Pediatrics Flashcards

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1
Q

How is TBW effected in pediatrics? What does this mean for Vd? What does this mean for plasma concentration of a drug? What does this mean for pediatric dosing of induction agents?

A

TBW is increased to about 80-90%. This means that water soluble drugs will have a higher volume of distribution, that plasma concentration will be “diluted” in ‘typical doses’ and thus higher doses of induction agents are required

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2
Q

Why do drugs tend to last longer in pediatric populations?

A

Children typically have decreased phase II metabolism thus the half life of drugs is often prolonged

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3
Q

Why is onset of inhalation agents quicker in children (how does the pulmonary system and the vascular system play into this)?

A

Kids have an increased respiration rate, this in turn can hasten the alveolar concentration. Furthermore, children have more vessel rich blood flow - i.e. higher proportion of blood flow to the major organs

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4
Q

Why might opioids have a prolonged effect in children?

A

They have immature blood brain barriers which can prolong opioid effects

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5
Q

What is the major factor drug action of duration in children? What factors cause this?

A

Reduced drug clearance. This is due to immature phase 2 degradation and decreased GFR.

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6
Q

How are the following respiratory factors different in children: minute ventilation, respiration rate, FRC

A

Minute Ventilation = increased
Respiration Rate = increased
FRC = decreased

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7
Q

When is MAC the highest? What is the trend of MAC before and after this? What is the MAC of sevo and desflurane for a 6 month old?

A

MAC is highest at 1-6 months. It is lower at 0 days - 1 month but increasing, until after 6 months when it steadily decreases over time (age). The MAC of sevo for a 6 month old is 3%. The MAC of Des for a 6 month old is 9%

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8
Q

At what age and weight is 1 gram of Tylenol every 6 hours acceptable? What is the acceptable dosage of Tylenol before these parameters are reached?

A

13 years old and/or weighing 50 kg.

15 mg/kg every 6 hours

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9
Q

How is the NMJ different in children compared to adults? How does this effect dosing of paralytics (Depolarizers vs Non-depolarizers)

A

The NMJ is immature and structurally different. Depolarizer dosing is INCREASED in children. Non-depolarizer dosing is unchanged, but its effects may be prolonged due to receptor sensitivity and reduced drug clearance.

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10
Q

Why is succinylcholine avoided in children except for emergency use?

A

It has been associated with sudden cardiac arrest d/t undiagnosed muscular dystrophy, myopathy, and subsequent hyperkalemia associated with its use.

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11
Q

Speak to the following indicators in regards to cancelation of elective surgery for children: nasal drainage, cough, respiratory patterns, WBC

A

Nasal drainage: clear is ok, if green or tenacious reconsider and active infection
Cough: may be indicative of illness
Respiratory patterns: if respiratory wheezing, increased work of breathing, etc. then evaluate
WBC: an elevated WBC is indication of infection and elective surgery should be reconsidered

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12
Q

What is the PO dose for Midazolam in pediatrics?

A

0.25 - 1.0 mg/kg

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13
Q

How do you determine ETT size for children? How far should the tube be advanced?

A

(Age / 4) + 4

3 times the size of the ETT; a size 5 ETT should be advanced to 15cm

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14
Q

What is thoracoabdominal asynchrony? What are indications? How is it treated? What causes it?

A

It is indication of a completely obstructed airway. It is illustrated by chest retraction and abdominal expansion with attempted inspiration. There are NO audible indicators of obstruction b/c the obstruction is complete.

It can be treated by chin lift, mandibular protrusion, and/or the later decubitus position

It is caused by collapse of the tissues of the airway and muscle relaxation of the airway with general anesthesia

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15
Q

What nerve is responsible for laryngospasm? What can help break a laryngospasm? Which type of environmental exposure increases the risk of laryngospasm 10-fold?

A

The superior laryngeal nerve.

Breaking a spasm: cease stimuli, deepen anesthetic, positive pressure, Larson’s maneuver, use of succinylcholine.

Smoking

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16
Q

What is the emergency dosing of succs and atropine for laryngospasm; IM and IV

A

Succs 4 mg/kg IM and Atropine 0.02 mg/kg

Succs 2 mg/kg IV and Atropine 0.02 mg/kg

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17
Q

What is bronchospasm and how does it differ from laryngospasm? How should it be treated?

A

Bronchospasm is contraction of the smooth muscle of the bronchus leading to airway diameter restriction and turbulent air flow. It MAY result in substantial obstruction of the airway, but it is not glottis closure.

To treat: stop stimulation, deepen anesthesia, provide a bronchodilator, a corticosteroid may have long term benefits but not acute, consider use of epinephrine if aggressive reversal needed?

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18
Q

What is the treatment of choice for acute and emergent airway obstruction due to bronchospasm? How is it dosed?

A

Epinephrine. Give 0.1 mg to 0.2 mg IV.

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19
Q

Are children more prone to laryngospasm with induction or emergence?

A

Emergence

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20
Q

What Post conceptual age is associated with increased risk of central apnea? How long should these patients be kept for observation after anesthesia?

A

< 60 weeks post-conceptual age. They should be kept over night for observation

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21
Q

What is fluid replacement and maintenance in pediatric patients? If a child is 12 kg what is maintenance rate?

A

The 4-2-1 rule still applies; 4ml for first 10 kg, 2ml for next 10 kg, 1ml for rest of kg. For NPO it is maintenance rate x hours NPO.

4x10 + 2x2 = 44ml/hr

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22
Q

How can humidification of inhaled gases influence fluid maintenance?

A

Dry gases result in condensation, water loss, and heat loss from the respiratory system

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23
Q

What is the estimated rate of fluid loss from open cavity procedures? How should this be considered in fluid replacement? What then is the potential maintenance fluid rate for a 12kg child with open abdominal surgery?

A

Up to 10ml/kg/hr

This value should be added to the maintenance rate

Maintenance is 44 ml/hr, open cavity is an additional 120 ml/hr, so 164ml/hr may be indicated

24
Q

What is TBW of a premature infant? Term infant? A 1 year old? An adult?

A

80%
70%
60%
60%

25
Q

In what subgroup of pediatric patients should glucose be assessed with anesthesia?

A

Healthy kids who have been fasting do not develop hypoglycemia with surgery. There is, however, a subgroup that are at higher risk which includes critically ill infants, kids weighing <10 kg, premature newborns, newborns born to gestational diabetes, diabetic children

26
Q

In comparison to adults, do children have higher or lower intravascular volume? What is the consequence of this then for both homeostasis of organ perfusion and Vd of pharmacological agents?

A

Children have LESS intravascular volume and MORE extravascular volume in comparison to adults. This means Vd is higher. This also means perfusion of organs can be compromised earlier in pediatric patients.

27
Q

How is the intravascular volume estimated in pediatrics? (Preterm, Term, Infant, Child 6+ years)

A

EBV for children is determined by set values based on age multiplied by the Childs weight in kg:

Preterm = 90-100 ml/kg
Term = 80-90 ml/kg
3 months to 3 years = 70-80 ml/kg
6 years and older = 60-70 ml/kg

28
Q

How can blood loss soaked in surgical drapes and sponges be assessed?

A

Every 1kg = 1ml blood loss

29
Q

What is an appropriate fluid bolus for pediatric patients? How long should this be administered over?

A

20 ml/kg administered over 15-30 minutes

30
Q

How is allowable blood loss calculated in pediatric patients: what value is relied upon and how is it calculated?

A

Hct is the indicative factor for blood loss and typically 24 Hct is a lower limit

ABL = EBV x (Original Hct - Acceptable Hct) / The average of original and acceptable

31
Q

In general, what value of packed RBCs will raise Hgb by 1g/dL in the pediatric patient? How much blood then is required for a 12 kg patient who’s Hgb is 7 and you wish to raise it to 9?

A

4ml/kg

12kg x 4ml/kg x 2g/dL = 96ml of blood to raise Hgb by 2 g/dL

32
Q

Why are neonates at increased risk for hypothermia? What is their means of generating heat? How does this differ from an infant or adult?

A

Neonates have little insulation and a high surface area which translates into easy heat loss. Neonates produce heat via brown fat metabolism. Older pediatric patients and adults can shiver to generate heat, neonates can not (at least not sufficiently)

33
Q

What are consequences of hypothermia?

A

Delayed emergence, increased oxygen demand from shivering, reduced perfusion and wound healing, and impaired coagulation

34
Q

How low does the spinal cord go in the neonate and infant? What is the adult level and by what age is this achieved?

A

L3. By the age of 3 the cord is at the normal adult level of L1 to L2

35
Q

Where does the larynx sit in the pediatric patient? How does this compare to the adult?

A

It is more cephelad at C2-C3 where as the adult is C3-C4

36
Q

What is the oxygen consumption per kg in a pediatric patient compared to an adult? What does this illustrate about desaturation in the neonate?

A

The oxygen demand in a neonate is 6.5 ml/kg compared to 3.5 ml/kg in an adult. Because of their increased oxygen demand, children desaturated quicker. Furthermore they have less FRC and hypoxia is a precursor to bradycardia

37
Q

Which are the two most common types of congenital diaphragmatic hernia? Which is more common and why is it more severe?

A

Generally speaking, there is left sided herniation and right sided herniation. The left sided herniation is through the foramen of Bochdalek and is found in 80% of CDH. Right sided herniation is through the foramen of Morgani. Left sided herniation is associated with more severe pulmonary hypoplasia than right sided.

38
Q

What does CDH due to pulmonary vasculature in utero and what is the result in regards to pulmonary pressure? What factors increase PVR and why is this unfortunate considering CDH? How can all of this lead to a return to fetal circulation?

A

Pulmonary vasculature is abnormal and reduced, this leads to pulmonary hypertension and increased PVR. Hypoxia is the main factor that will increased PVR and children with CDH are often hypoxic, hypercarbic, and acidodic. Increased PVR can lead to R->L shunt through the PDA

39
Q

Is CDH an emergent procedure? What should be considered before surgery?

A

In short, no. Patients should be optimized cardio and respiratory. Children often on ECMO before undergoing surgery.

40
Q

What is the maximum PIP that should be observed with CDH and why?

A

Keep PIP <30 as pulmonary hypoplasia puts neonates at increased risk for barotrauma

41
Q

What factors should be avoided as to not increased PVR with CDH?

A

Hypoxia, hypercapnia, acidosis, hypothermia

42
Q

Describe the ventilation goals with CDH in regards to PaCO2, SaO2, and Peak Inspiratory Pressures

A

Permissive hypercapnia to 45-55 mm Hg
Ensure oxygenation of at least SaO2 >/= 85%
PIP < 25 mm Hg

43
Q

Physiologically, what is the difference in presentation between ompahalocele and gastroschisis? Which is associated more commonly with other congenial defects and what are the common defects?

A

An omphalocele is protrusion of abdominal contents through the umbilicus which is surrounded by a visceral sack. Gastroschisis is protrusion of abdominal contents through a hernia in abdominal wall (usually right side) that is NOT covered with a viscera

Omphalocele is associated more with other congenital defects; heart defects, pulmonary hypoplasia, and Bechwith-Wiedman Syndrome

44
Q

What is the immediate concern with gastroschisis and its exposure of abdominal contents to the enviornment?

A

Increased risk of infection and increased risk for dehydration from water loss through evaporation from bowel

45
Q

What characteristics are associated with Beckwith-Wiedman Syndrome and which disease (omphalocele or gastroschisis) is it associated with?

A

The disease is associated with hypoglycemia, a large tongue, and an Omphalocele

46
Q

Why is decompression of the stomach with omphalocele and/or gastroschisis imperative

A

Decompression of the stomach will help ensure decreased risk of aspiration and proceeding respiratory compromise

47
Q

What should be monitored with step-wise return of protruding contents back into the abdomen with fixture of omphalocele and gastroschisis (respiratory and circulatory, specifically)

A

A small abdominal compartment can be stretched and pressure in abdomen increased with return of contents into abdomen. As such the diaphragm can increase intrathoracic pressures and compromise ventilation on a possible hypoplastic lung (specifically with omphalocele). The increasing abdominal pressure can also decrease perfusion to organs and lower extremities by decreasing blood flow in the circulatory system)

48
Q

What type of tracheoesophageal defect is most common and how does it present anatomically?

A

Type C; a blind esophageal pouch and a fistula between the stomach and trachea via the esophagus connected just above the carina

49
Q

What, if any, anomalies are associated with Tracheoesophageal fistula?

A

Patients are increased risk for other congenital anomalies such as cardiac defects, VATER, etc.

50
Q

What are signs and symptoms of possible tracheoesophageal fistula in a new born? What is a key sign in utero?

A

Coughing, choking, cyanosis with feeding. Polyhydramnios is indicative of this defect in utero as the amniotic fluid is not ingested by the fetus

51
Q

Describe the pathology of pyloric stenosis. What does this lead to physiologically?

A

It is a thickening and narrowing of the outlet between the stomach and the small intestine.

The obstruction delays gastric emptying into the SI and leads to hypokalemia, hyponatremia, hypochloremia, and metabolic alkalosis

52
Q

Is pyloric stenosis a medical emergency? It is a surgical emergency? How should the request for surgery be handled?

A

It is a medical emergency, but not a surgical emergency. The patient should be optimized for surgery and electrolyte balances as well as volume status should be addressed before surgery.

53
Q

How should induction before correction of pyloric stenosis by handled?

A

The patients stomach should be suctioned with an OG or NG tube BEFORE induction as it is common for contents to back up in the stomach increasing the risk of aspiration.

Inhalation induction is NOT recommended

The airway should be secured via RSI or awake induction

54
Q

When is pyloric stenosis most often diagnosed (age)? What are the signs and symptoms?

A

At 2-8 weeks. Electrolyte abnormalities, dehydration, projectile vomiting

55
Q

How can pyloric stenosis be palpated?

A

It presents as a hard olive in the RUQ or epigastric region of the abdomen