Pediatric/Neonate

Question 1

What is the definition of the neonate, preterm and extremely low gestatonal age?

What are pre-terms at risk for in the perioperative period and some anesthetic considerations for those risks?

Answer 1

• neonate= Birth- 30 days
• preterm <37 weeks
• ELGAN-
  
  • 23-27 weeks gestations; all organs immature
  • most vulnerable peds patient

Pre-terms at risk for:

1. Respiratory distress
   
   • O2 consumption doubled with increased alveolar ventilation–> rapid desaturations especially during cold stress and airway obstruction
2. apnea
   
   • Former premature infants up to 60 weeks PGA are at increased risk for postoperative apnea and bradycardia
     
     • ​calculate PGA by #weeks gestation at birth + current age in weeks after birth
   • requires postop monitoring, admission, and 12 hour period free of apne
3. ​hypoglycemia

• ​minimal glycogen stores and have decreased reserve
• 1st case of day, minimize NPO time
  
  • ​Breastmilk 4 hours
  • formula 6 hours
  • solid foods 8 hours

1. electrolyte disturbance (particularly hypomagnesemia and hypocalcemia)

• dependence on ionized calcium and particularly vulnerable to effects of citrated blood producs
• lower Ca stores in CV muscle cells

1. infection
   * only innate immunity functioning, no acquired immunity
2. hyperbilirubinemia
   
   • reduction in glucuronyl transferase decreases bilirubin breakdown causing jaundice
3. polycythemia
   
   • higher threshold for transufion in preterm neonates (would transfuse to maintain Hct 30%)
     
     • ​INCREASED RISK FOR APNEA IN PRETERM INFANTS IF HCT <30%
   • higher risk for thrombotic compliacations
4. thrombocytopenia
   
   • decreased Vit K dependent factors, at birth 20-60% of adult values)
     
     • reach adult level clotting factors 1 week after birth
   • Decreased PLT function

Question 2

What are some major key points to fetal circulation, specifically describing pre-ductal, post-ductal circulation and the characteristics of each?

Answer 2

• (high o2 blood) Placenta → Umbilical vein (high pressure if contraction occurring)→ ductus venosus (DV) *high intrahepatic pressure* → most blood gets shunted away from liver → IVC (most blood)→ RA….
• PREDUCTAL Circulation (Parallel circulation): IVC→ RA (high rate of flow) → Foramen Ovale (FO)→ LA (high O2 []) → LV → aorta
  
  • HIGH O2 blood to head, neck, and RUE drained into SVC = then MIXED (high O2-RA→ FO→ LA→ LV)
    
    • Less oxygenated than blood that went straight to head, neck, arms
• Postductal Circulation: If stayed in RA → RV → pulmonary artery *high pulm resistance* (only 12% [10-15%] blood goes to lungs) → ductus arteriosus (DA) (~85% blood from RV) → aorta → goes systemic circulation (MIXED BLOOD)
  
  • Ductus arteriosus- keeps lungs from being overloaded by blood

OVERALL:

• Pre-ductal: More oxygenated blood going to head, neck, RUE
  
  • From IVC → RA → LA→LV→Aorta→ head, neck, RUE → SVC
• Post-ductal: More deoxygenated blood going to system circulation from DA!
  
  • Liver, kidney, lower extremities
• High pulmonary vascular resistance and low systemic circulatory resistance
• Minimal intrauterine pulmonary blood flow: only ~10% of the cardiac output

Question 3

What is transitional circulation in the neonate? What can cause the occurrence of transitional circulation and what are common prevention and treatment strategies for its occurrence?

Answer 3

Transitional circulation: occurs at birth for the first several weeks

• Functional Closure of FO and DA right after birth
  
  • → flap not permanently closed
  • Can reopen if introduced with high pressures or low O2
    
    • DA: true closure → 4-6 weeks after birth
    • FO: true closure→ few weeks after birth
      
      • 25-30% of adults have patent foramen ovale
        
        • L or R heart stress= flap opens
        • Easier with R heart stress (ex: pulm HTN, pulm vascular resistance)
          
          • R → L

Period of vulnerability: fetal circulation persists in times of stress

• Hypoxia (acidosis)
• Hypercapnia (acidosis)
• Hypothermia
  
  • (any stressful events) *why we need to avoid stress in neonate*
  • If any of those things happen, can lead to:
    
    • ↑ pulmonary artery pressure
      
      • → Reversal of flow through FO
      • → reopening of DA (bc functionally closed) & FO
    • Shunting (bc low pulm vascular resistance)→ hypoxia is difficult to correct
      
      • low pulm. vascular resistance and DA open → lots of deoxygenated blood bypassing lungs
      • If reopened will see:
        
        • Preductal (RUE): lower pulse ox and ABG (RV blood being shunted to DA)
        • Postductal (LLE): normal pulse ox and ABG
• FYI: Measuring on…
  
  • Pulse ox (pre-RUE, post-Lower extremity)
  • ABG (pre-RUE, post- Umbilical Artery/femoral artery)

Prevention:

• Optimal oxygenation
• Correct acidosis
• WARM
• Stress free

Treatment: hyperventilate to reduce PaCO2

Question 4

What CV changes occur at birth to transition from fetal to adult circulation, and why do these changes occur?

Answer 4

Changes that allow parallel circulation of the fetus to convert to the series circulation of the adult:

1. Pulmonary Vascular Resistance DECREASES
   
   1. 1^st breath → expansion of lung → pulm vascular resistance DROPS → increased alveolar O2 → increase in pH
   2. neurohumoral mediators and nitric oxide (NO) relaxes pulmonary vasoconstriction.
2. FO closes
   
   1. When placenta separates from uterine wall:
      
      1. placental BV constrict
      2. SVR & left ventricular afterload increase.
         
         1. Decrease PVR + increase SVR → increases left atrial pressure above right atrial pressure
            
            1. Pressure: LA > RA → functionally closes FO “flap valve”
               
               1. FO not close anatomically for months to years (if ever)
               2. Patent in ~15% adults.
3. Ductus Arteriosus closes
   
   1. decrease PVR causes flow through the ductus arteriosus to reverse.
      
      1. This exposes the ductus to oxygenated systemic arterial blood + rapid decrease prostaglandin E 2 (PGE2) after birth → closes ductus arteriosus
      2. Anatomic closure of the ductus requires several weeks.
   2. D/t Increase PaO2 exposure >60 mm Hg → cause vasoconstriction → functional closure of ductus arteriosus
4. Ductus Venosus Closes
   
   1. The ductus venosus closes passively with removal of the placental circulation and readjustment of portal pressure relative to inferior vena cava pressure.
5. There is a further gradual decline in PVR secondary to structural remodeling of the muscular layer of the pulmonary blood vessels. During fetal life, the central pulmonary vascular bed has a relatively thick muscle layer.
   
   1. After birth, the muscle coat thins and extends to the periphery of the lung, a process that takes months to years to complete
   2. Expansion of the lungs at birth decreases pulmonary vascular resistance, and the entire right ventricular output is diverted to the lungs

**Overall: Increase SVR + decrease PVR → functional closure of PFO & ductus arteriosus (blood not being oxygenated by lung is NOW going through lungs to be oxygenated) **

Question 5

What are some physiologic differences in the cardiovascular system of the neonate?

Answer 5

• ## Newborn heart: “extreme example”
  • Changes progressively get more adult like as ages
  • structurally immature- cells not organized in parallel yet
  • fewer myofibrils
  • sarcoplasmic reticulum immature
  • ↓ cardiac calcium stores
• ## Ventricles are less compliant:
  • ## ​Cardiac output → HR dependent****
    • Ex: Less responsive to volume loading than child & adult
• Baroreceptor reflex immature:
  
  • Ex: inability for reflex tachycardia when compensate for hypotension
• Parasympathetic dominance
  
  • Sympathetic nervous system immature
    
    • Ex: Tendency to have bradycardia with suctioning & laryngoscopy
      
      • → premed against brady when exposing them to those stressors
• Resting CO:
  
  • Neonate at birth: ~400 mL/kg per min
    
    • ↑ resting CO → reserve limited
  • Infant: 200 mL/kg per min
  • Adolescent: 100 mL/kg per min
• Dependence on ionized calcium: particularly vulnerable to effects of citrated blood products
  
  • d/t lower Ca stores in CV muscle cells → ↑ dependency in iCa
  • Citrate blood products bind to Ca → replace Ca
• ## Neonatal myocardium is not as compliant compared to an older child → “relatively noncompliant muscles”
  • ↑ preload does not increase SV to the same degree
  • Can’t generate great contractile force
  • ↑ Afterload → poorly tolerated
• Hypovolemia & bradycardia
  
  • → dramatic ↓ CO that threaten organ perfusion (d/t lack of compliance)
• ​Epinephrine >>> atropine
  
  • ↑ contractility
  • ↑ HR
    
    • preferred treatment of bradycardia & decreased CO in peds pts
    • 1^st 3 mo – not respond as well to inotrope support → *maturational changes in beta receptor fx (not capable of responding)
      
      • Ex: Adult increase CO x 300%
      • Ex: Newborns only increase CO 30-40%

Question 6

Describe some characteristics of the pulmonary system in the pediatric patient?

Answer 6

• *Alveoli increase in number & size up until 8 yo

·Infants:

​Highly compliant airway & chest wall

• Small airway diameter → ↑ resistance (with any swelling)

Swelling drastically increases resistance compared to adults (1 mm swelling→ ­ resistance x 32 fold)

• Chest wall: cartilaginous → more likely to collapse)
• ​Closing capacity >> FRC (in very young & very old)
  
  • AW closure can occur before end exhalation
• ### Early fatigue of diaphragmatic & intercostal muscles until age 2 (Type 1 muscle fibers not mature)
  • Type 1 (slow twitch)- long lasting/resistant to fatigue
  • Type 2- react quick but fatigue
    
    • → (Why they wear out fast, not mature Type 1)
      • oInfants T1 muscle fibers: 10%
      • oAdults: 55%
• ### ​​​​Angulation of right mainstem bronchus → more likely to have R mainstem intubation
• ## O2 consumption 2-3x’s HIGHER than adult with increased alveolar ventilation
  • ## leads to rapid desaturations especially during cold stress and in the case of airway obstruction
• MV:FRC ratio 2-3x higher than adult
• Faster for induction/emergence
• Less O2 reserve

Question 7

Describe the differences in airway anatomy in infants compared to adults?

Answer 7

Infant:

• larger tongue in smaller submental space
• higher larynx
  
  • infant= C2 to C4
  • adults C4-C6
• short stubby (omega shaped) epiglottis, stiff (apex says long and stiff)
  
  • ​may need miller blade in peds
  • ​adults short and floppy “leaf shaped”
• angled vocal cords (slant caudally)
  
  • ​looks like anterior airway, Miller blade more appropriate
• funnel shaped larynx with narrowest region @ cricoid ring
  
  • need various ETT sizes available
  • Age +16/4 standard calculation for uncuffed tube. if cuffed tube needed, decrease by 1/2
• obligate nasal breathers
  
  • 5 month switch to mouth breathing– periods of stuffy nose can be poorly tolerated
• large occiputs & the “sniffing” position is favored for axis alignment
  
  • shoulder roll useful. large head c/t body, no hyperextension!
• endentulous
  
  • ​Tooth eruption normally occurs between 4 and 12 months of age for the first tooth; eruption of the 20 primary teeth should be complete between 24 and 30 months of age.
• short trachea (4-5 cm)
  
  • easily can right main stem
    *

Question 8

Why might an infant have decreased thermoregulation in the OR? What are some anesthesia considerations to maintain normothermia in the OR, including implications of both hypo and hyperthermia.

Answer 8

Infant decreased thermoregulation d/t:

• Large surface area to body weight
• Lack of subcutaneous tissue as an insulator
• < 3 mo →Inability to shiver:metabolize brown fat to increase heat production
  
  • can lead to metabolic acidosis & increased O2 consumption
    
    • Brown fat: tissues in neck, vertebral column, around adrenal glands → Metabolically stressful!

Anesthesia considerations

• warm the OR (dec convection) 72-76^{o (or 80’s)}
• head coverings (up to 60% of heat loss)
• transport in isolette
  
  • use a warming mattress
  • use incubators
  • cover with blankets- dec radiation
• humidify gases- dec evaporation
  
  • single limb circuit**- gases getting warmed up by exhaled air
• use plastic wrap on the skin
• warm prep & irrigation solutions
• change wet diapers & remove wet clothing
• Forced air warmers: the most effective strategy to minimize heat loss in surgery in children > 1 hr
  
  • Careful w/ injury!
• Anesthetics alter non-shivering thermogenesis in neonates

Temperature monitoring is Essential for all pediatric cases

• Mid-esophageal placed probe- best core temp!
  
  • precodial stethoscope has attachment for temp!
• Axillary temp: Advantage - if properly positioned:
  
  • proximity to deltopectoral group improves recognition of elevated temp in MH
• NO FOREHEAD TEMP- not advised
  
  • 10 MH episodes occurred that were unrecognized with forehead temp (Barash)
• Hypothermia: consequences →
  
  • delayed emergence- metabolism of drugs slower
  • reduced degradation of drugs
  • increased infection
• Hyperthermia: MH? → primary presentation not always fever (1^st see ETCO2)
  
  • Stop VA, high flow on, switch to TIVA, evaluate (stop anesthetic d/t Ca dysregulation getting worse)

Question 9

Neuraxial considerations in pediatrics

Answer 9

• The conus medullaris ends at approximately L1 in adults and at the L2–L3 level in neonates and infants.
• In infants, the line across the top of both iliac crests (the intercristal line) crosses the vertebral column at the L4–L5 or L5–S1 interspace, well below the termination of the spinal cord
• The dural sac in neonates and infants also terminates in a more caudad location compared to adults, usually at about the level of S3 compared to the adult level of S1
• Infants: lack of a lumbar lordosis compared to older children predisposes the infant to high spinal blockade with changes in positioning

Question 10

Renal characteristics of infants?

Answer 10

• GFR is significantly impaired at birth but improves throughout the 1st year
  
  • greatest impairment is in 1st 4 weeks of life
  • renal maturation will be delayed further with prematurity
    
    • UOP low at birth x 24 hours then increases to 1-2mL/kg/hr
    • be concerned after 24 hours with low UOP
    • in utero kidney only receives 3% blood flow. adult 25%.
• Renal tubular concentrating abilities do not achieve full capacity until ~2years
  
  • difficulty with concentrating and diluting urine
  • does not respond as well to aldosterone
    
    • hypo/hypernatremia can easily become an issue
• Half-life of medications excreted by glomerular filtration are prolonged in the very young (antibiotics; etc.)
• In contrast, during childhood, renal clearance rate may increase to levels higher than even adult clearance rates
  
  • higher CO, more blood flow in childhood

Question 11

Liver function in infants?

Answer 11

• Enzyme systems are still developing up until 1 year of age
• Phase I Cytochrome P450 system is 50% of adult values at birth
  
  • 3A4 50% drugs
  • 2D6= 10-20% drugs
• Phase II (conjugation reactions) are impaired in neonates
  
  • Long half life of BZD and morphine
  • Decreased bilirubin breakdown due to reduction in glucuronyl tranferase (leading to jaundice)- also metabolize tylenol
• Hepatic synthesis of clotting factors reach adult levels within a week of birth
  
  • ​Vit K dependent factors (II, VII, IX, X)
    
    • ​at birth 20-60% adult values
    • preterm values even less
• Lower levels of albumin/ other proteins for drug binding in newborns- larger proportion of unbound drug circulating
  
  • increases effect of highly protein bound drugs.
• Minimal glycogen stores- prone to hypoglycemia

Question 12

GI system in pediatrics?

Answer 12

• Obligate nose breathers
  
  • Coordination of swallowing with respiration not mature until 4-5 months of age (grow out of it eventually)
  • high incidence of reflux especially in pre-terms
    
    • coanal atresia- blockage of nasal to trachea
      
      • resp depression bc want to breathe through nose! Will breath better when crying
• Gastric juices are less acidic (more neutral) up to ~3 years of age
  
  • Less absorption of drugs
• Absorption of oral medications is generally slower compared to adults (less effective)
  
  • The gastrointestinal tract is generally slower in children than in adults
  • Children have differences in gastric pH, emptying time, intestinal transit, immaturity of secretions, and activity of both bile and pancreatic fluids

Question 13

How can body composition of infants alter pharmacokinetics?

Answer 13

• Water soluble drugs have a larger volume of distribution (have higher TBW)
  
  • Need a larger initial dose (Sch; abx- higher dosing of water soluble drugs)
  • Delay excretion – from larger volume of distribution
• Half-life of medications in >2 years of age is shorter than adults or equivalent due to significant CO to liver & kidneys
  
  • More fentanyl/propofol mg/kg
• Pharmacokinetics in children varies with body composition, renal and hepatic function, and with altered protein binding
• Neonates have less fat & muscle
  
  • Drugs that depend on redistribution to fat for termination of action will have prolonged effects (fentanyl; propofol)
• Protein binding: < 6 months old have reduced albumin & alpha-1 acid glycoprotein (AAG)
  
  • higher free-fraction of protein bound drugs → higher risk of toxicity!!
    
    • Free fraction of lidocaine will be higher in the very young!
    • Acidic drugs tend to bind mainly to albumin (e.g., diazepam, barbiturates)
      
      • plasma protein binding of many drugs is decreased in the neonate relative to the adult in part because of reduced total protein and albumin concentrations.
    • Basic drugs bind to globulins, lipoproteins, and glycoproteins. (e.g., amide local anesthetic agents)

“In general, most medications will have a prolonged elimination half-life in preterm and term infants, a shortened half-life in children older than 2 years of age up to the early teenage years, and a lengthening of half-life in those approaching adulthood.” – patient to patient variability ***

Question 14

Difference in drug pharmacokinetics in infant, childhood to adulthood?

Answer 14

• Preterm/infants: prolonged elimination half-life
• >2 yo to early teenage yrs: shorted half-life
• Adulthood: lengthened half-life

Question 15

Difference in hematocrit and blood volume in infant?

How do we dose blood transfusions in infants?

Answer 15

Fetal Hgb:

• Lower P50 (19 mmHg vs. adult normal of 26 mmHg) → left shift = Holds onto O2!
• Low levels of 2,3 diphosphoglycerate
  
  • This lower P 50 allows the fetus to load more oxygen at low placental oxygen tension, but it makes unloading oxygen in tissues more difficult.
  • 3- 6 months after birth → fetal hemoglobin has been replaced with adult hemoglobin.
    
    • Tolerate Anemia more poorly bc left shift
    • Blood products helpful d/t having adult Hgb that allows released O2 to tissues
• Target hct in neonates is higher
  
  • Hct minimum 40% (instead of 30%)
  • Why?: bc
    
    • L shift
• Tx: 4-5 ml/kg of transfused PRBC’s increase hgb ~1g/dL
  
  • Order blood based on body weight
  • Ex: 15 kg pt = 75 ml blood
• Physiologic Natar: lowest point of anemia as fetal Hgb being replaced (PERIOD OF TRANSITION)
• Physiologic anemia at 2-3 months of age→ lower threshold to give blood products (low P50 & physiologic anemia)

Question 16

What are some considerations of glucose administration and hypoglycemia prevention in infants?

Answer 16

• Routine use of glucose-containing IVF in the perioperative setting in children is NOT recommended
  
  • Exception: Children at high risk of hypoglycemia- can use D5 1/2NS @ maintenance rates
    
    • Don’t use for BL or evaporative loss replacement (must use balanced Na solution)
  • Continuous TPN:
    
    • must NOT suddenly stop
    • consider leaving on at a reduced rate
    • some providers may use D10 to bridge- monitor glucose!!
  • Children with mitochondrial disease will definitely need glucose containing replacement fluid

Miller says cut the TPN rate by one third and leave running

Question 17

Why is uptake of VA more rapid in children?

Answer 17

Uptake (Wash-in) more rapid in children for several reasons:

• increased respiratory rate
• larger proportion of CO to VRG (heart, brain, GI, kidneys, endocrine)
• Reduced tissue/blood and blood/gas solubility in infants
• Increased Alveolar ventilation to FRC ratio
  
  • Infants: 5:1
  • Adults: 1.5:1
• *Increased risk of anesthetic overdose in infants/ toddlers
  
  • Faster equilibration to what set on dial (from co-exist lecture last semester)
    
    • Determinants of “wash in” of VA → FRC, inspired concentration, alveolar ventilation
      
      • Wash in is inversely related to solubility= lower solubility→ higher wash in
        
        • Less is binding to tissue, less dissolved in blood
    • Removal → CO, solubility, alveolar-venous partial pressure
• 18% BF to VRG in infants as opposed to only 8% in adults

Question 18

MAC for sevo and des in neonate, infant and children?

Answer 18

I doubt they’ll ask specific MAC differences for nenonate, infant and children. Instead they might want us to say Sevo MAC remains slightly elevated, but the same from neonate–> infant, then decreases in childhood. Desflurane increases from neonate–> 1 yo then steadily decreases?

• Sevoflurane:
  
  • Neonates: 3.3%
  • Infants (1-6 mo): 3.2%
  • Children (> 6 mo): 2.5%
• Desflurane:
  
  • Neonates: 9.2%
  • Infants (1-6 mo): 9.4
  • Infants (6-12 mo): 9.9%
  • 1-3 yo: 8.7%
  • 5-12 yo: 8%
• All VA: MAC increases until 2 to 3 months of age (max: 1 to 2 years old) and steadily declines with age thereafter
• Sevo (Exception): MAC remains constant in neonates and infants up to 6 months
  
  • MAC up to 6 months is ~3.2%
  • MAC 6 months to 12 years is constant at 2.4% (decrease)

Question 19

How do you determine how much blood to transfuse in infant?

Answer 19

• Once MABL is approaching, if blood loss is expected to continue then blood will be given
  
  • always use a blood warmer
• Calculation of blood to be transfused: (desired hct - current hct) x EBV

hct of PRBC’s (which is 60%)

• > 1 blood volume replaced → FFP will be needed
• Watch for ionized hypocalcemia & resultant CV depression (esp w/ rapid infusion of FFP)
  
  • Reasons for it being risk:
    
    • Ca stores already low in neonates
    • FFP has highest concentration of citrate
  • neonates & children with liver failure are at pronounced risk
• Platelets: need for replacement depends on starting platelet count- clinical oozing on the field is the typical indicator
  
  • Starting normal platelet count usually does not need platelets UNTIL EBL > 2 blood volumes

Question 20

Coagulation in newborns/infants?

Answer 20

• At birth, vitamin K-dependent coag factors are low ( 2,7, 9,10)
  
  • reach adult levles by 6 months age
• fibrinogen polymerization does not reach its full capacity during first few postnatal months
  
  • leads to prolonged thrombin time
• PLT number at birth comparable to adults
  
  • however, PLT function impaired in early life
• Postnatal period represents hypercoaguable state
  
  • d/t inhibitor of coagulation decreased by 30% to 50% in newborn
• Antithrombin III and protein S levels reach maturity by 3 months of age
  
  • protein C and plasminogen levels reach adult levels after 6 months of life
• higher risk for thrombotic complications in neonates and infants.

Question 21

Induction agent use in pediatrics?

Propoofl, ketamine, etomidate, thiopental, methohexital doses?

Answer 21

• Neonates: Immature BBB & decreased metabolism can increase sensitivity
  
  • increased permeability of BBB makes more sensitive

Older children & adolescents generally require increased doses of induction agents compared to adults

• Dosing:
  
  • Propofol (Diprivan): have extra available
    
    • < 2 yo: 2.9 mg/kg
    • 6-12 yo: 2.2 mg/kg
  • Ketamine:
    
    • 2 mg/kg IV
    • 4-8 mg/kg IM (plus atropine 0.02 mg/kg IM/IV → for hypersalivation)
  • Etomidate:
    
    • 0.25-0.3 mg/kg
  • Thiopental sodium (Pentothal):
    
    • neonates (< 1 month): 3 to 4 mg/kg
    • infants (1 m–1 yr): 7 to 8 mg/kg
    • Children: 5-6 mg/kg
  • Methohexital: ECT therapy
    
    • 2 mg/kg IV or 15-25 mg/kg of a 1% or 20-30 mg/kg of a 10% solution PR

Question 22

Propofol use in pediatrics?

Answer 22

• Most commonly used IV induction agent in children
• Greater Vd than adults
• More rapid redistribution
• Pain of injection can be reduced with a mini Bier block with 0.5-1 mg/kg of Lidocaine for 60 seconds (BP cuff)
• Antiemetic properties
• TIVA- lower rate of PONV/emergence delirium
  
  • Propofol infusion syndrome: long term infusions in ICU avoided in infants & children (acidosis); still appropriate for TIVA case
  • Egg/soy: only avoid if documented anaphylaxis with eggs

Question 23

Ketamine use in pediatrics?

Answer 23

• can be used IM, IN, PO, IV → hemodynamic compromised pts
  
  • Induction with ketamine preferred in
    
    • severe hypovolemia,
    • cyanotic heart disease,
    • septic shock, & induction for mediastinal mass (need spontaneous ventilation)
  • Increased secretions (premedicate w/ anticholinergic)
    
    • Ex: atropine
  • Emergence irritation
    
    • reduced with co-administration w/ Midazolam
    • waking up in a dark/quiet room

Question 24

Midazolam use as sedatives in pediatrics?

Metabolism?

Reversal agent?

Answer 24

most widely used anxiolytic pre-op

• Oral dosing:
  
  • dose increases in younger patients
  • poor oral bioavailability
  • bitter taste
  • allow 10-15 minutes
    
    • ORAL dosing: dose decreases w/ age
      
      • 18 mo-3yo: 0.75-1 mg/kg
      • 3-6 yo: 0.6-0.75 mg/kg
      • 6-10 yo: 0.5 mg/kg 6-10 yo
• IV: 0.1-0.2 mg/kg (immediate onset)
• Intranasal: 0.3 mg/kg
  
  • MAX DOSING: 15 mg
• Reversal:
  
  • flumazenil 0.01mg/kg IV
• Hepatic metabolism (CYP 3A4) & renal excretion

Question 25

Ketamine use in peds as sedatives?

Answer 25

• Severe cognitive/ behaviorally challenged older children → IM administered preop ** preferred
  
  • IM dose: 4-5 mg/kg
  • Onset: 3-5 minutes
  • Duration: 30-40 minute duration
• Oral onset: 15-20 min

Question 26

Dexmedetomidine as sedative in pediatric patients?

Answer 26

• hypotension with loading doses
• bradycardia with high dose infusion
  
  • (note biphasic response with transient hypertension initially) → then hypotension
• will not be adequate as a sole anesthetic but can be helpful as adjunct
• opioid sparing effects
  
  • Uses:
    
    • useful in awake FOB
    • radiological procedures
    • reduction of emergence delirium
• Dosing:
  
  • IV:
    
    • initial dose: 0.7-1.0 μg/kg administered over 10 minutes
    • → followed by infusion: 0.5-1 μg/kg/hr
  • Intranasal: 80% bioavailability!! great premed!! But takes long to peak
    
    • Dose: 1-2 mcg/kg
    • Peak: 30-40 min (long time)

Question 27

Considerations of opioids in pediatrics?

morphine? fentanyl? dilaudid? remi? demerol? codeine?

Answer 27

• Variety of choices: onset, potency, duration, & metabolism are factors just like in adults
  
  • Also consider previous exposure to opioids (tolerance), severity of pain, & other multi-modal strategies
• Morphine:
  
  • active metabolite (morphine-3- glucuronide)
    
    • → cause prolonged respiratory depressant effects in neonates and preterm and critically ill infants
  • Dosing: 50-100 mcg/kg (IV) per single dose
• Dilaudid dosing: 10-20 mcg/kg (IV) per single dose
• Fentanyl: most widely used opioid intra-op in children
  
  • stable CV profile
  • Caution: chest wall rigidity
  • Dosing variability
    
    • ~ 0.5-1 mcg/kg range
      
      • Work up to 1-3 mcg/kg range (IV) per single dose & titrated for effect
      • Safely go up to 10 mcg/kg depending on sx
• Remifentanil:
  
  • excellent for neonates
    
    • great choice in renal/hepatic failure/immaturity (due to metabolism via esterases → mature system in neonate)
    • predictable eliminiation
  • Caution:
    
    • bolus injections can cause significant bradycardia/hypotension
    • must have plan for analgesia once infusion discontinued
  • Dose: 0.05-0.1 mcg/kg/min
• Demerol:
  
  • Admin for shivering in small doses (0.25-0.5 mg/kg)
  • Metabolite: normeperidine
• Codeine:
  
  • historically very commonly prescribed postop
  • withdrawn from many markets due to respiratory events
    
    • SNP’s in ultra-rapid metabolizers confer risk of OD (CYP affected)→ BLACK BOX warning
    • Slow metabolizers- placebo

Question 28

Acetaminophen and ketorolac use in peds?

Answer 28

• Acetaminophen:
  
  • PO 10-15 mg/kg
  • IV: 15 mg/kg q 6 hours (10-15 min onset)
  • rectal absorption: SLOW (1-2 hours)
• Ketorolac:
  
  • Dose: 0.5 mg/kg IV
  • Ask surgeon before administration
  • CAUTION:
    
    • Severe asthma → caution all NSAIDs
      
      • Nasal polyps, eczema, and asthma → tend to have NSAID allergies

Question 29

What are some consideration for the use of muscle relaxants in pediatrics?*

Answer 29

• NMJ not fully mature until ~2 months of age
  
  • Infants: may be more sensitive to NDNMB but also have larger VD → so dose/kg is usually the same as adults
    
    • EXCEPTION: Rocuronium- dose is lower in infants
      
      • ex: infants 0.3 mg/kg
      • ex: children: 0.6 mg/kg
      • RSI: same
• Considerations:
• • Always use nerve stimulator → response is highly variable (neonates not have normal resp to NS)
    
    • Use small doses
    • Reassess frequently
    • May see a prolonged duration of action due to immature renal/ hepatic elimination

Use of succinhylcholine:

• Higher Sch doses needed in neonates & infants due to larger VD
  
  • < 1yo: (2-3mg/kg)
  • Older → dose gets smaller
• Sch is limited to RSI and emergency tx of laryngospasm in Peds
• Cardiac sinus arrest may follow 1st dose of succs → more common after repeated bolus admins in any age
  
  • Co-administer w/ vagolytic drug (atropine) should probably be intravenously administered just before the first dose of succinylcholine in all children, including teenagers
    
    • unless a contraindication to tachycardia (e.g., a cardiomyopathy) exists
• _RISKs***_:
  
  • Bradycardia
  • Hyperkalemia
  • masseter spasm
  • MH in children w/ undiagnosed myopathies

Question 30

NMB reversal in pediatrics?

Answer 30

• Routine reversal for TOFR < 0.9
  
  • Neostigmine: dose for infants & children 30-40% lower than adults
    
    • Dose: 0.02-0.04 mcg/kg
    • co-administered with anticholinergic
      
      • glycopyrrolate 0.01mg/kg
      • atropine 0.02mg/kg
• Sugammadex: not FDA approved in peds
  
  • Dose: 2 mg/kg
  • Always reverse peds pts!

Question 31

Local anesthetic use in pediatrics?

Answer 31

• Cardiac output and local blood flow: 2-3x greater in infants than in adults
  
  • → so systemic LA absorption is increased (higher chance of LA toxicity)
• Epinephrine is effective in slowing systemic uptake
• Very Low Plasma concentration of AAG at birth (0.2 to 0.3 g/L) and does not reach adult levels (0.7 to 1.0 g/L) before 1 year of age
• Free fraction of all local anesthetics is increased in infants

Maximum doses of all amino-amides must be reduced (KNOW DOSES!) → think about cumulative amount going to give

Extra key points about LA:

• Nonionized LA cross almost freely the capillary wall close to injection site
• rbc storage
  
  • In neonates, high HCT values (exceed 70%) and enlargement of erythrocytes cause entrapement of LA and lower peak plasma concentrations after a single injection, but increases secondary release. which increases half life of LA
  • in infants: a physiologic anemia reduces RBC storage of LA and protects against systemic toxicity.
• LA are metabolized by CYP45, CYP3A4 metabolizes lido and bupi. cyp1a2 metabolizes ropi. these hepatic systems are immature at birth

Question 32

Generic Preop eval for pediatric patient?

Answer 32

• Standard adult history and physical exam must be adapted; some topics that require further emphasis in children
• Birth history; prematurity
• Neurologic development- appropriate for chronological age? psychological issues?
• Airway anomalies, surgical history, previous intubations, and general medical health (heart, lung, endocrine, renal disorders)
• AW exam:
  
  • Indicators for Difficult AW:
    
    • check for facial dysmorphias
    • signs of stridor, dysphonia, swallowing disorders, difficulty in breathing, difficulty in speaking, and hoarseness
• Genetic or dysmorphic syndrome?
  
  • Potential for anomalies in the cervical spine (eg, Down syndrome) or craniofacial dysmorphia
    
    • Down syndrome- atlantoaxial subluxation at C1-C2 level
• Family history: fevers or troubles waking up? MH, PD
  
  • (1) malignant hyperthermia (MH)
  • (2) pseudocholinesterase deficiency
  • (3) postoperative nausea and vomiting
  • (4) congenital myopathies
  • (5) bleeding (brushing teeth)
• No laboratory work is indicated for healthy children undergoing a procedure with minimal blood loss anticipated
• Routine pregnancy testing: controversial; parents may decline; history alone can be unreliable
  
  • Have waver ready
  • Midaz- iatrogenic effect
• Higher risk for latex allergy in certain pediatric populations:
  
  • Ex: spina bifida, myelodysplasia, urinary tract malformations; multiple previous surgeries

Question 33

s/s of difficult airway in peds?

Answer 33

• Mandibular protrusion
• mallampati
• movement of atlantooccipital join
• reduced mandibular space
• increase tongue thickness
• age <1 yo
• ASA II-IV
• Obesity
• maxillofacial and cardiac sx

Question 34

What questions can you ask during preop eval focusing on respiratory system

Answer 34

• Frequent upper respiratory infections (URIs)?
  
  • Risk for post op resp complications/laryngospasm
  • Up to 6 weeks after URI
• History of wheezing? History of noisy breathing? Hospitalizations? History of intubations?
• History of eczema/skin allergy/atopy? → likely to have bronchospasms/AW issures
• In daycare? Immunization status? Smokers in the house? → prone to reactive AW dx
• Infant: Frequent vomiting after feeds/“choking” episodes? → reflux
• Child: Frequent tonsillitis? Ear infections? Snoring?

Airway history

• Presence of URI- risk of larynospasm
• Snoring or noisy breathing
• Presence and nature of cough
• Past episodes of croup
• Inspiratory stridor, usually high pitched
• Hoarse voice
• Asthma and bronchodilator therapy
• Repeated pneumonias
• Previous anesthetic problems, particularly related to the airway
• Atopy, allergy
• History of a congenital syndrome
• Parents smoke in the house? Increase risk of laryngospasm
• Suspicion of a C-spine anomaly?
  
  • down syndrome, klippel-feil, goldenhar
  • fracture/sbuluxation/neck burn
  • RA

Question 35

CV focused questions to assess during preop pediatric patient?

Infant vs older child?

Answer 35

Any family history of CHD/chromosomal abnormalities, sudden/premature death; maternal illness/infections (both chronic and during pregnancy); maternal medications/drug use

• Infant: look for clues on undiagnosed congenital heart defect →
  
  • Any problems with poor feeding, sweating (especially on the forehead) during feeding, poor weight gain, FTT, decreased activity level
  • Symptoms of CHD often occur with feeding because of increased oxygen consumption and the need for greater cardiac output.
    
    • Need further testing
  • Babies with cyanotic heart disease turn dark blue or ruddy in color when crying because of prolonged expiratory phase and resulting increase in right-to-left shunting.
  • Hypercyanotic spells are often associated with extreme irritability and rapid, deep, and sometimes labored respirations.
• Older child/ adolescent:
  
  • Any inability to keep up with the activity level of peers, need for frequent periods of rest, anorexia, cough, wheezing, rales, chest pain, leg cramps, syncope, light-headedness, palpitations; any history of drug use; any family history of sudden death, syncope, or arrhythmias
• Any changes in color or cyanosis when crying? → undiag congenital heart defect

Question 36

Considerations for known difficult airway in peds?

Answer 36

• Have LMA out & ready for back up
  
  • may use LMA as conduit for FOB

Sample plan: known difficult airway plan for nasal intubation with FOB → MAINTAIN SV!!! No apnea!!

• Apply standard ASA monitors; inhalational induction with sevoflurane, and maintain spontaneous ventilation (may require an oral airway)
• Obtain intravascular access if not previously obtained.
• Administer:
  
  • glycopyrrolate (5 mcg/kg)
  • propofol as needed to deepen anesthetic (larger doses may cause apnea) → don’t induce apnea
• Prepare nasal cavity with oxymetazoline → reduce bleeding
• Size both nostrils with a nasal pharyngeal airway (NPA). Keep the NPA in the smallest nostril and attach endotracheal tube connector to the end of the NPA. The patient can now entrain air : oxygen and sevoflurane during spontaneous ventilation.
• Place a fiberoptic scope with a previously loaded nasal RAE endotracheal tube through the opposite nostril. Suction should be attached to the suction port.
• Visualize the glottic opening. Spray the vocal cords with lidocaine (use 2% if over age 2 years, 4% if over age 8 years). Enter the trachea, and spray the trachea.
• Lubricate the endotracheal tube and slowly pass through the nose into the trachea. Downsize the endotracheal tube by 0.5. Apply slow, steady pressure.
• Place endotracheal tube connector from the NPA onto the ETT and confirm end-tidal CO2

Question 37

Ventilation considerations for peds?

Answer 37

• 6 to 8 mL/kg is typical
• Sustained plateau airway pressures > 35 cm H2O can lead to barotrauma:
  
  • Pneumothorax
  • Pneumomediastinum
  • subcutaneous emphysema
• Lung protective strategies apply
• Pressure control ventilation is proffered
• Peak inspiratory pressure: 15-18 cmH2O
  
  • Titrate as needed
• Resistance in circle system: unidirectional valves, kinking of ETT, CO2 absorbent, humidity and moisture exchanger
  
  • Issue with infant: sometimes need less valves, less resistance → use Mapleson circuit to limit resistance

Question 38

Laryngospasm, symptoms, risk, treatments?

Answer 38

• More frequent in infants; risk decreases with increasing age
• Reflex closure of false & true vocal cords
  
  • afferent limb- internal branch of SLN
  • Efferent limb- recurrent larngeal nerve (innervates all laryngeal muscles except cricothyroid) and External branch SLN (cricotyhroid muscle)
• Sx: stridor, retractions, flailing of lower ribs; “rocking horse” chest wall movement; stridor will be absent with complete closure “silent inspiratory effort” (NO FOGGING OF MASK)
  
  • Can lead to profound bradycardia & desaturation if unrelieved
• Risks:
  
  1. recent URI (w/in 3 wks),
  2. secondhand smoke,
  3. stimulation while “light,”
  4. secretions in airway (CRYING, BLOOD IN AW)
• Treatment: Continuous positive airway pressure,100% oxygen, jaw thrust at condyles of mandible (Larson’s Maneuver)- anterior displacement, suction secretions/ blood etc., deepen anesthesia (propofol)
  
  • Unresolved?
    
    • Atropine & Sch- if no IV access then give IM
• Severe Laryngospasm/Bit through ETT: → lead to negative pressure pulmonary edema especially in healthy, muscular adolescents- may have to remain intubated for 12-24 hours & may need furosemide (flash pulmonary edema)

Question 39

Bradycardia in pediatric patient?

causes?

treatment?

Answer 39

THINK VENTILATION & OXYGENATION

• Infants: <100 bpm
• 1-5 yo: <80 bpm
• >5 yo: < 60 bpm
  
  • If O2 and vent don’t help → chest compressions!
• Causes:
  
  • Hypoxia → leading cause of bradycardia in children (and asystole)
  • Single dose Sch
    
    • other causes: vagal stimulation, increased ICP, meds (Sch), CHD, hypothermia, air emboli, tension pneumothorax
• Treat cause: think oxygenation and ventilation first!! Then…
• → Atropine if vagal origin 0.02 mg/kg IV
• Epinephrine if decompensated 10 mcg/kg
• if HR <60 with s/s of poor perfusion, call for help and start chest compressions

Meds bradycardia: clonidine, beta blockers, Sevo esp in downs syndrome, propofol infusion syndrome, some eye drops, Sch without atropine

The most frequently encountered arrhythmia in pediatric populations is hypoxia-induced bradycardia that can lead to asystole, if not appropriately handled. Ventricular fibrillation is extremely rare in infants and children.

Question 40

Emergence in peds for awake extubation

Answer 40

• Neuromuscular function- check & reverse if appropriate
• Different techniques for extubation; always prioritize patient safety
  
  • light anesthesia is the most common cause of laryngospasm
• Awake extubation: must be awake & purposeful; laryngospasms happen when patients are extubated in the early & second phase, “if in doubt…don’t take it out!”
  
  • 3 phases waking up:
    
    • early phase- coughing intermittently, gagging, struggling, moving nonpurposefully
    • second phase- apnea, agitation, straining, breathholding, RR not regular
    • third (final) phase- regular respiratory rate, purposeful movement, coughing, opening eyes spontaneously → extubation now appropriate

Question 41

Deep extubation in peds?

Answer 41

• Deep Extubation:
  
  • Sevo increased to 1.5-2 MAC for at least 10 minutes
  • ensure no response (cough, breath holding) to suctioning or tube movement; & ensure regular respirations
    
    • place oral AW and allow them to breathe off gas or assist them
    • No deep extubate: DAW or aspiration risk
• Transport in lateral decubitus position “recovery position”
• Tx w/ O2
• PACU complications in ~5% of children:
  
  • vomiting 77% (more common in >8 yo), airway compromise 22% (more common in <1 yo); CV compromise is <1%

Question 42

Contraindication for neuraxial anesthesia in peds?

Answer 42

• (1) severe coagulation disorders (hemophilia, DIC)
• (2) severe infection such as septicemia or meningitis
• (3) hydrocephaly and intracranial tumoral process
• (4) true allergy to local anesthetics
• (5) certain chemotherapies (such as with cisplatin) prone to induce subclinical neurologic lesions that can be acutely aggravated by a block procedure
• (6) uncorrected hypovolemia
• (7) cutaneous or subcutaneous lesions, whatever their nature (infection, angioma, dystrophic or tumoral, tattoo) at the contemplated site of puncture
• Parental refusal is a non-medical absolute contraindication

Question 43

Caudal anesthetic technique?

Answer 43

• The most commonly used technique of epidural blockade in children
• Simple technique; low complication rate
• Anatomy of the sacral hiatus:
  
  • a U -shaped or V -shaped aperture resulting from the lack of dorsal fusion of the fifth and often fourth sacral vertebral arches
    
    • limited laterally by two palpable bony structures, the sacral cornua
    • covered by the sacrococcygeal membrane (sacral continuation of the ligamenta flava)
• 25-mm needles are long enough to reach the sacral epidural space and short enough to prevent inadvertent dural puncture in most patients
• Contraindications:
  
  • major malformations of the sacrum (myelomeningocele, open spina bifida)
  • meningitis
  • intracranial hypertension.
• Rare: unrecognized dural puncture can lead to cardiovascular collapse or respiratory arrest
• Position: lateral or prone position with the legs flexed in the “frog” position
• Single shot or placement of epidural catheter can be threaded to 2-3 cm (same as regular epidural block)
• Upper limit of dosing:
  
  • 1 ml/kg (1.25 ml/kg can lead to block above T4)→ resp consequences!

Question 44

PONV in kids?

high risk sx, prevention, treatment?

Answer 44

• Increased risk in certain surgeries: hernia; orchidopexy; T&A; strabismus; middle ear; laparoscopic
  
  • Strabismus sx pt- higher risk of MH (high risk of concurrent myopathies) (MD)
• Prevention:
  
  • Hydration
  • multi-modal analgesia (opioid sparing- use less)
• Peak incidence in females age 10-16
• Typical 2-3 agent strategy for prevention in at-risk (decreases risk by 80%):
  
  • Ondansetron 0.05-0.15 mg/kg IV (note risk in undiagnosed long QT syndrome)
  • Dexamethasone 0.0625-1 mg/kg IV

Question 45

Emergence delirium in kids?

Answer 45

• Agitation & inconsolability unrelated to pain
• Peaks in age 2-6 yo
• Most common after Sevo (then Desflurane); less common with TIVA
• Usually self-limiting (lasts ~ 10-20 minutes)
• Tx:
  
  • Small dose of fentanyl clonidine, or propofol
• Patient self-harm can be an issue (thrashing, etc.)
• need to go through and rule out hypoxemia/metabolic derangements
  
  • ​agitation may be due to pain, cold, full bladder, presence of casts, fear, anxiety, or having tantrum

Question 46

Describe similarities and differences between LTB and epiglottitis

Answer 46

• Both epiglottitis and croup have supraglottic swelling
• really nothing else in common
• epiglottitis 2-6 yo
  
  • stirdor uncommon
  • thumb sign on CXR
  • abx
  • need sx availability of airway, get airway secured
  • Epiglotittis review
    
    • Life threatening bacterial infection of the epiglottis, aryepiglottic folds, arytenoids, & sometimes the uvulas/s: high fever, severe sore throat, drooling, ill appearing, tripod positioning
    • Rapid deterioration may occur
    • Tx: antibiotics, securing AW!!
    • Technique:
      
      • Calm, sitting inhalational induction, maintain SV**
      • Do not manipulate the airway without a backup for surgical airway in place
      • Do not agitate the child (hold down for IV start; separate from parents)
• LTB (aka croup) <2 yo
  
  • stridor common
  • steeple sign (subglottic narrowing) on CXR
  • use things to decrease swelling but typically don’t need to intubate.
  • Croup= (Laryngotracheobronchitis)- LTB review
    
    • Viral infection of the subglottic structures; more gradual onset
    • S/S: barky or seal-like cough along with hoarse voice and inspiratory stridor
    • Technique:Most cases resolve with simple management
    • Tx: humidified air or oxygen, steroids
    • <10% require hospitalization

Question 47

What are some similarities and differences between tracheomalacia and laryngomalacia?

Answer 47

Both can lead to airway collapse

Laryngomalacia

• most common airway problem in infants & children
• Immature cartilage of the supraglottic larynx leads to symptoms
  
  • slowly resolves by 12–18 mo
  • self-limiting & resolves w/ age
• Symptoms: Inspiratory stridor w/ activity/feeding that IMPROVES when the child is calm

Tracheomalacia

• Weakened/ “floppy” trachea that leads to symptoms
• Symptoms:
  
  • Harsh noise/stridor on expiration caused by airway collapse
  • Onset: early neonatal period
• Dx: bronchoscopy

Question 48

Asthma considerations in pediatric patients?

Answer 48

• Optimize patients preoperatively
• Pre-op review: ever been hospitalized for asthma? intubated? ER visits (last 6 mo)? age of onset? treatments used (today)? need for steroids?
• Assessment:
  
  • Auscultate for wheezing
• Cancel elective cases for ACTIVE wheezing!
• Technique:
  
  • Admin pre-op bronchodilators in mild/moderate asthma even if not wheezing
• Avoid intubation where facemask or LMA can be used (think sx type and aspiration risk)
• Have bronchodilators present in OR
  
  • Refractory asthma (not moving air) → admin IV epi w/ refractory bronchospasms bc inhaled bronchodilators cant pass

Question 49

How can you assess the degree and severity of OSA in the pediatric population? What are some anesthetic considerations for a pediatric patient with OSA?

Answer 49

• Prolonged upper airway obstruction and/or intermittent complete obstruction (obstructive apnea) that disrupts normal ventilation during sleep
  
  • altered response to CO2
• Anesthesia concerns:
  
  • opioid sensitivity
    
    • CONSIDER NON-OPIOID ALTERNATIVES:
      
      • local anesthetics
      • tylenol
      • ketorolac
      • ketamine
      • dexmedetomidine
    • When opioid is given: REDUCE DOSE! (usually by 1/2)
    • Admin in small doses and assess for response
  • post-op respiratory complications
    
    • post-op admission for monitoring depending on results of sleep study
    • High risk patient?
      
      • Safest route: Admit for postoperative monitoring even if no sleep study has confirmed diagnosis
    • Council family members about transporting child home → watch for obstruction
• Primary cause of OSA in children: large tonsils & adenoids → T&A sx most likely for OSA
  
  • Other: craniofacial abnormalities, neuromuscular disorders, obesity

Assessment of risk factors:

• loud snoring, witnessed apnea, nocturnal enuresis, ADHD, behavioral problems, inattention at school; increased risk in African American
  
  • Daytime somnolence is not a common feature of OSA in children (opposite than adult pts)
  • AHI score- apnea-hypopnea index (AHI)
    
    • graded by # of apnea and hypopneic episodes during 1 hour obs
    • Mild >5 but <15/hour
    • moderate 15-30/hr
    • severe >30/hour

BIG concern with OSA in peditrics:

• Intermittent hypoxia → may lead to remodeling
  
  • Consequences: pulmonary hypertension & right heart failure (cor pulmonale)
    
    • Preop: Echocardiography recommended when severe OSA suspected to have CV involvement
  • Red flags:
    
    • systemic hypertension
    • right ventricular dysfunction (s/s: peripheral edema, hepatic enlargement (below 1-2 cm costal margins), elevated liver enzymes)
    • frequent severe desaturations (<70%)

Question 50

URI considerations in pediatrics? When to proceed or cancel a case?

Answer 50

• Most common co-morbidity in children presenting for surgery
• Increased risk complications/ bronchospasm at induction/emergence
  
  • Laryngospasm, bronchospasm, excess secretions
    
    • The most common perioperative respiratory adverse events (PRAEs) associated with URI are:
      
      • **laryngospasm, bronchospasm, breath holding, atelectasis, arterial oxygen desaturation, bacterial pneumonia, and unplanned hospital admission
• Caution but proceed: clinically look OK
  
  • clear runny nose
  • no fever
  • playful
  • clear lungs
• Cancel:
  
  • purulent nasal discharge
  • fever
  • lethargy- ill looking
  • persistent cough, wheezing/ rales
  • previous preemie
  • <1 yo
• Consider waiting at least 2 weeks for elective surgery
  
  • Complications can persist up to 6-8 weeks

Question 51

Anesthetic considerations with recent URI?

Answer 51

• Airway manipulation (ETT) increases the risk of bronchospasm
  
  • Techniques:
    
    • ensure deep plane of anesthesia before manipulate AW
      
      • (risk of airway reflex response: face mask < LMA < ETT)
    • Avoid intubation if case can be done with less invasive airway (mask case; LMA)
    • Add propofol/local anesthetic
• Considerations:
  
  • Tx for bronchospasm available @ bs
  • anticipate increased potential for laryngospasm
• Most common perioperative respiratory adverse events associated w/ URI are:
  
  • laryngospasm
  • bronchopasm
  • breathholding
  • atelectasis
  • arterial oxygen desat
  • bacterial pna
  • unplanned hospital adm

Question 52

Anesthesia for tonsillectomy

Indications, considerations, technique, complications?

Answer 52

• One of the most commonly performed pediatric surgeries

Indications:

• recurrent infections
• OSA
• Most tonsillectomy patients have enlarged tonsils without other airway deformities
• Must consider presence of sleep apnea
  
  • potential need for admission
  • use of multi-modal analgesia (reduce opioid doses)

Technique:

• LMA used by some but majority still intubate
• RAE tube

Complications:

• Post-op hemmorhage
  
  • occurs in 0.1-3% of T&A
  • can be primary (day of surgery) or 7-10 days later
  • Consider: active bleeding in airway →
    
    • visualization difficult
    • full stomach- swallowing blood
      
      • RSI**
    • hypovolemic shock potential

Question 53

Considerations for congenital heart disease?

L to R and R to L shunting?

Answer 53

• most common birth defect
  
  • incidence: 1:25 live births
• L-to-R shunting:
  
  • increases pulmonary BF → potentially decreases systemic blood flow
• R-to-L shunting:
  
  • Blood bypasses pulm circulation → Deoxygenated BF into systemic circulation → causes reduced pulmonary blood flow and increased cyanosis
    
    • *deoxygenation BF into periphery
• PDA present
  
  • have pulse ox on RUE (preductal oxygenation) and any other extremity (postductal oxygenation)
    
    • Preductal: BF feeds head, neck, and RUE
    • Postductal: any other extremity

Question 54

General L to R shunt managmenet in pediatrics?

Answer 54

• Management is dependent on specific anatomy and physiology
• Attempt to maintain pt baseline (same SpO2 and other vital signs)
• L-to-R shunts:
  
  • Avoid increases in SVR and decreases in PVR (which will increase shunt)
  • Avoid negative inotropes
  • Avoid hypervolemia
  • Desaturation → Could be reversal of shunt
  • Anesthetic considerations:
    
    • minimal impact on uptake of volatile anesthetics

Question 55

General R to L shunt management

Answer 55

R-to-L shunts:

• Maintain high SVR to decrease shunt:
  
  • Ex: Ketamine, phenylephrine
• Avoid increased PVR
• Minimize intrathoracic pressure
• Avoid air bubbles in IV
• Anesthetic Considerations:
  
  • decreased wash-in of VA
    
    • → IV supplementation may be required

Question 56

What is tetralogy of fallot?

What are tet spells?

What do we want to avoid?

Answer 56

• Most common cyanotic CHD
  
  • primary repair done at 3-12 months
• Anatomy:
  
  • Right ventricular outflow (RVOT) obstruction
  • Infundibular narrowing, pulm stenosis, PA hypoplasia, pulm atresia
  • Ventricular septal defect (VSD): Large, unrestrictive
  • Overriding aorta
  • RV hypertrophy
• Tet spells: (Left unrepaired) → cyanotic episodes!!!
  
  • Crying and agitation leading to tet spell leading to more hypoxemia, hypercarbia, acidosis (avoid)
  • Consequences: lead to RVH, RV failure, and death (50% in first year of life)
• Increased R-to-L shunting caused by:
  
  • decreased SVR or
  • increased PVR
• Avoid hypoxia, acidosis, high airway pressures, excitement, and agitation

Question 57

Anesthetic considerations for repaired CHD?

Single ventricle? Williams syndrome?

Answer 57

• Can be associated with the later development of dysrhythmias (esp if approach was ventriculotomy → conduction system violated)
  
  • repaired single-ventricle physiology → high risk sudden death as a result of pathologic arrhythmias
  • any intraoperative arrhythmias must be reported to cardiologist → may require RF ablation
• Children with a single-ventricle physiology (Fontan) require very specific anesthetic management:
  
  • well hydrated
  • avoid PEEP
  • avoid laparoscopic surgery (avoid intrathoracic/intraabdominal pressure)
• Williams syndrome → high risk sudden death with anesthesia
  
  • Anatomy: aortic stenosis, abnormal coronary arteries, pulmonic stenosis
• Former cardiac transplantation:
  
  • must rule out small vessel coronary artery disease

Question 58

What is sickle cell?

Possible complications?

Answer 58

• Hgb SS homozygous: Hgb S permits deoxygenated Hgb molecules to polymerize into rigid insoluble fibers → resulting in sickled erythrocytes
  
  • Sickled erythrocytes = shortened life span → leading to chronic hemolysis and anemia

Complications:

• anemia, stroke,
• acute chest syndrome- lead to sig pulm failure
  
  • A vascular occlusive crisis in the lungs leads to acute chest syndrome (ACS). ACS is leading cause of death and second most common complication in sickle cell disease.
• , myonecrosis, CHF, MI, splenic sequestration, retinal hemorrhage, hematuria, ESRD, seizure, wound infection, UTI, and unexplained death

Question 59

What should we avoid in sickle cell patients?

Answer 59

AVOID:

• Dehydration
• Stasis
• Hypoxia
• Hypothermia
• Acidemia
• pain

ANY OF THESE LEADS TO → Vaso-occlusive crises

• Vaso-occlusive crisis → lead to subsequent end-organ ischemia
  
  • Ex: Bone, chest, brain- may have significant sequelae from previous crises

Question 60

Preop, intraop and postop considerations in sickle cell disease?

Answer 60

Pre-op:

• warm, well-oxygenated, and hydrated!
• Thorough multi-system assessment
  
  • may have chronic pain, hx of stroke, pulmonary complications from infection or acute chest syndrome, anemia, infections, renal disease, AVN of hips
• Consult hematologist preop:
  
  • Possible preop transfusion to target hgb (10 g/dL)
  • ensure pre-op hydration- admit night before to hydrate
  • IV access can be challenging

Intra-op:

• Maintain euvolemia & normothermia
• avoid tourniquets

Post-op:

• Adequate IV hydration; early mobilization and incentive spirometry; supplemental O2; consider multimodal analgesia (many are opioid tolerant)

Question 61

Malignant hyperthermia considerations?

Answer 61

• Blood relative or muscle biopsy
• Technique:
• First case of the day
• Remove vaporizers from machine
  
  • flush per manufacturer guidelines (w/ charcoal filter)
• Use trigger-free anesthetic: propofol, opioids, BZD’s, NDNMB’s, N2O, regional
• Mandatory Monitoring:
  
  • EtCO2*
    
    • increased etCO2 earliest indicator
  • temp monitoring*
• MH-susceptible children can have outpatient procedures as long as trigger-free anesthetic is used * (no Succs or VA)

Question 62

Definition for childhood obesity?

LBW calc? IBW?

Answer 62

• Definitions for obesity in children are based on BMI
  
  • obesity = BMI >95th percentile
  • morbid obesity= BMI >99th percentile
  • IBW calculation for children:
    
    • < 8 years: 2 x Age (years) + 9
    • >8 years: 3 x Age in years
• LBW calculation= IBW + 1/3(TBW-IBW)

Question 63

Consequences of childhood obesity?

Answer 63

• Consequences:
  
  • Restrictive pulmonary pattern
  • Increased O2 consumption
  • decreased chest wall compliance
  • FRC
  • vital capacity
• CV effects:
  
  • Htn
  • LVH
  • premature atherosclerosis
• Insulin resistance is common

Question 64

Drug dosing consideraitons in obese children?

anesthetic considerations?

Answer 64

• Drug dosing is complex (see chart)**
  
  • Ex: Induction
    
    • TBW: succs, sugammadex
• Technique:
  
  • Airway:
    
    • position HOB 25 degrees
    • plan for possible difficult mask ventilation
    • note rapid desaturation
  • Consider Desflurane for maintenance (least fat soluble) if airway reactivity is not a concern

Question 65

How does the lung develop in the fetus?

Answer 65

• Lung development begins in utero at approximately 4 weeks’ gestation but lungs are functionally immature until nearing term
• occurs in five stages:
  
  • embryonic,
  • pseudoglandular,
  • canalicular,
  • saccular, and
  • alveolar
• growth of the pulmonary parenchyma and surfactant system occurs during the saccular phase occurring from week 24 through week 40 (36 weeks: magic # for surfactant)
  
  • maturation & expansion of alveoli occur during the alveolar period which begins near term & continues to mature through childhood
    
    • 24 mil alveoli at birht, 300 mil by age 8
  • surfactant can be adminitered via ETT in premie infant
• Alveoli must transition from fluid filled state to air-filled (gas exchanging) parenchyma

Question 66

What are some respiratory variations in the newborn?

Answer 66

Respiratory system newborn variations:

• Diaphragm is flatter;
• more compliant chest with cartilaginous ribs;
  
  • poorly compliant lungs; may see paradoxical breathing;
    
    • paradoxical breathing= inward movement of chest during inspiration
• predominantly nose breathers until 4 weeks of age;
• chest circumference very close in size to head circumference at birth

Question 67

What is persistent fetal circulation?

What are some precipitating conditions?

Treatment?

Answer 67

Also called Persistent Pulmonary Hypertension of the Newborn

• PA pressures abnormally elevated causing the ductus arteriosus & foramen ovale to remain open (or re-open):
  
  • leads to hypoxia due to R to L shunting
• Hypoxia & acidosis with concurrent inflammatory mediators are primary causes
• Precipitating conditions:
  
  • severe birth asphyxia,
  • meconium aspiration,
  • sepsis,
  • congenital diaphragmatic hernia,
  • mom’s use of NSAIDS,
  • idiopathic
• Response to treatment is unpredicatable
• Initial tx: provide optimal oxygenation
  
  • ​(PaO2 60-100,
  • correct stressors like hypoglycemia or polycythemia
• Other tx: surfactant, inhaled nitric oxide, HFOV, ECMO
  
  • inhaled nitric oxide only FDA approved treatment

Question 68

What might cause an infant to have persistent fetal ciruclation in the early weeks of life?

Answer 68

• Period of vulnerability:
  
  • Hypoxia (acidosis)
  • Hypercapnia (acidosis)
  • Hypothermia
  • Infection
  • Prematurity
• Preterm infants: ductus arteriosus may remain open for several weeks & can cause hemodynamic instability
  
  1. tx: prostaglandin inhibitor (indomethacin)
  2. surgical ligation
     
     • ex: if see sudden hypoxia < 10 days old → suspect flip flow circulation occurring
       
       • tx: hyperventilate & hyperoxygenate – difficult to correct
• Phenomenon leads to sudden increases in pulmonary artery pressure and shunting of blood past the lungs through a patent foramen ovale or the ductus arteriosus, which may reopen, particularly during the first 10 days of life

Question 69

What are the components that make up APGAR scoring? What is the significance of APGAR socring?

Answer 69

APGAR scoring:

• five signs measured/observed in neonates 1 minute & 5 minutes after delivery
  
  • PREDICTIVE on neonatal distress and need for intervention
  • Components:
    
    • Most important:
      
      • heart rate
        
        • HR < 100 bpm: signifies arterial hypoxemia
      • quality of respiratory effort
    • Least informative:
      
      • color –
        
        • healthy neonates have acrocyanosis @ 1 min from cold ambient temps (peripheral vasoconstriction)
        • Persistent cyanosis- acidosis and pulm vasoconstriction most likely causes
• Scores 3–7: Mild to moderately depressed function
  
  • may respond to oxygen administration by face mask
  • with or without positive pressure ventilation
• Score < 3: CONCERN
  
  • consult NRP algorithm

Score 0-10

Question 70

What are some essentials to the newborn resuscitation program (NRP)

Answer 70

Initial actions for newborn in distress:

• Clear infant airway
• Warm/dry them
• Stimulate
• Position- sniffing
• Evaluate: HR, respirations, color
  
  • Ex: labored breathing and persistent cyanosis- suction
  • HR < 100 bpm- assist w/ PPV
  • HR < 60: intubate, PPV, chest compressions
    
    • O2 & chest compressions not effective → IV Epi

Question 71

Airway assessment in newborn

Answer 71

• assess mucous membranes;
• look at tongue size/ mobility- look at frenulum of tongue (impact feeding);
  
  • a short tight lingual fenulum attached to inferior tip of tongue may impede movement of tongue and breastfeeding
• evaluate chin (retrognathia?- diff intubate);
• nasal patency/ discharge;
• intact hard and soft palate?;
• presence of natal teeth (< 1 mo old- fall out easily)?
  
  • teeth that erupt in first month of life, typically central incisors
  • similar to normal teeth but lack developed root system and may fall out
  • no indication for removal unless concern for aspiration or interference with feeding
• unrestricted neck movement
  
  • congenital torticollis- means that a baby is born with an odd position of the neck. The odd position is because of a tight, short neck muscle

Question 72

Heart and lung assessment in newborn/neonate?

Answer 72

• assess for tachypnea, flaring grunting, retractions
  
  • respirations may be “regularly irregular” with pauses (pauses should not last >20 seconds)
  • Periodic breathing: more common in infants, particularly preterm infants; probably due to inadequate development of the medullary respiratory centers
    
    • Assess length of pause
• assess clavicles
  
  • Clavicular fractures are a common birth injury occurring in 0.2%–3.5% of births. Usually left untreated
• assess upper & lower extremity pulses
  
  1. risk of CHD- impact perfusion to extremities
• Murmurs common in newborns
  
  1. Systolic murmur- not as concerning
  2. Diastolic murmur – concerning!!
     
     • PDA: murmur best heard along the left lower sternal border

Question 73

Neuro and musculoskeletal assessment in newborn/neonate

Answer 73

• Neuro assessment:
  
  • Posture,
  • muscle tone,
  • movement,
  • seizure activity;
  • head control,
  • quality of cry;
  • response to light and sound;
  • fontanelles (Anterior and posterior)
  • Back: Spinal contour; presence of cysts, sinuses, dimples, tufts of hair
• ·Musculoskeletal:
  
  • Normal: Inward flexion resting position of upper and lower extremities
  • Abnormal: rigidity or extension
    *

Question 74

Pharmacokinetic difference in newborn/neonate?

Answer 74

• Larger volume of distribution: increased dose for water soluble meds
  
  • Ex: AntiX and Succs
• Decreased protein binding: increased free fraction of primarily protein bound drugs
  
  • Ex: More drug available to exert effects
• Decreased body fat percentage: higher levels of drugs that are primarily redistributed to muscle and fat
  
  • Less redistribution that takes place
• Immature renal and hepatic function

Question 75

Pharm reminders and “pearls?

Versed and opioid use?

Propfool?

Morphine?

remi?

NDNMB? Vec? Cis?

NMB Reversal?

Lidocaine

Answer 75

• Versed and opioids combined in neonates can lead to severe hypotension- titrate carefully
• Propofol: variability in elimination in neonates and preterm infants
  
  • may see longer elimination times
• Morphine clearance directly correlated with gestational age
  
  • r/t immaturity of kidneys
  • → reduce frequency of admission
• Remifentanyl has similar PK to older children making it a reliable choice for an intraoperative opioid
  
  • Independent of liver/kidneys
• Sch dose increased
  
  • DOSE: 3 mg/kg
  • Pretreatment: w/ atropine
• NDNMB:
  
  • have significant variability and unpredictability in this population- titrate carefully
  • Will always need reversal in neonates**
• Vecuronium: considered a “long acting” NDNMB in infants <1 yo due to liver immaturity
• Cisatracurium produces reliable recovery due to Hoffman elimination
  
  • TEMP & PH MUST BE NORMAL
  • laudanosine → can decrease seizure threshold
• Lidocaine has a longer half life and volume of distribution in the neonate

Question 76

What was historic txmt of meconium aspiraiton?

Current treatment/recommendations?

Answer 76

• Historic tx: ETT immediately after delivery with suctioning of meconium from newborn’s airways
• Roughly 10% of newborns have meconium staining- routinely intubating all leads to complications of advanced airway in many who do not need it.
• Currently tx: more conservative
  
  • NRP guidelines updated (2010): do NOT recommend routine oropharyngeal/nasopharyngeal suctioning with either clear or meconium-stained amniotic fluid
• Endotracheal suctioning IS indicated for nonvigorous meconium-stained newborns
  
  • Recommendation: meconium present →
    
    • Tx:
      
      • 1^st: orally suction
        
        • vigorous & crying- no further action.
      • If still depressed:
        
        • intubate & suction
          
          • If vigorous → pull the tube and reintubate (don’t want merconium in tube)
          • If not → keep tube → move to PPV.

Recommendation: meconium present- 1st orally suction, if vigorous and crying- no further action. If still depressed then intubate and suction- if then vigorous, pull the tube and reintubate. If not- keep tube and move to PPV.

Question 77

What is respiratory distress syndrome in neonate/newbown? What are some treatments and long term effects of RDS?

Answer 77

• Primary Cause: Lack of surfactant
  
  • decreased number of branching airways and alveoli
  • atelectasis
  • impaired gas exchange
  • hypoxemia
  • poor lung compliance & propensity for alveolar collapse
• Incidence inversely proportional to gestational age & birth weight (< 36 wks → more likely to have RDS b/c less surfactant in alveoli)
• S/S:
  
  • Tachypnea
  • Tachycardia
  • Cyanosis
  • Grunting
  • Retractions
  • flaring
• Tx: surfactant (delivered via ETT)Anesthesia: Limit hypoxemia while avoiding hyperoxia
  
  • follow ABG’s
• Consequences:
  
  • Long term: bronchopulmonary dysplasia
• Surfactant initially appears at 23 to 24 weeks and increases in concentration during the last 10 weeks.
• Surfactant is released into the alveoli at about 36 weeks’ gestation, thus making normal extrauterine life possible.

Question 78

What is choanal atresia?

s/s?

Answer 78

• Abnormal embryogenesis (formation) of neuroectodermal cell linen → obstructing nasal passage
  
  • functional atresia may also occur resulting from obstruction (blood, mucus, or meconium)
    
    • ~90%: bony
    • 10% : membranous

Considerations:

• Nasal obstruction should be suspected when good breathing efforts but in whom air entry is absent
  
  • Recall- infants are obligate nasal breathers

1. 40% of term infants can convert to oral breathing if nasal airway is obstructed (60% cant)
2. 5 mo- Almost all infants can easily convert to oral breathing

*

Question 79

s/s and treatment of choanal atresia?

Answer 79

s/s:

• cyanosis (develops if these infants are forced to breathe with their mouths closed)
• Respiratory distress at birth
  
  • worsen w/ feeding
• Improve w/ crying (bc breathing out mouth)
• Airway obstruction
• stridor
  
  • paradoxical cyanosis (normally, newborns turn pink when crying as they begin to breathe through their open mouth).
• 1/2 of children with choanal atresia have other congenital issues – also look for ear defomiries. can be s/s of other congenital syndromes
  
  • CHARGE association:
    
    • Coloboma- eye deformity
    • heart disease
    • atresia [choanal]
    • retarded growth
    • genital abnormalities
    • ear deformity
• Unilateral atresia: rarely a surgical emergency,
  
  • often intervention can be delayed.
• Dx: Unilateral or bilateral choanal stenosis
  
  • based on inability to pass a small catheter through each nare
• Tx:
  
  • Congenital choanal atresia requires surgical treatment during the neonatal period
    
    • Use of an oral airway may be necessary until surgical correction can be accomplished
  • Functional choanal atresia is treated by nasal suctioning

Question 80

What is a congenital diaphragmatic hernia?

Location? Consequences? s/s?

What are some initial treatments for CDH in delivery room?

Answer 80

• Herniation of abdominal viscera through a defect in diaphragm
  
  • Locations of Herniations:
    
    1. Foramen of Bochdalek (on the left side): most common site
    2. Anterior foramen of Morgagni herniation: occurs in only 2%.
• Consequences: Lungs are underdeveloped d/t compression in utero
  
  • Alveolar & Vascular hypoplasia
• S/S:
  
  • Severe respiratory distress at birth
  • Cyanosis
  • scaphoid abdomen (collapsed abdomen)
  • Chest x-ray: abdominal contents in thorax
  • Associated anomalies (40%-50% pts)
    
    1. CNS- meningomyelocele
    2. CHD- most common
• Initial treatment in delivery room:
  
  • avoid aggressive mask ventilation
  • urgent intubation
  • decompress stomach
  • maintenance of PaCO2 <40
  • optimal oxygenation
• Problems: must avoid iatrogenic volutrauma (over ventilating)!!!
  
  • High risk pneumothorax on the side opposite the hernia if attempts are made to expand the ipsilateral lung
  • Hypoxemia secondary to pulmonary hypoplasia & pulmonary hypertension
  • Hypotension d/t overdistention of stomach & mechanical kinking of great vessels

Question 81

Treatment and management of congenital diaphragmatic hernia

Answer 81

• Tx:
  
  • Supportive care rather than immediate surgery after birth: ECMO, HFOV, & nitric oxide (manage PHTN)
• Management:
  
  • awake intubation without positive pressure ventilation
  • adequate IV access
  • a-line
  • opioids
  • muscle relaxation
  • maintain optimal oxygenation (PaO2 >100)
  • ventilation
  • avoid nitrous oxide (d/t bowel distention)
    
    • anticipate ICU postop

Question 82

What is apnea of prematurity? treatmnt?

Answer 82

• Inversely proportional to gestational age
• Immaturity of the respiratory control centers of the brainstem → decreased sensitivity to elevations in CO2
• Both central apnea & obstructive apnea
  
  • Dx:
    
    • apneic periods >15-20 seconds
    • apnea with HR < 80-100
    • apnea with desaturation
• Tx:
  
  • Methylxanthines- primary tx
  • Others:
    
    • aminophylline
    • caffeine

Question 83

Pathology behind neontal hypoglycemia?

Answer 83

• The most common problem in newborns & young infants
• Patho:
  
  • Early in gestation, the fetal liver begins to store glycogen while a continuous supply of glucose is delivered by transplacental transfer from the mother.
  • In the third trimester, glycogen stores begin to develop in fetal skeletal and cardiac muscle, as well as in the kidneys, intestines, and brain. (but still immature)
    
    • Birth → neonatal glucose concentrations decrease rapidly to 30 mg/dL w/in 1st 1-2 hrs
      
      • → stimulates glycogenolysis & gluconeogenesis
      • → glucose flux usually stabilizes at values > 45 mg/dL by 12 hours post birth

Question 84

S/S or neonatal hypoglycemia

Highest risk for neonatal hypoglycemia?

Answer 84

• S/s:
  
  • Hypotension
  • Tremors
  • Seizures
    
    • can be masked by anesthesia
    • Other sx: respiratory distress, apnea, cyanosis, high-pitched cry, irritability, limpness, lethargy, eye-rolling, poor feeding, temperature instability, and sweating
• Highest risk: Infants with intrauterine growth restriction; diabetic mothers; severe intrauterine fetal distress
  
  • Premature infants:
    
    • prone to hypoglycemia owing to immature glucoregulatory mechanisms,
    • reduced levels of glycogen storage,
    • increased energy demands,
    • limited adipose stores (reduced free fatty acids and ketones available as alternative sources of energy)
  • Also at risk: Full-term infants who have been excessively fasted, small-for-gestational-age (SGA) infants, and infants of diabetic mothers

Question 85

What is hypoglycemia defined as in the full term and preterm infants?

Prevention of hypoglycemia?

Answer 85

• Full term neonates:
  
  1. < 40 mg/dL glucose [] during 1^st 24 hours after birth
  2. < 60 mg/dL at 36 hours
• Premature infants:
  
  1. < 45 mg/dL at 1^st 24 hrs
  2. < 50 mg/dL > 24 hrs after birth
• Prevention:
  
  • 1^st 48 hours MIVF:
    
    • contains 10% glucose in 0.2% saline with 20 mmol/L K
  • > 48 hours:
    
    • 5% glucose supplementation is usually okay
    • preterm infants will have increased requirement

Question 86

Treatment for hypoglycemia?

Answer 86

• Acute dose: bolus 0.25 - 0.5 g/kg (1–2 mL/kg of D25 W or 2.5–5 mL/kg of D10 W)
  
  1. → then increase glucose in MIVF (to prevent stimulation of insulin production)
     
     • A single bolus of glucose without subsequent infusion can stimulate insulin production with consequent return to the hypoglycemic state
• All other fluids (e.g., to replace third-space losses, blood loss, and fluid deficits) should be glucose-free to avoid hyperglycemia
• Check blood sugar frequently
• TPN- do not stop suddenly without bridging with a glucose containing fluid

Question 87

What are the 3 main forms of calicum in the body?

what causes hypocalcemia in neonates?

s/s

Answer 87

• 3 forms of Ca in body:
  
  • 1. Protein bound
  • 2. Chelated to bicarb, phos, and citrate
  • 3. Free or Ionized- physiologically active component
       * Not always clear relationship b/t total serum Ca and iCa (correlation is poor with hypoalbuminemia or acid-base disturbances, as seen in premature and critically ill neonates)
• Hypocalcemia:
  
  • iCa: < 1 mmol (in both premature and neonate pop)
  • Hypocalcemia is defined as a total serum calcium concentration less than 8 mg/dL (2 mmol/L) in full-term infants and less than 7 mg/dL (1.75 mmol/L) in premature infants. An iCa 2+ less than 4 mg/dL (1 mmol/L) defines hypocalcemia in both populations.
• At birth → abrupt loss of maternal calcium
  
  • by 3^rd day of life, serum calcium concentrations in the full-term neonate to return to normal
    
    • Infants who are born prematurely do not benefit from the transfer of maternal calcium
• Hypocalcemia present in nearly 40% of critically ill neonates
  
  • Causes: PTH insufficiency, inadequate calcium supplementation, and altered calcium metabolism caused by transfusion with citrated blood products, bicarbonate administration, or diuretics (e.g., furosemide)
• Hypocalcemia s/s:
  
  • asymptomatic or…
  • nonspecific symptoms such as neuromuscular irritability (myoclonic jerks, exaggerated startle, or seizures), tachycardia, prolonged QT interval, and decreased cardiac contractility

Question 88

Treatment of symptomatic hypocalcemia in neonate?

Answer 88

• Tx:
  
  • Slow IV infusion over 5-10 min w/ → (2 txs)
    
    • 1. 90 mg/kg calcium gluconate
      
      • May be given IV but is vesicant!! (tissue necrosis and subcutaneous calcification deposits with extravasation)
    • 2. 30 mg/kg calcium chloride
      
      • Infused through central line**
    • Monitor for bradycardia!!! (seen with rapid increases in the serum concentration of calcium)
• Consider need for Magnesium supplementation as well

Question 89

What is a meningomyelocele?

Anesthesia considerations?

Treatment?

Answer 89

• Hernial protrusion of a part of the meninges and spinal cord through a defect in the vertebral column
  
  • To protect the defect, it is placed on a “doughnut” and towels are placed under the head
• Anesthesia:
  
  • Plan for positioning for intubation to protect defect
  • Anticipate larger insensible losses – membranous sac
  • High possibility of hydrocephalus
  • Possibility of cranial nerve (vocal cord) palsy leading to respiratory distress/ stridor
  • Potential for brainstem herniation
  • Higher incidence of latex allergy:
    
    1. always use latex precautions
• Meningomyelocele usually have an Arnold-Chiari malformation and may have stridor from vocal cord paralysis
  
  • caudal displacement of the medulla
  • treatment:
    
    1. relief of the hydrocephalus
    2. possible cervical decompression of the herniation
    3. tracheotomy and long-term mechanical ventilation may be required (if VC paralysis)

Question 90

What is esophageal atresia or TEF? when to suspect it

s/s?

dx test?

what other anomalies might be present?

anesthesia consideraitons?

Answer 90

• The inability to swallow amniotic fluid in utero results in polyhydramnios
• Five plus different configurations
  
  • esophageal communication with trachea causes aspiration pneumonitis
• Suspect in polyhydramnios
• Esophageal atresia: the esophagus ends in a blind pouch
• s/s: Copious amounts of oropharyngeal secretions are usually present
• Diagnostic test: inability to pass a suction catheter into the stomach
• Suspect other anomalies:
  
  • VATER association ( V , vertebral; A , anal; TE , tracheoesophageal; R , renal) or
  • VACTERL association (VATER and C , cardiac; and L , limb).
• Echocardiogram advised before anesthesia

Prematurity and polyhydramnios are associated with TEF. The inability to swallow amniotic fluid in utero results in polyhydramnios

Question 91

What are the types of tracheoesophageal fistulas?

Answer 91

• Classification by Gross
• Type C is the most common (~ 85% of TEFs)

A—Esophageal atresia without fistula

B—Esophageal atresia with communication of the upper esophageal segment to the trachea

C—Esophageal atresia with communication of the lower esophageal segment to the trachea

D—Esophageal atresia with both upper and lower esophageal segments communicating with the trachea

E—No esophageal atresia but TEF

F—Esophageal stenosis without fistula

Question 92

Anesthesia managment of esophageal atresia?

Answer 92

• Anticipate presence of aspiration pneumonia
  
  • may have to receive treatment before stable for surgery
  • g-tube may be placed for nutrition
• Airway management:
  
  • withhold feedings
  • place soft suction in esophagus to drain saliva
  • position prone in a head-up position
    
    • Plan:
      
      1. awake intubation with sedation (fentanyl/ versed/ topicalization)
      2. Intentional right mainstem then back out to Bil BS → hope is that ETT is past fistula
  • ETT placement is CRITICAL- it is possible to ventilate one lung, both lungs, and/or the fistula depending on tube placement with 1-2 mm movement
    
    • Ventilation:
      
      1. spontaneous assisted ventilation → best to avoid stomach over distention until the fistula is ligated or g-tube placed
  • SpO2 placement should be pre-ductal and post-ductal
  • Consider left precordial stethoscope (under left axilla)
    
    • continuously monitor for endobronchial intubation
  • May require postoperative ventilation but may trial extubation depending in surgeon preference
  • Postoperative pain may be managed with a caudal catheter

Miller suggestion: 0.5 to 1 μg/kg of fentanyl and 25 to 50 μg/kg of midazolam and topicalizes the tongue, larynx, and vocal cords with no more than 5 mg/kg of lidocaine (1.0%)

Stomach can rupture if large volumes of air are being instilled with positive pressure ventilation

Question 93

What is an omphalocele? Gastrochisis?

complications?

Answer 93

• Major defects in the closure of the abdominal wall that result in exposure of viscera
  
  • omphalocele: covered by peritoneum
    
    • typically ass. w/ anomalies (very sick)
    • W/in umbilical cord
  • gastroschisis: not covered by peritoneum
    
    • not ass. w/ anomalies
    • periumbilical
• Complications:
  
  • severe dehydration and massive fluid loss from the exposed visceral surfaces
  • heat loss
  • complex surgical closure
• High association with prematurity and other congenital defects
  
  • cardiac abnormalities common (omphalocele ∼20%)

Question 94

Management of omphalocele/gastroschisis?

Answer 94

• ECHO before anesthesia
• Anticipate need for postop ventilation
• May be a staged repair
  
  1. Early repair: reduces the potential for infection and compromise of bowel function; minimizes fluid & heat loss
• Must optimize fluid and electrolyte balance before surgery
• Obtain good IV access
  
  1. anticipate need for TPN postop- central line placement
• Expect invasive monitoring if associated cardiac defect is present
• Expect liberal use of muscle relaxants for closure of the defect
• Anticipate hypotension secondary to tension on a major organ (liver) or caval compression (tight space fitting everything)
• Increased abdominal pressure after a tight closure
  
  1. Impairs ventilation
  2. Risk of abdominal compartment syndrome → may alter hepatic/ renal function & metabolism
• Omphalocele has association with Beckwith-Wiedemann syndrome
  
  • → profound hypoglycemia, hyperviscosity syndrome, congenital heart disease, and associated visceromegaly

Question 96

What is hirschprung disease?

S/S? Tx?

Answer 96

• The absence of parasympathetic ganglion cells in the large intestine- a nonperistaltic segment in gut of variable length, a tonically contracted anorectal sphincter, and delayed passage of meconium
  
  • Functional obstruction occurs at the level of the affected segment
  • ~ 60% of patients will have an associated anomaly.
• S/S:
  
  • consistent with bowel obstruction
    
    • bilious vomiting
    • abdominal distention
• Left untreated it can lead to toxic megacolon
• Tx:
  
  • volume replacement
  • vasopressor support
• Surgical repair
  
  • varies: anorectal myomectomy, mucosal resections, diverting colostomies, and transanal pull-throughs

Question 97

Lower GI obstruction in neonate?

s/s?

mgmt?

anesthesia?

Answer 97

• Lower GI obstruction usually develops 1-7 days after birth
  
  • Ex: Imperforate anus, duodenal atresia, jejunoileal atresia, intussusception, malrotation, volvulus, choledocal cyst, meconium ileus
• S/s: Vomiting secondary to obstruction → fluid shifts
  
  • Increased intra-abdominal pressure can lead to respiratory compromise
• Management:
  
  • Optimize pre-op:
    
    1. Na+ 130mEq/L
    2. UOP 1-2 ml/kg/hr
• Anesthesia:
  
  • fluid and electrolyte resuscitation
  • full stomach precautions (awake intubation or RSI)
  • N2O avoided
  • adequate muscle relaxation req
  • consider remifentanil infusion if planning to extubate → indep of renal/liver for metabolism
• Look for other congenital anomalies:
  
  • association w/ trisomy 21, cystic fibrosis, imperforate anus, or renal abnormalities

Question 98

What is pyloric stensosi? considerations? mgmt?

Answer 98

• Not a surgical emergency, correct metabolic derangement before surgery
  
  • normally revealed in the first 3 to 6 weeks of life
  • have severe projectile vomiting
• Considerations: ALL electrolytes/fluids SHOULD BE CORRECTED
  
  • full stomach
  • metabolic alkalosis with hypochloremia and hypokalemia
  • sodium deficits
  • severe dehydration
• Management:
  
  • NGT BEFORE induction: suction stomach in the supine and the right and left lateral positions
  • Awake intubation or RSI w/ cricoid pressure after →
    
    • atropine (0.02 mg/kg)
    • propofol (3 mg/kg)
    • succinylcholine (2 mg/kg) administration

Question 99

What is NEC?

Answer 99

Necrotizing enterocolitis

• Typically affects premature infants but may be seen in term newborns
  
  • Patho: immature intestine has decreased absorptive ability leading to stasis
    
    1. the stasis promotes bacterial proliferation and sepsis;
  • ischemia and infection can lead to intestinal necrosis and perforation
• Medical management:
  
  • NPO
  • Antibiotics
  • OG tube
  • F&E
  • hemodynamic support
• Unresponsive to medical management: Ex lap
  
  • Extremely ill patient
    
    1. RSI with cardiac stable agent (ketamine)
    2. caution with Sch if hyperkalemic from dead bowel
  • 25-50% mortality
• Maintenance:
  
  1. avoid nitrous oxide
  2. very judicious with inhalational agent if unstable (use opioids as primary anesthetic) low VA
  3. Anticipate need for blood products; expect massive fluid losses
  4. Anticipate postoperative continuation of intubation and ventilation

Question 100

Use of NMB iin neonatal pt?

Answer 100

• Neonatal (term and preterm) response to muscle relaxants varies greatly from patient to patient
  
  • Best practice: titrate to response
  • Dose:
    
    1. reduce 30%-50% trach intubation dose w/ potent inhaled agent
  • atracurium/ cisatracurium: advantage is Hoffman elimination since renal/ hepatic are immature
  • vecuronium: very prolonged duration in newborns (approaching pancuronium)
    
    1. good b/c no histamine

Question 101

Caudal anesthesisa in neonates?

Answer 101

• Landmarks:
  
  • Coccyx
  • the two sacral cornua
  • posterior superior iliac spines
• The sacral cornua are identified.
• A styletted needle is introduced into the caudal space through the sacral hiatus.
• A “pop” is felt as the sacrococcygeal ligament is accessed. After aspiration, 0.8 to 1 mL/kg of local anesthetic solution is injected.
• Most common: 0.125% bupivacaine, 0.25% bupivacaine, or 0.2% ropivacaine. Epinephrine, 1:200,000, is added for recognition intravascular injection
• This provides analgesia for hernia repair, circumcisions, and lower abdominal surgeries
• Analgesia lasts 6-8 hours

Question 102

Considerations for room setup in peds?

Answer 102

• Always have a range of sizes of airway equipment (face masks, OPA’s, ETT’s, LMA’s, blades)
  
  • Need size up and size down from anticipated size
  • Straight blades are most commonly preferred in infants due to anatomical differences (get both out)
  • Appropriate size LMA should always be available even if intubation is planned in case of unanticipated difficult airway
• Ensure appropriate sized BP cuff and pulse oximeter is present & functional
• Calculate drug doses, allowable blood loss, & fluid requirements
• Have primed bag of IV fluid ready and all supplies to start & secure IV set up & accessible
• Prepare a pediatric circuit/bag
  
  • 0.5, 1, 2 L bag → use peds circuit if < 5-8 yo
  • If can pull TV > than volume of bag → negative pressure in system (switch over to bigger bag)
• Preset vent settings appropriate for size (& program in weight to anesthesia machine if applicable)
  
  • Pressure control better
  • Volume control- TV/kg can be calculated
  • Appropriate sized mask- injury, eyes, bad seal, VAGAL response!
• Emergency drugs for every pediatric case:
  
  • Sch & Atropine + IM needle: Weight appropriate doses with a small gauge needle appropriate for IM injection
    
    • Laryngospasm, take on every transport
  • Propofol syringe – have backup
    
    • facilitate intubation, break laryngospasm, increase depth of anesthesia quickly
  • Epi diluted to 10mcg/ml: not always drawn up but definitely consider drawing up in a sick patient/ complex case (cardiac arrythmias→ bradycardia not responsive to O2—ex: O2 typically primary tx )
    
    • Comes 100 mcg/ml → need to dilute down to 10 mcg/ml
• Plan for age appropriate distractions: have flavors for masks; consider parental presence if facility allows (cover supplies to hide anxiety)
• Warm the room

Question 103

Mask ventilation considerations in peds?

Answer 103

• Sniffing position is critical – no hyperextend neck
  
  • Tongue bigger/oral AW smaller → prone to obstruct
    
    • Align oral, pharyngeal, laryngeal axis – slightly displace mandible forward/neutral
    • Put little pillow behind to put nose to ceiling
    • Shoulder roll
• Avoid pressure on the soft tissue in the submental triangle – might cause obstruction
• Jaw thrust
• Low threshold for 2-person ventilation

Question 104

Inhalational induction in peds?

Answer 104

Inhalational induction is common: seated or supine position

One approach:

• Higher flows with 70% N2O and 30% O2 (7L N2O and 3L O2)
• Fully open APL
• Allow a few breaths of N2O mixture and then incrementally turn on Sevo to 8% (some providers turn up sevo to 8% without using incremental technique after a few breaths of N2O- especially if crying)
• Turn off N2O to provide 100% O2
• Assist spontaneous ventilation PRN- caution about high inspired volatile agent with assisted or controlled ventilation (keep spontaneously breathing!)
  
  • Decrease inspired anesthetic if need to ventilate
    
    • ​do not want to get to this point!
• Obtain IV
• Once IV is in, induction proceeds- give some propofol, narcotic, +/- NMB, etc at this point and then proceed with airway management appropriate for case (LMA, ETT)
  
  • NOTE: intubation is often completed without NMB’s
• Be sure to turn down Sevo to normal MAC range for the child; watch VS closely during induction

Question 105

RSI in children?

Answer 105

• Same principle as adults to prevent aspiration
  
  • Cricoid pressure in infants/ children is +/- (Barash says no) → increased likelihood of obstructing an infants airway with little proven benefit
  • Note that children will have rapid desaturation with hypoxia (limited reserve) and often hard to preoxygenate an uncooperative child
• Equipment: ETT (pre-stylet) age calculated plus 0.5 smaller & 0.5 larger; laryngoscope (working), suction immediately available at HOB, functioning IV, pre-drawn drugs
  
  • Propofol 2-4 mg/kg (stable) vs. ketamine 1-2 mg/kg or etomidate 0.2-0.3 mg/kg (unstable)
    
    • plus Sch 2 mg/kg (premed with Atropine 0.02 mg/kg)
    • consider Rocuronium 1.2 mg/kg if Sch contraindicated (45 to 75 minute duration)
  • Calcium (IV) should be immediately available in the event Sch leads to unanticipated hyperkalemia w/ ventricular arrhythmias
    
    • Succs used in DAW patient → have Ca available

the younger the pediatric patient, the less reserve they have

Question 106

Airway management in children?

Answer 106

• Mask management is more critical skill in peds airway
• Always have ranges of ETT sizes
  
  • (0.5 smaller than calculated & 0.5 larger)
• Short trachea favors right mainstem intubation
• Breath sounds are often referred → bilateral chest rise and fall/w/ sounds
• Common formula over 2 yo
  
  • (Age + 16)/4
  • Cuffed tubes: reduce size by 0.5 mm
• Cuffed tubes are fine as long as cuff pressures are monitored
• Rough estimate of depth is 3x ID
  
  • Ex: using 4 tube → depth should be 12 cm
• A leak should be maintained around cuff regardless @ 20-30 cmH20 (not want pressure on trachea)
  
  • If turn APL to 20, should hear leak
  • If leak at 10- will be polluting OR and wont get TV

Question 107

Considerations for appendicitis, managmeent?

Answer 107

• One of the most common abdominal emergencies
  
  • most likely in teen years
  • > 24 hrs delaying dx → increased risk perforation
  • s/s: classically RLQ pain
• Risks of intraabdominal perforation:
  
  • Abscess
  • Ileus
  • sepsis

Considerations:

• Aspiration risks
• active nausea and vomiting
• tachycardia due to pain, dehydration, or sepsis

Management:

• Preop IV antibiotics w/ gram negative coverage
• correct fluid deficits
• use full stomach precautions – RSI
• evacuate stomach with NG/ OG

Question 108

What is down syndrome? physical exam findings?

What may they require surgery for?

Considerations for induction?

Answer 108

• 3rd copy of chromosome 21
  
  • 1:1000 live births
  • increased incidence in moms over 35
• Physical exam findings: Midface hypoplasia, brachycephaly, epicanthal folds, simian crease, downward medial slant of eyes, high-arched palate, glossoproptosis, and murmur (DAW)
• May require surgery for tympanostomy, strabismus, CHD repair, duodenal/esophageal atresia, marrow aspiration/biopsy, cervical spine fusion
• Considerations:
  
  • **5-fold risk of bradycardia during Sevo induction (first 6 minutes) in children with Downs (Barash)
  • Difficult intubating d/t macroglossia & glossoproptosis
  • Difficult masking d/t midface hypoplasia
  • Chart →
    
    • Keep neck neutral (d/t subluxation of C1/2)

Question 110

Down syndrome anesthetic considerations?

Answer 110

• Airway
  
  • Have variety of devices available (e.g., oral and nasal airways, laryngeal mask, glidescope, fiberoptic) to manage airway obstruction.
  • Avoid neck extension during laryngoscopy if possible.
  • Smaller endotracheal tube may be necessary for narrowed subglottic space.
• Vascular Access
  
  • Meticulously avoid injected air due to likelihood of CHD
• Anticipated Problems/Concerns
  
  • Bradycardia with inhalational induction (sevo)
  • Resistance to separation from caregiver