Neonatal Anesthesia Flashcards
Children < 1 year have higher incidence of complications than older children often related to
Ooxygenation, ventilation, airway management, and response to anesthetic agents and medications
The transition from fetal to neonatal physiology takes place during the first __-__ hours of life
24-72.
First 72 hrs the most important for cardiac, pulmonary, and renal systems.
A premature infant is born less than ___ weeks gestation
37
A postmature infant is born over ___ weeks gestation
42
Growth and development is massive in the first year of life. Body weight alone will increase by a factor of
3
Importance of catecholamines at birth
- Helps them prepare for birth, adapt to extrauterine life, and cope with hypoxia
- Animals deprived of a catecholamine surge at birth less likely to survive hypoxia
- Catecholamines aid in the clearance of liquid from the lungs, which improves lung compliance after birth
- Are important for the release of surface-active material from alveolar type II cells
- During asphyxia, catecholamines maintain cardiac output and redistribute blood flow from the periphery to the heart, brain, and adrenal glands
- They also increase arterial blood pressure and slow the heart rate, which reduces myocardial oxygen consumption
- Infants delivered by cesarean section without maternal labor have lower blood glucose concentrations and less blood flow to peripheral organs than after vaginal delivery and is related to plasma catecholamine concentrations
- Neonates with elevated catecholamine concentrations have higher Apgar scores than those who have low concentrations
- Catecholamines help to redistribute CO. Causes preferential redistribution to brain, heart, etc.
Immediate physiologic changes at birth
- Cessation of umbilical circulation
- Initiation of ventilation/lung expansion
- Stress and associated catecholamines
Fetal circulation
Fetal Circulation:
Oxygenated blood comes from placenta through the umbilical vein to IVC to Right Atrium
In RA, about 40% of this oxygenated blood mixes with desaturated blood returning from the upper body/head via the SVC. Then goes through the Right Ventricle and into the PA. Only 5-10% of this goes to the fetal lungs since PVR is HIGH. The rest is shunted through the DUCTUS ARTERIOSUS to the descending aorta
The remaining 60% of oxygenated blood that came from the placenta is shunted through the FORAMEN OVALE to the LA the LV and the ascending Aorta
Based on this, overall 60% of oxygenated blood goes to the upper body and 40% goes to the lower body.
Why is the pressure so high in the fetal pulmonary circulation?
1) Low pH promotes vasoconstriction
2) Low PaO2 promotes vasoconstriction
3) The alveoli are full of fluid, which compresses the blood vessels
The ductus arteriosus is dilated by
Low O2.
This is why it is open during fetal life, and closes once the lungs start functioning and the newborn experiences higher O2 concentrations.
Permanent closure of the foramen ovale occurs
after a few months.
However, 10-20% of the population will never have a truly anatomically closed FO.
True fibrotic closure of the ductus arteriosus doesn’t occur until
2-3 weeks of age
It can take longer if the child was born premature
What causes the ductus venosus to close?
Drop in portal pressure due to removal of the placenta
PVR decreases dramatically at birth due to
lung expansion, breathing, increased pH, and the increase in alveolar oxygen tension that occurs at birth
These factors can increase PVR
Hypoxia, acidosis, hypovolemia, hypoventilation, atelectasis, and cold increase PVR
Fetal circulation can be re-established if these factors occur during the first 2 weeks of life
Hypoxia, hypothermia, or acidosis
Why is hydration important in keeping normal circulation?
Because dehydration would drop the SVR and re-establish fetal circulation
Closure of the ductus arteriosus
Functional closure: within 1-2 days after birth.
–> O2(most important), catecholamines, and PSNS activation all encourage functional closure.
Anatomical closure: In 10-14 days in healthy neonate (up to several months in premature infants) the ductus arteriosus is replaced by connective tissue and is known as the ligamentum arteriosum.
How can we prevent the patient from reverting to fetal circulation?
Keep the patient warm, hydrated, normal PaO2, PaCO2, minimize myocardial depression related to anesthetic agents, maintain SVR*****
Myocardial depression will also cause BP to drop.
A baby’s first breath requires
40-60 cmH2O negative intrathoracic pressure.
Thus, if we have to ventilate, it’s a better idea to do so by intubating than mask ventilating
Surfactant production in the fetus and its importance in the newborn
Surface active material important for normal lung function. By 20 weeks’ gestation it is present within the alveolar lining cells,and by 28-32 weeks gestation, is present within airway lumens. Significant amounts don’t appear in terminal airways until 34-38 weeks gestation, unless SAM production and release stimulated by stress or steroids.
Administration of SAM decreases the incidence of hyaline membrane disease and the incidence of serious cardiopulmonary complications. Giving SAM at birth reduces the inflammatory response to mechanical ventilation and improves lung function.
Stimulation for breathing immediately after birth
. Stimulation of the respiratory centers by mild acidosis, hypercarbia, hypoxia, pain, cold, touch, noise, and clamping of the umbilical cord initiates and sustains rhythmic respiration. Severe acidosis, hypoxia, CNS damage, and maternal drugs (e.g., narcotics, barbiturates, local anesthetics, magnesium, alcohol) depress breathing. A few minutes after birth, the respiratory rate is 30 to 60 bpm - removes the increased CO2 produced by the high oxygen consumption of the neonate (about 6 mL/kg/min) and helps maintain a normal FRC by not allowing sufficient time for the FRC to be expired.
Normal FRC and ABG values are obtained within __ minutes after birth
10-20 minutes
Normal TV and MV are established within __ minutes after birth
5-10 minutes
Immediately after birth, it is normal to see sats in the ____
and PaO2 in the _____
Sats 20s-30s%
PaO2 40s-50s
How do babies establish their FRC?
By not fully exhaling. They breath in more than they exhale. This helps to establish FRC. Also their rapid RR doesn’t allow enough time for full exhalation, resulting in the buildup of FRC.
RBF and GFR in the fetus
Minimal d/t
1) Low SVR
2) High renal vascular resistance
3) Lower permeability of capillaries in the glomerulus
4) The glomeruli present are few and small
GFR will double in the first 2 weeks of life and reaches adult values in 2 years.
At 1 month of age, the kidneys are __% mature
60%
Be careful giving drugs that rely on renal excretion for termination of effect
Is fetal urine output important for removing waste?
No, the placenta does this
Proper laryngoscopy of the newborn
Head neutral- “sniffing” position during bag-&-mask ventilation & intubation. Extension can cause the airway to be very anterior.
Laryngoscope held with thumb and index finger & chin grasped with ring and middle fingers of left hand. This allows the head and hand to become a single unit, reducing the likelihood of lacerations if the neonate moves.
Pressure applied over hyoid bone with small finger of the left hand (moves the larynx posteriorly and exposes the VC).
ETT tip of the tube placed 1- 2 cm below the VC and 1-2 cm above carina.
Remember that babies have STRONG vagal presence. Atropine often given prophylactically before DVL to prevent bradydysrhythmias.
EtCO2 monitoring in neonates
Often difficult because proper readings require large TVs.
The combination of low TVs and low pulmonary blood flow in some infants at birth can make EtCO2 readings inaccurate.
LMA size in neonates
Size 1 for 1- 5 kg
Size 1.5 for 5-10kg
Masking vs. intubating neonates
Masking is rare. Large pressures needed, and can cause insufflation of stomach. Usually place ETT with RSI
When do we extubate neonates?
Awake! This helps avoid laryngospasm.
Awake enough when eyes are open, attempts to cry, and grasps at tube.
If a fiberoptic scope is to be used, the ETT must be AT LEAST this size
3.5
Generic NeonatalVentilator Parameters for Neonates
Vt 10ml/kg
RR 20-25 bpm
PIP ~ 20 cmH2O
PEEP 3-5 cmH20
Fluid distribution of neonates vs. infants and young children
Fetus and neonate ECF ~ 40% TBW; ICF ~20% TBW
Infant & young child ICF ~40% TBW, ECF ~20% TBW
The high ECF means they have large fluid shifts and less buffer against dehydration. The ICF usually serves as a reserve to draw on.
These will increase insensible water loss
radiant warmers and phototherapy (jaundice lights)
These will decrease insensible water loss
heated humidifiers and warm air mattresses preserve body heat and reduce insensible water loss
Why do immature babies have more insensible water losses?
The more physically immature the patient, the higher the skin permeability, the ratio of BSA:weight, and the metabolic demand
Daily fluid requirements for the term neonate in the first few days of birth
day 1, 70 mL/kg/24 hours
day 3, 80 mL/kg/24 hours
day 5, 90 mL/kg/24 hours
day 7, 120 mL/kg/24 hours
Slightly higher for a premature infant d/t even thinner skin, BSA ratio, higher ECF%, etc.
Newborns have a lot of extra ECF when born, and it takes a few days for their kidneys to get rid of it. Therefore, they have a smaller fluid requirement during their first week of life.
ECF is comprised of
Plasma volume and interstitial fluid
Newborns are usually started on this type of fluid
10% glucose. This is continued for several days until glucose values are stable.
Started on either 5% or 10% dextrose solutions
Neonates of diabetic mothers or mothers who were given large amounts of glucose right before delivery may be (more/less) prone to hypoglycemia.
More prone to hypoglycemia.
Why are neonates prone to hypoglycemia? What are some s/s of hypoglycemia in neonates?
Neonates have low stores of hepatic glucose and immature gluconeogenesis mechanisms, so they can develop hypoglycemia with fasting.
Symptoms include apnea, cyanosis, respiratory distress, seizures, high-pitch cry, lethargy, limpness, and sweating.
Neonates and IV fluid requirements during surgery
Maintenance 4:2:1 rule – essentially 4ml/kg/hr
Deficit – 50% 1st hr, 25% 2nd hr, 25% 3rd hr
3rd space – 1-15ml/kg/hr depending on procedure
Glucose containing fluids are controversial
A balanced salt solution (LR) for deficits and third-space losses
D5 in 0.45% NS for maintenance requirement (remember, maintenance fluid always has glucose!)
Use a buretrol filled 25-50ml at a time!
Blood product transfusion in neonates
Newborn major surgery, keep Hgb => 10 g/dl
Severe cardiac or pulmonary disease, keep Hgb= >13 g/dl
We want platelets >50,000
Make sure PRBCs are irradiated in the neonate – 6 mo old to prevent graft vs host disease
When ordering blood products for neonates, we order a certain volume, not a certain number of units
Some reasons why pharmacology is different in neonates
1) Body composition –> Body compartments (fat, muscle, water) change with age. Total-body water content is significantly higher in premature than term infants and in term infants than 2-year-olds. Fat and muscle content increases with age.
2) Protein binding – lower
3) Body temperature– fluctuates more and can influence drugs
4) Distribution of cardiac output – higher % going to brain, heart, and lungs
5) Functional maturity of the heart – impairs ability to compensate
6) Maturation of the blood-brain barrier – immature
7) Relative size/maturity of the liver and kidneys
8) Congenital malformations
9) Pre-maturity, Sepsis, CHF, increased intra-abdominal pressure, controlled ventilation, and poor nutrition
10) Larger Vd, causing delayed excretion
11) Immature hepatic and renal function
12) Neonates have a larger distribution of their cardiac output to vessel-rich tissues. Neonates often require a larger initial dose of medication and then have prolonged elimination times
Concerns regarding anesthetics and development
Concerns for anesthetics influencing development only theoretical and only shown in extreme cases in animal studies
Neonates and their larger Vd
TBW content is significantly ↑ in the neonate
1) H20 soluble drugs have larger Vd (sux); larger initial dose to achieve the desired blood level (e.g., most antibiotics, succinylcholine); delayed excretion occurs as well
2) A drug that depends on redistribution into fat for termination of its action will have a longer clinical effect (e.g., thiopental)
3) A drug that redistributes into muscle may have a longer clinical effect (e.g., fentanyl)
Neonates and a balanced technique
The CV system of a premature infant rarely tolerates the cardiovascular depressant effects of volatile anesthetics. Synthetic narcotics (e.g., fentanyl, sufentanil, alfentanil, remifentanil) are usually well tolerated by even critically ill infants. Must be carefully titrated to response – keeping in mind the possibility of narcotic-induced bradycardia and its consequences on cardiac output. Low concentrations of potent inhaled anesthetics can be used with narcotics to provide a way of controlling hemodynamic responses without significantly depressing the myocardium. The relative merits of one anesthetic technique over another are not clear, and the few studies examining this issue are poorly controlled. Narcotics and inhaled anesthetics suppress the hormonal responses to pain.
Preemies and inhalational agents
POORLY TOLERATED BY PREEMIES! Use with extreme caution, and consider a balanced technique (inhaled + opioid)
Term neonates and inhalational agents
With iso, des, and sevo, will see similar drop in SVR as in adults.
N2O –> does cause myocardial depression, but less than in adults. Remember risk of demyelination!
Why do neonates have a faster uptake of inhalational agent and have increased risk of overdose?
Reasons for faster uptake:
1) The ratio of alveolar ventilation to FRC is 5:1 VS 1.5:1 in adult
2) More cardiac output to vessel rich group of organs (heart and brain)
3) Greater CO/kg in general
4) Infant has a lower blood gas partition coefficient for volatile agents
Rapid rise plus immaturity of the heart places the neonate prone to OD
MAC for anesthetic agents in neonates
Sevoflurane: MAC = 3.3% for neonates- fewer hemodynamic changes compared with iso
Desflurane: MAC = 9.2% for neonates
Isoflurane: MAC = 1.6% for neonates – keep in mind need to decrease muscle relaxants when iso used.
Vagal predominance in neonates
Strong vagal predominance, especially in those < 6 months old.
Bradycardia can follow induction, suctioning, DVL, and succinylcholine, so give atropine to these patients!!**
Vagal predominance can also cause excessive salivation. Clear that shit up with glyco or atropine (10mcg/kg IV)
Infant less than ____g is low birth weight
2500g (2.5kg)
Infants can have breast milk ___ hours before induction
4
Something to remember when taking care of infants and neonates is that they may have undiagnosed
congenital abnormalities
About 15-25% of those with TEF, and 25-30% of those with congenital diaphragmatic hernia also have
associated cardiac defects
Assessment of fluid status in neonates
BP not always reliable assessment tool Anterior fontanelle (sunken?) Skin turgor Tear-less crying Cap refill big toe*** > 5seconds Skin color (pale, mottled, cyanotic?) Mucus membranes Extremity temp (drastically cooler than trunk?)
At a MINIMUM, neonates need these labs
CBC** and glucose**
(Remember they have HgF)
Add other labs indicated by disease processes and surgical procedure
Glucose less than ___mg/dl is considered hypoglycemic in this population and need supplemental glucose
45
It is common for sodium and calcium in neonates to be (high/low/same)
low
Normal coag values in neonates are 10% (longer/shorter) than adults
longer
Monitoring required for the neonate
1) Precordial or esophageal stethoscope
2) NIBP cuff (normal SBP 60-70 mm Hg)
3) ECG (HR normal 120-160 bpm)
4) Temperature probe
5) Pulse oximeter (consider pre and post ductal). Sat is probably 2% less than what’s reading d/t HgF
7) ETCO2
8) Anesthetic concentration analyzer
9) Arterial and central venous catheters if indicated by pt. status or procedure
Basically just ASA monitors with the addition of a precordial or esophageal stethoscope
How can the severity of pulmonary shunt d/t atelectasis or severe pulmonary disease be estimated?
By examining the difference between arterial expired CO2
Children with congenital heart disease are particularly vulnerable to the cardiac depressant effects of
potent inhaled anesthetics
Pulmonary artery flow-directed catheters are rarely indicated in pediatric patients because
Right- and left-sided cardiac pressures are almost identical
However, occasionally, the occurrence of pulmonary artery hypertension or severe multisystem failure may require the use of this monitor
BP cuff shouldn’t be cycled more than every __ minutes
3 minutes
Cycling more than every 3 minutes can cause trauma and venous stasis
Hyperoxia can be damaging to a neonate. Sat goals should be between
93-95%
How can you help sooth infants that are freaking out in the OR?
Give them a rubber nipple or gloved finger to suck on
Why is mask induction especially dangerous in neonates?
Easy to misjudge the depth of anesthesia, combined with high cardiac depression and no IV
A child MUST be kept spontaneously ventilating until
an IV is in place
Do changes made to the concentration of inhaled anesthetics equalize within the circuit faster with circle system or Mapleson D?
Mapleson D because gases are delivered right at the ETT
Benefits of regional blockade in neonates
Reduces dose or eliminates need for opioid, volatile anesthetic & muscle relaxant!
Effect of spinals on blood pressure in neonates
Not too much effect d/t immature SNS. They already have strong vagal tone!
Falling sats after placement of spinal can indicate
High spinal
Caudal Anesthesia, indications, technique, and dosing
For thoracic or abdominal anesthesia (good choice). Can place cont. catheter here, but risk of infection d/t location.
22 G short bevel needle with LOR technique. Penetrate the sacrococcygeal membrane aspirate to check for CSF or blood. Epi added to r/o IV injection look for peaked T waves, increased HR, and ST changes. Use incremental injection as additional safety precaution. Ropivicaine is not officially approved for infant use – however, it demonstrates potential to be superior to bupivicaine because of its more favorable cardiotoxicity profile.
Dosing:
- 0.125%-0.25% Bupivicaine or 0.2% Ropivicaine with 5mcg/ml epinepherine
- Loading dose 0.2-0.25 mg/kg followed 1-2 hrs later by infusion of 0.2mg/kg/hr
Dose of intralipid for LA toxicity in neonates
1.5mL/kg
These neonates are highly prone to post-op apnea
Especially pre-mature, multiple congenital abnormalities, history of apnea and bradycardia, and chronic lung disease.
Most widely accepted guideline is to monitor all infants <50 weeks post-conceptual age for apnea for at least 12 hours post-op regardless of anesthetic technique utilized.
Reasons for post-op apnea may be decreased ventilatory control and a decreased responsiveness to hypercarbia/hypoxia compared with older people. When you add sedatives and anesthetic agents – obviously this gets worse. Also, decreased type I fibers in respiratory muscles = earlier fatigue.
Risks of keeping neonate intubated after surgery
Subglottic trauma, stenosis, and edema
These two CNS stimulants can be used to increase central respiratory drive and lower threshold for response to increased CO2, and increase diaphragmatic contractility, thus preventing post-op apnea
Caffeine and Theophylline
Immediate interventions after the delivery of an unstable newborn
Have a specialized team ready to receive and treat the baby with people specially trained in neonatal resuscitation. Baby goes straight from vag to team rather than vag to chest.
Have two anesthesia providers present. One for airway management and one for lines.
Suction its holes (mouth and nose)
Vigorously dry it (helps to decrease heat loss and stimulate it to breath)
Warm that baby
Put it in slight T-berg (promotes drainage of lung fluid and reduces the likelihood of aspiration of gastric contents)
Apgar at 1 and 5 minutes
Basics of Apgar scoring
Score at 1 and 5 minutes
1 minute = acidosis and survival
5 minute = predictive of neurologic outcome
Looks at 5 predictors: HR, respiratory effort, muscle tone, reflex irritability, and color
What is the primary purpose of apgar scoring?
To ensure that each neonate is closely evaluated during the first few minutes of life.
Cause of excessive pinkness/redness to newborns
Neonates whose skin is entirely pink within 2 minutes of birth may be intoxicated with alcohol or magnesium, or they may be alkalotic (pH >7.50). Rubrous neonates are usually polycythemic.
Meconium
10 – 12% of all deliveries
Amnioinfusion prenatally can decrease severity
Chronic Fetal Hypoxia during the 3rd trimester leads to passage of meconium in utero –> “THICK MEC”**
Meconium will be detected with rupture of membranes
Treatment: Suction oropharynx before ventilation
Intubate and suction trachea of newborn only for thick meconium, mechanical airway obstruction, and/or Apgar <8
Empty the stomach stomach
Basically, thin mec = thoroughly suction
Thick mec = suction with head delivery, and then intubate with head poking out of the vag before the baby is delivered to avoid inhalation of mec into the lungs
Preparing the delivery room for newborn resuscitation
KDC bed/radiant warmer
Suction (w/small ETT compatible catheters), Wall Oxygen with Flow Meter
Infant Facemask, Oral Airways
Pencil Handle Laryngoscope with Blades Size 0 and 00
ETTs 2.5, 3.0, 3.5, 4.0 mm with Stylets
Modified Jackson-Rees vs. Ambu t give PEEP, which is not good because these newborns usually have atelectasis)
Monitoring Equipment
Umbilical Artery Catheterization Tray (allows BP monitoring, blood draws, and fluid resuscitation)
Line Insertion Equipment -bright lights with focal points
Pharmacy (needles, syringes, epi, narcan, bicarb, volume)
Normal SaO2 of neonates is
87-95%
Normal ABG at birth
SaO2 21%, pH 7.24, pCO2 56
Physiologic effects of asphyxia in the newborn
PaO2 < 5 mmHg, causes shift to
Anaerobic Metabolism
Respiratory and Metabolic Acidosis (pH < 7)
Peripheral Vasoconstriction/Core Distribution of C.O. (to heart, brain, and adrenals)
Myocardial depression (d/t acidosis) and failure = bradycardia (HR < 100)
Increased PVR – risk a return to fetal circulation
Increased circulation of endogenous opiates
Increased “stress” hormone release (ACTH, Glucocorticoids, Catecholamines, ANF, Renin, Arginine Vasopressin)
Decreased response to catecholamines
Decreased Insulin secretion
Shift of oxyhemoglobin curve to the right
Early cord clamping results in
Hypovolemia, because the blood that should have been transferred naturally to the fetus is stuck in the placenta
Dose of surfactant
5mL/kg directly into ETT
May cause initial decrease in sats, but then followed by increase in sats and lung compliance
Chest compressions should be started for HR less than
100bpm
Pulmonary resuscitation of the neonate
Intubate immediately – brain damage at 4 min.
Positive-pressure ventilation at 30 - 60 bpm
Every 5th breath should be held 2-3 seconds to expand atelectatic lung and remove lung fluid
PIP <25 cmH2O; PEEP 3-5 cmH2O
Avoid excessive pressures or volumes when ventilating the neonate
Ventilation of the newborn
Breath sounds may be normal despite pneumothrorax or a congenital lung anomaly. This is d/t transmission of sounds waves within the very small chest.
Signs of adequate ventilation = pink color, initiation of rhythmic breathing, normal heart rate, normal blood gas levels
40-60 bpm for bradycardia or inadequate ventilation
Initial breath may need _______ cm H20 pressure
If PaO2 >80 mm Hg (SaO2 > 94%), the FiO2 reduced in 5-10% increments
Goal = PaO2 50-80 mmHg (SaO2 = 87-94%)
Great chart Barash 6th pg 1164
Too much oxygen in newborns can cause
Retinopathies
Circulatory resuscitation of the newborn
Assessment (i.e., skin color, perfusion, cap. refill, pulse volume, MAP –> this is better indicatory of volume than SBP or DBP, urine output, and extremity temp.)
Is volume resuscitation needed?
NO AIR IN THE LINES!!!
To bicarb or not to bicarb? What are potential hazards? Bicarb turns into CO2 (not an issue as long as ventilated), ends up giving the babies a lot of sodium
Glucose? (0.5 – 1.0 mL/kg of D10% followed by infusion and q 5 minute glucose check until stable). Low glucose, like acidosis can decrease cardiac function.
Chest compressions if HR < 100 after 30 seconds of PP ventilation (correct the hypoxia first! Remember that hypoxia can CAUSE bradycardia)
Why is acidosis so bad in the newborn?
pH < 7 can cause severe myocardial depression and heart failure
Issues surrounding giving bicarb
- Sodium bicarbonate is hypertonic, about 1800 mOsm/L. If a large volume of sodium bicarbonate is administered rapidly (>1 mEq/kg/min), the intravascular volume may expand rapidly and cause intracranial hemorrhage.2. The complete reaction of hydrogen ions with 50 mEq of bicarbonate generates approximately 1250 mL of CO2. If ventilation is adequate, the CO2 is quickly exhaled, and the Paco2 rises 1 to 3 mm Hg. If ventilation is inadequate, as it is in asphyxiated neonates, the Paco2 increases significantly, and because the CO2 freely diffuses into cells, it may lead to cardiac arrest. Because it dilates cerebral vessels, Paco2 increases cerebral blood flow and may cause intracranial hemorrhage. To prevent the rise in Paco2, ventilation should be controlled. Sodium bicarbonate should not be infused to correct metabolic acidosis unless ventilation is adequate.3. Administering bicarbonate also may induce hypotension. This occurs because acidotic, hypovolemic neonates have intense peripheral vasoconstriction, which preserves their arterial blood pressure. Correcting the acidosis reduces the PVR and induces hypotension because the neonate’s blood volume is inadequate to fill the expanded vascular space.
Hypervolemia can cause
HTN and ICH (babies have poor cerebral autoregulation)
Volume expansion in neonates
Avoiding transfusions is best practice – If you have a healthy neonate and blood loss is less than 25-30% of circulating blood volume and Hgb does not drop below 8-9g/dl then can usually avoid transfusion.
Whole Blood, PRBC O negative
Placental blood if baby is bleeding out in front of you and need blood right away
NS 10 mL/kg
Plasma 10 mL/kg
Albumin (Barash says AVOID secondary to increased mortality)
Problems with polycythemia in neonates
The hyperviscosity that accompanies polycythemia also increases PVR, reduces pulmonary blood flow, and increases right-to-left shunting of blood through the ductus arteriosus and foramen ovale. Hyperviscosity also increases the systemic vascular resistance
Causes of hypotension in the newborn
Hypovolemia Hypoglycemia Hypocalcemia Hypermagnesemia** Polycythemia (increases R to L shunt)
Issues with pulmonary HTN
PaO2, pH, & nitric oxide levels influence PVR
Hypoxia, acidosis, & inflammation can cause vasoconstriction of pulmonary vasculature= persistent pulmonary HTN
The pulmonary vascular system can be normal or contain excessive smooth muscle in distal airways
In infants with PPH (persistent pulmonary HTN) - a right to left shunt develops via foramen ovale and/or ductus arteriosus
KEY: Don’t let their PaO2 drop!! It will cause a downward spiral of pulm constriction, T to L shunting, etc.
Treatment therapies and goals for pulmonary HTN
Therapy goals:
PaO2 50-70 mmHg
PaCO2 50-55 mmHg
Therapies = surfactant, high frequency ventilation, inhaled nitric oxide, extracorpeal membrane oxygenation (ECMO)
Remember, it’s ok to allow some permissive hypercarbia. Don’t just do things to make your ABG look pretty.
Possible causes of retinopathy of prematurity (ROP), and guidelines to prevent it
Common cause of blindness
Proposed causes:
Hyperoxic vasoconstriction of retinal vessels, induction of vascular endothelial growth factor, & damaged spindle cells by oxygen-free radicals. Abnomal CO2 may also play a part (recent development).
Guidelines for premature infants
- maintain PaO2 at 60-80 mmHg =SaO2 of 90-95% (6th ed. Barash says 96-99% OK)
- min. FiO2 needed to maintain SaO2 of 95% good practice
- Normal ETCO2 may be associated with ↓ ROP
What is a meningiomyelocele?
A sac that contains both meninges & neural components herniates through defect in spinal column. It IS associated with deficits, as opposed to meningocele = no neural component usually no deficits.
Happens at 4th week of gestation. Associated with folic acid deficiency.
Other co-abnormalities associated with meningiomyelocele
Highly associated with Arnold-Chiari II malformation (most will have it)
Cerebellar tonsils herniate into foramen magnum. Only 20% sympomatic
Other associated congenital defects = clubfoot, hydrocephalus (most with meningiomyelocele will develop this. VP shunt often placed with correction), hip dislocation, extrophy of the bladder, prolapsed uterus, Klippel-Feil Syndrome, cardiac defects
Intubation for those with meningiomyelocele
Intubation in lateral position. Or donut can be placed around the sac and intubated supine. Surgery will be prone.
Pre-op considerations for meningiomyelocele
Usually pre-op stabilization period Prevent infection – antibiotics Prone position Cover defect w/warm saline soaked gauze to prevent desiccation Evaluate for and prevent dehydration Identify other congenital defects Replace CSF leakage with normal saline Type and Cross – PRBCs in OR
Anesthesia concerns for meningiomyelocele
(1) special positioning for endotracheal intubation (defect on a “doughnut” and towels under the head), (2) the possibility of underestimating fluid and blood loss from the defect, (3) the high association of this condition with hydrocephalus, (4) the possibility of cranial nerve palsy resulting in inspiratory stridor, and (5) the potential for brain stem herniation. IV access crucial and invasive monitoring; replace all fluid deficits, including loss from the defect (usually with normal saline); and ensure that cross-matched blood is available. Latex allergy precautions should be used with these patients for their first and all subsequent anesthetics
More anesthesia Intra-op concerns for meningiomyelocele
Full latex precautions on all patients (High risk of development of latex allergy in this population related to intense exposure to latex early in childhood with repetitive surgeries and catheterizations)
Induction position – lateral or supine w/donut
Operative position - prone
Inhalational or IV induction appropriate
Succinylcholine OK (without hyperkalemia)
Maintenance with inhaled agents
Avoid NDMR – surgical nerve stimulation common
Give cisatracurium if NDMR needed
Caution with narcotics – abnormal brainstem function (bradycardia and apnea more likely)
Regional Anesthesia ? –> Spinal with tetracaine has been successfully reported
Surgeon may ask for valsalva to detect CSF leak
Post-Op concerns for meningiomyelocele
Monitor carefully, especially if VP shunting did not occur as well (hydrocephalus)
Brain stem involvement (Chiari malformation) = high risk for stridor, apnea, bradycardia, cyanosis, respiratory arrest
Post-op hydrocephalus/increased ICP = lethargy, vomiting, sz, apnea, bradycardia/CV instability. These babies have open sutures/fontanelles, so s/s of high ICP do not manifest until much later***
Post-op intubation for hydrocephalus = RSI d/t N/V associated with IICP
Do TIVA to avoid gas which can increase ICP.
However, the open sutures of the newborn help blunt increases in ICP.
Basics of diaphgragmatic hernia
Herniation of abdominal contents into the chest
Delay/incomplete closure of the diaphragm, or premature return of the gut to the peritoneal cavity restricting normal closure of the diaphragm
Abdominal contents compress developing lung – hinder growth and vascularization – “a spectrum”
–> Pulmonary hypoplasia & pulmonary hypertension
Eventration of the diaphragm (abnormal elevation of the dome of the diaphragm)
Scaphoid abdomen/ barrel shaped chest
Decreased or absent breath sounds and/or bowel sounds on affected side
Cardiac involvement possible (23%)
Should you mask ventilate kids with congenital diaphragmatic hernias?
NO! The stomach may be above the hernia. Insufflation of the stomach can prevent full lung expansion and inhibit cardiac filling as well. Get an NG or OG to decompress the stomach.
Pre-op goals for CDH
After birth = decompress the stomach and intubate immediately - awake intubation without bag and mask ventilation
AVOID excessive airway pressures – PTX will be a disaster in these patients
Permissive hypercarbia – conventional ventilation to prevent iatrogenic lung injury
For these patients, we prefer to wait and optimize the patient before taking them to surgery.
Goals = SaO2 > 85%, PIP <25 cm H2O, PaCO2 45-55 mmHg
Intra-op concerns for CDH
The goal is to adequately ventilate without causing barotrauma
Usually arrive intubated
Need arterial line and adequate IV access – a must!
Carefully watch surgical field to anticipate issues
Expect reactive pulmonary HTN
Keep patient warm (cold babies have a higher O2 demand, and run the risk of worsening pulm HTN
Detect PTX early!! (sudden drop in O2)
Avoid anesthetics that depress heart until the chest is decompressed
Combined Opioid/ Volatile Agent/NDMR for maintenance anesthesia – BLUNT the stress response!
NDMR often needed for closure of the abdomen
No N2O – hinders abdominal closure
For repair of minor defects – regional, post-op extubation possible choices
Type of anesthesia that must be done if patient is on ECMO
TIVA
Two places to place a pre-ductal a-line
Right radial and temporal arteries
Post-op concerns for CDH
ICU- to watch for sudden deterioration
Most remain intubated
Honeymoon period rapid improvement followed by severe hypoxia, hypercarbia and acidosis (often fatal)
Control of pulmonary HTN important – accounts for 25% of post-op deaths
What is an oomphalocele?
External herniation of abdominal viscera through the base of the umbilical cord
The abdominal contents are covered by the amnion (protects from infection and ECF loss)
Associated with 75% incidence of co-existing congenital defects
1/3 pre-term birth
20% cardiac defect
Lung hypoplasia & thoracic deformity possible
30% mortality related to associated cardiac defects and pre-maturity
Highly associated with Beckwith-Wiedemann syndrome which consists of mental retardation, hypoglycemia, heart defects, and large tongue.
What is gastroschisis?
Herniation of abdominal viscera via a 2-5cm defect in the anterior abdominal wall lateral to the normal umbilical cord insertion point
NO Membrane covers defect – higher infection risk and loss of ECF
Rarely associated with other congenital defects***
Higher rate of pre-term birth
Is surgery delayed with gastroschisis?
NO! It is not associated with other abnormalities (other than GI abnormalities), so the patient doesn’t have to be optimized. Also, there is high risk of infection and fluid loss, so surgery should be done to correct right away.
Pre-op considerations for gastroschisis and oomphalocele
Gastroschisis
Lower body placed in sterile clear plastic bag filled with warm saline
Minimize fluid/temperature loss and prevent infection
Often need ventilatory support
IV access important
ABG, serum albumin, & CBC
6-12 ml/kg fluid deficit (replace ¼ of this deficit with protein containing fluid)
OG or NG stomach decompression d/t high risk of aspiration
Assess for associated anomalies – pre-op echocardiogram
Are both of these conditions surgical emergencies????
No, with omphalocele we want to spend a little time diagnosing other anomalies and optimizing the patient. Gastroschisis is an emergency!
Intra-op considerations for oomphalocele and gastroschisis
Pre-oxygenate before awake intubation
Maintenance w/opioids and volatile anesthetics appropriate
Hydration! Replace w/full-strength balanced salt solution using U.O. & peripheral circulation to guide
Omphalocele – when membrane removed large amt of ECF often lost
Art line important for BP, ABG
No N2O
Use air to reduce O2 concentration
NDMR to allow for closure (but too much can mask if the abdominal wall will be too tight once relaxant is reversed). Intragastric pressure of 20mmHg the limit for primary closure.
Size of defect and developmental level of peritoneal cavity determine ability to close
If peritoneal cavity too small - attempted closure can impair circulation to bowel, kidneys, lower extremities and inhibit ventilation – SaO2 on foot helpful to monitor during abdominal wall closure
also if liver blood flow compromised may slow down metabolism of drugs. Tight closure will impair the diaphragm and venous return.
Once the surgeons begin to put the viscera into the abdomen to ventilatory requirements of the neonate can change. Hand ventilation is a good idea at this point to feel the changes in compliance and peak pressures – if the pressure exceeds 40cmH20 – the surgeon should be notified.
Post-op considerations for oomphalocele and gastroschisis
Usually to PICU intubated to allow the abdominal wall to stretch and accommodate viscera.
If defect too large for primary closure - a Dacron silo is incorportated into the abdominal wall to contain and cover the abdominal viscera
Staged repair – every 2-3 days the size of silo reduced (like a toothpaste tube is squeezed) - stretches the peritoneum and skin (consider ketamine 0.5-1.0 mg/kg)
Pt. may remain intubated or extubated
SaO2/artBP/pulse monitoring in the ICU to see how they are tolerating the expanding size of their abdomen
After several silo adjustments patient is taken back to the OR for final closure under GA w/ NDMR
Post-op ventilation for 24-48 hours up to a week following closure (especially w/omphalocele related lung hypoplasia)
Post-op peripheral edema & HTN secondary to kidney compression & renin release
Liver compression can alter post-op drug metabolism
Parenteral nutrition (TPN) improves survival rates
Basics of Tracheoesophageal Fistula (TEF) (esophageal atresia)
Blind upper esophageal pouch w/distal esophagus that forms a fistula with the trachea
Suspected when polyhydramnios present because normal babies will swallow the amniotic fluid
Catheter inserted into esophagus can not be passed into the stomach – confirm w/CXR
Copious oropharyngeal secretions are present
Cyanosis & coughing w/PO feeds
50% w/another congenital defect
15-25% w/associated cardiac defect (PDA)
30-40% born pre-maturely
Is TEF an emergency?
Yes, this is another emergency, but we have time to optimize first.
If pt is aspirating a bunch pre-op we can decompress the stomach with a PEG tube.
Where does the ETT have to end when intubating a neonate with TEF?
Below the level of the fistula. Intubation is done fiberoptically to ensure this.
Pre-op concerns for TEF
Aspiration & dehydration are the primary concerns
Blind upper pouch is decompressed
Head of bed increased
Optimization of fluid, electrolytes, and pulmonary system pre-op
If optimized…. surgery 24-48 hours after birth
Primary repair = extrapleural approach w/ ligation of fistula and anastomosis of 2 ends of esophagus
Operative position – left lateral decubitus
After TEF repair, do we want the baby to be extubated or remain intubated?
Extubated. If the baby is thrashing around, the ETT could damage the repair
Intra-op concerns for TEF
Leave gastrostomy, if present, open to air
Spontaneously breathing intubation (mild sedative or following inhalational induction) VS traditional induction & intubation
Intubation of the fistula must be avoided and ruled out when ventilatory status changes
ETT should be above the carina & below TEF. One way to do this is to right mainstem on purpose and gradually pull out until BS are heard bilaterally.
If adequate hydration – volatile agents for maintenance
N2O best avoided
Caudal anesthesia useful if extubation planned
Miller suggests threading a catheter to thoracic level
Art line – frequent ABGs; precordial left chest
Endoscopic repair – new/challenging…. Need to keep patient spontaneously breathing until fistula ligated
Post-op concerns for TEF
Decreased tracheal cartilage – may require re-intubation d/t tracheal collapse
May need post-op ventilation/ ETT with PEEP secondary to associated defects, pre-existing aspiration pneumonitis, RDS, etc.
Extubation desirable to avoid suture line pressure
Trial of extubation after surgery in those with healthy lungs who have received short acting anesthetics
Basics of pyloric stenosis
Hypertrophy of pyloric smooth muscle w/edema of pyloric mucosa & submucosa
Persistent vomiting w/fluid & electrolyte imbalance
Hyponatremic, hypokalemic, and hypochloremic metabolic alkalosis, with compensatory respiratory acidosis
Same profile as anyone who has been vomiting excessively
Usually start to detect during second week of life
Optimization (fluids and electrolytes) is very important in these patients. Increased M&M if not optimized.
Pre-op optimization for pyloric stenosis patients
Medical NOT surgical emergency We want: Normal skin turgor Na > 130 mEq/L K > 3 mEq/L Cl > 85 mEq/L Urine output 1-2 ml/kg/hr
These kids are high aspiration risk. Pre-op NG/OG usually indicated. Stomach should be suctioned in supine and R and L lateral positions
Intubation is done awake or with RSI
Intra-op concerns for pyloric stenosis
High aspiration risk (full stomach – barium?) – empty the stomach pre-induction
Awake VS RSI anesthesia
Muscle relaxation needed to meet surgical goals while accessing the pylorus (beginning) and while replacing the pylorus in the abdomen (end) cisatracurium is preferred agent
Caudal anesthesia great option (1.25ml/kg of 0.25% ropivicaine with epi)
Extubation after eyes open, reach for ETT, crying
Post-op apnea monitor, pulse oximeter *
