and limiting the PIP and Inspiratory time, if the infant remains on conventional ventilation

If PIE is one side only

Turn baby bad side down to splint the over-inflated lung

Tape the effected side (put effected side down)

Front 35

Persistent Pulmonary Hypertension of the Newborn (PPHN)

Back 35

A syndrome that occasionally occurs in infants who are typically term or post-term.

When giving the patient oxygen doesn't do the trick..

Primary PPHN: vessels don't want to dilate; patient desats, dutus stays open. This is usually in a term/ post term kid.

Front 36

PPHN can also be seen in patients suffering from what?

Back 36

Prenatal asphyxia

MAS

Diaphragmatic hernia

Pneumonia

Congenital heart disease

Pulmonary Hypoplasia

Front 37

Pathogenesis of PPHN:

Pulmonary vasoconstriction is?

Meconium may trigger what?

Back 37

Pulmonary vasoconstriction is exacerbated by hypoxia, acidosis, and hypercapnia resulting in intrapulmonary right to left shunting.

Meconium may trigger vasoactive process to exacerbate this. (Increase deadspace = decrease in PO2)

Front 38

PPHN: Anatomic abnormality of the pulmonary vascular bed

Back 38

pulmonary hypoplasia with pulmonary smooth muscle hypertrophy

chronic in-utero hypotension following chronic intrauterine hypoxia may also play role.

Front 39

PPHN:

Birth asphyxia is associated with what?

Structural lung abnormalities?

Back 39

Birth asphyxia with hypoxia, acidosis and shock is clinically associated with increased responsivness of the pulmonary vascular bed.

Group B streptococcal sepsis via Strep polysaccharide toxins.

Structural lung abnormalities such as congenital diaphragmatic hernia are frequently associated with PPHN.

Front 40

Diagnosis of PPHN

Back 40

This is essentially one of exclusion of significant cyanotic congenital heart disease and severe parenchymal lung disease.

This is usually called primary PPHN

However, PPHN may coexist with significant parenchymal lung disease.

This is sometimes called secondary PPHN

Have a high index of suspicion for a term baby with respiratory distress and cyanosis with:

Group B strep pneumonia

A history of intrauterine hypoxia

Meconium exposure

Birth asphyxia

Front 41

PPHN Echocardiographic diagnosis

What can it rule out or determine?

Back 41

Allows accurate diagnosis of PPHN and should be done as soon as PPHN is suspected.

With echocardiography one can Exclude congenital heart disease

Determine the pulmonary artery pressure.

Determine the presence, degree and direction of shunt through the duct and foramen ovale.

Determine ventricular outputs. These are commonly very low in the early course.

Front 42

PPHN Clinical Investigations

Back 42

Additional helpful clinical investigations include:

Chest X-ray

Serial arterial blood gases (simultaneous pre and post ductal samples may be helpful)

Pre and post ductal SpO2

CBC

Blood cultures

Front 43

PPHN Goals of Management

Back 43

Lower pulmonary vascular resistance.

Maintain systemic blood pressure. Reverse right to left shunting.

Improve arteriolar oxygen saturation and oxygen delivery to the tissues.

Minimize barotrauma.

Front 44

Treatment of PPHN

Two most potent nature pulmonary vasodilators are what?

Back 44

The two most potent natural pulmonary vasodilators are oxygen and lung inflation.

Front 45

Treatment of PPHN:

Oxygen

Conventional ventilation

Back 45

Oxygen

Keep PaO2 between 100-120 mmHg

Optimal pulmonary vasodilatation occurs with a pO2 around 120mmHg.

No benefit is likely from PaO2 > 120 mmHg, which may also contribute to secondary lung injury.

Conventional ventilation

Sedate and paralyze (if necessary) term and near term babies to ensure optimal ventilator efficiency.

Aim to maintain normal to low normal PaCO2 in the 35 to 40 mmHg range.

PaCO2 lower 35 mmHg than this may cause cerebral vasoconstriction.

Front 46

Treatment of PPHN:

HFOV

Back 46

High Frequency Oscillatory Ventilation (HFOV)

Randomized studies comparing HFOV with conventional ventilation in babies with severe hypoxic respiratory failure have shown that HFOV gives better oxygenation.

The best effect is seen in babies with secondary PPHN.

HFOV probably works in this situation by allowing better lung inflation and alveolar recruitment.

Front 47

Treatment of PPHN: ***

INO

Back 47

Nitric oxide (INO) : more specific and has more evidence to support its use and has largely superseded these drugs.

NO is the vasodilator of choice in term in babies with PPHN.

Evidence to support its use in preterm babies is not yet available.

Randomized trials in term babies with primary and secondary PPHN have shown that:

INO significantly improves oxygenation.

INO significantly reduces the need for rescue with ECMO.

Response to INO depends on the underlying pathophysiology.

Marked improvement is seen with NO alone in babies with primary PPHN.

In babies with secondary PPHN, the effects of INO are augmented by HFOV.

Front 48

Treatment PPHN:

Systemic vasodilators

Back 48

Systemic vasodilators:

Tolazoline and Prostacycline have been widely used in PPHN although there are no randomized trials to support their use.

Both drugs have similar vasodilator effects on the systemic and the pulmonary circulation and so may cause systemic hypotension.

Front 49

Treatment PPHN:

ECMO

Back 49

Extracorporeal membrane oxygenation (ECMO).

This is essentially prolonged cardio-pulmonary bypass Since the introduction of NO and HFOV, the need for ECMO has declined.

Usual criteria are infants who have an Oxygenation Index (OI) >40.

The neurological status of the infant may be an important factor in determining if ECMO is offered.

Very, Very Expensive.