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Neonatology I June 19, 2014
variability becomes more pronounced. (which may lead to insults B. CONTRACTION STRESS TEST (CST)
to the fetus, one of which is hypoxia which may lead to acidosis Observes fetal response to spontaneous, nipple-stimulated or
and FHR variability ) oxytocin-stimulated uterine contractions-Nelson
Contraindicated in women with preterm PROM, previous uterine
HOW HYPOXIA (LOW OXYGEN) LEADS TO ACIDOSIS AND DECREASED FHR scar from a classic cesarean section, multiple gestations,
VARIABILITY incompetent cervix & placenta previa-Nelson
Fetus uses oxygen to burn molecules and release energy Used by some antepartum testing centers to evaluate placental
Reaction: glucose + oxygen carbon dioxide + water + energy function under stress. The test is performed by placing transducers
Poor blood flow from the uterus and placenta causes the fetus to (ultrasound and toco), on patient’s abdomen as with the nonstress
constrict blood vessels in nonvital peripheral areas such as the test
arms and legs in order to supply more blood flow to vital organs The tracing is then observed for late decelerations which suggest
such as the heart and brain fetal compromise
With a limited supply of oxygen (hypoxia) the peripheral tissues The test requires three contractions in 10 minutes to be present
can only partially break down the sugar and converts it to lactic with the contractions lasting 40 – 60 seconds
acid (always refers to Kreb’s Cycle-aerobic and anaerobic If uterine activity is absent then oxytocin is infused or nipple
oxygenation) stimulation is used
Significant levels of acid in the blood (acidemia) may suppress the Positive Test: if late decelerations are consistent and present with
fetal nervous system and eventually lead to cardiovascular more than 50% of the contractions
collapse. Positive CST associated with an increased incidence of intrauterine
death, late decelerations in labor, low 5-minute Apgar scores, and
PRESENCE OF MODERATE FHR VARIABILITY IS REASSURING intrauterine growth restriction.
Persistently minimal/Absent FHR variability appears to be the CST is equivocal or suspicious if there are intermittent late
most significant intrapartum sign of fetal compromise. decelerations.
Presence of good FHR variability may not always be predictive of a
good outcome (such as may occur with an abruption). C. BIOPHYSCIAL PROFILE (BPP)
Normally, the baseline FHR is variable. Variability is classified as follows: Assess movement, fetal breathing, body movement, tone, heart
absence variability (amplitude change is undetectable); minimal rate, and amniotic fluid volume; improve accurate and safe
variability (amplitude range is ≤5beats/min); moderate variability identification of fetal compromise-Nelson
(amplitude range 6-25 beats/min); marked variability (amplitude range 24-28 weeks gestation: approximately 50% of NSTs are
˃25 beats/min. The presence of moderate variability predicts the nonreactive
[1]
absence of fetal metabolic acidemia. In contrast, sonographically evaluated variables are valid early in
gestation and account for 3-5 components of the biophysical
CAUSES OF DECREASED VARIABILITY profile
Fetal metabolic acidosis May be used to verify fetal well-being when the nonstress test is
CNS depressants not reactive
Fetal sleep cycles Fetal movement and fetal tone develop between 7.5 and 9 weeks
Congenital anomalies menstrual age.
Prematurity Fetal breathing movements are detectable by, at least 17-18
Fetal tachycardia weeks gestation.
Preexisting neurologic abnormality Amniotic fluid may be reduced as early as 17.5 weeks by fetal
Normal variant acidosis.
Betamethasone The components of the biophysical profile develop sequentially. In
order of appearance: (1) tone, (2) movement, (3) breathing,
LATE DECELERATIONS (4)reactivity
Late associated with no variability (where loss of variability has not
been caused by drug administration) COMPONENTS OF THE BIOPHYSCIAL PROFILE SCORE
o With progressing hypoxia the decelerations become Component Definition
deeper. Non-stress Two or more fetal heart rate accelerations peak (but do
o As acidosis develops the brain stem reflexes become test not necessarily remain) at least 15 beats per minute
blunted and direct myocardial depression causes shallow above the baseline and last 15 seconds from baseline to
decelerations (20.22) baseline within a 20 minute period with or without fetal
o If myocardial depression is severe enough, lates may be movement discernible by the woman.
absent all together Amniotic A single 2 cm x 2 cm pocket is considered adequate or
Causes fluid volume AFI greater than 5.0 cm.
o Excessive uterine contraction (hyperstimulation), Fetal One or more episodes of rhythmic fetal breathing
maternal hypotension, or maternal hypoxemia breathing movements of 30 seconds or more within 30 minutes.
o Reduced placental exchange as in hypertensive movements Hiccups are considered breathing activity.
disorders, diabetes, IUGR, abruption Fetal At least three discrete bodies or limb movement.
o Response to any maternal, placental, umbilical cord, or movements Episodes of continuous movement are considered as a
fetal factor that limits effective oxygenation of the fetus- single movement.
Nelson Fetal Tone One or more episodes of extension of a fetal extremity
or trunk with return to flexion, or opening or closing of
a hand.
FETAL LUNGS
Fluid filled
Resistant
Nourishment depends on placenta
NEWBORN CIRCULATION
At birth, with the onset of respiration, due to the presence of oxygen,
the muscle layer in the Ductus Arteriosus would contract, functionally
closing the Ductus Arteriosus. With the inflation of the lungs, blood
would now flow to the lungs and would be oxygenated. Oxygenated
blood now would go to the Left Atrium, thereby increasing the pressure
Figure 1. Fetal Circulation-Blue: deoxygenated; Red-Oxygenated &Purple-
inside. With the increasing pressure, the septum primum would be
Mixed Blood
pressed onto the more rigid septum secundum, essentially closing the
Blood from placenta, which is about 80% oxygenated, returns to
Foramen Ovale. Blood would now flow from the Left Atrium, to the Left
embryo via the Left Umbilical Vein. Most of the blood goes to the
Ventricle, to the aorta, to be distributed to the Systemic Circulation.
Ductus Venosus to enter the Inferior Vena Cava. Some of the blood
When the umbilical cord is clamped, there is cessation of blood flow in
enters the liver sinusoids and would be mixed via the vein returning
this area from the placenta. With this, the Left Umbilical Vein becomes
from the Portal Circulation. In the Ductus Venosus, close to the
the Ligamentum Teres Hepatis or the Round Ligament of the Liver. The
entrance of the left umbilical vein, a sphincter mechanism is present.
Ductus Venosus becomes the Ligamentum Venosum. On the other
This sphincter mechanism prevents the sudden overloading of the heart,
hand, the distal portion of the umbilical arteries becomes the Medial
especially when there are uterine contractions, wherein too much blood
Umbilical Ligaments, whereas the proximal portion becomes the
would flow to the placenta. The sphincter mechanism would contract
Superior Vesicle Arteries to supply the urinary bladder.
and would close, so that the heart of the fetus would not be overloaded
Anatomically, the Ductus Arteriosus completely closes during the 2nd-
with blood.
3rd week (some CVS books) or 1-3 months (Langman’s Medical
Blood returning from the lower extremities mixes with blood in the
Embryology) while the closure of the Foramen Ovale, forming the fossa
Inferior Vena Cava (but still well-oxygenated). From the Inferior Vena st
ovalis, occurs within the first year of life. (1 year Anatomy Trans)
Cava, blood would go to the Right Atrium. Most of the blood coming
Postnatal circulation
from the Inferior Vena Cava is directed to the Left Atrium via the valve
Right atrium, SVC, IVC
of the Inferior Vena Cava, the Eustachian valve. This valve would direct
most of the blood to the Left Atrium. Some of the blood would be Poorly oxygenated blood
prevented from entering the Left Atrium by the Septum Secundum, but Right ventricle, pulmonary artery, pulmonary circulation
most of the oxygenated blood would flow to the Left Atrium. In the Left Oxygenated blood
Atrium, blood is mixed with deoxygenated blood from the Pulmonary Left atrium, pulmonary veins
veins (blood coming from the lungs), and from the Left Atrium, would Left ventricle, aorta, systemic circulation
go to the Left Ventricle, to the aorta. Since the initial portion of the Keeping those in mind, in premature babies the ductus arteriosus will not be
ascending aorta has the coronary arteries and the carotid arteries, this closed and there are factors that will keep the ductus close or patent.
ensures that the brain and the heart receive well-oxygenated blood. Therefore, knowledge in neonatal resuscitation is needed. This would be
[4]
Blood then flows to the aorta and then to the descending thoracic time- dependent.”
aorta.
The well-oxygenated blood that was prevented from entering the Left NEWBORN RESUSCITATION
Atrium now remains in the Right Atrium. This is mixed with *See IMAGE 1 on index page
deoxygenated blood from the head via the Superior Vena Cava. Blood At birth, questions asked are the following:
from the Right Atrium would go to the Right Ventricle, to the Is meconium clear?
Pulmonary Trunk. Since the pressure is great in the lungs, only a small o if there is hypoxic insult there would be relaxation of
amount of blood would go to right and left pulmonary trunks. Most of sphincteric muscle leading to passage of meconium
the blood would be shunted through the Ductus Arteriosus, to be mixed o In utero, meconium would be sterile but once it is already
with the blood coming from the arch of the aorta. Blood would now go in the post natal circulation or when the patient starts to
to the Descending Thoracic Aorta, to the Descending Abdominal Aorta, breathe, meconium will be contaminated
and finally, would return via the Umbilical Artery, to the placenta. o May lodge in the lungs and cause chemical pneumonitis
Breathing or crying?
Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 4 of 15
Pediatrics 1.1
Good muscle tone?- differentiate if term or pre-term The inverted triangle gives you priorities in initial resuscitation
Is the baby pink? - No longer asked due to presence of Only 10% needs aggressive resuscitation-resuscitation in the
acrocyanosis which is due to constriction of vessels to conserve delivery room and emergency room mainly involves the drying,
heat stimulation and suctioning if needed
Is the patient term or preterm? Lowest is the medication
If the answer to any of the of the questions is no,
o Provide warmth by drying, stimulate, reposition and ASSESSMENT
provide oxygen if necessary to clear the airways ASSESSMENT BEFORE: APGAR SCORE
o Evaluate HR and color This is a postnatal assessment for newborns which assesses and
If HR is less than 100, provide positive pressure grades the neonate’s 1st minute to 5th minute of life, based on
ventilation (ambulatory bag) Appearance, Pulse, Grimace, Activity, and Respiration.
[4]
If HR is less than 60, initiate cardiac “Still the best tool to evaluate physiologic parameters”
compression 10 is the highest score which equates to the best possible
condition but infants do not get 10 points because of acrocyanosis
in the 1st minute or even in the 5th minute of life.
Normal score of 7-10
Intermediate score of 4-7
Poor score of 0-3 (requires immediate resuscitation)
The 1st minute of life signifies the need for resuscitation while
the 5th minute of life tells the CNS outcome.
APGAR score has limitations and is affected by gestational age,
maternal medications, resuscitation, congenital anomalies and
trauma.
Figure 2. Primary and Secondary Apnea Low APGAR score on the 1st minute does not correlate with future
outcomes.
If there is apneic episode determine if it is more than 20 seconds Low APGAR score from 0-3 minutes may correlate with neonatal
then classify whether it is: mortality but not with neurologic dysfunction.
o Primary apnea APGAR scores of 0-3 in the 10th, 15th and 20th minute increases
[2]
None of the HR and BP are affected; happens the possibility of a neurologic problem.
during transitional period, the newborn adapts
to new environment Table 1. FACTORS AFFECTING THE APGAR SCORE
spontaneous post-natal breathing, causing the FALSE-POSITIVE (NO FETAL ACIDOSIS OR HYPOXIA; LOW APGAR SCORE
fluid out of the alveoli and stops fetal Prematurity
respiration Analgesics, narcotics, sedatives
o Secondary apnea Magnesium sulfate
a drop in HR and BP; tells you that you are not Acute cerebral trauma
successful in helping the patient in transition, Precipitous delivery
WHAT YOU WANT TO PREVENT Congenital myopathy
o Blood Pressure is affected to ensure stimulation of the Congenital neuropathy
patient to avoid lagging in secondary apnea, affecting the Spinal cord trauma
heart rate and making the patient bradicardic Central nervous system anomaly
Lung anomaly (diaphragmatic hernia)
Airway obstruction (choanal atresia)
Always Assess baby’s response to birth Congenital pneumonia and sepsis
Needed Previous episodes of fetal asphyxia (recovered)
Keep baby warm, Position, clear airway, Hemorrhage-hypovolemia
stimulate to breathe by drying, and give oxygen FALSE-NEGATIVE (ACIDOSIS; NORMAL APGAR SCORE)
(as necessary) Maternal acidosis
High fetal cathecholamine levels
Needed Less Establish effective ventilation Some full term infants
Frequently Bag and mask
Endotracheal intubation ASSESSMENT NOW
Provide chest Physiologic parameters (Apgar is still the best tool)
Compression Breathing
Rarely Needed Heart rate
Administer Color
meds Questions to ask yourself
Clear of meconium
Breathing or crying
Good muscle tone
Term gestation?
Figure 3. Inverted pyramid of the priorities in initial resuscitation
INITIAL MANAGEMENT: FOR ALL DELIVERIES Keep the mouth slightly open
Provide warmth- to prevent evaporation as a loss for heat Delivering good and adequate pressure: chest rise is seen
Position and clear airway The manometer indicates pressure given
Dry don’t go beyond 40mmHg because it can cause
Give oxygen (as necessary) barotrauma leading to pneumothorax
o in premature babies: they at risk for retinopathy of Indications for intubation
prematurity if you give 100% oxygen Meconium and baby is not vigorous
o now it is accepted to do resuscitation in room care PPV by bag-mask does not result in good chest rise
PPV needed beyond a few minutes
Chest compressions necessary
Route to administer epinephrine
Special indications
prematurity
lack of surfactant making lungs atelectatic
Congenital Diaphragmatic Hernia - migration of GI
content into thoracic cavity. Thus, when you use ambu-
bag which distends the bowels, you compromise
respiratory status; clinically seen as scaphoid abdomen
Indications for compressions
Heart rate<60 bpm after 30 secs of PPV
Figure 4. Providing Warmth: The Cycle of Hypothermia. Hypothermia will
Coordinated with ventilation
increase oxygen utilization causing depletion of oxygen. This will increase
4 events in 2 seconds
accumulation of lactic acid causing acidosis.
90 compressions and 30 breaths per minute
MEDICATION: EPINEPHRINE
Indication: HR <60 after 30 sec of coordinated ventilation and
compressions
1:10,000 (0.1 mg/ml)
Get 1 ml of 1:1,000 dilute in 9ml to make 1:10,000
Route: Endotracheal tube or IV
0.1-0.3 ml/kg
1ml Term
0.5 ml Preterm
0.25 ml extreme preterm
EXTENDED ALGORITHM
Endotracheal intubation if not already accomplished
Establish IV access with UVC (Umbilical Venous Catheter)
Stat Chest x-ray- to know if endotracheal tube is properly placed
and situated above the carina
Discontinue efforts if no heart rate after 15 minutes
Discussion for Figure 5: Patient A is a 35-weeker with a BW of 2kg-AGA; Chronic fetal infections (cytomegalic inclusion disease,
Patient B is full term with a BW of 2kg-SGA. congenital rubella, syphilis)
Better to have patient A, since the problem with patient B may already be Congenital anomalies – syndrome complexes
chronic and there may also be a lot of problems even in the intrauterine Irradiation
[4]
period. Classification based on weight is for PROGNOSTICATION. Multiple gestation
Pancreatic hypoplasia
LARGE FOR GESTATIONAL AGE (LGA) Insulin Deficiency
th th
Appropriate for Gestational Age = 10 – 90 centile Insulin-like growth factor type 1 deficiency
th
Small for Gestational Age – below the 5 centile
th
Large Gestational age – above the 95 centile Placental
*the evaluation of the newborns will predict complications which Decreased placental weight or cellularity, or both
may occur during the fetal and neonatal transition period and Decrease in surface area
closely monitor them Villous placentitis (bacterial, viral and parasitic)
Appears large and plump Infarction
LGA babies are at risk for difficult delivery that can result in birth Tumor (chorioangioma, hydatidiform mole)
injuries/ distress Placental Separation
Prone to hypoglycemia; polycythemia Twin transfusion Syndrome
Ex. Infants of diabetic mother; fetal hydrops; Beckwith-Weidmann
(chronic hypoglycemia with omphalocele); postterm infants; Maternal
constitutionally large infants Toxemia
Hypertension or renal disease
SMALL FOR GESTATIONAL AGE (SGA) Hypoxemia (high altitude, cyanotic cardiac or pulmonary
Accounts for 1/3 of low birth weight (<2500) in western countries disease)
Appear scrawny with large head; alert; more mature than what Malnutrition (micro/macro deficiencies)
their BW would suggest Chronic Illness
Babies who either have not received enough nutrition in utero to Sickle cell Anemia
grow appropriately or have poor use of nutrients, such as those Drugs (narcotics, alcohol, cigarettes, cocaine, anti-
with chromosomal defects metabolites)
Higher risk of mortality than AGA or LGA babies
PROBLEMS OF IUGR/SGA INFANTS
They have experienced chronic stress in utero and diminish
Problem Pathogenesis
reserves to withstand stresses of labor and delivery
Intrauterine Fetal Demise Hypoxia, acidosis, infection and
Premature SGA infants are at lower risk for RDS
lethal anomaly
They are at risk for hypoglycemia; need higher caloric
Perinatal Asphyxia Decreased utero- placental
requirements
perfusion during labor with or
* If you have a mother with chronic hypertension or pregnancy-induced
without chronic fetal hypoxia
hypertension, the effect of hypertension on pulmonary maturity is
resulting to acidosis, meconium
hastened. Therefore, these patients do not have an increased incidence
[4] aspiration syndrome
of hyaline membrane or respiratory distress.
Hypoglycemia Decrease tissue glycogen stores
and gluconeogenesis,
IDENTIFICATION OF SGA/IUGR
hyperinsulinism, increased
An infant may be small at birth due to genetic factors. Non genetic glucose needs due to hypoxia,
factors may not be apparent before 32-34 weeks of gestation and hypothermia and large brain
this could be due to: Polycythemia – Hyperviscosity Fetal hypoxia with increased EPO
1. Placental insufficiency from maternal disease involving small production
blood vessel as seen in maternal conditions such as pre- Reduced oxygen Hypoxia, hypoglycemia starvation
eclampsia or primary hypertension, renal disease or long consumption/hypothermia effect, poor subcutaneous fat
standing diabetes stores
2. Placental involution which is noted in post-mature babies Dysmorphology Syndrome anomalads,
3. Infectious agents such as cytomegalovirus, rubella virus or chromosomal-genetic disorders,
toxoplasma gondii oligohydramnios- induced
4. Small head circumference: head bigger than chest by >3 cm deformation, TORCH infection
5. Physical characteristics such as skin appearance (loose folds
of skin), ear cartilage (small amount of ear cartilage), sole IUGR VS SGA
creases (less creases) lack of subcutaneous tissues SGA IUGR
6. Patient’s behavior? Does he have a vigorous suck? Alert? BW less than population norms BW less than expected inhibition of
7. Feeding behavior normal growth potential
8. Maternal History: opioid or cocaine user? Alcohol and th
<10 % OR Implies pathology
smoking during pregnancy? < 2 SD below the mean A term used by OB to describe a
9. Growth restriction pattern of growth over a period of
time
FACTORS ASSOCIATED WITH IUGR Pathologic or non-pathologic causes
Fetal A term used by PEDIA
Chromosomal disorders UENT MANAGEMENT OF ASP
Good supportive care is essential in the first 48 hours after asphyxia to SUBSEQUENT MANAGEMENT OF ASPHYXIATED NEONATES
prevent ongoing brain injury in the penumbra region
Strict monitoring and prompt correction is needed for common
problems including temperature maintenance, blood sugars, blood
pressure and oxygenation to see if patients are showing signs of
improvement/deterioration
[2]
Guidelines to be followed in managing patients with HIE
Meconium stained, amniotic fluid
o If the patient is vigorous and crying, there’s no need for intubation
and suctioning
o If the patient is depressed, you need to suction the amniotic fluid
even before the first breath to avoid aspiration. If aspiration lodges
in the lungs, chemical pneumonitis may be a complication. Figure 9. Subsequent Management
o Meconium aspiration syndrome is the end result if patient is not
able to recover from this condition A. Ventilate if there is respiratory depression especially in the setting
Avoid hyperthermia of:
o Full-term patients: 100% FiO2 is recommended but if supplemental Severe encephalopathy
oxygen is not available room air can be utilized. Frequent seizures
o Pre-term patients: 100% FiO2 is detrimental because it can lead to Post anticonvulsant medication-ie. Phenobarbital can
blindness or retrolental fibroplasia. cause respiratory depression, although a high dose of this
Chest compression is given when seizure is intractable
o Initiated if the heart rate is absent or remains to be <60 bpm. B. Aim for O2 Saturation= 90-93% in the term baby to minimize the
o If it is <100 bpm, just do positive pressure ventilation. risk of pulmonary hypertension
Give epinephrine: 1:10,000 at 0.01 to 0.03mg per kg C. Avoid hypocapnia (pCO2<50mmHg) will worsen cerebral
vasoconstriction
Prevent Further Organ Damage D. Consider crystalloid boluses (10-20ml/kg of 0.9% saline)
Maintain oxygenation, ventilation and perfusion Perfusion is poor
Correct and maintain normal metabolic and acid base milieu Lactate not improving
Prompt management of complications Mean BP <40mmHg in a term baby
In the NICU set-up, if your patient shows metabolic acidosis,
Clinical Monitoring sodium bicarbonate is not the answer.You must evaluate the
HR, RR, color, CRT (Capillary Refill Time), O2 saturation, BP and fluid status of your patient first before you administer
temperature bicarbonate infusion.-Dr. Salazar
Assessment of neurologic status-tone, seizures, consciousness, E. Consider blood transfusion if there has been fetal blood loss and
pupillary size & reaction, sucking and swallowing poor perfusion and metabolic/ lactic acidosis persists-
Abdominal circumference-since GI is not a priority organ F. If hypotension persists start inotropes
Urine output-good output is 1cc/kg Dobutamine (5-20 micrograms/kg/minute)
Biochemical Monitoring Dopamine (5-20 micrograms/kg/minute)
Blood gases & pH G. Acidosis usually improves with improved ventilation and
Bedside blood sugar by Destrostix perfusion. Consider a half bicarbonate correction, if severe
Hematocrit metabolic acidosis persists. However, persisting acidosus suggests
S electrolytes (Na, K) impaired cardiac output and attention should be directed towards
S calcium treating this
H. Restrict fluids to 40-50 ml/kg/day until urine output (of
BUN, creatinine
1ml/kg/hour) is established.
Other Investigations
I. Give 10% glucose in the first 24 hours and monitor blood glucose
Neuroimaging
levels. Once renal function is stable sodium and potassium
1. CT scan
additives can be commenced
o Brain edema as suggested by small compressed vessels
J. If oliguria/anuria, consider:
o Hemorrhage
Urinary catheterization
2. Ultrasound
Fluid challenge (20ml/kg 0.9% saline over 30 mins.) with
o Small compressed vessels
diuretic (Furosemide 1-2 mg/kg IV)
o Intraventricular hemorrhage
Dopamine (renal dose 2.5-5 micrograms/kg/minute)
3. EEG
Withholding aminoglycoside antibiotic if prescribed.
*Sepsis Screen should be part of your work-up to exclude in utero or acquired
infections during resuscitation esp. if you have utilized your umbilical cord as
[4] AIMS OF SPECIFIC MANGAMENT
your vascular access.
Maintain temperature, perfusion, oxygenation and normal metabolic
*Sometimes if you suspect barotrauma (intubated patient doing all right
state
then suddenly experiences desaturation, becomes cyanotic and there is o
1. Temperature: 36.5- 37.5 C
absence of breath sounds on auscultation-PNEUMOTHORAX), you can do
2. Perfusion:
transillumination. Transillumination is when you put a bright source light on
BP: Mean 40-60 mmHg
the chest and the area of pneumothorax lightens up. Documentation of this
[4] CRT: Maintain <3 sec.
should be done through chest x-ray. Thoracocentesis can also be done.
SEIZURE MANAGEMENT
Peaks on the first 48 hours
Anticonvulsant therapy-AE: respiratory depression
A. Phenobarbital
st
1 line anticonvulsant, drug of choice for maintenance
monotheraphy in the first 6 months of life due to its
relale absorption and long safety record
Initial Dose: 20mg/kg/dose, if seizures continue, up to
40mg/kg can be given safely. Stop IV once seizure is
controlled
Maintenance: 5mg/kg/day once daily
B. Phenytoin
nd
2 line anticonvulsant
Loading Dose: 15-20mg/kg/dose IV
Phenytoin absorption orally is unreliable, thus this
agent is discontinued after the immediate stabilization
period
C. Midazolam
rd
3 line anticonvulsant can be titrated for continuous
The patient would actually meet the criteria for asphyxia. These are the infusion.
guidelines used for infants who are asphyxiated and usually apply for term D. Clonazepam
patients where they usually institute the HYPOTHERMIA THERAPY. Safe and effective alternative
INDEX
Image 2: Algorithm of New Born Resuscitation Image 3: Algorithm of New born Resuscitation