Neonatal Anesthesia

Anesthesie bij de Pasgeborene
Aandachtspunten bij Abdominale Heelkunde
M. Verhaegen
Ochtendkrans 27 mei 2016
Neonatal surgery: Topics
•
•
•
Definitions
Fetal to newborn transition
Physiology of the neonate
– Problems related to anesthesia
•
Anesthesia
– General remarks
– Abdominal (emergency) surgery
Neonatal anesthesia
Definitions
•
•
Neonate: first month of life
Infant: 1 month – 1 year (2 years)
•
Prematurity: < 37 weeks gestation at birth
•
RDS
Symptomatic
IVH
501 - 750 g
80 %
25 %
751 - 1000 g
65 %
12 %
1001 – 1250 g
45 %
8%
25 %
3%
Low birth weight: < 2500 g
• Prematurity
• Intrauterine growth retardation
•
•
Very low birth
weight
Very low birth weight: < 1500 g
1251 - 1500 g
Extremely low birth weight: < 1000 g
Morbidity and mortality are inversely related to birth weight
• Respiratory distress syndrome (RDS): 25 – 80 %
• Symptomatic intraventricular hemorrhage (IVH): 3 – 25 %
• High incidence of sepsis, necrotizing enterocolitis, bronchopulmonary dysplasia
Neonatal anesthesia
Term
Definition
Units of Time
Gestational
age
Time elapsed between the first day of the last
menstrual period and the day of delivery
Completed
weeks
Chronological
age
Time elapsed since birth
Days, weeks,
months, years
Postmenstrual
age
Gestational age + chronological age
Weeks
Corrected
age
Chronological age reduced by the number of weeks
born before 40 weeks of gestation
Weeks, months
Pediatrics 2004; 114 (5)
Morbidity and Mortality
Perioperative morbidity and mortality is higher in neonates than in older children and adults
• Emergent procedures
• Complex pathology
• Neonatal physiology
– Fetal
neonatal transition
– Immature organ systems
•
Neonatal anatomy
– Intubation
•
Neonatal pharmacology
– Narrow margin of safety
– Dosing errors
•
Technical challenges for monitoring and management
– Size matters!
•
Lack of experience
Neonatal anesthesia
FETAL TO NEWBORN TRANSITION
Fetal Anatomy and Physiology
•
Fetal circulation: parallel, shunt-dependent
–
–
–
Ductus venosus
Foramen ovale
Ductus arteriosus
Schematic drawing of the fetal circulation. Red indicates blood
with a high SO2 and blue indicates blood with a low SO2.
Before birth blood from the placenta enters the infant through
the DV and passes into the right atrium. 2/3 of the blood shunts
through the open FO and 1/3 passes through to the right
ventricle and into the pulmonary artery (PA). 90% of the blood
shunts through the DA and only 10% enters the lungs due to
the high PVR.
Van Vonderen et al. Neonatology 2014; 105: 2030 - 242
•
Fetal pulmonary system
–
Fluid filled alveoli
Neonatal anesthesia
Hemodynamic parameters of human fetal pulmonary circulation at term compared with
the 2- to 3-day-old newborn. The fetus is relatively hypoxic with hemoglobin oxygen
saturations (numbers in black circles) of 65, 55, and 45% in the aorta (AO), pulmonary
artery (PA), and pulmonary vein (PV), respectively (98, 108, 331). The fetal pulmonary
circulation is characterized by high vascular resistance (PVR) and low blood flow (499),
due to thick-walled pulmonary arteries (258, 259) and high vasomotor tone (499). Wall
thickness of pulmonary arteries with external diameters of 200 µm in term fetuses
(PAWT, expressed as % of 2 times wall thickness/external diameter) is twice that in the
newborn. High PVR in the fetus prevents the major portion of the cardiac output from
entering the lungs, and blood flow is diverted to other organs via the foramen ovale
(FO) and the ductus arteriosus (DA). After birth, PVR is markedly reduced by increased
vasodilator activity, stimulated in particular by oxygenation and shear stress (499), and
also by a rapid increase in vessel diameter of resistance arteries due to reduced
overlapping of smooth muscle cells and cytoskeletal remodeling (258, 259). The
numbers in black are the percentages of the combined cardiac output of the left and
right ventricles that flow through the pulmonary arteries, FO, and DA. SVC, superior
vena cava; IVC, inferior vena cava. Pulmonary hemodynamic data in the fetus and the
newborn are from studies by Agata et al. (12), Emmanouilides et al. (163), and
Rasanen et al. (481). PAWT data, from pulmonary arteries with 200 µM external
diameter, are from Hislop and Reid (258, 259).
Yuansheng Gao, and J. Usha Raj Physiol Rev 2010;90:1291-1335
Fetal to Newborn Transition
•
Ligation of umbilical cord
– Passive closure of ductus venosus
•
Lungs filling with air
Perfusion of lungs and oxygenation of blood
– Normal tidal ventilation within 10 min
– Normal FRC within 20 min
– Stabilization of blood gases within 1 hr
Barash, Clinical Anesthesia 7th ed.; Chapter 41: 1181
Neonatal anesthesia
Fetal to Newborn Transition
•
Ligation of umbilical cord
– Passive closure of ductus venosus
•
Lungs filling with air
perfusion of lungs and oxygenation of blood
– Normal tidal ventilation within 10 min
– Normal FRC within 20 min
– Stabilization of blood gases within 1 hr
Decrease of pulmonary vascular resistance
Increase of left atrial pressure > right atrial pressure
Neonatal anesthesia
Before birth
Figure 2: Schematic drawing of the fetal circulation. Red indicates
blood with a high SO2 and blue indicates blood with a low SO2.
Before birth blood from the placenta enters the infant through the DV
and passes into the right atrium. 2/3 of the blood shunts through the
open FO and 1/3 passes through to the right ventricle and into the
pulmonary artery (PA). 90% of the blood shunts through the DA and
only 10% enters the lungs due to the high PVR.
After birth
Schematic drawing of the neonatal circulation just after birth. Red
indicates blood with a high SO2 and blue indicates blood with a low
SO2. After birth the umbilicus is clamped and there is loss of 30-50%
of total venous return. Pulmonary resistance decreases due to
aeration of the lungs causing increased pulmonary blood flow through
the pulmonary artery (PA). Blood flow through the DA and FO
becomes bidirectional. Up to 50% of the pulmonary blood flow arises
from the DA through via a left-to-right shunt.
Van Vonderen et al. Neonatology 2014; 105: 2030 - 242
Fetal to Newborn Transition
•
Decrease of pulmonary vascular resistance
– Reversal of flow through ductus arteriosus and functional closure of DA
• Starts to close in the first day of life (PaO2 > 50 mmHg, fall in PGE2)
– Ductus of preterm infant is less responsive to oxygen
• 95 % is functionally closed by day 4, mechanical closed (fibrosis) at 2 – 3 w
– Normalization of PVR within 3 – 4 days
PAPm
Barash, Clinical Anesthesia 7th ed.; Chapter 41: 1182
Neonatal anesthesia
Fetal to Newborn Transition
•
Decrease of pulmonary vascular resistance
– Reversal of flow through ductus arteriosus and functional closure of DA
• Starts to close in the first day of life (PaO2 > 50 mmHg, fall in PG E2)
– Ductus of preterm infant is less responsive to oxygen
• 95 % is closed by day 4
– Normalization of PVR within 3 – 4 days
•
Increase of left atrial pressure > right atrial pressure
– Functional closure of foramen ovale
• Within the first hour of life
• Anatomic closure within the first year of life (probe-patent in 10 – 20 % of adults)
Neonatal anesthesia
Fetal to Newborn
Circulation
Copyright © 2011 John Wiley & Sons, Inc.
All rights reserved.
Fetal to Newborn Transition: Problems
•
Patent ductus arteriosus
– Risk factors: asphyxia and respiratory distress syndrome (RDS)
•
Persistent pulmonary hypertension of the neonate
– Primary
– Secondary to hypoxia, hypercarbia, hypothermia, acidosis, pain, hypo- or hyperglycemia
Constriction of respiratory smooth muscle
• Meconium aspiration, sepsis, pneumonia, RDS, congenital diaphragmatic hernia
• Anesthesia and airway problems (hypoxia, hypercarbia, acidosis)
• Goal: pO2 > 50 mmHg and pCO2 < 60 mmHg
Foramen ovale and ductus arteriosus remain open or reopen
Right-to-left shunting
Profound hypoxemia and right heart failure
– Treatment
• Causal
• Improvement of oxygenation: standard mechanical ventilation, high-frequency ventilation, exogenous surfactant,
inhaled nitric oxide, ECMO
Neonatal anesthesia
Fetal to Newborn Transition: Problems
•
Respiratory distress syndrome
– Decreased surfactant production
•
Surfactant maintains distensibility of alveoli and maintains FRC at exhalation
– Alveolar collapse, decreased lung compliance, hypoxia, increased work of breathing, respiratory failure
– Risk factors: prematurity, maternal diabetes, perinatal asphyxia
– Endotracheal surfactant (Curosurf®)
•
•
•
Treatment of RDS
Prevention of RDS (preterm births)
Improved gas exchange in the absence of RDS (sepsis, heart failure, systemic problems)?
– Long-term risk: evolution to bronchopulmonary dysplasia (BPD)
•
Need for additional O2 at > 28 d of age or > 36 w postconceptional age
Lauer et al., Br J Anaesth, 2012;
109 (suppl 1): i47 – i59
Neonatal anesthesia
Bronchopulmonary Dysplasia
Chronic disease of lung parenchyma and airways
•
•
•
•
•
Mostly infants born at 24 – 28 w of gestation (rarely > 32 w)
Causes: lung irritation and inflammation
– Barotrauma, volutrauma, O2 administration, infection
Airway smooth muscle hyperplasia, peribronchiolar fibrosis, enlarged alveoli, disorganized pulmonary
vasculature
Symptoms: rapid breathing, labored breathing, wheezing, hypoxemia, repeated lung infections, poor growth
Evolution
– Many patients improve with age
– Other patients suffer from pulmonary problems for years
• Reactive airways, recurrent pulmonary infections, prolonged need for O2
– Severe cases: pulmonary hypertension
Neonatal anesthesia
Bronchopulmonary Dysplasia
•
BPD and Anesthesia
– Increased risk of morbidity and mortality
• Bronchospasm, alveolar collapse, rapidly developing hypoxemia
• Cardiac dysfunction
– Preoperatively asses oxygenation, presence of active bronchoconstriction, respiratory infection
– Avoid triggering bronchospasm
• Induction: cardiac depression vs risk of bronchospasm
• No histamine releasing drugs
• Tracheal intubation: appropriately sized ETT (1 intubation!)
– Mechanical ventilation strategy
• Generally: patients with V/P mismatch and compensated respiratory acidosis
• Goals: O2 sat > 90, pH > 7.25 (permissive hypercapnia)
• High respiratory rate: risk of gas trapping
Lauer et al., Br J Anaesth, 2012;
109 (suppl 1): i47 – i59
Neonatal anesthesia
Organ Systems
NEONATAL PHYSIOLOGY
Neonatal Upper and Lower Airways
•
•
•
Obligatory nasal breathing
Greater anatomical dead space in infants than in older children and adults
More compliant pharynx, larynx, trachea and bronchial tree
– Forceful inspiration
•
dynamic airway collapse
Smaller airway diameters
higher resistance
– Luminal blood, secretions, presence of an ETT: increased work of breathing
– Increased risk of airway collapse
• Mechanical ventilation: PEEP
– Airway resistance decreases continuously during the first year of life
Neonatal anesrhesia
Neonatal anesthesia
Neonatal Respiratory System
•
High O2 consumption: 6 - 7 mL/kg/min
–
–
•
Adult: 3 mL/kg/min
High minute volume: increased respiratory rate (x 3 – 4 vs adults)
Static lung volumes
–
Tidal volume (mL/kg) in neonate ≈ child ≈ adult
•
–
High MV by high respiratory rate
FRC in neonate ≈ child ≈ adult
High MV:FRC ratio: 5 to 1 (adult 1.5 to 1)
•
•
Faster induction/emergence with volatile anesthetic
Less O2 reserve and fast desaturation (apnea, hypoventilation)
– High closing volume (> FRC)
•
•
•
Normal tidal ventilation
terminal airway closure
From Benumof JL, et al. Anesthesiology 1997; 87:979–982
Infants maintain and dynamically increase FRC by
– Self-recruitment maneuver (postinspiratory activity of intercostal and diaphragmatic muscles)
– Auto-PEEP (high respiratory rates with short expiration times)
– Functional PEEP (laryngeal adduction in expiration increased airway resistance)
Anesthesia and mechanical ventilation: PEEP (laparoscopy!)
Neonatal anesrhesia
Neonatal anesthesia
Barash, Clinical Anesthesia 7th ed.; Chapter 41: 1181-1182
Neonatal Respiratory System
•
Respiratory system compliance
– Lung compliance is relatively low
– Chest wall compliance is higher than in older children
• Pliable rib cage with chest retraction
Functional airway closure
Less efficient gas exchange
Increased work of breathing
•
Diaphragmatic breathing pattern
– Intercostal muscles are poorly developed at birth
– Neonatal diaphragm: less type 1 fibers
• Type1: slow twitch, high-oxidative, sustained contractions, very little fatigue
– 25 % in the neonate vs 55 % in mature diaphragm (2 y)
– 10 % in the premature newborn
• Type 2: fast twitch, low-oxidative, quick contractions, fatigue easily
Risk of diaphragmatic fatigue in the presence of resistance to ventilation
Miller’s Anesthesia, 8th ed,
(Data from Keens et al: J Appl Physiol 44:909-913, 1978.)
Neonatal anesrhesia
Neonatal anesthesia
Neonatal Respiratory System
•
Control of breathing: less stimulated by hypoxia and hypercapnia
– Paradoxical response to hypoxia: hyperventilation (1 - 2 min) followed by hypoventilation/apnea
• Term infants: 1st week of life
• Preterm infants: 2 - 3 weeks
Neonatal anesrhesia
Neonatal anesthesia
Neonatal Apnea
•
•
Apnea > 20 s, or apnea < 20 s with oxygen desaturation and/or bradycardia
Apnea of prematurity (< 37 w gestation), apnea of infancy (onset at > 37 w gestational age)
– Incidence is inversely proportional to gestational age
• Gestational age < 28 w: almost 100 % incidence
– Rare in healthy term infants
•
Immature ventilation control processes
• Brainstem respiratory rythmogenesis
• Peripheral and central chemoreceptor responses
•
Differentiate from periodic breathing
– Cycles of breathing and respiratory pauses of 5 – 10 s (= common)
•
•
Central, obstructive, mixed
Increased risk of postoperative apnea
Neonatal anesrhesia
Neonatal anesthesia
Neonatal Postoperative Apnea
•
•
Pause in breathing for more than 20 s (15 s), or more than 10 s if associated with oxygen
saturation less than 80 % or bradycardia (20 % decrease in heart rate)
Reported incidences vary widely: 5 – 49 %
– Incidence is highest 4 – 6 hrs postoperatively (up to 12 hrs)
– Most apneas occur in the PACU but it can occur hours later
•
Mechanisms
– Immature brainstem respiratory control mechanism
– Decreased responsiveness to hypoxia and hypercarbia
Increased sensitivity to respiratory depressant effects of anesthetics, sedatives and analgesics
– Exaggerated inhibitory response to afferent laryngeal stimulation or to exessive inflation of the lungs
– Increased work of breathing, respiratory muscle fatigue
Neonatal anesthesia
Neonatal Postoperative Apnea
•
Risk factors for postoperative apnea regardless of anesthetic technique
– Decreasing gestational and postconceptional age
• No uniform guidelines on postoperative monitoring
– History of apnea
• Postoperative apnea can occur without a history of apnea
– Anemia (hematocrit < 30 %)
– Co-existing disease
• Multiple congenital anomalies
• Chronic lung disease
– Hypothermia
Neonatal anesthesia
Predicted probability of apnea for all children by gestational age and weeks postconceptual age. Children with anemia are shown as the horizontal solid black line.
Bottom marks indicate the number of data points by postconceptual age. The risk for apnea diminishes in infants born at a later gestational age. The shaded boxes
represent the overall rates of apnea for infants within that gestational age range. The probability of apnea was the same, regardless of postconceptual age or
gestational age, for infants with anemia (horizontal solid black line).
Miller’s Anesthesia 8th ed., Chapter 93: Pediatric Anesthesia, from Coté CJ, Zaslavsky A, Downes JJ, et al: Postoperative apnea in former preterm infants after inguinal herniorrhaphy.
A combined analysis, Anesthesiology 82:809-802, 1995.
Neonatal Postoperative Apnea
• CNS stimulants
– Caffeine base (10 mg/kg iv)
– Theophylline (higher risk of toxicity) (6 mg/kg iv)
• Spinal vs general anesthesia?
– Limited data (inguinal herniorrhaphy)
• Small studies
• Variability in defining and identifying apnea
• Different general anesthetics
– Regional (spinal, epidural, caudal) versus general anesthesia in preterm infants undergoing inguinal
herniorrhaphy in early infancy (Review).
Jones et al., Cochrane Database of Systematic Reviews 2015, Issue 6
– Davidson et al, Anesthesiology 2015; 123: 38 – 54 (GAS study)
Neonatal anesthesia
Neonatal Postoperative Apnea
Regional (spinal, epidural, caudal) versus general anesthesia in preterm infants undergoing
inguinal herniorrhaphy in early infancy (Review).
Jones et al., Cochrane Database of Systematic Reviews 2015, Issue 6
There is no statistically significant difference in the risk of postoperative apnea/bradycardia,
postoperative oxygen desaturation, the use of postoperative analgesics or postoperative
respiratory support between infants receiving spinal or general anesthesia.
– 7 small trials
– Subgroup analysis
•
•
Spinal anesthesia without sedation: reduced risk for postoperative apnea
No history of preoperative apnea: reduced risk of postoperative apnea with spinal anesthesia
– High RA failure rate
Neonatal anesthesia
Neonatal Postoperative Apnea
Apnea after awake regional and general anesthesia in infants.
The General Anesthesia Compared to Spinal Anesthesia Study—Comparing Apnea and Neurodevelopmental
Outcomes, a Randomized Controlled Trial
Davidson et al, Anesthesiology 2015; 123: 38 – 54 (GAS study)
– Postmenstrual age ≤ 60 w, gestational age ≥ 26 w
– RA: variety of techniques, GA: inhalation anesthetic, no opioids, nerve block
– Incidence of apnea
RA (n=355)
GA (n=356)
P
Overall
3%
4%
0.21
Early (0 – 30 min)
1%
3%
0.04
Late (30 min – 12 hrs)
2%
2%
0.77
– Strongest predictor of apnea: prematurity
• 96 % of patients with apnea were premature
– RA + GA or sedation: no increase in apnea
• 19 % in RA group: sevoflurane or sedation
– Anemia: no risk factor for apnea
Neonatal anesthesia
From: Apnea after Awake Regional and General Anesthesia in Infants:The General Anesthesia Compared to Spinal
Anesthesia Study—Comparing Apnea and Neurodevelopmental Outcomes, a Randomized Controlled Trial
Anesthesiology. 2015;123(1):38-54.
Figure Legend:
Time to apnoea events in RA and GA. Times of all apnoea events in all infants in RA and GA allocated groups with RA group further
divided into those with no sedation or sevoflurane (closed circles) and those exposed to sevoflurane or sedation (closed squares).
Each horizontal dashed line represents one infant. GA = general anesthesia; RA = regional anesthesia.
Copyright © 2016 American Society of Anesthesiologists. All rights reserved.
Neonatal Oxygen Toxicity
•
Immature antioxidative systems
– Preterm > term infants
•
High FiO2 in premature infants
– Retinopathy
– Contribute to development of BPD
– Absorption of O2
atelectasis and FRC decrease
•
Preductal target SaO2: 90 – 95 %
– SaO2 85 – 89 %: reduced survival and increased risk of NEC in infants up to 36 w PCA
Neonatal anesthesia
Neonatal Mechanical Ventilation
•
Avoid O2 toxicity
–
–
•
Avoid volutrauma
avoid excessively high VT
Avoid barotrauama
use minimal PIP
Avaid atelectotrauma
start PEEP 4 – 6 cm H2O, increase if necessary
Normocapnia, permissive hypercapnia
–
–
–
•
•
•
Goal: SaO2 90 – 95 %
Constant SaO2
Strategies to avoid ventilator induced lung injury and BPD.
–
–
–
•
FiO2 as low as possible to
PaCO2 35 – 55 mmHg, pH > 7.25
Avoid hypocapnia (periventricular leucomalacia)
Increased risk of IVH (preterm infants, first 4 d of life): PaCO2 < 35 mmHg, PaCO2 > 60 mmHg, great PaCO2 fluctuations
I:E = 1:1
40 – 60 breaths/min
Recruitment maneuvers
Neonatal anesthesia
Neonatal Cardiovascular System
•
Immature myocardium
– Decreased contractility
• Fewer and less organized myofibril elements: 50 % of contractile tissue compared to adults
• Undeveloped sarcoplasmatic reticulum system and decreased Ca2+ - ATP activity
Highly dependent on ionized plasma calcium
– Reduced compliance
Small, fixed SV (1 – 2 mL/kg)
•
Parasympathetic > sympathetic influence
– Risk of bradycardia
– Inadequate response to hypovolemia
– Inadequate response to inotropics
•
Immature baroreceptor response
– Limited ability to compensate for hypotension
– Anesthesia depresses baroreceptor reflex more than in adults
Neonatal anesthesia
Neonatal Cardiovascular System
Neonatal cardiac output depends mainly on heart rate
– Resting cardiac output is high in the neonate
– Resting cardiac output is close to maximal cardiac output
•
•
Adult: 300 % increase is possible
Neonate: 30 – 40 % increase
Barash, Clinical Anesthesia 7th ed. Fig 41-2. From: Friedman and George, J Pediatr 1985; 106: 700
Neonatal anesthesia
Neonatal Cardiovascular System
Neonatal cardiac output depends mainly on heart rate
Neonatal myocardium is very susceptible to myocardial depression by volatile anesthetics
The neonate does not tolerate hypovolemia or hypervolemia
The neonatal heart does not respond well to increasing preload or high afterload
Neonatal anesthesia
Neonatal Neurological System
•
Immature cerebral blood vessels
–
–
–
–
Risk of intraventricular hemorrhage (IVH)
First 72 h of life
Premature babies
Blood pressure fluctuations, hypoxia, hypercarbia, low or high hemoglobin, pain
Anesthesia: no increased risk?
• Awake intubation in the past
•
Determinants of cerebral blood flow: arterial CO2 and arterial O2
– Important interindividual variability in cerebral blood vessel reactivity
– Absent under certain circumstances
Neonatal anesthesia
Neonatal Neurological System
•
Cerebral blood flow: autoregulation
– Cerebral autoregulation is present in healthy neonates
• MAP 40 – 80 mmHg?
– Lost cerebral autoregulation
• Sick neonates (e.g. sepsis)
• Effect of anesthetics?
• Blood pressure range ensuring adequate cerebral perfusion in the neonate is unknown
– Role for NIRS?
•
Anesthesia and neurotoxicity?
– Concerns about long-term consequences
– Currently there is no evidence to support a change of practice
Neonatal anesthesia
Neonatal Hepatic System
•
Immature metabolic liver functions
– In utero: drug elimination by maternal circulation and metabolism
– Most enzyme system are present but have not been induced
– Different hepatic metabolic pathways mature at different rates
• Some pathways achieve maturity only at 1 year of age
Prolonged elimination half-life of some drugs
•
Immature synthetic liver function
– Low levels of albumin and other protein
• Greater levels of free drugs: e.g. synthetic opioids, local anesthetics
– Need for exogenous vitamin K
– Reduced glycogenesis and risk of hypoglycemia
Neonatal anesthesia
Neonatal Renal System
•
Fetal kidney: passive
– Fetal waste is removed by maternal placenta
– Low renal blood flow (RBF)
• In utero: 3 % of cardiac output (adults: 25 %)
– Low glomerular filtration rate (GFR)
•
Renal changes at birth
– GFR: Low at birth but almost doubles in the first 2 weeks
• Newborn: limited ability to concentrate or dilute urine
– Improves during the first 3 – 4 days
• 1 month: kdineys are 60 % mature
• Adult levels only at 2 years of age
Miller’s Anesthesia, 8th ed,
(Data from McCrory WW: Developmental nephrology,
Cambridge, Mass, 1972, Harvard University Press.)
– RBF: progressive increase (increased systemic arterial pressure, decreased renal vascular resistance)
– Diuresis
• First 24 hrs: low (< 1 mL/kg/hr)
• > 1 d: postnatal diuresis (2 – 3 mL/kg/hr of dilute urine)
Neonatal anesthesia
Neonatal Renal System
•
Neonatal renal function and anesthesia
– Medication excreted via the kidneys: prolonged half-life
– Neonates < 1 week of age
• Limlited ability to conserve water
Do not tolerate fluid restriction / deficit
• Inability to excrete large amounts of water
Do not tolerate fluid overload
• Newborn kidney: better able to conserve than to excrete sodium
Neonatal anesthesia
Neonatal Body Fluid Compartments
•
Total body water (TBW) varies by age and gestational status
Gestational age
(weeks)
Body weight (BW)
(g)
Total body water
(% BW)
ECF volume
(% BW)
23 – 27
500 – 1000
85 – 90
60 – 70
28 – 32
1000 – 2000
82 – 85
50 – 60
36 - 40
> 2500
71 - 76
~ 40
O’Brien and Walker, Ped Anesth 2014; 24: 49 - 59
– Term newborn: TBW ≈ 75 % of BW, first year of life: progressive decrease to 60 – 65 % of BW
•
Intracellular Fluid (ICF) / Extracellular Fluid (ECF) distribution
– Newborn: ECF 40 - 45 % of body weight, ICF 30 - 35 % of body weight
• Infants, children, adults: ECF 20 % of BW, ICF 40 % of BW
• Neonate cannot maintain intravascular volume during fasting, diarrhea, fever, other causes of abnormal fluid loss
– ECF/ICF approach adult values at 1 year of age
Neonatal anesthesia
Friis-Hansen, Acta Paediatrica 1983; 72 (s305)
Neonatal Body Fluid Compartments
•
Intracellular Fluid (ICF) / Extracellular Fluid (ECF) distribution
– Postnatal diuresis
ECF decrease
• Pulmonary vascular resistance decrease, pulmonary venous return increase, atrial natriuretic peptide release
• Healthy newborns lose 5 -10 % of body weight during the first week of life
• Excessive fluid (and sodium) administration has an adverse effect on outcome
– Increased risk of patent ductus arteriosus and NEC
– Possibly increased risk of BPD, IVH and mortality
– Cell growth
•
ICF increase
Plasma volume in infants and children ≈ 5 % of BW (≈ 50 mL/kg)
– Preterms ≈ 10 % of BW
•
Blood volume in the newborn (full-term, hematocrit = 45 %) ≈ 8 % of BW (≈ 80 mL/kg)
– Preterm: 90 – 100 mL/kg
Neonatal anesthesia
Neonatal Thermoregulation
•
Non-shivering thermogenesis from brown adipose tissue (BAT)
– Only neonatal mechanism to preserve body heat
• Impaired shivering
• No effective vasoconstriction
– Neonatal BAT: 5 % of body weight
• Neck, axillae, back, mediastinum, around kidneys
• Extensive vascularisation, high mitochondrial content
Neonatal anesthesia
Neonatal Thermoregulation
•
Non-shivering thermogenesis from brown adipose tissue (BAT)
– Only neonatal mechanism to preserve body heat
– Impaired by anesthesia
– Negative effects
• Metabolic acidosis
• Osmotic diuresis
• Diversion of cardiac output to BAT
Thermoreceptor stimulation (skin)
Hypothalamic stimulation
Norepinephrine release
Brown fat: Lipolysis
FFA
Expression of uncoupling protein 1
Uncouples respiration from ATP production
Increased O2 consumption
Production of ketone bodies
Heat
production
Neonatal anesthesia
Neonate and Hypothermia
•
High risk of developing hypothermia
– Inadequate shivering mechanism
– High body surface area / weight
• Term infants: 3 x adult ratio
– Thin skin
– Low body fat
•
Adverse effects
–
–
–
–
Pulmonary hypertension
Delayed drug metabolism
Hyperglycemia
Apnea
Measures to maintain normothermia are absolutely necessary
Neonatal anesthesia
NEONATAL ANESTHESIA
Neonatal anesrhesia
Neonatal Anesthesia: General Attention Points
•
Thermoneutral environment
– Warm room
– Warming devices
•
•
No sedative premedication
Atropine before induction
– Dominance of parasympathic nervous system
•
bradycardia
Blood (products)?
– Normal neonatal hemoglobin: 15 – 18 g/dL
•
Drugs: careful dosage calculation and dilution
– IV drug administration: clear all air from syringes, needles, IV tubing, stop cocks (paradoxal air emboli)
Neonatal anesthesia
Neonatal Anesthesia: General Attention Points
•
Monitoring and installation
– Pulse oximetry
• Preductal O2 saturation may be different from postductal saturation
• Fetal hemoglobin: left shifting of oxyhemoglobin dissociation curve
– Pulse oximetry does not compensate for left shift
≈ 2 % higher than arterial blood O2 saturation
ODC (continuous line) and factors that influence its shape
Sotirios Fouzas et al. Pediatrics 2011;128:740-752
Neonatal anesthesia
Neonatal Anesthesia: General Attention Points
•
Monitoring and installation
– Capnometry: accuracy?
– Invasive blood pressure monitoring?
• Surgical procedure, status of the neonate
• Advantages
– Accurate blood pressure monitoring
– Blood sampling
Ventilation adjustment
– Central venous catheter?
• Surgical procedure, status of the neonate
• Advantages
– Good IV access
– Blood sampling
– Vasoactive drugs
– TPN
Neonatal anesthesia
Neonatal Airway
Differences with adult airway
•
Preferential nasal breathing
–
•
•
Large tongue
smaller pharyngeal space
Epiglottis easily obscures view of the vocal cords
–
•
Large, floppy, U-shaped
Premature neonate: C3
Adult: C5 - C6
Funnel shaped larynx and trachea
Vocal cords slant anteriorly
Narrowest part at cricoid cartilage
–
–
•
Barash, Clinical Anesthesia 7th ed,
(Modified from: Smith RM. Anesthesia for Infants andChildren, 4th ed.)
Larynx at level of C3 – C4 and more anterior
–
–
•
•
•
Small nares
Adults: glottis
Until age 5
Trachea is less rigid
Barash, Clinical Anesthesia 7th ed,
(from: Ryan JF, Coté CJ, Todres ID, eds. A Practice of Anesthesia for
Infants and Children, 2nd ed.)
Neonatal anesthesia
Neonate: Intubation
•
Positioning may be difficult
– Large occiput
•
Obstruction of the upper airway
– Too much flexion due to large occiput
– Large tongue
•
Laryngoscopy and visualization of the vocal
cords may be more challenging
–
–
–
–
•
Large tongue
Large, floppy, U-shaped epiglottis
Larynx at level of C3 – C4 and more anterior
Anterior-slanting vocal cords
Passage of endotracheal tube may be more difficult
– Narrow funnel-shaped trachea with narrow cricoid ring
– Anterior slanting vocal cords
Neonatal anesthesia
Neonatal Fluid Management during Surgery
Not sufficiently studied
• Volume: inadequate or excessive fluid volume
poor outcomes
– First day of life: low diuresis, problems with handling fluid load
• High levels of vasopressin at time of birth
– High insensible losses
– Immature kidney: limited concentration capacity
• Risk of hypovolemia
– Controlled administration of IV fluids
mL/kg/24 hr
Day 0
60
Day 1
80
Day 2
100
Day 3 - 30
120 - 150
• Infusion pump
• Syringe bolus
Neonatal anesthesia
Neonatal Fluid Management during Surgery
•
Maintenance fluid: glucose-containing fluid
– Risk of hypoglycemia
• Insufficient glycogen stores
• Risk factors: diabetic mothers, premature babies, small for gestational age, post-resuscitation
• Continue maintenance glucose-containing fluid intraoperatively
– Hypoglycemia threshold?
• Glycemia < 30 mg/dL first 24 hrs, < 45 mg/dL first 3 days of life, 60 mg/dL thereafter
• Neonates seem to tolerate hyperglycemia better than adults in ischemic injury
– Metabolization of ketones
– Hypotonic fluids: risk of hyponatremia and cerebral edema
• Controlled administration (syringe pump)
•
Replacement fluids: balanced electrolyte solution
– First 24 – 48 hrs: newborn has difficulty handling sodium load
– Inadequate sodium intake: hyponatremia
• Poor long-term neurological outcome in preterm babies
• Monitoring plasma sodium
Neonatal anesthesia
NEONATAL GASTROINTESTINAL
EMERGENCIES
Neonatal Gastrointestinal Emergencies
•
First day(s) of life
– Abdominal wall abnormalities
• Gastroschisis
• Omphalocoele
– GI (sub)obstruction
•
•
•
•
•
Duodenal or jejunal atresia
Meconium ileus, meconium peritonitis, meconium plug
Intestinal malrotation
Imperforate anus
First month of life
– Necrotizing enterocolitis (NEC)
– Pyloric stenosis
– Inguinal hernia
Neonatal anesrhesia
Neonatal anesthesia
Neonatal Gastrointestinal Emergencies
•
•
•
•
•
≈ 1/1500 life births
Prematurity
Associated pathology
Nasogastric tube prior to induction
Rapid sequence induction?
– Modified
•
•
Avoid N2O
Postoperative ventilation may be indicated
Neonatal anesthesia
Neonatal Abdominal Wall Abnormalities:
Omphalocele and Gastroschisis
•
Omphalocele
– Covered (amnion) abdominal wall defect
– Frequently associated with other anomalies
• Congential heart lesions (20 %)
• Beckwith – Wiedemann syndrome (mental retardation,
congenital heart disease, large tongue, hyperviscosity,
omphalocele
Cardiac and neurological evaluation
•
hypoglycemia,
Gastroschisis
– Uncovered abdominal viscera
– Full thickness abdominal wall defect due to interruption
of omphalomesenteric artery ( abdominal wall
ischemia and atrophy)
Neonatal anesthesia
Neonatal Abdominal Wall Abnormalities:
Omphalocele and Gastroschisis
•
Problems
–
–
–
–
•
Severe dehydration
Significant heat loss and hypothermia
Prematurity
Other congenital defects
Antenatal diagnosis
– High levels of maternal serum α-fetoprotein (AFP)
– Ultrasonography
Neonatal anesthesia
Neonatal Abdominal Wall Abnormalities:
Omphalocele and Gastroschisis
•
Treatment: surgical closure
– Small defect: primary closure
• Intragastric pressure monitoring? (≤ 20 mmHg?)
– Moderate to large defect: staged closure (silo)
Neonatal anesthesia
Neonatal Abdominal Wall Abnormalities:
Omphalocele and Gastroschisis
•
Anesthesia: attention points
–
–
–
–
Arrive generally intubated and ventilated
Major insensible fluid loss
Muscle relaxation is absolutely necessary
Preservation of visceral blood flow
• Additional pulse oxymeter on foot
– Postoperative ventilation
Neonatal anesthesia
Neonatal Bowel Obstruction
•
Upper GI tract obstruction:
– Rare in the newborn (congenital web)
– Persistent vomiting
• Fluid and electrolyte disturbances
– Stomach: 100 – 130 mEq/L sodium, 5 – 10 mEq/L potassium
• Aspiration of gastric contents
•
Lower GI tract obstruction
– Imperforate anus, anal atresia, duodenal atresia, jejunoileal atresia, intussusception, malrotation,
volvulus, choledochal cyst, meconium ileus
– Problems develop within 1 – 7 d after birth
• Fluid and electrolyte disturbances
– Sequestration of fluid in the GI tract
– Vomiting
• Increased intraabdominal pressure
– Respiratory problems
Neonatal anesthesia
Neonatal Bowel Obstruction
•
Intestinal atresia
– Duodenal atresia
• Shortly after birth: bilious vomiting without abdominal distension
• Associated pathology
– Annular pancreas, vertebral defects, congenital cardiac lesions, esophageal atresia
– Up to 60 % trisomy 21
– Jejunal/ileal atresia
• Bilious vomiting with abdominal distention/ileus
• Associated with cystic fibrosis, Hirschprung’s disease
•
Meconium ileus
– Medical treatment is first attempted
– Association with cystic fibrosis
Neonatal anesthesia
Neonatal Bowel Obstruction
•
Bowel malrotation/midgut volvulus
– Diagnosis is easily missed at birth
– Risk of bowel ischemia, bowel perforation, sepsis
– True surgical emergency
• Derotation: vasoactive mediator release, acidosis, hypotension
Neonatal anesthesia
Necrotizing Enterocolitis
•
Affects primarily premature infants
–
•
•
•
Multifactorial pathophysiology
Bowel ischemia, necrosis, perforation, peritonitis, and sepsis
Critically ill infants
resuscitation
–
•
•
Abdominal distention, acidosis, coagulopathy and bleeding, hemodynamic instability, hyperkalemia
Conservative management is often attempted
Surgery: decompressive laparotomy +/- bowel resection and ileostomy
–
–
–
–
•
Very low birth weight: 5 – 15 %
Inotropic support is often necessary
Major fluid losses
• Balanced electolytes
• RBCs, FFP, platelets
Arterial and central venous line
Postoperative intubation and ventilation
Poor outcome
–
Weight < 1500 g: 25 – 50 % mortality
Neonatal anesthesia
Pyloric Stenosis
•
Pyloric hypertrophy, progressive obstruction, persistent projectile vomiting
–
–
–
–
•
2 - 3/1000 live births
Usually 4 – 6 weeks of age (possible at 2 w of age)
Male > female
Early diagnosis: clinical signs and symptoms
ultrasound
Dehydration, electrolyte disturbances, acid-base disturbances
– Hypochloremic metabolic alkalosis (+ compensatory respiratory acidosis)
– Hyponatremia, hypokalemia
Correction before surgery
•
•
Surgery: open or laparoscopic extramucosal pyloromyotomy
Gastric tube and evacuation of the stomach before induction
– Gastric content: significant volume
– Aspiration in supine, right and left lateral decubitus position
•
Minimal postoperative discomfort
Neonatal anesthesia
Neonatal Inguinal Hernia
•
•
Emergency: incarcerated inguinal hernia
Preterm infants: semi-elective surgery
– 20 – 30 % incidence
– High risk of incarceration
• Elective repair prior to discharge
– Infants with RDS
Residual chronic lung disease: BPD
• Hypoxemia
• Reactive airways and increased risk of bronchospasm
• Parenchymal damage
– Postoperative apnea risk
• Caffeine 10 mg/kg IV
• Guidelines for postoperative monitoring: no consensus
– General (+ caudal) or spinal anesthesia?
Neonatal anesthesia