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Neonatal Resuscitation

Neonatal Resuscitation

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OS 215 Reproductive

Ma. Esterlita Villanueva-Uy Exam 2

Neonatal Resuscitation and Depressed Infant
OUTLINE How does a baby receive oxygen after birth? Before birth (in utero) Transition to neonatal circulation At completion of this normal transition What can go wrong during transition? How can you tell if a newborn had in utero or perinatal compromise? Risk factors associated with need for resuscitation APGAR Score A Depressed Infant

I. A. B. C. D. E. F. II. III.

resistance < Systemic Vascular resistance – note: There is only functional closing of the foramen ovale and ductus arteriosus during delivery. The actual closing of these two shunts takes several days to complete.
Pulmonary hypertension in the newborn happens if there is no increase in PBF and no decrease in PVR. The lungs remain constricted and the baby becomes cyanotic.

How does a baby receive Oxygen after birth?
A. Before birth (in utero)

C. At completion of this normal transition Baby breathing and using his lungs Crying moves the fluid out of his lungs Oxygen and gaseous distension make pulmonary vessels relax Baby turns from blue to pink D. What can go wrong during transition?

Lungs

have no ventilatory purpose, gasless (because it is fluid-filled), and have decreased blood flow - only 10% of the blood goes into the pulmonary circulation (due to high resistance in the lungs) while the other 90% is shunted through the ductus arteriosus and goes to the systemic circulation Fetal PO2 = 24-28mmHg; Adult PO2=5060mmHg

90%

Placenta is the gas-exchange organ- “lungs” - it has very low resistance compared
resistance of the peripheral circulation Right to left shunts: - foramen ovale - ductus arteriosus

to high

of the time, transition is very smooth. 10% would need resuscitation. But what could possibly go wrong? Baby does not breathe sufficiently to force fluid or foreign material (meconium) from the alveoli, thus lungs will not be filled with air.

Excessive Lack

blood loss (ex. Abruption placenta) or poor cardiac contractility (ex. Due to infection) will result to no increase in blood pressure hence the shunts remain open of oxygen or gaseous distension will cause sustained constriction of the pulmonary arterioles hence not enough blood will be brought to the lungs(Persistent Pulmonary Hypertension of the Newborn) E. How can you tell if a newborn had in utero or perinatal compromise? In an experiment done in the 60s, they observed newly born baboons whose heads were wrapped in plastic after being born. The following changes (in chronological order) were observed as they desperately gasped for air and progressive hypoxia occurred:
Breathing

Figure 1. Fetal Circulation. Maternal blood carrying food and
oxygen for the fetus goes to the umbilical vein (vessel with highest oxygenation) and into the ductus venosus. From the inferior vena cava, blood goes to the right atrium and is shunted through the foramen ovale into the left atrium. From the left atrium, blood goes to the left ventricle and eventually to the aorta. Blood from the superior vena cava goes to the right atrium, into the right ventricle and into the pulmonary artery. Blood is then shunted into the ductus arteriosus and then goes to the aorta.

Rapid breathing

Primary apnea

Irregular gasping

Secondary apnea

Heart rate

Blood pressure

B. Transition to Neonatal Circulation Table 1.Changes occurring during delivery and their effects. Changes Effects Umbilical cord is clamped Eliminate the placenta Expansion of the lungs resulting in a ten-fold First breath is taken increase Pulmonary Blood Flow (PBF) and a ten-fold decrease in Pulmonary vascular resistance (PVR) Blood flow increases to the Lung fluid gradually lungs  pulmonary vein  leaves the alveoli left atrium Blood flow to lung Closes foramen ovale increases and Left atrial pressure > Right atrial pressure Pulmonary vascular Closes the ductus arteriosus

Rapid breathing Primary apnea Irregular gasping Secondary apnea HYPOXIA
Figure 2. Physiologic changes associated with primary and secondary apnea. Initial oxygen deprivation results in a transient period of rapid breathing. If such deprivation persists, breathing movements cease (primary apnea). This is accompanied by a decrease in heart rate and loss of neuromuscular tone. Blood pressure compensates and increases. If oxygen deprivation and asphyxia persists, the infant will develop deep gasping respirations, followed by secondary apnea. This is associated

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OS 215 Reproductive

Ma. Esterlita Villanueva-Uy Exam 2

Neonatal Resuscitation and Depressed Infant

with a further decline in heart rate, falling blood pressure and loss of neuromuscular tone.

pink Mnemonic: A – appearance (color) P – pulse rate (heart rate) G – grimace (reflex irritability) A – activity (muscle tone) R – respiration 1 minute APGAR Score - more of a measure of state of infant in utero, or how bad his or her condition in the womb was - use to identify the need for immediate resuscitation 5 minute APGAR Score and particularly the change in the score between 1 and 5 minutes - useful index of the effectiveness of resuscitation efforts - a score of less than 3 could lead to the development of cerebral palsy
Most infants at birth are in excellent condition, as indicated by APGAR Scores of 7 to 10, and they require no aid other than perhaps simple nasopharyngeal suction. Median score is 9 due to acrocyanosis related to temperature instability Scoring an infant should be logical. An infant would logically not have good activity if heart sounds are not present. An infant with a score of 4 to 6 at 1 minute demonstrates depressed respirations, flaccidity and pale to blue color. Heart rate and reflex irritability, however, are good. Infants with scores of 0 to 3 usually have slow and inaudible heart rates and depressed or absent reflex responses.

The same response can be said about newborns in utero or perinatal compromise. An objective measure that can tell you whether the newborn is in perinatal compromise or not can be obtained through APGAR Score. Apnea is the best indicator of neonatal compromise because it is the earliest manifestation. Blood pressure is the last to go. In primary apnea, when hypoxic stimulus is removed, the baby will start breathing. In secondary apnea, removing hypoxic stimulus will not make the newborn breathe. In the clinics, primary and secondary apnea cannot be differentiated, so when faced with an apneic newborn, always assume that the baby might already be in secondary apnea so resuscitate aggressively. F. Risk Factors Assoc. with Need for Resuscitation - be aware of these Risk Factors so you can have all equipment ready in the OR 1. Maternal infection Lungs heart blood blood vessel uterus others aminionitis pneumonia, asthma, ARDS (Adult respiratory distress syndrome) arrythmia, structural defects, failure anemia, hemoglobinopathies SLE, DM, HPN hypertonus, rupture genetic, drugs, PTL (Preterm labor) , MG (multiple gestation), abnormal FP (fetal presentation) postmaturity abruption, previa

2. Placenta age size, morphology 3. Fetal umbilical cord blood metabolic others

A Depressed Infant
The only way to check if infant is depressed is through the APGAR score. Low APGAR score (0-5) in 5 minutes May be due to a lot of reasons: - Maternal sedation or anesthesia - Substance abuse - Trauma - Infection - Congenital anomalies - CNS disorders - Cardiovascular disorders - Neuromuscular disorders Does not necessarily mean that infant is asphyxiated A. Perinatal asphyxia

knot, prolapse, compression, thrombosis anemia IEM (Inborn errors of metabolism) infection, hydrops, MG

APGAR Score
Objective method of quantifying the newborn’s condition Conveys information about the newborn’s overall status and response to resuscitation

Not

used to decide how or when to resuscitate – it is measured in the 1st and then 5th minute after delivery of the baby. If sufficient distress is noted before the 1st minute, when APGAR scoring hasn’t yet been done, then infant must be resuscitated. Assigned at 1 and 5 minutes of life When <7, additional scores every 5 min for up to 20 minutes APGAR SCORE SIGN 0 1 2 Heart Rate Absent <100 >100 Respiration Absent Slow, Good, irregular crying Muscle Limp Some Active Tone flexion Motion Reflex No Grimace Cough, irritability response sneeze, cry Color Blu or pale Pink body Completely

Interference in gas exchange between organ systems of mother and fetus resulting in impairment of tissue perfusion and oxygenation of vital organs in the fetus Lactic acidosis and hypercapnea Multi-organ damage New ACOG/AAO Definition All four requirements must be met 1. Evidence of antenatal distress - Meconium stained fluid, electronic fetal heart rate abnormality, fetal tachycardia 2. Low APGAR score (3 or less in the first 5 mins.) 3. Evidence of end organ damage - Brain, lungs, gastrointestinal and kidney damages 4. Acid-base abnormality (ph <7.0)

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Ma. Esterlita Villanueva-Uy Exam 2

Neonatal Resuscitation and Depressed Infant

B.

Criteria that Suggest an Intrapartum Nonspecific to Asphyxial Insults

Timing

but

3.

Pulmonary blood flow decrease in hypoxemia and asphyxia

A sentinel hypoxic event occurring immediately before or during labor A sudden and sustained fetal bradycardia or absent fetal variability in presence of late decelerations Apgar score of 0-3 beyond 5 minutes Onset of multi-system involvement within 72 hours of birth Early imaging study showing evidence of acute non-focal cerebral abnormality

=from this point on, these are the slides in the powerpoint which were skipped by Dr. Uy, except those in bold. So please read these parts. =) D. Injury from Asphyxia

C.

Changes in Cardiac Output, Percentage Distribution, Heart Rate, and Pulmonary Blood Flow During Asphyxia - What happens during asphyxia? absence of blood flow from placenta to baby will lead to hypoxia carbon dioxide is not released hypoperfusion will cause baby to undergo anaerobic metabolism and thus develop acidosis fetus becomes a preferential organ organism: blood flow to brain, heart and adrenal glands are increased while blood flow to other organs will be compromised: Fetal cardiac output and percentage distribution during asphyxia

-

1.

Cardiac Output (ml/min/kg)
700 600 500 400 300 200 100 0 Normal Asphyxia

New development regarding mechanism of brain injury in the term neonate due to asphyxia: cell death occurs during oxidative stress, inflammation, and DURING REPAIR STAGE. Why is there injury during the repair stage? Cytotoxic effects of oxygen radicals after blood flow to the tissues is re-established and molecular oxygen is re-introduced into the tissue.  REPERFUSION INJURY 1. Generation of Oxygen Radicals


• •

Hypoxanthine degradation by hypoxanthine oxidase and oxygen  oxygen radicals Blood vessels dilated by and oxygen radicals generated by prostaglandin Proteases and lipases eat up plasma membrane and lead to radical oxygen species generation
ATP AMP

Figure 3. Difference in total fetal cardiac output in normal and asphyxiated newborns

Distribution of Cardiac Output (%)
60 50 40 30 20 10 0 Placenta Brain U. Body Adrenals L. Body Spleen Lungs Heart Gut Kidney Normal Asphyxia

Adenosine Inosine

Hypoxanthine

Figure 5. Conversion of ATP into hypoxanthine. When ischemia occurs, ATP is converted into hypoxanthine after a series of steps.

Figure 4. Distribution of cardiac output in normal and asphyxiated newborns. In asphyxia, placenta has greatest allocation of blood. There is also preferential perfusion to the brain, the heart, and the adrenals. 2. Heart rate response to hypoxemia and asphyxia - Heart rate decreases in response to hypoxemia and asphyxia

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OS 215 Reproductive

Ma. Esterlita Villanueva-Uy Exam 2

Neonatal Resuscitation and Depressed Infant

Release of Reactive Oxygen Species Pathophysiology
Ischemia ATP depletion Calcium influx Phospholipase activation Arachidonic release Prostaglandins Vasodilation Reperfusion ROS release Proteases, lipases Increase microvascular permeability

Sarnat scoring determines/ predicts how severe the cerebral palsy is/ will be Not rare for sarnat score to increase and progress G. Neonatal Encephalopathy and Cerebral Palsy The Report of ACOG’s Task Force Encephalopathy and Cerebral Palsy 1. on Neonatal

ROS
DNA strand breakage Membrane damage Lipid peroxidation Neutrophil accumulation

Release of proteases, myeloperoxidase, prostaglandins

PMN plugging of capillaries

Cell death Tissue damage

Phagocytosis

Ischemia

Neonatal encephalopathy - Defined clinically on the basis of findings to include a combination of abnormal consciousness, tone and reflexes, feeding, respiration or seizure and can result from a myriad of conditions - May or may not result in permanent brain damage - Term or near term Cerebral Palsy - Chronic disability of the CNS characterized by aberrant control of movement and posture, appearing early in life and not as a result of a progressive neurologic damage - Spastic diplegia - Pathway from intrapartum hypoxic-ischemic injury to subsequent CP must progress through neonatal encephalopathy - Why do we need to predict the development of cerebral palsy?  This disease is usually detected around 1-2 years of age. Early detection and intervention like physical therapy and maternal counseling lead to less sequelae Epidemiology Neonatal encephalopathy - Majority (70%) of NE due to events arising before labor

Figure 6. The release of reactive oxygen species and its effects. Ischemia leads to the production of reactive oxygen species, which in turn causes tissue damage and further cell death. 2. Neurotoxicity is secondary to increase in: • Increase turnover of NA into MHPG (3methoxy-4-hydroxyphenylglycol) • Excitatory amino acids - Glutamate and aspartate • Adenosine and gamma aminobutyric acid

2.

E.

Resuscitation:Immediate Treatment of Asphyxia! 1. Airway 2. Breathing room air vs. 100% oxygen bad effects of excessive oxygen: decreased cerebral blood flow and increased oxygen radicals - new studies showing that room air leads to higher 5th minute APGAR score, shorter time to first breath, and less neurologic impairment 3. Circulation 4. Drugs Risks of Permanent Sequelae

3.

H.

Criteria to Define an Acute Intrapartum Event Sufficient to Cause Cerebral Palsy

F.

Table 2. Classifying the Degree of Encephalopathy to Establish the “Pretest” Probability of Poor Outcome.

Essential Criteria Evidence of a metabolic acidosis in fetal umbilical arterial cord blood obtained at delivery Early onset of severe or moderate neonatal encephalopathy in infants at 34 or more weeks of gestation Cerebral palsy of the spastic quadriplegic or dyskinetic type Exclusion of other identifiable etiologies such as trauma, coagulation disorders, infectious conditions or genetic disorders I. Possible Post Resuscitation Strategies 1. Hypothermia Decrease of 2-6% below baseline

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Ma. Esterlita Villanueva-Uy Exam 2

Neonatal Resuscitation and Depressed Infant

Started <6 hours after hypoxic insult Decrease brain metabolism Better neurologic outcome

(eg. Dopamine) or volume replacement Kidneys • Acute tubular acidosis • • • Brain • • Apnea Seizures • • • • Gastrointestinal • • Ileus Necrotizing enterocolitis • • • Metabolic/ HematoloGic • Monitor urine output Restrict fluids if oliguria is present Monitor serum electrolyte levels Monitor for apnea Monitor glucose and electrolyte levels Avoid hyperthermia Consider anticonvulsant Delay initiation of feeding Administer intravenous fluids Consider parenteral nutrition Monitor blood glucose Monitor electrolyte levels Monitor hematocrit Monitor platelets

2.

Selective Head Cooling (Gunn 1998) In selective head cooling, the hypothermic baby is said to have a band around his/her head that is maintained at a temperature of 33oC. Minimal(6) 2 1 1 3 2 1 1 1 2 Mild(6) 0 2 4 0 6 0 0 0 6

Infants Control (10) CT scan Severe 1 Mild changes 4 Normal 2 EEG Abnormal 2 Normal 4 Dead 2 Severe 1 handicap Mild to 2 moderate Normal at 6-12 5 mos

3.

Whole Body Cooling (Shankaran Pediatrics 2002)

In a study done, it was noted that there were improvements in the following parameters: hypotension, renal failure, length of hospital stay, oxygen use, and seizures; however, the samples are still too small since it is an ongoing study. Hypotension PPHN Renal failure Hepatic dysfunction DIC Death Days on oxygen Length of stay Discharge status Gavage feeding Abnormal Neuro exam Seizure (on meds) Abnormal MRI Hypothermia (9)Normothermia (10) 8 10 3 2 3 5 1 1 1 1 2 3 6.8 8.4 14.9 21.6 0 1 0 3 2 4 2 3

Hypoglycemi • a • Hypocalcemi • a/ Hyponatremi • a • • Anemia • Thrombocyt openia Neonatal Resuscitation Algorithm (next page)

Table 3. Neonatal Postresuscitation Complications and Actions Organ Potential Post Resuscitation System Complication Action Lungs • Pulmonary • Maintain adequate Hypertensio oxygenation and n ventilation • Pneumonia • Consider antibiotics • Pneumothor • Delay oral feeding ax if respiratory • Transient distress is evident Tachypnea • Consider • Meconium surfactant therapy aspiration syndrome • Surfactant deficiency Cardiovascular • Hypotension • • Monitor blood pressure and heart rate Consider inotrope

Notes: • Mnemonic for the first questions to ask: Nucleotides TACG • Routine Care o Warmth: Equipment to be used such as radiant warmers should be pre-warmed before delivery o Aiway: semi-sniffing head position (to align airway, slightly chin-up) o Dry: dry with linen; replace wet linens with dry ones o Assessing Color: note for acrocyanosis(pink but with pale nailbeds) which may be secondary to mechanical problems after birth

To stimulate: flick the toes or rub the back but don’t take too long to avoid compromising the baby. If the baby doesn’t breathe immediately, assume secondary apnea. Things to assess to decide whether to resuscitate o Color o Heart/Pulse Rate o Respiration PPV without chest compression o Breathe-2-3-breathe-2-3 o 40 breaths/min o 100% O2 ideally Types of Positive Pressure Ventilation o Bagmask  Ambubag: self-inflating w/ oneway valve therefore cannot be used for free-flow O2

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OS 215 Reproductive

Ma. Esterlita Villanueva-Uy Exam 2

Neonatal Resuscitation and Depressed Infant

Anesthesia Bag: needs O2 for inflation o Laryngeal mask: used when the baby cannot be intubated PPV w/ Chest Compressions o Heart rate is checked for 6seconds (multiplied by 10) because you have to do everything in 30s. o Cadence: 1-and-2-and-3-and-breathe o 90 compressions,30 breaths per min 2 Methods of Chest Compression o Two-finger: 1 hand at the back of the baby for support;  Pointer + middle  Middle+ ring o Two- thumb: more stable *depth: 1/3 of AP diameter Epinephrine o IV: 0.1ml/kg, 1cc syringe o ET(endotracheal tube): 1ml/kg, 3-5cc syringe (1:10,000 dilution) 

Withdrawing resuscitation: • If there are no signs of life with continuous and adequate resuscitation, rescue efforts are stopped after ten minutes Jeopardy Notes:


• • • • •

Most important single step in resuscitation is pulmonary ventilation Three indications for PPV 1. Apnea 2. Heart rate <100 3. Persistent cyanosis despite O2 support Indications for chest compressions: HR<60 after 30 sec of PPV Landmark for chest compressions: imaginary mammary line Room air resuscitation is sometimes better than the 100% O2 Best way to asses if endotracheal tube is in: increase in HR Causes of bradycardia o Adult: MI o Child: Myocardial hypoxia secondary to pulmonary cause

Neonatal Resuscitation Algorithm

If preterm: A. Oxygenation • O2 blender • O2 sat goal 90-95% • Ambu w/o reservoir: 40% (mixed w/ room air) • Ambu w/ reservoir: roughly 100% B. Thermoregulation • Preterms are at risk for hypothermia • Use radiant warmer, dry baby and replace wet with dry linen • If <28 weeks, ziplock is used as a warming back

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OS 215 Reproductive

Ma. Esterlita Villanueva-Uy Exam 2

Neonatal Resuscitation and Depressed Infant

If meconium stained:

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