Pediatric/Neonate Flashcards
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?
- neonate= Birth- 30 days
- preterm <37 weeks
- ELGAN-
- 23-27 weeks gestations; all organs immature
- most vulnerable peds patient
Pre-terms at risk for:
- Respiratory distress
- O2 consumption doubled with increased alveolar ventilation–> rapid desaturations especially during cold stress and airway obstruction
- 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
-
Former premature infants up to 60 weeks PGA are at increased risk for postoperative apnea and bradycardia
- 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
- 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
- infection
* only innate immunity functioning, no acquired immunity - hyperbilirubinemia
- reduction in glucuronyl transferase decreases bilirubin breakdown causing jaundice
- 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
-
higher threshold for transufion in preterm neonates (would transfuse to maintain Hct 30%)
- 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
-
decreased Vit K dependent factors, at birth 20-60% of adult values)
What are some major key points to fetal circulation, specifically describing pre-ductal, post-ductal circulation and the characteristics of each?
- (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
-
HIGH O2 blood to head, neck, and RUE drained into SVC = then MIXED (high O2-RA→ FO→ LA→ LV)
-
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

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?
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
-
25-30% of adults have patent foramen ovale
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
- ↑ pulmonary artery pressure
-
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
What CV changes occur at birth to transition from fetal to adult circulation, and why do these changes occur?
Changes that allow parallel circulation of the fetus to convert to the series circulation of the adult:
-
Pulmonary Vascular Resistance DECREASES
- 1st breath → expansion of lung → pulm vascular resistance DROPS → increased alveolar O2 → increase in pH
- neurohumoral mediators and nitric oxide (NO) relaxes pulmonary vasoconstriction.
-
FO closes
- When placenta separates from uterine wall:
- placental BV constrict
- SVR & left ventricular afterload increase.
-
Decrease PVR + increase SVR → increases left atrial pressure above right atrial pressure
- Pressure: LA > RA → functionally closes FO “flap valve”
- FO not close anatomically for months to years (if ever)
- Patent in ~15% adults.
- Pressure: LA > RA → functionally closes FO “flap valve”
-
Decrease PVR + increase SVR → increases left atrial pressure above right atrial pressure
- When placenta separates from uterine wall:
-
Ductus Arteriosus closes
- decrease PVR causes flow through the ductus arteriosus to reverse.
- This exposes the ductus to oxygenated systemic arterial blood + rapid decrease prostaglandin E 2 (PGE2) after birth → closes ductus arteriosus
- Anatomic closure of the ductus requires several weeks.
- D/t Increase PaO2 exposure >60 mm Hg → cause vasoconstriction → functional closure of ductus arteriosus
- decrease PVR causes flow through the ductus arteriosus to reverse.
-
Ductus Venosus Closes
- The ductus venosus closes passively with removal of the placental circulation and readjustment of portal pressure relative to inferior vena cava pressure.
- 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.
- After birth, the muscle coat thins and extends to the periphery of the lung, a process that takes months to years to complete
- 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) **
What are some physiologic differences in the cardiovascular system of the neonate?
- ## 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
- ## Cardiac output → HR dependent****
- 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
- Ex: Tendency to have bradycardia with suctioning & laryngoscopy
- Sympathetic nervous system immature
-
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
- Neonate at birth: ~400 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
- 1st 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%
Describe some characteristics of the pulmonary system in the pediatric patient?
- *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%
-
→ (Why they wear out fast, not mature Type 1)
- ### 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
Describe the differences in airway anatomy in infants compared to adults?
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
*
-
easily can right main stem

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.
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!
- can lead to metabolic acidosis & increased O2 consumption
Anesthesia considerations
- warm the OR (dec convection) 72-76o (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 (1st see ETCO2)
- Stop VA, high flow on, switch to TIVA, evaluate (stop anesthetic d/t Ca dysregulation getting worse)
Neuraxial considerations in pediatrics
- 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

Renal characteristics of infants?
-
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
Liver function in infants?
- 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
-
Vit K dependent factors (II, VII, IX, X)
-
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
GI system in pediatrics?
- 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
- coanal atresia- blockage of nasal to trachea
-
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
How can body composition of infants alter pharmacokinetics?
- 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)
- higher free-fraction of protein bound drugs → higher risk of toxicity!!
“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 ***
Difference in drug pharmacokinetics in infant, childhood to adulthood?
- Preterm/infants: prolonged elimination half-life
- >2 yo to early teenage yrs: shorted half-life
- Adulthood: lengthened half-life
Difference in hematocrit and blood volume in infant?
How do we dose blood transfusions in infants?
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)
What are some considerations of glucose administration and hypoglycemia prevention in infants?
- 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
- Exception: Children at high risk of hypoglycemia- can use D5 1/2NS @ maintenance rates
Miller says cut the TPN rate by one third and leave running
Why is uptake of VA more rapid in children?
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
- Wash in is inversely related to solubility= lower solubility→ higher wash in
- Removal → CO, solubility, alveolar-venous partial pressure
-
Determinants of “wash in” of VA → FRC, inspired concentration, alveolar ventilation
- Faster equilibration to what set on dial (from co-exist lecture last semester)
- 18% BF to VRG in infants as opposed to only 8% in adults
MAC for sevo and des in neonate, infant and children?
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)

How do you determine how much blood to transfuse in infant?
- 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
- Reasons for it being 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

Coagulation in newborns/infants?
- 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.
Induction agent use in pediatrics?
Propoofl, ketamine, etomidate, thiopental, methohexital doses?
-
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
-
Propofol (Diprivan): have extra available
Propofol use in pediatrics?
- 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
Ketamine use in pediatrics?
- 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
- Induction with ketamine preferred in
Midazolam use as sedatives in pediatrics?
Metabolism?
Reversal agent?
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
- ORAL dosing: dose decreases w/ age
- 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









