PEDS Flashcards

1
Q

The oxyhemoglobin dissociation curve of the newborn is shifted to the left or the right? Why?

A

Left. Fetal Hgb does not bind with 2,3 DPG. Thus, the newborn’s oxyhe- moglobin dissociation curve will be shifted to the left. This gives the fetus the advantage ofloading more oxygen at low fetal oxygen partial pres- sures (fetal arterial PCh of20-30 mmHg). [Ped. Anesthesia, George Greg- ory, M.D., Vol!, p52j

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2
Q

What happens to the oxyhemoglobin disso- ciation curve during the first few months of life1 Why?

A

The oxyhemoglobin dissociation curve shifts right. As fetal Hgb is re- placed by adult Hgb (at 3-4 months of age, infants have increased levels of2,3 DPG as compared to adults), the infants l\0 increases (the curve shifts right) to approximate that of the adult, enhancing 0 2 delivery. [Gregory, Ped. Anesthesia, Vol!, p52]

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3
Q

An infant is considered premature if born before what gestational age and has what weight? In what five ways is the premature infant different from the full-term neonate?

A

Prematurity is defined as less than 38 weeks gestation and less than 2500 gm at birth. As compared to the term infant, the premature infant is less able to: (1) suck, (2) maintain body temperature, (3) swallow, (4) eat, and (5) sustain ventilation. [Gregory, Ped. Anes., pp30-31]

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4
Q

At what conceptual age is surfactant devel- oped?

A

Surfactant appears initially between 23 and 24 weeks gestational age and increases in concentration during the last 10 weeks of gestational life. [Miller, Anesthesia, 1994, p2451]

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5
Q

What pressure is needed to open airways at birth?

A

Inspiratory pressures more negative than 25-40 mm Hg are required to overcome the surface tension when opening the alveoli for the first time. [Guyton, TMP, 1996, pp1049-1050; Barash, Clinical Anesthesia, 1997, pl082]

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6
Q

Identify the two limitations of kidney func- tion in the newborn. What is the significance of these limitations?

A

GFR at birth is 15-30% of the normal adult on a weight basis, and the ability to concentrate the urine is diminished. Hence, infants do not toler- ate large volumes of water and salts because oflow GD\ and decreased tubular concentrating ability. [Davison, Eckhardt, and Perese, Mass Gen- eral, 1993, p387]

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7
Q

When do liver enzymes become completely functional in the neonate?

A

During the first week oflife the liver functions poorly and is incapable of conjugating significant quantities of bilirubin with glucuronic acid. Re- duced quantities of blood clotting factors are also synthesized. The cyto- chrome P450 enzyme system isfully functional at one month ofage. Sum- mary: Liver metabolism is decreased in the neonate until one month of age.[Guyton, TMP, 1996, ppl052-1053; Morgan and Mikhail, Clinical Anesthesiology, 1996, p730]

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8
Q

Where does the spinal cord end in the neo- nate?

A

The spinal cord of the newborn ends at the lower border of L3. [Ellis & feldman, Anatomyfor Anaesthetists. 8e. 2004 pp126]

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9
Q

What are the angles of the left and right bronchi in a child less than three years of age?

A

Left, 55 degrees. Right, 25 to 70 degrees. [Smith, Anes. for Infants and Children, p12, Adriani and Griggs]

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10
Q

Why is subglottic stenosis potentially more severe in the pediatric patient than in the adult?

A

The pediatric airway has a relatively small cross-sectional area in a nor- mal pediatric patient. With the presence of a subglottic stenosis, which may be congenital or acquired, even a small amount of swelling can rapid- ly occlude the opening. [Rasch and Webster, Clinical Manual of Ped. Anes., 1994, p19; Steward, Manual ofPed. Anes., 1995, p246; Authors]

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11
Q

What factors contribute to the decreased functional residual capacity (FRC) in the neonate and infant during general anesthe- sia?

A

The chest wall in infants is less rigid (more compliant) because ribs are cartilaginous and not bony. In addition, the boxlike configuration of an infant’s thorax permits less elastic recoil than the dorsoventrally flattened thoracic cage of the adult does. Additionally, an infant is more vulnerable to muscle fatigue, which may further decrease the stability of the chest wall. As a result of all these factors, an infant’s chest wall is extremely compliant. The net effect of the compliant chest wall and the poorly com- pliant lungs is a reduced functional residual capacity (FRC). [Miller, Anesthesia. 6e. 2005 pp2842; Davis & Motoyama, Smith’s Anes. for In- fants and Children. 7e. 2006 pp34; Cote, PA1C. 3e. 2001 pp13]

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12
Q

In newborns, the closing capacity is higher than FRC. What does this mean?

A

Some airways close during the expiratory phase of normal tidal breathing. [Barash, Clinical Anesthesia, 1997, pp1095-1097]

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13
Q

How is the in children calculat- ed? What is the dead-space of a 30 kg child?

A

Dead-space is 2.0-2.5 mL/kg. Multiply patient weight by 2.0 or 2.5 to get dead-space. The dead-space of a 30 kg child is 30 kg x 2 mL!kg = 60 mL. [Davison, Eckhardt, and Perese, Mass General, 1993, p568; Barash Hand- book, Clinical Anesthesia, 1997, p407; Barash, Clinical Anesthesia, 1997, p1097]

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14
Q

What is the tidal volume of a neonate in mL/kg?

A

A neonate should have a ventilator setting for tidal volume of7 mL!kg (6-8 mL/kg is the normal range). This is the same as the adult range. [Barash, Clinical Anesthesia, 1997, p1097]

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15
Q

What is the minute volume per kg for the neonate?

A

Tidal volume in the neonate is 7 mL/kg and respiratory rate is 30-50 per minute. Ventilation “” tidal volume x respiratory rate. An estimate of minute ventilation in the neonate is: minute ventilation::::: 7 mL!kg x 30- 50 per minute= 210-300 mL!kg/min. 250 mL!kg!min is a reasonable nwnber to remember. Minute ventilation is 250 mL!kg. [Barash, Clinical Anesthesia, 1997, p1097; Authors]

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16
Q

Calculate the minute volume of a newborn who weighs 3 kg and has a respiratmy rate of 40 breaths per minute?

A

Minute volume::::: respiratory rate (breaths per minute) x tidal volume. Tidal volume is 7 rnL!kg (tidal volume is the same in the adult and the infant). If respiratory rate is 40 and the newborn weighs 3 kg, minute ventilation is 40 x (3 kg) x (7 mL!kg) = 840 mL/min. [Clinical Anesthesia, 2e, 1992, Barash, p1314]

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17
Q

How does chest wall compliance and pul- monary (lung) compliance differ in the in the neonate compared with the young, healthy adult’

A

In the neonate, chest wall compliance is increased and pulmonary coiTt- pliance is decreased. This means the chest wall is easier to distend (it is less rigid) but the lung is more difficult to distend (it is more rigid). [Bell and Kain, Peel. Anes. Handbook, 1997, p113]

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18
Q

What is the length of the infant trachea from the cords to carina?

A

The length of the trachea (vocal cords to carina) in infants and neonates and children up to one year of age varies from 5-9 em. [Cote, PAIC. 3e. 2001 pp92]

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19
Q

What is the distance from the teeth (alveolar ridge) to midtrachea in the newborn? In the infant who is six month to one-year-old? In the two-year-old, three-year-old, and four- year-old?

A

Newborn::::: 10 cm;6 mo to 1yr = ll cm; 2yr= 12 cm; 3yr::: 13-14 cm; 4 yr = 15 cm; 5 yr = 15-16 cm. [Cote, PAlC. 3e. 2001 pp93t]

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20
Q

lis the infant larynx located higher, at the same, or at a lower level in the neck com- pared to the adult larynx? Identify the level of the infant larynx.

A

The infant larynx is located higher in the neck, at the level of C3-4 than in the adults, where the larynx is located at the level of C4–5. Author’s com- ment: I find these text statements somewhat misleading-as you know, the cricoid cartilage-certainly part of the larynx-lies at C6, and many texts (Miller, for example) state that the adult larynx ranges from C3-C6. Perhaps the more accurate statement is: the thyroid cartilage is located at C3–4 in infants compared to C4-5 in adults. [Miller & Stoelting, Basics. 5e. 2007 pp233; Cote, PAIC. 3e. 2001 pp81; Authors]

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21
Q

How does the longue differ in the child compared with the adult?

A

A child’s tongue is relatively larger in proportion to the rest of the oral
cavity, compared to the adult tongue. [Cote, PAlC. 3e. 2001 pp81 I

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22
Q

Why are infants more prone to airway ob- struction?

A

Infants have a proportionately larger tongue than adults. [Gregory, Ped.
Anes., 2002, p223]

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23
Q

What part of a child’s airway has the small- est diameter?

A

The cricoid cartilage is the narrowest part. [Davison, Eckhardt, and Perese, Mass General, 1993, p434; Morgan and Mikhail, Clinical Anesthe- siology,1996,p730;Miller,AHesthesio, 1994,p2l01]

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24
Q

What is the blood volume (mL!kg) of the preterm neonate, term neonate, infant, child, and adult? What is the estimated blood volume of a 3.5 kg neonate?

A

Pre term neonate) 95-100 mL!kg; term neonate, 85-90 mL/kg; infant, 80 mL!kg; child, 75 mL!kg; adult, 65-75 mL!kg. The estimated blood volume of a 3.5 kg term neonate is: 85-90 mL!kgx 3.5 kg= 297.5-315 mL. [Da- vison, Eckhardt, and Perese, Mass General, 1993, p387; Morgan and Mikhail, Clinical Anesthesia, 1996, p7281

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25
Q

What is the hemoglobin (Hgb) concentra- tion at 2 weeks of 2-3 months of age? 2 years of age?

A

At 2 weeks, Hgb is !3-19 gllOO mL blood; at 2-3months, Hgb is less than !O-Il g/100 mL blood; at 2 years, Hgb is less than 12.5 gllOO mL blood. [Bell and Kain, Ped. Anes. Handbook, 1997, pp16, 2811

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26
Q

Describe the physiological anemia of the neonate and pediatric patient.

A

Normal hemoglobin levels in the full-term newborn infant range between 14-20 g/dL. The hemoglobin concentration progressively “bottoms out” during the 9th to 12th week reaching a minimum of 10-ll g/dL, with a hematocrit of 33%. Afler the third month ( 12 weeks) the hemoglobin levels stabilize at 11.5-12.0 gldL until about 2 years of age. After 2 years of age, the hemoglobin levels gradual increase to reach adult levels of 14.0- 15.5 gldL by puberty. [Cote, PA/C, 2001, ppl9-20; Gregory, Ped. Anes., 2002, p124]

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27
Q

Compare the physiological anemia in the preterm neonate to the full-term neonate.

A

In preterm infants, the decrease in hemoglobin levels is greater and earli- er, reaching the minimum hemoglobin concentration of8 g/dL by 4-8 weeks (hemoglobin “bottoms out” earlier and lower). At about l year old, the preterm and full-term infants hemoglobin levels are comparable and pre term infants following the same progression, reaching normal adult levels at puberty. [Cote, PAIC, 200l, pp19-20; Gregory, Ped. Anes., 2002, p124]

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28
Q

Below what hemoglobin concentration is anemia sufficient to jeopardize oxygen carrying capacity (and hence cause you to cancel elective surgery) in the neonate? Infant older than three months?

A

Less than I3 g/dL in the newborn and less than 10 g/dL in the pediatric patient older than three months.(Steward, Manual ofPed. Anes., 1995, p3IS; Stoelting and Miller, Basics, 1994, p381 I

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29
Q

A three-month-old infant, who is scheduled for surgery, has a hemoglobin of 10.5 mg/dL. What action should be taken?

A

None; this hemoglobin level is normal for this age. At three months of age, hemoglobin concentration normally decreases to this level. “It is rare for infants to develop any clinically significant symptoms from physiolog- ic anemia of the newborn.” [Bell and Kain, Ped. Anes. Handbook, 1997, p282l

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30
Q

During the preoperative evaluation of a 6- month-old surgical candidate, you note physiologic anemia. What is a likely cause for the physiologic anemia?

A

he infant with physiologic anemia at 6 months of age is most likely a formerly premature infant (expremie). “Even at several months of age,
expremies remain anemic because of poor nutrition and delayed hemato- poiesis that is induced by earlier transfusions.” Reminder: the nadir (low point) of physiologic anemia typically occurs at 2-3 months for full-term infants. [Gregory, Ped. Anes., 4e, 2002, p373; Cote, PAIC, 3”1 ed., 2001, p20; Yemen, Ped. Anes. Handbook, 2002, p139]

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31
Q

How are maintenance fluid requirements calculated for the pediatric patient?

A

4 mL!kg/hr. for first 10 kg; 2 mL!kg/hr. for second 10 kg; 1 mL!kg/hr. for each additional kg. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p728]

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32
Q

For a 3-week-old, 4 kg newborn undergoing prolonged surgery, maintenance fluids should be delivered at how many mL!hr.?

A

Maintenance fluid delivery rate for a 4 kg newborn is: 4 mL/kg/hr. x 4 kg = 16 mL!hr. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p728]

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33
Q

What is the fluid deficit of a normal66lb child NPO for 5 hours? Hint: first calculate the weight of the child in kg.

A

The fluid deficit is 350 mL. There are 2.2lb per kg. 66lb divided by 2.2 Jb/kg = 30 kg. Maintenance fluid for 30 kg child = (4 mL!kg/hr. x 10 kg) + (2mL/kg/hr. x 10 kg)+ (1 mL!kg/hour x IO kg)= 40 mi./hr.+ 20 mL!hr. + 10 mL!hr. = 70 mL!hr. 70 mi./hr. x 5 hrs. = 350 mL deficit. [Rasch and Webster, Clin. Manual ofPed. Anes., 1994, pl49]

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34
Q

Pediatric fluid replacement for blood loss is best determined by which method of moni- toring?

A

Hematocrit. Blood loss is typically replaced with crystalloid (3 mL of lactated Ringer’s per mL of blood loss) or colloid (1 mL of 5% albumin per mL of blood loss) until hematocrit falls to a pre-determined level. [Mor- gan and Mikhail, Clinical Anesthesiology, 1996, p728; Pediatric Anes., pp475-476]

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35
Q

Why is the cardiac output in infants de- pendent on heart rate and not stroke vol- ume?

A

Infants cannot alter stroke volume, so the only way to alter cardiac output is to change heart rate. Stroke volume cannot be altered because of the low contractile mass per gram of cardiac tissue, which results in limited ability to increase myocardial contractility, and also because left ventricu- lar compliance is reduced which makes ventricular fil!ing difficult. [Ba- rash, Clinicnl Anesthesia, 1997, p1097]

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36
Q

What is the normal heart rate of the term infant?

A

Heart rate of the term infant is reported to be 100-180 beats per minute {Mass General). Bell and Kain indicate that the normal heart rate of the neonate is greater than 120 beats per minute. 120-180 beats per minute might be considered an appropriate range for the term infant. [Davison, Eckhardt, and Perese, Clinical Procedures of the Massachusetts General Hospital, 1993, p.438; Bell and Kain, Ped. Anes. Handbook, !997, p420; Authors]

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37
Q

List two ways the physiology ofthe cardio- vascular system of the neonate differs from that of the adult.

A

In the neonate: (1) cardiac output is heart-rate-dependent, and (2) left ventricular compliance is decreased. [Morgan and Mikhail, Clinical Anes- thesiology, 1996, p726]

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38
Q

At what age is basal metabolic rate normally the highest?

A

Basal metabolic rate (BMR) peaks somewhere between 6-12 months old. In a full-term infant, BMR rises progressively during the first 10 days of life. After the first few weeks of life, BMR decreases nearly linearly throughout life (Nagelhout & Zag!aniczny). However, if you look at calor-ic requirements, infants under 1year old require about 100 cal!kg/day, whereas older infants require 75 cal/kg/day, and adults require 35 cal!kg/day. [Nagelhout and Zaglaniczny, NA, 2001, p397; Gregory, Ped. Anes., 2002, p87]

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39
Q

Give four reasons why it is so difficult to keep newborns warm?

A

(l) Newborns readily lose heat because of their greater surface area to body weight ratio. (2) They cannot compensate by shivering. (3) They have limited subQ fat for insulation. (4) They have limited stores of brown fat and unstable thermoregulatory systems. [Davison, Eckhardt, and Perese, Mass General, 1993, pp387,512]

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40
Q

By what route do infants lose most of their body heat?

A

Most heat loss is lost by radiation. [Davison, Eckhardt, and Perese, Mass General, 1993, p389; Barash Handbook, Clinical Anesthesia, 1997, p330; Stoelting, PPAP, 1987, p638]

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41
Q

Newborns produce heal primarily by what mechanism?

A

Newborns produce heat by non-shivering thermogenesis by metabolism of brown fat. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p727; Steward, Manual ofPed. Alles., 1995, p37]

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42
Q

What is the significance of brown fat? Where is brown fat located?

A

Infants respond to cold stress by increasing norepinephrine production, which enhances metabolism of brown fat and increases body heat, i.e., chemical thermogenesis. Brown fat is located in the interscapular space and around large blood vessels, around the neck, behind the sternum, and around the kidneys and adrenals. [Steward, Manual ofPed. Anes. 4e. 1995 pp37]

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43
Q

What controls non-shivering thermogenesis in infants?

A

The autonomic nervous system activates non-shivering thermogenesis in infants. [Steward, Manual ofPed. Anes., 1995, p37]

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44
Q

INon-shivering (cellular) thermogenesis is a crucial heat -generating mechanism in the neonate and infant, as you know. At approx- imately what age does non-shivering ther- mogenesis cease to be clinically significant?

A

Clinically and physiologically significant non-shivering thermogenesis persists up to the age of 2 years. Non-shivering thermogenesis may con- tinue into adulthood, but generally is not a relevant and significant source of heat generation in the adult. [Davis & Motoyama, Smith’s Anes.Jor Infants and Children. ?e. 2006 pp162; Gregory, Pediatric Anes. 4e. 2002 pp67]

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45
Q

What is the best way to maintain an infant’s body heat? What is the best way to warm an infant in the operating room?

A

The best way to maintain an infant’s body heat is to maintain high ambi- ent temperature. Increasing operating room temperature is the best way to warm an infant. [Cote, PAIC. 3e. 2001 pp628]

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46
Q

Premature infants may require what ambi- ent temperature to maintain a normother- mic state?

A

26’C. [Cote, PAlC. 3e. 2001 pp628]

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47
Q

At what rate do infants consume oxygen? How does this compare with the adult?

A

Resting 0 2 consumption in healt-hy infants is 7 mL!kg/min (twice that of the adult). [Davison, Eckhardt, and Pcrese, Mass General, 1993, p387]

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48
Q

To what do preductal or postductal coarcta- tion of the aorta refer?

A

Coarctation of the aorta refers to a discrete narrowing of the aorta imme- diately distal to the origin of the left subclavian artery. A preductal coarc- tation refers to a coarctation in a neonate or infant in which the narrow- ing occurs proximal to the opening of the ductus arteriosus. Postductal coarctations supposedly present in adulthood long after closure of the ductus arteriosus. [Rasch and Webster, Clin. Manual ofPed. Anes., p435; Morgan and Mikhail, Clinical Anesthesiology, 1996, p402]

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49
Q

Should upper extremity blood pressure be monitored in the neonate with preductal coarctation of the aorta on the right or the left side?

A

Monitoring of blood pressure is best achieved in a patient with a preduc- tal coarctation by placing a catheter in the right radial artety. [Stoelting, Co-Existing, 1993, p52; Bell, Kain, and Hughes, Ped. Anes. Handbook, 1997, pp158-159]

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50
Q

Blood shunts through what two structures in the neonate with persistent fetal circulation?

A

Blood shunts through the ductus arteriosus and the foramen ovale. [Mor- gan and Mikhail, Clinical Anesthesiology, 1996, p702]

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51
Q

What causes the foramen ovale to close in the newborn?

A

The closure of the foramen ovale is due to the decrease in pulmonary vascular resistance and increased pulmonary flow that occurs as the infant takes his/her first breaths and the alveoli expand. The decrease in pulmo- nary vascular resistance is accompanied by constriction of the ductus arteriosus secondary to oxygenation. This results in an increase in pul- monary blood flow and an increase in left atrial pressure. The increased ptessureintheleftatriumshutstheflap, locatedontheleftsideofthefo- ramen ova/e. [Barash, Clinical Anesthesia, 1997, pl09I; Guyton, TMP, 1996, pl05l]

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52
Q

Name the physiologic factor most responsi- ble for closure of the ductus arteriosus after birth.

A

Nonnal closure of the ductus arteriosus occurs in response to increased arterial oxygen tension (PnOJJ, as well as to reduction in circulating pros- taglandins that follow separation of the placenta. (Realize that a number ofother substances such as eicosanoids and factors such as PaC02 and pH have been implicated, but that increased oxygen tension seems to be the major factor precipitating ductus arteriosus closure.) [Cot, PAIC, yd ed. 2001, p356; Gregory, Ped. Anes., 4th eel. 2002, p424]

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53
Q

What is a patent ductus arteriosus? When does the ductus arteriosus normally close?

A

Patent ductus arteriosus is the abnormal persistence in the newborn of blood flow through the ductus arteriosus, an opening between the pulmo- nary artery and aorta. Normally, the ductus closes within a few hours to a few days after birth due to changes in the pressures of the pulmonary vasculature. [Guyton, TMP, 1996, p1051]

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54
Q

Is the shunt of a patent ductus arteriosus right-to-left or left-to-right?

A

The shunt is left-to-right. [Stoelting, Co-Existing, 1993, p40]

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55
Q

With a patent ductus arteriosus, what cardi- ovascular changes occur?

A

A patent ductus arteriosus allows blood to flow from the aorta into the pulmonary artery. The additional blood is reoxygenated in the lungs and returned to the left atrium and left ventricle and this causes increased workload on the left side of the heart and left ventricular hypertrophy, and increased pulmonary vascular congestion and resistance. Most pa- tients are asymptomatic. [Stoelting, Co-Existing, 1993, p41]

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56
Q

hat hemodynamic alteration may wors- en (increase flow through) a left-to-right intracardiac shunt?

A

An increase in systemic vascular resistance (SVR) may increase left-to- right intracardiac shunt flow, such as occurs in atrial septal defect. Avoid interventions that may increase SVR in the patient with an ASD. [Mor- gan, Mikhail, and Murray, Clinical Anesthesiology, 4e, 2006, p481]

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57
Q

What is the probable problem if the pediat- ric patient has a systolic and diastolic murmur?

A

Patent ductus arteriosus. A continuous systolic and diastolic murmur is often the only manifestation of patent ductus arteriosus. [Stoelting and Miller, 1994, p260; Guyton, TMP, 1996, pp276-277]

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58
Q

Where are pulse oximeters placed on the neonate to monitor preductal and postductal oxygenation?

A

Preductal oxygenation should be measured with a pulse oximeter on the right hand orfinger. Postductal oxygenation should be measured with a pulse oximeter on the left foot or a left toe. [Cote, PAIC, 2001, p395; Duke, Secrets, 2000, p302]

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59
Q

What is the purpose of a preductal pulse oximeter in the neonatal patient undergoing cardiac surgery?

A

Measurements of arterial oxygen saturation taken at a preductallocation (right hand/finger) are a better index of neonatal cerebral oxygenation than are those taken at a postductallocation (left foot/toes). The right-to- left shunt at the ductus arteriosus persists for some time after birth and this shunt may affect oxygen saturation readings, thus preductal place- ment of the pulse oximeter is preferred. A postductal pulse oximeter may be used in addition to the preductal pulse oximeter to quantitate the severity of the right-to-left shunt. [Birnbach, Textbook Ob. Anes., 2000, p7l4; Norris, Ob. Anes., 1999, pp680-68l; Duke, Secrets, 2000, pp301- 302]

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60
Q

Where should arterial blood pressure be measured in a patient undergoing repair of a patent ductus arteriosus (PDA)?

A

The catheter for measuring blood pressure should be placed in a periph- eral artery such as the femoral. [Stoelting, Co-Existing, 1993, p 42; Au- thors]

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61
Q

Identify the best site to obtain arterial blood gases from in the neonate.

A

Arterial blood gases in the neonate are best obtained from the radial arte1y.ln additional to ease of access, this site will reflect preductal oxy- gen saturation, which better reflects cerebral oxygenation. [Gregory, Peel. Anes., 2002, p257]

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62
Q

Which two sites are to be avoided when obtaining arterial blood gases in the neo- nate? Why?

A

Arterial blood gases samples are usually not obtained from the brachial or femoral arteries. Obtaining blood samples from a brachial artery has been associated with nerve damage. Obtaining blood samples from a femoral artery has been associated with femoral head necrosis and limb shorten- ing. The artery of first choice for obtaining arterial blood gas samples is the radial artery. [Gregory, Ped. Anes., 2002, p257]

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63
Q

Identify 4 factors that may cause a neonate/infant to return to fetal circulation.

A

Persistent fetal circulation (or a return to fetal circulation) is common in pre term infants and infants with metabolic derangements (asphyxia, sepsis, meconium aspiration, congenital diaphragmatic hernia). Hypox- emia, acidosis, pneumonia, and hypothermia are 4 primary precipitating factors in persistent fetal circulation. The pathologic mechanism common to all4 factors is increased pulmonary vascular resistance (PVR) and to-left shunting. [Nagelhout and Zaglaniczny, NA, 2”’ eel. 2001, pll35; Gregory, Ped. Anes., 4th ed. 2002, pp424-425]

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64
Q

What is the usual cause of persistent pulmo- nary hypertension (persistent fetal circula- tion)? Is the shunt associated with persistent pulmonary hypertension left-to-right or right-to-left?

A

Hypoxia, acidosis, and other factors cause a high pulmonary vascular resistance; the resulting pulmonary hypertension causes blood to shunt from right-to-left. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p702; Barash, Clinical Anesthesia, 1997, p1092)

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65
Q

List three congenital defects in which there isaright-to-leftshunt.

A

(1) Tetralogy ofFallot; (2) pulmonary atresia with ventricular septal defect;and(3)patentforamenovale.[Miller,Anesthesia, 1994,pp1815- 1816)

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66
Q

What is the anesthetic concern for the pedi- atric patient undergoing repair of a ventricu- lar septal defect (VSD) without significant pulmonatyhypertension?

A

Ventricular septal defect (VSD) without significant pulmonary hyperten- sion should be managed to avoid arrhythmias, RV dysfunction, pulmo- nary vascular obstructive disease, and paradoxical embolus. [Kaplan, CardiacAnesthesia, 1999,pp809-810)

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67
Q

What is the anesthetic concern for the pedi- atric patient undergoing repair of a ventricu- lar septal defect (VSD) with significant pulmonary hypertension?

A

The patient with an unrepaired VSD and irreversible pulmonary hyper- tension often displays right-to-left shunting through the VSD (Eisen- menger’s physiology). Manipulations that may increase PVR can cause rapid deterioration and include hypoxia, hypercarbia, acidosis, hypo- thermia, atelectasis, sympathetic stimulation and polycythemia. Early closure ofVSD before I year old results in normal ventricular function and ejection fraction. [Kaplan, Cardiac Anesthesia, 1999, pp809-810)

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68
Q

A right-to-left intracardiac shunt is pre- sent in the patient with a ventricular septal defect (VSD with Eisenmenger’s syndrome). What hemodynamic alterations may worsen (increase shunt Oow) the right-to-left shunt ofVSD with Eisenmenger’s syndrome?

A

An abrupt increase in pulmonary vascular resistance (PVR) or a decrease in systemic vascular resistance (SVR) is poorly tolerated in the patient with ventricular septal defect {VSD). Avoid interventions that may increase PVR or decrease SVR in the patient with a right-to-left intracardiac shunt. [Nagelhout & Zaglaniczny, NA, 3’’ ed., 2004, p432)

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69
Q

List three conditions that increase right-to- left shunt (tetralogy ofFallot).

A

Acidosis, hypercarbia, and hypotension {decreased SVR) increase right-to- left shunt. In general, increases in pulmonary vascular resistance or de- creases in systemic vascular resistance (caused by acidosis or hypercarbia) increase right-to-left shunt. Volatile anesthetics and histamine release decrease SVR. [Stoelting and Mil!er, Basics, 2000, p258; Hurford, Bailin, Davison, Haspel, Rosow, Mass Gen Handbook, 1998, p411; Morgan and Mikhail, Clinical Anesthesia, 1996, p370)

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70
Q

List four congenital heart defects involved with tetralogy of Fallot (cyanotic heart dis- ease).

A

(1) Ventricular septal defect, {2) right ventricular outflow tract obstruc- tion (pulmonary stenosis), (3) right ventricular hypertrophy, and
(4) dextroposition (to the right) of the aorta with overriding of the ven- tricular septal defect. [Morgan, Clinical Anesthesiology, 1996, p370)

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71
Q

Does blood shunt right-to-left or left-to- right through the ventricular septal defect in tetralogy of Fallot (cyanotic heart disease)?

A

Blood shunts right-to-left, permitting unoxygenated blood to mix with oxygenated blood, resulting in cyanosis. [Morgan and Mikhail, Clinical Anesthesiology, !996, p370)

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72
Q

An infant has Tetralogy of Fallot (cyanotic heart disease). Which of the following arte- rial blood gas parameters will not typically be changed: 1’,02, pH, P,CO,?

A

pH and P.C02 are likely to be in the normal range. P,02 is usually marked- lydecreased (

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73
Q

What are the goals of anesthetic

management for the patient who has tetralogy of Fallot (cyanotic heart disease)?

A

The goals of anesthetic management should be to maintain intravascular volume and systemic vascular resistance (SVR). Increases in pulmonary vascular resistance also should be avoided. [Morgan and Mildlail, Clinical Anesthesiology, 1996, pp370-371]

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74
Q

What change in systemic vascular resistance and in pulmonary vascular resistance in- crease shunt in the patient with tetralogy of Fallot? What drugs increase shunt in the patient with tetralogy of Fallot by altering systemic vascular resistance or pulmonary vascular resistance?

A

Shunt increases when systemic vascular resistance decreases or pulmo- nary vascular resistance increases. Volatile anesthetics, drugs that cause histamine release, ganglionic blockers, alpha blockers, or other vasodila- tors (nitroprusside) decrease systemic vascular resistance, increase right- to-left shunt, and worsen arterial hypoxemia. Increased pulmonary vascu- lar resistance increases shunt in a child with cyanotic heart disyase. N20 increases pulmonary vascular resistance, which is detrimental to children with right-to-left shunts. [Greg01y, Pediatric Anes., 2e, p857; Stoelting, Co-Existing, 1993, p44]

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75
Q

What pharmacologic agent decreases a right to left shunt?

A

A decrease in the magnitude of a righHo-left shunt (tetralogy of Fallot is a right-to-left shunt) occurs if systemic vascular resistance (SVR) increas- es. Phenylephrine increases SVR and decreases a right-to-left shunt. [Stoelting and Miller, Basics, 2000, p258; Hurford, Bailin, Davison, Haspel, Rosow, Mass Gen Handbook, 1998, p411]

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76
Q

During the case, oxygen saturation decreas- es, apparently because of increased shunt* ing. The patient has tetralogy ofFallot. What agents might be selected to decrease shunt and increase oxygen saturation?

A

Intravascular fluid volume must be maintained with IV fluid
administration since acute hypovolemia will tend to increase the magnitude of the righHo-left intracardiac shunt. A n alpha- agonist drug such as phe- nylephrine must be promptly available to treat an undesirable decrease in systemic blood pressure caused by a decrease in SVR. [Stoelting, Co- Existing, 1993, pp44-45]

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77
Q

Will a intracardiac shunt theo- retically slow or accelerate inhalation induc- tion? Is the effect be clinically significant?

A

A right-to-left intracardiac shunt will theoretica!ly slow inhalation induc- tion, because less anesthetic is absorbed from the lung, and mixing will further dilute blood passing to the left, decreasing the arterial concentra- tion of the blood going to the brain, especially the less soluble agents. This effect is rarely problematic. [Fleisher, Anesthesia and Uncommon Disease, 5e, 2006 p91]

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78
Q

Will a intracardiac shunt theo- retically slow or accelerate intravenous induction?

A

An intravenous induction will be theoretically accelerated with a
right to left intracardiac shunt. [Fleisher, Anesthesia and Uncommon Disease, 5e, 2006 p91]

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79
Q

Will a intracardiac shunt theo- retically slow or accelerate inhalation indue· Lion? Why is this phenomenon rarely evi- dent clinically?

A

A inlracardiac shunt shou!d accelerate the speed of inhalation induction because the rate of transfer of anesthetic agent from the lungs to the blood is increased. However, this effect is rarely clinically evident because decreased delivery of anesthetic to the target tissues negates the increased uptake of agent with a left -to-right inlracardiac shunt. [Fleisher, Arwsthesia and Uncommon Disease, 5e, 2006 p9l; Barash, Clinical Anes- thesia, Se, 2006, pp1209-1210]

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80
Q

Will a intracardiac shunt theo· retically slow or accelerate intravenous induction? Why is this phenomenon rarely evidentclinically?

A

Intravenous induction should be slowed by a lefHo-right shunt; however, unless cardiac output is very poor, the effect is clinically irrelevant. [Fleisher, Anesthesia and Uncommon Disease, Se, 2006 p91; Barash, ClinicalAnesthesia,Se, 2006,pp1209-1210]

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81
Q

Where is the fistula usually located in a patient with a tracheal-esophageal fistula?

A

In 90% of tracheal-esophageal fistulas, the lower segment of the esopha- gus inserts just above the carina onto the posterior wall of the trachea. [Barash, Clinical Anesthesia, 1997, p1107; The Physiologic Basis ofSur- gery, 1993, p63; Yao and Artusio, Problem Oriented Patient Management, 1993]

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82
Q

Where is the proper placement of the endo- tracheal tube in a patient with a tracheal- esophageal fistula? Describe the procedure for intubating the patient with a tracheal- esophageal fistula.

A

The tip of the endotracheal tube can be placed just distal to the tracheal- esophageal fistula (between the fistula and the carina). The endotracheal tube can be inserted until it enters one or the other mainstem bronchi. Look for unilateral expansion of the chest and unilateral breath sounds. The endotracheal tube is then slowly withdrawn until bilateral breath sounds are present. [Barash, Clinical Anesthesia, 1997, pll07; Morgan and Mikhail, Clinical Anesthesiology, 1996, p735]

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83
Q

What is trachea malacia (also known as tracheobronchomalacia)? What patients are at risk for developing tracheomalacia?

A

Malacia” means abnormal softening of tissue, therefore tracheomalacia would be softening of the tracheal tissue, especially the cartilaginous rings. Tracheoma!acia is sometimes seen in neonates/infants, often in association with esophageal atresia (e.g., tracheoesophageal fistula, TEF) or with extrinsic compression by vascular anomalies or mediastinal mass- es. Tracheomalacia may also be associated with hyperthyroidism. [Bissonnette, Ped. Anes., 2002, p1203; Barash, Clinical Anesthesia, 4th ed. 2001, p1188; Barash, Handbook, 4th ed. 2001, p596; Authors]

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84
Q

What is the anesthetic concern for the pa- tient with tracheomalacia?

A

Airway obstruction, possibly requiring urgent intubation, is of great con- cern for the patient with tracheomalacia. Airway obstruction due to tra- cheomalacia may be intrathoracic or extrathoracic; flow-volume loops will differentiate between intra-and extrathoracic obstruction. [Bis- sonnette, Ped. Anes., 2002, p1203; Barash, Handbook, 4th eeL 2001, p596; Yao, POPM, Sthed. 2003, pp700-701]

85
Q

The key to successful anesthetic manage- ment of the neonate with a tracheal- esophageal fistula is correct positioning of the endotracheal tube. What is the im- portant consideration for intubating the infant with a tracheal-esophageal fistula? What intubation techniques are appropri- ate?

A

An important issue is to avoid positive pressure ventilation, which will distend the stomach, thereby increasing the risk for reflux and ventilatory compromise. There are two approaches to tracheal intubation after indue- lion of anesthesia. One is to use an inhalation induction, followed by topical application of lidocaine and intubation while the infant is breath- ing spontaneously. The other technique is to use an IV or inhalation induction and intubate the trachea after muscle paralysis. This latter technique may lead to distention of the fistula and stomach after onset of positive pressure ventilation. [Barash, Clinical Anesthesia, 1997, 1107]

86
Q

Compare gastroschisis and omphalocele with regard to location, hernial sac, and associated congenital anomalies?

A

Gastroschisis: location is lateral to umbilicus; hernial sac is absent; associ- ated congenital anomalies are absent. Omphalocele: location is at the base of umbilicus; hernial sac is present; associated congenital anomalies are present and include trisomy 21 (Down’s syndrome), cardiac anomalies, diaphragmatic hernia, and bladder anornalies. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp736-737J

87
Q

Perioperative management of gastroschisis and omphalocele centers around what three preventative measures?

A

Perioperative management of gastroschisis and omphatocele is aimed at prevention of: (1) hypothermia, (2) dehydration, and (3) infection. [Barash, Clinical Anesthesia, 1997, p11051

88
Q

In which disorder, gastroschisis or

omphalocele, are hypothermia, dehydration, and infection most serious? Why?

A

These problems are more serious in gastroschisis because the hernial sac
is absent. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p736]

89
Q

List three congenital anomalies associated with prune-belly syndrome.

A

Prune-belly syndrome is associated with (1) cryptorchidism (undescend- ed testicles), (2) club feet, and (3) genitourinary tract abnormalities. Tip: even though the syndrome is called prune-belly, there are no associated gastrointestinal anomalies, notwithstanding the underdevelopment of the abdominal musculature. [Morgan, Milduil, and Murray, Clinical Anesthe- siology, 3’’ ed., 2002, p866; Authors]

90
Q

Name four conditions in which the patient presents with a large tongue. What is the concernifthepatienthasalargetongue?

A

Down’s syndrome, Pierre Robin syndrome, acromegaly, and hypothyroidism. Patients with large tongues are prone to respiratory obstruction. [Miller,Anesthesia, 1994,pp1406-1407]

91
Q

Mandibular hypoplasia is associated with what three congenital diseases? Should these patients generally be intubated awake or asleep?

A

Patients with Pierre Robin syndrome, Treacher Collins syndrome, and Goldenhar syndrome have mandibular hypoplasia and may be difficult to intubate. These patients are more often intubated after induction of anes- thesia with a volatile anesthetic. While awake intubation can sometimes be accomplished, awake intubation of these patients may produce severe trauma to the upper airway and does not eliminate the risk of pulmonary aspiration. [Stoelting, Co-Existing, 1993, p605]

92
Q

What is Pierre Robin syndrome? What are the concerns and how should this patient be managed? What intubation technique should be used?

A

Pierre Robin syndrome is a combination of a cleft palate, micrognathia (small lower jaw with receding chin), glossoptosis (downward retraction or displacement of the tongue). Respiratory obstruction may occur (the tongue may cause total airway occlusion) and can lead to cor pulmonale; maintain airway by placing prone on a frame; may require tongue suture, intubation, or tracheotomy. [Steward, Manual ofPeel. Anes., 1995, p379]

93
Q

Describe the suggested tracheal intubation technique for a patient with Treacher- Collins syndrome.

A

Treacher-Collins syndrorne is the most common of the mandibulofacial dystoses, a group of syndromes that feature mandibular hypoplasia. In addition, up to 30% ofTreacher-Collins patients have an associated deft palate. An awake tracheal intubation (oral or nasal) with aid of a fiberop- tic laryngoscope after adequate topical anesthesia is recommended. Miller advocates: (1) topicalization with 1% lidocaine, {2) LMA insertion, fol- lowed by (3) fiberoptic intubation through theLMA. Also consider fiber- optic tracheal intubation after induction with a volatile agent. [Stoelting & Dierdorf, Handbook ofAnesthesia and Co-Existing Disease, 4e, 2002, p709; Miller, Anesthesia, 6e, 2005, pp2384-2388]

94
Q

Treacher-Collins syndrome is associated with cleft palate, as you know, indicating a difficult airway. What congenital heart disease is associated with Treacher-Collins syndrome?

A

Treacher-Collins syndrome is frequently accompanied by congenital heart disease, most prominently ventricular septal defect. Concept: ventricular septal defect is the most commonly occurring congenital heart disease, therefore VSD is frequently associated with many other congenital anom- alies. [Hines, Stoelting’s Co-existing. Se. 2008 pp6l3; Yao, Yao & Artusio’s POPM. 6e. 2008 ppl053]

95
Q

At what age is cleft palate usually repaired?

A

Cleft palate repair is usually undertaken when the infant is 12-18 months old, but sometimes younger. [Steward, Manual ofPed. Anes., 1995, p255]

96
Q

What is the concern with an infant who has a cleft palate?

A

In infants with a large cavernous defect of the palate, intubation of the trachea becomes difficult if the blade slips into the cleft and cannot be adequately manipulated. [Stoelting, Co-Existing, 1993, pp604-605]

97
Q

What intubating techniques would you use on a child with a cleft palate?

A

Insert a small piece of sponge or dental roll to fill the gap of the cleft and thus reduce the likelihood of the blade lodging in the gap. Tape the endo- tracheal tube to the lower lip in the midline. Use a preformed RAE tube to reduce the chance of tracheal tube occlusion by the palate retractor during palatoplasty. [Stoelting, Co-Existing, 1993, pp604-605; Steward, Manual ofPed. Anes., 1995, p255]

98
Q

What causes myelomeningocele? What is the difference between a meningocele and a meningomyelocele?

A

Myelomeningocele is caused from failure of the neural tube to close in the fetus during development. Failure of the caudal end to close results in spina bifida. A sac is present which contains meninges and neural ele- ments. A meningocele is a sac containing only the meninges. [Rasch and Webster, Clin. Manual ofPed. Anes., 1994, p498; Steward, Manual ofPed. Anes., 1995, pp201-202]

99
Q

List 7 anomalies often co-existent with myelomeningocele.

A

Myelomeningocele is often associated with: (I) club foot, (2) hydrocepha- lus (along with stenosis of the aqueduct ofSylvius and Arnold-Chiari malformation), (3) dislocation of hips, (4) exstrophy of bladder (possible incontinence), (5) prolapsed uterus, (6) Klippel-Peil syndrome, and (7) congenital cardiac defects. [Stoelting, Co-Existing, 3’” ed. 2002, p705]

100
Q

What are the concerns for anesthetizing the newborn with meningomyeloce!e?

A

The patient may not be able to lay supine for intubation due to possible sac disruption. The awake lateral decubitus position may be necessary. [Rasch, p498; Steward, Manual ofPed. A11es., 1995, pp20!-202; Stoelting, Co-Existing, 1993, p600]

101
Q

What is Arnold-Chiari malformation? What are four symptoms of Arnold-Chiari mal- formation?

A

Arnold-Chiari malformation is a malformation consisting of an elongated cerebellar vermis that herniates through the foramen magnum and also compresses the brain stem. Symptoms of Arnold-Chiari malformation are: (1) difficulty swallowing, (2) recurrent aspiration, (3) stridor, and possibly (4) apneic episodes. [Steward, Manual ofPed. Anes., 1995, p203]

102
Q

A seven-year-old patient with spina bifida comes to the operating room for a ventricu- lar-peritoneal shunt. What is the primary concern?

A

The major concern for this patient is the high probability of a latex aller- gy, which may trigger an anaphylactic episode in the operating room. While the incidence oflatex allergy among medical personnel is 6-7%, 18-34% of patients with spina bifida have a latex allergy. Most children who have had intraoperative anaphylaxis had spina bifida. [Motoyama and Davis, Smith’s AIC, !996, p; Stoelting, Co-Existing, 1993, p601]

103
Q

In addition to cleft palate and ventricu- loseptal defects, what other conditions are associated with Treacher-Collins syndrome? Is a macroglossia (large tongue) associated with Treacher-Collins syndrome?

A

Treacher-Collins syndrome is associated with cleft palate (30%), ventricu- loseptal defect (VSD), malar hypoplasia, colobomas (notching of the lower eyelids), macrostomia (large mouth), malocclusion, and a small oral cavity. Treacher-Co!lins syndrome is not associated with macro- glossia (large tongue) or mental retardation. [Hines, Stoeltiug’s Co- existing. Se. 2008 pp613; Yao, Yao & Artusio’s POP/vi. 6e. 2008 ppl053]

104
Q

What is the most frequent pediatric surgical emergency?

A

Foreign body aspiration into the airway or esophagus is the most frequent pediatric surgical emergency. [Roizen & Fleisher, Essence ofAnesthesia Practice, 2”’ ed. 2002, p144]

105
Q

Children with long-standing obstructive sleep apnea (caused by hypertrophied ton- sils, for example) show what anatomic changes in the heart?

A

In children with long-standing hypoxemia and hypercarbia, pulmonary artery hypertension and right ventricular hypertrophy develop. [Barash, Clinical Anesthesia, 1997, p929]

106
Q

Children of what ages get croup (laryngotra- cheobronchitis)?

A

Croup usually occurs in children aged 2 or less. [Cote, PAIC, 2e, pp251- 254, 1992]

107
Q

What are four signs and symptoms of croup?

A

The affected child demonstrates: (1) a low-grade fever, (2) a “croupy” cough with inspiratory stridor and chest retractions, (3) fever rarely above 39’ Celsius, and (4) cyanosis. [Cole et al., PAIC, 2”’ ed. 1992, pp251-254]

108
Q

List three (3) treatments for postintuba- tion laryngeal edema (postintubation “croup”).

A

Treatment ofpostintubation laryngeal edema (“croup”) is aimed at reduc- ing airway edema. Mild cases often improve with cool, humidified mist and oxygen therapy, ideally administered by a face tent. More severe cases require hourly administration of aerosolized racemic epinephrine, 0.05 mL!kg of2.25% epinephrine in 3.0 mL of saline. Intravenous dexame- thasone mg/kg) may prevent the edema, but the effect takes up to 4-6 hours to manifest. [Hines, Stoelting’s Co-existing. Se. 2008 pp616; Barash, Clin. Anes. 6th. 2009 pp1313; Hagberg, Benumofs Airway Man- agement. 2e. 2007 pp796; Morgan, et al., Clin. Anesth. 4e. 2006 pp939]

109
Q

What is the usual cause of croup (laryn- gotracheobronchitis )?

A

The cause is usually viral. [Cote et al., PAIC, 211d ed. 1992,

110
Q

What is the pathogenesis of post-intubation croup? Identify 6 risk factors for post- intubation croup.

A

Post-intubation croup is due to glottic or tracheal edema. Post-intubation croup is associated with: (l) early childhood (age 14 years), (2) repeated intubation attempts, (3) large endotracheal tube, (4) prolonged surgery, (5) head and neck procedures, and (6) excessive movement of the endo- tracheal tube. [Morgan el al., Clinical Anesthesiology, 3’’ ed. 2002, p863]

111
Q

What is the appropriate treatment for post- intubation croup.

A

Post-intubation croup is treated with inhalation of nebulized racemic epinephrine (0.25-0.50 mL of2.25% solution in 2.5 mL ofNS). Intrave- nous dexamethasone (0.25-0.50 mg/kg) may prevent edema. [Morgan et al., Clinical Anesthesiology, 3’” ed. 2002, p863j

112
Q

What is the etiology of epiglottitis?

A

Epiglottitis is due to life-threatening infection by Haemophilus irifluenza type ll bacteria. [Cote et al., PA/C, 2”’ ed. 1992, pp251-254j

113
Q

List nine signs and symptoms of epiglottitis

A

Signs and symptoms of epiglottitis include: (1) upper airway obstruction, (2) inspiratory stridor, (3) chest retractions (4) tachypnea, (5) cyanosis, (6) drooling, and (7) difficulty swallowing. The child also (8) insists on sitting and (9) is restless. [Cote et al., PAIC, 2”” ed. 1992, pp25l-254]

114
Q

Children of what ages get epiglottitis?

A

Affected children are usually I to 7 years old. Epiglottitis occurs with greater frequency in children less than 3 years of age. [Cote eta!., PAIC. 2”“ed.1992, pp25l-254)

115
Q

Where is the optimal hospital location for intubation of a patient with epiglottitis? Why?

A

Intubation should occur in the operating room. Total obstruction of the airway could occur at any moment. An attempt to visualize the epiglottis should not be undertaken until the child is in the operating room where intubation of the trachea and possible emergency tracheostomy should be performed. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p736; Stoelting and Miller, Basics, 1994, p390)

116
Q

What induction agent and what endotrache- al tube size should be used in the patient with epiglottitis?

A

An inhalation induction is followed by intubation with an endotracheal tube 1/2 to 1size smaller than usual. [Morgan and Mikhail, Clinical Anes- thesiology, 1996, p736)

117
Q

How long might one expect the endotracheal tube to be left in place in the patient with epiglottitis? What is one signal suggesting it is time for extubation?

A

The endotracheal tube is left in place for 24-96 hours. At this time an air leak usually appears around the endotracheal tube (because swelling has gone down) signaling the possibility of extubation. [Cote, PAJC, 211(1 ed. 1992, p253)

118
Q

Where and when should the patient with epiglottitis be extubated?

A

Extubation of the trachea is performed in the operating room only after direct laryngoscopy has confirmed resolution of the swelling of the epi- glottis. [Stoelting and Miller, Basics, 1994, p390; Cote eta!., PAIC, 2”” eel. 1992, p253)

119
Q

How is general anesthesia induced in the child with acute epiglottitis?

A

Parents should be present until the airway is secure. The operating room should be quiet. Monitors should be applied as tolerated, especially the pulse oximeter. Initiate induclion with 100% Ot/halothane or 02/sevoOurane with the patient in a sitting position. Start an IV, give fluids and atropine and ora!!y intubate. Do not use muscle relaxants. Avoid touching the epiglottis with the laryngoscope blade. Go into the vallecula. If oral intubation fails, try with a bronchoscope. If that fails then a tracheostomy is performed. [Rasch, p246; Cote, Ryan, Todres and Goudsouzian, pp252-253]

120
Q

In what position would you induce the patient with epiglottitis?

A

A parent should hold the child on his/her lap, and after mask induction the d1ild is placed supine with head slightly up. [Cote, Ryan, Todres and Goudsouzian, p252]

121
Q

List four anesthesia considerations for the patient with congenital diaphragmatic her- nia?

A

(l) Use ketamine 0.5-1.0 mg/kg or fentanyll-3 meg/kg. (2) Avoid nitrous oxide. (3) Gently atlempt tore-expand the lungs under direct vision using pressures no greater than 30 em I-hO after repair. (4) Antici- pate the need for postoperative support of ventilation. [Barash Handbook, Clinical Anesthesia, !997, pp1!04-1!05)

122
Q

In the patient with diaphragmatic hernia, what lung is usually involved?

A

Herniation on the left side through the foramen ofBochdalek occurs in 80% of congenital diaphragmatic hernias. Hence, the left lung is involved. [Morgan eta!., Clinical Anesthesiology, 2002, pp734-735)

123
Q

What peak inspiratory pressure should be used with a patient who has a diaphragmatic hernia? Why?

A

Peak inspiratory pressure should be less than 30 em I·hO. Pneumothorax of the contralateral (usually right) lung can occur if peak inspiratory pressure is too high. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp734-735]

124
Q

Is the infant with a diaphragmatic hernia with bowels extending into the chest an emergency? List seven anesthetic considera- tions for managing an infant with a dia- phragmatic hernia with bowels extending into the chest.

A

This is an emergency. Anesthetic considerations for managing this patient include: (1) Place a nasogastric tube, (2) do not apply positive ventilation via mask, (3) intubate with controlled ventilation, (4) do not use N20,
(5) monitor PaC02 and Sa02, (6) use 100%02, (7) give muscle relaxants and opioid after the chest is opened. [Davison, Eckhardt, and Perese, Mass General, 1993, pp404-405]

125
Q

During the intraoperative period of a con- genital diaphragmatic hernia repair, the Sa02 suddenly falls to 65% and heart rate decreas- es to 50 beats/min. What is the likely cause and what should be done?

A

Any sudden deterioration in lung compliance, heart rate, oxygen satura- tion, or blood pressure suggests a tension pneumothorax on the contrala- teral side. Absent or diminished breath sounds confirm the diagnosis of pneumothorax, and a chest tube should be inserted immediately. [Yao, Yao & Artusio’s POPM, 5e, 2003, p112; Gregory, Ped. Anes., 4e, 2002, p437]

126
Q

What might be signaled by a sudden fall in lung compliance (reflected by an increased peak inspiratory pressure), blood pressure, or oxygenation during repair of a congenital diaphragmatic hernia?

A

A contralateral (usually right-sided) pneumothorax should be suspected. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p735]

127
Q

What nerves are blocked for repair of an inguinal hernia?

A

The ilioirzguinal and iliohypogastric nerves are blocked for inguinal hernia repair. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p271j

128
Q

What two electrolyte abnormalities will be seen with projectile vomiting?

A

(l) Hypokalemia and (2) hypochloremia. [Stoelting and Miller, Basics, 1993, pp 226, 392]

129
Q

What acid -base disturbance will be seen with significant loss of bile vomitus?

A

Significant loss ‘of bile vomitus will result in metabolic acidosis. [Katz, Anesthesia and Uncommon Diseases, pp430-43l]

130
Q

What acid-base and electrolyte abnormali-
ties develop in the patient with pyloric ste-
.1 !lOSIS.

A

As a result of persistent vomiting, the infant becomes alkalotic (metabolic alkalosis), hypochloremic, hypokalemic, and possibly hyponatremic. 71ze infant is dehydrated with a hypokalemic, hypochloremic metabolic alkalo- sis. [Stoelting, Co-Existing, 1993, p597; Miller, Anesthesia, 1994, p2118; Barash Handbook, Clinica Anesthesia, 1997, pp607-608j

131
Q

What serum sodium, potassium, and chlo- ride concentrations and what urine output are needed before surgery in the patient with pyloric stenosis?

A

Electrolytes need to be: sodium > 130 mEq/L, potassium> 3 mEq/L, chloride> 85 mEq/L and a urinary output ofat least 1-2mL/kglhr. [Mil- ler, Anesthesia, 1994, p21!8; Stoelting and Miller, Basics, 1994, p392; Davison, Eckhardt, and Perese, Mass General, 1993, p400J

132
Q

A neonate diagnosed with pyloric stenosis presents with aNa’ of 120, C! of 84, and a respiratory rate of 16. What is the appropri- ate course of action for this patient?

A

Pyloric stenosis is characterized by persistent vomiting which depletes sodium, potassium, chloride, and hydrogen ions, causing hypochloremic metabolic alkalo- sis. In this particular presentation the disturbances are moderately severe and the patient should be given IV 5 percent dextrose in 0.45 percent normal saline with 20-40 mEq/L potassium chloride administered at a rate of 10 mL!kg/hr. Avoid lactated Ringer solution, because lactate is metabolized to bicarbonate. [Gregory, Pe(i. Anes., 2002, pp579-580; Morgan et aL, Clinical Anesthesiology, 2002, pp866- 867j

133
Q

What happens to the oxyhemoglobin disso- ciation curve in pyloric stenosis? Why?

A

The oxyhemoglobin dissociation curve shifts to the left because of meta- bolic alkalosis secondmy to vomiting. [Stoelting, Co-Existing, 1993, p597; Stoelting and Miller, Basics, 1994, pp392, 230]

134
Q

Is pyloric stenosis a medical emergency or a surgical emergency?

A

Pyloric stenosis is a medical, but not a surgical, emergency. Surgery should be postponed for 24-48 hours until fluid and electrolyte abnor- malities are corrected. [Stoelting, Co-Existing, 1993, p597; Yao and Artu- sio, POPM, 1993, pp318-19; Barash, Clinical Anesthesia, 1997, pp 1117- 1118; Authors]

135
Q

How is the infant with pyloric stenosis pre- pared for surgery?

A

The emergent therapy for pyloric stenosis is to stop oral intake (stop formula feeding or breast feeding) and metabolically reconstitute the child with intravenous sodium chloride, potassium, and glucose (dextrose). The metabolic abnormalities can be corrected in 12 to 24 hours by IV therapy.
Surgery should be postponed for 24-48 hours. [Stoelting, Co-Existing, 1993, p597; Longnecker et al., PPA, 1998, p21 OS]

136
Q

What concentrations of sodium chloride (saline), potassium, and glucose are used to prepare the infant with pyloric stenosis for surgery?

A

The dehydration and hyponatremia can be corrected with IV saline (0.45% to 0.9%). When urine output is restored, potassium (usually 40 mEq/L) must be added to this to correct the hypokalemia. Maintenance fluid should be added to this regimen, and for this purpose 5% dextrose in 0.225% saline is usually adequate. [Yao and Artusio, POPM, 1998, p427]

137
Q

What is the major concern for inducing an infant who is scheduled for a pyloromyoto- my? What do you need to do before induc- ing a patient with pyloric stenosis?

A

Pulmonary aspiration is the rnajor concern darir1g induction. The stomach is emptied as much as possible with a large-bore catheter prior to induc- tion. [Barash Handbook, Clinical Anesthesia, 1997, p608; Stoelting, Co- Existing, 1993, p597; Yao and Artusio, POPM, 1993, pp318-l9; Barash, Clinical Anesthesia, 1997, pp 1117-1118; Authors]

138
Q

In addition to emptying the stomach, list three actions that should be taken to manage a patient with pyloric stenosis.

A

In addition to emptying the stomach, (1) use rapid sequence induction, (2) perform awake intubation, and (3) extubate awake. [Miller, Anesthe- sia, 1994, p2118; Stoelting and Miller, Basics, 1994, p392; Davison, Eck- hardt, and Perese, Mass General, 1993, p400]

139
Q

How might you intubate a lethargic infant scheduled for pyloromyotomy? An alert infant with an IV line in place? An alert infant without an IV line in place?

A

An awake intubation may be performed for a lethargic infant. If the infant has an IV in place, intubation can be done after rapid-sequence induction with cricoid pressure. If there is no IV line, the patient may be induced wilh 50%02, 50% N20, and 1.5-3% halothane or 3-6% sevoflurane. [Stoelting, Co-Existing, 3”1 ed, 1993, p597; Yao and Artusio, POPM, 1993, pp318-l9; Barash, Clinical Anesthesia, 1997, pp 11!7-1118; Authors]

140
Q

The newborn has undergone a pyloromyo- tomy. What might you be concerned about in the postoperative period?

A

Neonates who have undergone pyloromyotomy maybe at increased risk for respiratory depression and hypoventilation in the recovery room because of persistent metabolic or cerebrospinal fluid alkalosis. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p736]

141
Q

What are six primary anesthetic considera- tions for the pediatric patient with hyper- trophic pyloric stenosis?

A

(1) Postpone surgery until volume and electrolyte deficiencies have been corrected; (2) correction of the volume deficit and metabolic alkalosis requires hydration with sodium chloride solution supplemented with potassium; (3) do not use lactated Ringer’s because lactate is metabolized to bicarbonate, which would aggravate the metabolic alkalosis; (4) thestomach should be emptied prior to surgery; (5) there is a high risk of aspiration during induction; (6) postoperative respiratory depression secondary to cerebrospinal fluid alkalosis should be anticipated. [Morgan and Mild1ail, Clinical Anesthesiology, 1996, p736]

142
Q

What is the average amount of blood lost (in mL/kg) during tonsillectomy?

A

During tonsillectomy, blood loss averages 4 mL!kg and must be carefully monitored. In terms of percentage, Gregory states lhat 5-10% of blood volume may be lost during tonsillectomy. [Longnecker, Tinker, and Mor- gan, PPA, 2e, 1998, p2209; Waugaman, PPNA, 3’’ ed., 1999, p740; Grego- ry, Ped. Anes., 4e, 2002, p674]

143
Q

What are three complications of tonsil and adenoid surgery?

A

Bleeding; laryngospasm; emesis. [Barash, Clinical Anesthesia, 1997, pp930-932]

144
Q

Should extubation be performed while the patient is awake or asleep after a tonsillec- tomy? Why?

A

An awake exlubation is preferred by most anesthetists because risk of aspiration is reduced. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p737]

145
Q

What actions are taken if the tonsillectomy patient begins bleeding? What are the major considerations if the patient needs to be taken back to the operating room?

A

Initial attempts to control bleeding may be made using pharyngeal packs and cautery. If the patient needs to be taken back to the operating room, (1) intravascular volume must first be restored, and (2) the patient must be considered to have a full stomach because large quantities of blood can be swallowed. [Barash, Clinical Anesthesia, 2001, p991; Atlee, Complica- tions in Anesthesia, 1999, p633; Morgan and Mikhail, Clinical Anesthesi- ology, 1996, p737]

146
Q

Postoperative bleeding after tonsillectomy is suggested by restlessness, pallor, tachycar- dia, or hypotension. If reoperation is neces- sary, what should be done first? Second? How should the patient be induced?

A

First, restore intravascular volume. Second, empty the stomach with a nasogastric tube. Morgan and Mikhail recommend a rapid sequence induction with cricoid pressure. Barash recommends an awake intubation or ketamine or an inhalation induction. [Morgan and Mikhail, Clinical Anesthesiology, 1992, p639; Barash Handbook, Clinical Anesthesia, 1996, p737]

147
Q

What causes kernicterus?

A

Kernicterus, also known as bilirubin encephalopathy, affects neonates and is caused by the toxic effects of unconjugated bilirubin on the central nervous system. The signs and symptoms of kernicterus include hyperto- nicity, opisthotonus, and spasticity. Unconjugated bilirubin doesn’t readi- ly cross the normal blood-brain barrier, but neonates have an immature blood-brain barrier. [Stoelting & Dierdorf, Co-Existing, 4th eeL 2002, pp694-695]

148
Q

What drugs may cause kernicterus in the neonate?

A

Bilirubin is normally conjugated to albumin, therefore any drug that competes for albumin binding sites may increase unconjugated bilirubin and increase the risk of kernicterus. Commonly used drugs that may displace bilirubin from albumin include furosemide, suifonamides, and diazepam (the preservative, benzyl alcohol, in diazepam is actually the culprit). [Duke, Secrets, 2”’ ed. 2000, p295; Barash, Clinical Anesthesia, 4th ecl.200Lp1158]

149
Q

Which type of shock is most frequent in the pediatric patient?

A

Hypovolemic shock, often due to blood loss from trauma, is the most common cause of shock in children. Appreciate that the compensatory mechanisms (vasoconstriction and tachycardia) in children are very efficient at maintaining perfusion; children may lose as much as one- fourth of their blood volume without significant cardiovascular changes in the supine position. Hypovolemic shock due to plasma loss can be seen with burns and peritonitis, and may be a component of septic shock. [Cote, PAIC, 2001, p325; Gregory, Peel. Anes., 2002, pp102-103]

150
Q

What is the best fluid replacement for the pediatric patient in hypovolemic shock?

A

Crystalloid solutions (e.g., lactated Ringer solution) are effective in the initial treatment of hypovolemic shock in pediatric patients. Crystalloids administered early in the management of hypovolemic shock wi!l prevent renal failure and also prevent renal collapse. If indicated, blood should be transfused as soon as crossmatching has been done. [Cote, PAIC, 2001, p325; Gregory, Peel. Anes., 2002, pp102-I03]

151
Q

dentify ten (10) factors associated with postintubation laryngeal edema (“croup”),

A

The following ten factors are associated with postintubation laryngeal edema (“croup”): (I) age younger than 4 years, (2) tight-filling endotra- cheal tube, no audible leak at 15-25 ern 1-hO, (3) traumatic or repeated intubation, (4) prolonged intubation, (5) high-pressure, low-volume cuff, (5) patient “bucking” or coughing during intubation, (6) head reposition- ing while intubated, (7) history of infectious or postintubation croup, (8) neck/airway surgery, (9) upper respiratory infection, and (10) Trisomy 21. [Hines, Stoelting’s Co-existing. 5e. 2008 pp617; Hagberg, Benumofs Airway Managernent. 2e. 2007 pp796; Morgan, eta!., Clin. Anesth. 4e. 2006 pp939]

152
Q

What is the most common cause for liver transplantation in children?

A

In children, the most common cause for liver transplantation is cholestatic liver disease secondary to biliary atresia, particularly in infants (SO%). [Cole, PAIC. 4th. 2009 pp606]

153
Q

What may be the most important considera- tion for anesthetizing the Down’s patient?

A

Intubation of the trachea is generally not too difficult to accomplish. Hence, the most important consideration may be the atlanta-occipital (cervical spine) instability. [Authors]

154
Q

What are three major concerns related to anesthetizing the Down’s (trisomy 21) pa- tient?

A

(1) Intubation may be difficult owing to the large tongue, short neck, small mouth, and subglottic stenosis (select endotracheal tube one size smaller than anticipated); (2) neck flexion during lmyngoscopy and intu- bation may result in atlanta-occipital (cervical spine) dislocation because ofcongenitally weak ligaments (considergettingcervical-spinefilms);
(3) congenital heart disease is present in 40% of patients (anesthesia compatible with the patient’s congenital heart defects should be deliv- ered). [Bell and Kain, Ped. Anes. Handbook, 1997. p537; Longnecker e l al., PPA, 1998, p428; Hurford, Bailin, Davision, Hospd, Rosow, Mass General, 1998, p206; Morgan and Mikhail, Clinical Anesthesiology, 1996, p738]

155
Q

What are four pathophysiological features associated with Down’s syndrome, in addi- tion to difficult airway, atlanto-occipital instability and congenital heart defects?

A

Pathophysiological features of Down’s syndrome also include; (I) irregu- lar dentition; (2) mental retardation; (3) hypotonia; (4) tracheoesophageal fistula; (5) chronic pulmonary infections; and (6) seizures. [MorgcHl and Mikhail, Clinical Anesthesiology, t996, p738]

156
Q

Describe the preoperative fasting (NPO) guidelines for children: (1) 36 months.

A

Fasting guidelines are: (l) Children 36 months old: restrict solids for 8 hours and clear liquids for 3 hours. The American Academy of Pediatrics/American Society of Anesthesiologists task force has set recommendations that “advise restriction of clear fluids for 2 hours, breast milk for 4 hours, formula or light meals for 6 hours, and fatty solid meals for 8 hours.” The pattern is to start NPO at 2 hours for clear liquids add 2 hours for each increasingly “fatly” meal. [Cote, PA/C, 2001, p225; Barash, Clinical Anesthesia, 2001, p1196; Authors]

157
Q

ositive pressure ventilation by bag and mask has been instituted on the neonate during resuscitation. When is endotracheal intubation indicated?

A

During neonatal resuscitation, prompt endotracheal intubation is indicat- ed if there is no immediate (

158
Q

When should imrnediate endotracheal intubation be considered during neonatal resuscitation?

A

Immediate endotracheal intubation of the neonate should be considered for situations in which bag and mask ventilation is likely to be ineffective, for example, extreme prematurity with low pulmonary compliance sec- ondary to surfactant deficiency. Other situations in which bag and mask ventilation may be ineffective are large bilateral pleural effusions and congenital diaphragmatic hernia. [Hughes, el a!., Anes.Jor OB. 4e. 2002 pp662j

159
Q

What is the appropriate internal diameter of the endotracheal tube for the premature newborn? For the full-term newborn?

A

The appropriate internal diameter of the endotrachdic tube is 2.5-3.0 mm for the premature newborn and 3.0-3.5 mm for the full-term new- born. [Davison, Eckhardt, and Perese, Mass General, 1993, p441; Barash Handbook, Clinical Anesthesia, 1997, pp1119-1120J

160
Q

What endotracheal tube size and length are required for the neonate, 2-year-old, 6-year- old and 10-year-old?

A

Neonate== 3.0-3.5 and 10 em length; 2-year-old = 4.5 and 13 em length; 6-year-old = 5.5 and 15 em length; 10-year-old = 6.5 and 17 em length. [Barash Handbook, Clinical Anesthesia, 1988, p49]

161
Q

Write the formula for calculating the inter- nal diameter of the endotracheal tube for the child who is greater than 20 months of age. Calculate the appropriate internal diameter of the endotracheal tube for a 5-year-old child.

A

Par children over 20 months, 4.0 +age (years)/4 = Lhe internal diameter (ID) needed. 4.0 + 5/4::::: 5.0 mm internal diameter endotracheal tube, for the 5-year-old. [Davison, Eckhardt, and Perese, Mass General, 1993, p441]

162
Q

How is the length of the endotracheal tube from the mouth determined, in em?

A

[10 +age (years)]/2. [Davison, Eckhardt, and Perese, Mass General, 1993, p441]

163
Q

How is the French size of the endotracheal tube determined for a child? What endotra- cheal tube size is required by a six-year-old?

A

The French size for a child is age (years)+ 18. Example: A six-year-old will require a 24 French ET tube (6 + 18 24). [Davison, Eckhardt, and Perese, Mass General, 1993, p441]

164
Q

W h a t size (French) suction catheter should be used to clear the endotracheal tube of the intubated neonate? The intubat- ed 2-year-old? The intubated 6-year-old?

A

The appropriate size (French) of suction catheter for clearing the endotra- cheal tube of the intubated child is: neonate-S Fr, 6 months to 2 years old-10 Fr, and 2 to 12 years old-14 Fr. [Nagelhout & Zaglaniczny, NA, 3’d ed., 2004, p1109]

165
Q

How many days post gestation is it safe for surgery in the full-term infant? For the preterm infant, surgery should be delayed how long post-conception?

A

Surgery is safe from the 15th through 56th day post-gestation in the full- term infant. Elective or outpatient procedures should be deferred until the preterm infant reaches the age of at least 60 weeks post-conception. [Ba- rash, Clinical Anesthesia, 1997, pp1084-l087; Morgan and Mikhail, Clini- cal Anesthesiology, 1996, p734]

166
Q

Surgery in neonates poses a major con- cern-development of apnea in the postop- erative period. Which neonates are at the highest risk for postoperative apnea?

A

Neonates at highest risk for postoperative apnea are those born prema- turely, those who have multiple congenital anomalies, those with a history of apnea and bradycardia, and those with chronic lung disease. [Barash, Clinical Anesthesia, Se, 2006, p1193]

167
Q

Woutd a formerly premature infant be a candidate for outpatient surgery? What are the anesthetic concerns for the formerly premature infant?

A

No, the formerly premature infant is not an appropriate candidate for outpatient surgery. Formerly premature infants (less than 46 weeks post- conceptual age), even if healthy, have an increased rate of post-anesthetic apnea and bradycardia. These formerly premature infants should have cardiorespiratory monitoring for a minimum of24 hours postoperatively and thus are not good candidates for ambulatory day surgery. [Morgan, Mild1ail, and Murray, Clinical Anesthesiology, 4e, 2006, pp1006-!007; Dunn, eta!., Mass Gen Handbook, 7e, 2007, p516]

168
Q

The infant patient is high-risk for postop- erative apnea what agent may be given prophylactically to decrease the risk of ap- nea?

A

The infant at risk for postoperative apnea may be given caffeine prophy- lactically to ensure adequate serum levels exist prior to surgery and dur- ing the postoperative period. Caffeine is a respiratory and CNS stimulant and is generally preferred to theophylline because caffeine has a wider therapeutic margin and a decreased propensity for toxicity. The recom- mended loading dose is 10 mg/kg of caffeine base, which is often obtained from 20 mg of caffeine citrate. The clinical effects of caffeine may last several days after a single dose, but do not administer caffeine and then discharge the patient, assuming that the caffeine will prevent apnea (Cote). [Barash, Clinical Anesthesia, Sc, 2006, p1193; Gregory, Ped. Anes., 4e, 2002, pp376-377; Cote, PAIC, 3’d ed., 2001, p47]

169
Q

W h a t is retinopathy of prematurity?

A

Retinopathy of prematurity (ROP), formerly known as retrolental fibro- plasia, is a fibrovascular proliferation overlying the retina that leads to progressive visual loss. ROP occurs almost exclusively in preterm infants. The risk of ROP is inversely proportional to birth weight, and is associat- ed with neonatal oxygen exposure, apnea, blood transfusion, sepsis, and fluctuating levels of carbon dioxide. [Cote, PAlC. 4th. 2009 pp64; Hines, Stoelting’s Co-existing. Se. 2008 pp588 J

170
Q

Neonatal retrolental fibroplasia is a result of oxygen toxicity above what% inspired oxy- gen?

A

Above 40% oxygen. Physiological studies indicate that the premature infant is probably safe with up to 40% oxygen but some believe that com· plete safety can be achieved only at the normal inspired oxygen concen- tration. [Guyton, TMP, 1996, p10SS]

171
Q

At what gestational age does the risk of retinopathy of prematurity become negligi- ble? Why?

A

The risk of retinopathy of prematurity becomes negligible after 44 weeks postconception because retinal vasculogenesis is complete between 42-44 weeks postconception. [Cote, PAlC. 4th. 2009 pp64; Hines, Stoelting’s Co- existing. 5e. 2008 pp588]

172
Q

What Pa02 and Sa02 are appropriate during anesthesia for the premature infant?

A

There appear to he no clearly established guidelines in the anesthesia literature. S,O, in the 90-95% range (P,O, = 60-80 mm Hg) is believed to be reasonable for the premature infant. The goal specified by guidelines of the American Academy of Pediatrics and the American College of Obste- tricians and Gynecologists is a PaOz between 50 and 80 mm Hg in
premature infants. [Barash, Clinical Anesthesia, 1997, pl112]

173
Q

A neonate is undergoing a surgical proce- dure with the use of a spinal blockade. What sign would indicate a “high” or “total” spi- nal?

A

Decreasing oxygen saturation is the earliest sign of a high or total spinal
i n the neonate. A high or total spinal, produced either with a primary spinal technique or secondary to an attempted epidural, presents as res- piratory insufficiency rather than hypotension owing to the relatively immature sympathetic nervous system in the neonate. With an immature sympathetic nervous system, the cardiovascular parameters are remarka- bly stable in the neonate with a high or total spinal. [Gregory, Ped. Anes., 2002, pp276-277]

174
Q

How do infants react to hypoxia?

A

Infants react to hypoxia with bradycardia progressing to cardiac arrest. [Davison, Eckhardt, and Perese, Mass General, !993, pp249, 400, 508]

175
Q

Whatl\Oz is desirable when ventilating a premature infant for surgery?

A

60-80 mmHg. [Morgan and Mikhail, Clinical Anesthesia, !996, p732]

176
Q

Where should PaO2 be maintained during intracranial surgery in children?

A

For children, PaC02 may be reduced to 20-25 mmi-Ig. [Steward, Manual ofPed. Anes., 1995, p193]

177
Q

What drugs will have a larger volume of distribution in the infant compared with the adult? What drugs will have a smaller vol- ume of distribution in the infant compared with the adult?

A

The infant’s extracellular body fluid compartment is large compared to the adult, so water soluble drugs will have a larger volurne of distribution in the infant compared with the adult. Conversely, lipid soluble drugs will have a smaller volume of distribution in the infant compared with the adult. [Steward, Manual ofPed. Anes., 1995, p43j

178
Q

What is the most prominent muscarinic action of a bolus of succinylcholine in the pediatric patient? How can this action be prevented?

A

Bradycardia develops in response to succinylcholine; for this reason, atropine should be administered prior to succinylcholine. [Stoelting and Miller, Basics, 1989, p399; Morgan and Mikhail, Clinical Anesthesiology, 1996, p732]

179
Q

How much nondepolarizing muscle relaxant does a pediatric patient require compared with adults on a weight basis?
succinylcholine?

A

Neonates, infants and children require the same dose of nondepolarizing neuromuscular relaxant as adults. Neonates require twice as much suc- cinylcholine on a body weight basis than older children or adults. [Stoelt- ing and Miller, Basics, !994, p384j

180
Q

Given that the infant has greater sensitivity to non depolarizing neuromuscular relaxants than the adult (because the neuromuscular junction of the neonate is immature), why is the dose admin- istered on a weight basis the same for infants and adults?

A

Infants have a greater volume o f distribution for muscle relaxants. The increased volume of distribution, normally requiring a greater amount of drug, is by the increased sensitivity of nondepolarizing muscle relaxants at the neuromuscu- lar junction. Thus, the infant dose of nondepolarizer is the same as the adult dose on a weight basis. [Barash llundbook, Clinical Anesthesia, 1997, pp609-610]

181
Q

State two reasons why neonates require more succinylcholine on a mg/kg basis than adults.

A

(1) Neonates have a larger volume of distribution for succinylcholine than adults. 40-50% of body weight of neonate is extracellular fluid (ECF) whereas in the adult ECF is only 20-25% of body weight. Succinylcholine distributes in the extracellular volume so more drug is needed on a per kg basis. (2) Also, the neuromuscular junction is immature (less sensitive) in the neonate, so more drug is needed on this basis. [Stoelting and Miller, Basics, 1994, p384]

182
Q

Define ED90. Stale if the ED90 for succinyl- choline is increased, decreased, or un- changed in the neonate compared with the adult, and indicate what this means.

A

ED90 is the dose of drug that is effective in 90% of the population (ED9o = effective dose in 90% of population), The ED90 for succinylcholine is in- creased in the neonate compared with the adult. An increased ED90 means that a larger dose ofsuccinylcholine must be given to the neonate to achieve adequate paralysis. [Goodman and Gilman, PET, 1996, pp48-49; Au- thors]

183
Q

As you know, neonates require a higher dose of succinylcholine compared to adults. This is due to both an immature neuromuscular junction and greater body water content per unit weight. How would the ED95 for suc- cinylcholine compare between a neonate and an adult-the same, higher, or lower?

A

The ED95 of succinylcholine for the neonate would be greater than that for the adult. Specifically, for succinylcholine the ED,5 = 620 meg/kg for the neonate and the ED95 = 290 meg/kg for the adult. This simply states the need for greater dosing of succinylcholine in the neonate, compared to the adult. [Nagelhout and Zaglaniczny, NA, 2”” ed. 2001, p1!42l]

184
Q

Compare the actions ofvecuronium (Norco- ron) in the infant and the adult with respect to potency, onset, duration of action, and recovery.

A

Vecuronium (Norcuron) has similar potency in infants and adults. Onset is more rapid in infants, duration of action is longer in infants, and recov- ery is slower in infants, compared to adults. [Stoelting, PPAP, yd ed. 1999, p211]

185
Q

How does an infant’s quantity of plasma proteins, body fat, and muscle differ from the adult?

A

Plasma proteins, body fat, and muscle are reduced in the infant compared with the adult. Decreased plasma proteins mean more free drug is available to produce clinical effects. A lower dose ofdrug may be indicated. [Steward, Manual ofPed. Anes., 1995, p43]

186
Q

A two-year-old develops laryngospasm postoperatively and becomes bradycardic. Should atropine be given prior, concurrent- ly, or after succinylcholine? Explain your answer.

A

If continuous positive pressure of 10-15 em I-hO does not break the laryngospasm, then atropine 0.02 mg/kg followed by succinylcholine ( l mg/kg IV; 4 mg/kg IM) is needed. Succinylcholine mimics the effect of acetylcholine at cardiac muscarinic receptors, which can precipitate more severe bradycardia, junctional rhythms, or sinus arrest. [Stoelting, PPAP, 1989, piSO; Rasch, p!23]

187
Q

What is the appropriate volume for a pediatric epidural blood patch?

A

In the child who is awake, the practitioner should stop the blood infusion once the child feels discomfort of pressure in the back In the anesthetized patient, no more than 0.3 mL/kg of blood should be injected into the epidural space. [Motoyama and Davis, Smiths Anesthesia for Infants and Children, 7e, 2006, p468)

188
Q

For the pediatric patient weighing between 2 and 20 kg, what volume (m!Jkg) of0.25% bupivacaine (mL/kg) should be adminis- tered caudally for a block to I.-I or T-12? To T-10? To T-4 or T-5?

A

0.35 mL/kg for L-1 to T-12level block; 0.5-0.75 mL/kg for aT- 10 level block; 0.75-1.25 mL/kg for a T-4 orT -Sieve! block. [Ped. Anes. Hand- book, 1991, p520]

189
Q

What is the maximum dose of0.25% bupivacaine that should be used for pediatric caudal anesthesia?

A

upivacaine (0.25%) at a volume of 1 mL/kg up to a maximum of25 mL can provide 3 to 6 hours of anesthesia for surgical procedures below the level of the diaphragm. [Steward, Manual ofPed. Anes., 1995, p123]

190
Q

Is elimination of amide local anesthetics shortened or prolonged in the neonate compared with the adult?

A

The half-time of elimination of amide local anesthetics is prolonged 2-3 times in the neonate but approaches adult values after six months of age. [Barash Handbook, Clinical Anesthesia, 1997, p220 J

191
Q

Which local anesthetic is not metabolized in neonates?

A

Mepivacaine is not metabolized in neonates; this is controversial, but generally accepted. “The neonatal enzyme systems are adequately devel- oped to metabolize most drugs, with the possible exception of
mepivacaine.” [Stoelting & Miller, Basics, 4e, 2000, p347]

192
Q

Of the following drugs administered to the pediatric patient for sedation, which will have the shortest duration of action: keta- mine (rectal or lM), chloral hydrate (PO), methohexital (rectal), or propofol (IV)?

A

Propofol has the shortest duration of action because it is administered IV. The duration of action of a bolus ofpropofol is 5-10 minutes. Ketamine has a duration of 12-25 minutes when administered rectally or IM. azolam has a duration of2-6 hours when administered IM. Methohexital has a duration of 30-90 minutes when administered rectally. Chloral hydrate, the most commonly used hypnotic for monitored conscious sedation by nonanesthetists, has a duration of 30-60 minutes (PO). Note: IV thiopental has a duration of 5-15 min, which is similar to the duration of propofol. [Omoigui, Anesthesia Drugs Handbook, 1995, ppl72,210,231,298,345; Bell and Kain, Peel. Anes. Handbook, 1997, p447]

193
Q

Compare the onset and duration of intrave- nous morphine in the neonate with the onset and duration of intravenous morphine in the adult?

A

The onset of action of morphine is faster in the neonate compared with the adult, possibly because of greater penetration of morphine through the blood:brain barrier and greater sensitivity of the respiratory centers to morphine. The duration of action of morphine will be longer in the neo- nate because, during the first month, metabolism of morphine by the immature cytochrome P450 system is reduced. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p730]

194
Q

Compare the duration of intravenous mor- phine in the infant and child with the onset and duration of intravenous morphine in the adult?

A

The duration of action of morphine is shorter in the infant and child because, after the first month, metabolisrn of morphine by the mature cytochrome P450 system is increased as a result of greater hepatic blood Oow. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p730]

195
Q

IIState 3 reasons why the uptake of anes- thetic drugs is typically faster in children than in adults.

A

Uptake of anesthetic drugs is faster in children than adults for the following 3 reasons. (I) The child’s higher alveolar ventilation per weight accounts largely for this effect. (2) Increased cardiac output with greater distribution to the vessel-rich groups combined with lower muscle mass aUows more of the agent to concentrate in vital organs, especially the brain. (3) Anesthetic agents appear to be less blood soluble in children than in adults, that is, the agents work (aster in children than adults.[Nagelhout & Zaglaniczny, NA, 3’d eel., 2004, p78]

196
Q

Nitrous oxide (N20) should be avoided in what pediatric procedures?

A

Nitrous oxide should be avoided in numerous procedures including: diaphragmatic hernia, bowel obstruction, pneumoencephalography, tympanoplasty, congenital emphysema, lung cysts, pneumothorax, ne- crotizing enterocolitis, patent ductus arteriosus (PDA), and omphalocele repair. [Motoyama and Davis, Smith’s A1C, 1996, ppl80,457,458,469; Cote et al., PAIC, 2001, p142; Bell and Kain, Ped. Anes. Handbook, Mosby, 1997, p370; Steward and Lerman, Manual ofPed. Anes., 2001, p44]

197
Q

Give the two most important reasons why children are induced faster than adults with inhalational agents.

A

Children have (1) a smaller functional residual capacity per unit of body weight and (2) a greater blood flow to the brain. [Stoelting and Miller, Basics, 1994, pp382, 383I

198
Q

What is the most common type of delirium in children?

A

In children, emergence delirium is more common. Emergence delirium occurs within minutes of regaining consciousness. [Stoelting & Miller, Basics, 4e, 2000, p384l

199
Q

Which fluid is most appropriate for a nor- mal six-month-old patient requiring sur- gery?

A

For short procedures, DSlactated Ringer’s is appropriate. For long proce- dures, lactated Ringer’s is appropriate with separate DSW or DlOW at a rate of4-6 mL!kg/min after blood glucose levels are checked. [Steward, Manual ofPed. Anes., 1995, p106l

200
Q

How many breaths per minute should be produced by the ventilator for the neonate? For the adult?

A

30-50 breaths per minute for the neonate and 12-16 breaths per minute for the adult. [Barash Handbook, Clinical Anesthesia, 1997, p1097l

201
Q

What are two advantages of using Randal- Baker masks in pediatrics?

A

The Randal-Baker mask is designed to fit the facial contours more closely and to reduce dead space (firm rubber). [Smith, p97l

202
Q

The child becomes unruly and combative in the pre-operative period. What agents are appropriate in this situation? Specify the dose and routes of administration of each agent on the list.

A

(1) Methohexital (10% solution): 25-30 mg/kg rectally, produces sleep in 8 - 1 0 minutes if the child weighs less than 20 kg. (2) Ketamine: up to lO mg/kg IM: 10 mg/kg rectally: 6-10 mg/kg orally; 3-6 mglkg intranasally. (3) Midazolam: IM (.025-.05 mglkg): oral (0.5-0.75 mglkg), rectal (.75- !.0 mglkg), nasal (0.2 mg/kg), sublingual (.2 mglkg). (4) Scopolamine: 0.1 mg IM for 6-12 mo.; 0.15 mg for 1-5 yrs. [Miller, Anesthesia, 1994, pp2104-05; Barash, Clinical Anesthesia, 1997, plll7; Morgan and Mi- khail, 1996, p732l

203
Q

What is the best criteria for determining premedication dosages in kids?

A

Body weight of child. [Barash, Clinical Anesthesia, 1997, pp1116-1117l

204
Q

What 9 cardiovascular signs indicate fetal cocaine toxicity in the newborn ofa cocaine- addicted mother?

A

Nine cardiovascular signs of fetal cocaine toxicity are: (I) arterial hypox- emia, (2) increased blood pressure, (3) increased heart rate, (4) increased cerebral blood flow, (5) reduced cardiac output, (6) reduced stroke
ume, {7) right ventricular conduction delay, (8) right ventricular hyper .. trophy, and (9) ST segment and T-wave changes. [Norris, Ob. Anes., 1999, p652; Barash, Clinical Anesthesia, 2001, p1t83I

205
Q

What is the most commonly used analge- sic for pediatric outpatients?

A

Acetaminophen is the most commonly used mild analgesic for pediatric outpatients. The initial dose is often administered rectally (up to 45 mg/kg) prior to awakening from anesthesia. Supplemental doses nre then given orally (10 mg/kg every 4 hours or 20 mg/kg every 6 hours) to main- tain adequate blood levels and effective analgesia. [Cot, PAIC, 3rt! ed., 200!, p61l

206
Q

What is the drug ofchoice and dosing for prophylaxis for pediatric endocarditis?

A

Standard general prophylaxis for pediatric endocarditis is amoxicillin, 50 mg/kg orally I hour prior to procedure. [Nagelhout & Zaglaniczny, NA, 3’” ed., 2004, 229tl

207
Q

The pediatric patient is scheduled for a radiofrequency ablation of an aberrant conduction pathway (e.g., Wolff-Parkinson- White syndrome). Why is a general anes- thetic typically required for this scenario?

A

Radiofrequency ablation is a nonsurgical approach designed to eliminate atrial or ventricular re-entrant tachyarrhythmias. The technique requires mapping and precision ablation of the aberrant pathway, using a radiof- requency ablation catheter. During the ablation, unexpected movement may result in catheter dislodgment and damage to normal conducting tissue; therefore, general anesthesia is usually required in younger chil- dren. Anesthetic agents and techniques should be chosen to maintain circulating catecholamines and avoid suppression of arrhythmogenesis, for identification of the aberrant pathway. [Miller, Anesthesia. 6e. 2005 pp2043]

208
Q

Describe the 4 steps to treating hyper- kalemia in the neonate.

A

Emergent treatment of hyperkalemia in the neonate centers around an- tagonizing the cardiac effects of excess potassium-administer calcium as calcium chloride (O.l mL!kg of 10% solution) or calcium gluconate
0.3-1.0 mL!kg 10% solution) over minutes. Return potassium to the intracellular space by correcting acidosis through administration of sodi- um bicarbonate, mild hyperventilation, and a Maintain potas- sium in the intracellular space by glucose + insulin infusion, 0.5-1.0 g/kg glucose with 0.1 U/kg insulin over minutes). Remove whole-body potassium burden by Kayexalate or dialysis and correct the underlying etiology. [Cote, PA/C. 4th. 2009 pp172-173]

209
Q

An infant has a life-threatening succinyl- choline-induced hyperkalemia: what is the definitive treatment?

A

The definitive treatment of succinylcholine-induced hyperkalemia is IV calcium (10 mg/kg calcium chloride or 30 mg/kg calcium gluconate or more). This restores the gap between the resting membrane potential of the cardiac cells and the threshold potential for depolarization. Repeated doses of calcium must be administered together with cardiopulmonary resuscitation, epinephrine, sodium bicarbonate, glucose and insulin, and hyperventilation until the arrhythmias abate. [Cote, PAIC. 4th. 2009 pp128]