Neonatal Pharm Flashcards
1
Q
Gestational Age
Definition
3 ways to determine GA
A
Estimated time since conception
- LMP
- Early ultrasound
- Dubowitz/Ballard – done within first 48 hour
2
Q
Corrected Age
A
(actual age – weeks premature = Corrected age)
Helps anticipate complications and expectations
3
Q
General Principles for Pharm (2)
A
Age – consider GA and PMA
Weight – update weekly (if not daily)
4
Q
Normal weight gain
A
20-40grams/day in first 6 months
5
Q
Enteral absorption
pH affects gastric absorption
A
o pH approaches neutrality at birth
o Highest gastric pH within first 1-10 days
o Lowest gastric pH within first 10-30 days
o Gastric secretion approaches lower limit of adult values by 3 months of age
o Better absorption of weak bases (Penicillin, ampicillin, erythromycin)
o Poor absorption of weak acids (Phenytoin, phenobarbital)
6
Q
Enteral Absorption
Decreased Intestinal Motility
(3)
A
o Possible increase absorption of drugs absorbed in the stomach
o Delayed absorption of drugs absorbed in small intestine
o Gastric emptying normalizes quickly but intestinal emptying lags behind until 4-6 months of age
7
Q
Enteral Absorption
Pancreatic Enzyme Activity (2)
A
- Important for meds that require cleavage from its salt form prior to absorption (clindamycin)
- Absorption is highly variable during the first 3 months of life
8
Q
Enteral Absorption
Preemies should be receiving ½ of total fluid intake enterally before PO meds are introduced (2) WHY?
A
- Indicates GI function = tolerating feeds
- Provides diluent and buffer for medications
9
Q
Intramuscular absorption (5)
A
- Pain
- Low blood flow/supply Slower absorption rates
- Decreased muscle mass in newborns (especially preemies)
- Immobility
- Volume of administration reserved for emergencies or situations in which slower absorption is desired and /or safer (ie-vitamin K at birth)
10
Q
Absorption
Increased topical absorption (5)
A
o Increased skin hydration
o Low fat stores
o Immature epidermis (thinner stratum corneum)
o Increased risk of toxicity (povidone iodine)
o Sensitive to environmental changes
11
Q
Absorption
Rectal (2)
A
o Useful for N/V, induction of anesthesia, status epilepticus
o Avoids first pass effect
12
Q
Distribution
Volume of distribution (2)
A
o Hydrophilic drugs (vanco, gentamicin) are confined to extracellular fluid or total body water (low Vd)
o Lipophilic drug (digoxin) widely distribute to all tissues (large Vd)
13
Q
Distribution
Volume of distribution in neonates (7)
A
- Increased total body water (85% vs 50%) – may need higher doses (mg/kg) to achieve same outcome
- Increased extracellular water (40% vs 20%)
- Decreased fat in neonates/infants
- Lipophilic drugs (digoxin) may have lower Vd
o 1% in 29 week preterm neonate
o 12%-16% in full term neonate
o 2-%-25% at 1 year of age
14
Q
Distribution
Decreased protein binding (2)
A
o Decreased albumin and decreased affinity for drug binding
o Therefore – increased free drug
15
Q
Albumin bound meds (4)
A
Phenytoin, phenobarbital, PCNs, morphine
High affinity for albumin – may displace drugs and increase free drug levels
Ex. Sulfonamides, ceftriaxone, may displace bilirubin = kernicterus
16
Q
Distribution
Increased concentrations of (2)
A
Free fatty acids
Unconjugated (indirect) bilirubin
17
Q
Metabolism (3)
Hepatic enzyme activity is…
A
- Hepatic enzyme activity is decreased
- Enzymatic microsomal systems responsible for drug metabolism are present at birth
- Their activities increase with advancing gestational age
18
Q
Metabolism
Phase I hepatic reactions (3)
A
- Oxidation, reduction, hydroxylation develop rapidly during infancy
- Adult capacities by 6 months of life
- Ex.prolonged elimination for phenobarbital and cocaine
19
Q
Metabolism
Phase II hepatic reactions (3)
A
- Synthesize a more water soluble compound to augment elimination
- Glucuronidation, Acetylation, Sulfation
- Glucuronidation – takes up to 1 year to develop= leads to decreased glucoronide = decreased GFR= leading to accumulation of drug (and can lead to death)
EX- chloramphenical – gray baby syndrome
20
Q
Metabolism (4)
A
- Different metabolic pathways
- Enzymatic systems responsible for metabolism
- Mature at different times – this coupled with the diminished volume of distribution in the newborn = prolonged effect of certain drugs
- Local anesthetics during delivery
21
Q
Elimination (4)
A
- CrCl is proportional to gestational age
- Nephrons begin forming in utero at 9 weeks and formation is complete at 36 weeks- but functionally immature
- Infants born before 34 weeks have a more pronounced decrease in renal function
- Drugs are often dosed according to post conceptual and postnatal age
22
Q
Normal CrCl = in newborns
A
newborns ~40-65ml/min
23
Q
Elimination reaches 50% of adult GFR by 1 month of age
3
A
Fullterm newborns have decreased renal function which approaches adult by 3-5 months
Decreased daily doses of meds which are renally eliminated
Gentamicin – Q12-24 hours
24
Q
Decreased ability to concentrate urine
3
A
Normal urine output – 1-2 cc/kg/hour
Renal insufficiency - <1cc/kg/hr
Drugs dosing has to be adjusted with decreased urine output
25
Calculation of CrCl – Schwartz Method
```
CrCl (ml/min/1.73m2)= K x length (cm)
// SCr
```
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K- age specific proportionally constant
preterm – 0.34 (1st year)
fullterm – 0.44 (1st year)
L- length in cm
SCr- serum creatinine in mg/dl
```
26
Elimination REMEMBER (4)
Adjust medications based on GA and weight
Aminoglycosides, cephalosporins
GFR changes with age
Premature infant -11ml/min
Fullterm infant -33ml/min
1 month old - 50ml/min
Look at what your patient is doing clinically
Reasons for renal impairment?
Always check your dosages
27
Factors leading to ADRs in neonates
| 5
1. Decreased plasma proteins- result in increased free (unbound) drug
2. Immature renal function – decreased elimination of renally excreted drugs
3. alteration in number of drug receptor sites
4. immature hepatic metabolism
5. increased permeability of skin
28
Common conditions Preterm Neonates (8)
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Respiratory Distress Syndrome (RDS)
Bronchopulmonary dysplasia (BPD)
Patent Ductus Arteriosus (PDA)
Apnea of Prematurity (AOP)
Sepsis
Necrotizing Enterocolitis (NEC)
Seizures
PPHN
```
29
Respiratory Distress Syndrome (RDS)
| 3 requirements
Hyaline membrane disease
Requirements
- Central cyanosis in room air
- Requiring supplemental oxygen to maintain a pulse oximeter saturation over 85%
- Characteristic chest Xray – uniform reticulogranular pattern to lung fields with or without low lung volumes/air bronchogram- within the 1st 24 hours of life
30
Patho RDS (4)
1. Surfactant deficiency is the primary cause of RDS
2. Complicated by overly compliant chest wall
3. Leads to progressive atelectasis – failure to develop effective FRC
4. Surfactant is a surface active material produced by epithelial cells
31
Type II pneumocytes (4)
- Begins at 24-28 weeks gestation
- Type II cells are sensitive to/decreased by… asphyxial insults in the perinatal period
Maturation of this cell line is delayed in presence of fetal hyperinsulinemia (DM)
Type II enhanced by
Administration of antenatal corticosteroids
Chronic intrauterine stress (HTN, IUGR)
32
Surfactant (3)
- Composed of phospholipids (75%) and protein(10%)
- Produced and stored in the Type II pneumocytes
- This lipoprotein is released into the airways where it functions to decrease surface tension and maintain alveolar expansion
33
what happens when neonates
| LACK surfactant
The small airways collapse- each expiration results in progressive atelectasis – cell damage – debris build up in the airway – directly decrease total lung capacity
34
RDS
| Prematurity leads to....
Prematurity leads to overly compliant chest wall – weak structural support- allows negative pressures cause retraction of the chest wall – (instead of inflation)- collapse!
35
Risk factors for RDS (5)
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Prematurity
Male sex
C-section without labor
Perinatal asphyxia
Maternal diabetes
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36
RDS Physical Exam (5)
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Tachypnea
Grunting
Flaring
Retractions
Cyanosis in room air
```
37
Management RDS(4)
Administer surfactant
Reduces surface tension in lungs (anti-stick)
Improves gas exchange
? Decrease in BPD. LOS, or mechanical ventilation- ??
38
Surfactant Products
| Synthetic (1)
Surfaxin
39
Surfactant Products
| Natural (3)
Curosurf – porcine
Infasurf - bovine
Survanta – bovine
40
Natural surfactant characteristics (3)
- Natural ( derived from animal lungs) surfactant preparations are better than synthetic (protein free)
- They have a quicker onset of action and reduced number air leaks (pneumothorax)
Natural are treatment of choice
41
Surfactant Replacement Therapy
| Early administration
Key to restore pulmonary function
Prevents tissue injury
Decreased mortality
42
Surfactant Replacement Therapy
| Composition
Animal origin
| All contain hydrophilic surfactant properties SpB and SpC
43
Surfactant Replacement Therapy
Actions
(3)
Intended to replace missing or inactivated natural surfactant
Surface tension reduction and stabilization of the alveolar air-water interface are the basic functions
Air-water interface stability lower alveolar surface tension--> prevents atelectasis
44
Surfactant Replacement Therapy
| Efficacy (3)
Can be seen with clinical conditions with both early and long-term effects
Early: reduction in Fio2 need-improved PaO2-improved lung function decreased ventilator pressure
Long-Term: decreased length of respiratory support, less severe CLD
45
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Surfactant Replacement Therapy
Side effects (2)
```
```
Pulmonary hemorrhage (low)
Air leak (pneumothorax) – change in tidal volume
```
46
Surfactant Admin (5)
- Administered through the ETT into each lobe of the lung- (direct tracheal instillation for all)
- Administer through the ETT using a premeasured 5 french end hole catheter
- Position the infant properly – gently inject the first dose through the catheter over 2-3 seconds
- Remove the catheter from the ETT
- Do Not Suction the infant for 1 hour after dosing unless signs of significant airway obstruction
47
Surfaxin (Lucinactant)
5.8 ml/kg – every 6 hours (up to 4 doses in 48 hours)
48
Curosurf (Poractant)
Initial 2.5ml/kg – may repeat with 1.25ml/kg every 12 hours up to 2 times
49
Infasurf (Calfactant)
3ml/kg – may repeat every 12 hours up to 3 times
50
Survanta (Beractant)
4ml/kg – may repeat every 6-8 hours up to 4 times
51
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Surfactant
Recommended prophylaxis (5)
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- Recommended prophylaxis if <26 weeks gestation within 15 minutes of birth
- Early rescue dose – should be given to all infants with evidence of RDS -- X-ray and oxygen
- Effect is better the earlier in the course of RDS it is given
- Can give a 2nd (and 3rd) dose if needed – based on clinical presentation
- Inhaled surfactant under investigation – clinical trials
52
Bronchopumonary dysplasia
BPD
Patho
Patho – Secondary development of a persistent lung injury is associated with an abnormal repair process and leads to structural changes in the alveoli –
Inflammation occurs in an exaggerated form d/t the alveolar influx of cytokines and macrophages)
53
BPD Definition (4)
- Respiratory failure during 1st week of life requiring mechanical ventilation for >/= 3 days
- Persistent respiratory symptoms
- Oxygen dependence after 28 days
- Consistent X-ray findings
54
BPD
Risk factors
(4)
Prematurity
LBW
Aggressive mechanical ventilation (barotrauma)
High Fio2 – Oxygen is a drug!!
55
BPD
| Manifestations (5)
```
airway hyper-reactivity (bronchospasms)
Pulmonary edema
Fibrosis
Shifting atelectasis
Airway hyperinflation (X-ray)
```
56
BPD Treatment (3)
1. optimize nutrition(24 cal/oz formula or EBM)
2. Fluid restrict (120ml/kg/day),
3. Oxygen
57
BPD Treatment
| Corticosteroids (9)
```
4. Corticosteriods (controversial)
Decrease pulmonary edema
Increase surfactant synthesis
Short term improvements in oxygenation
Earlier extubation
Decreased long term risks of BPD
- Pulmonary complications
- Poor growth
- Neurodevelopmental problems
Decreased risk of death
```
58
BPD Treatment
Corticosteroids
Dexamethasone
Dexamethasone
0.25mg/kg/dose IV BID x 3 days –gradually taper by 10% every 3 days …
Taper over 12-21 days – total of 42 days is possible
Long t ½
59
ADE of Corticosteroids for BPD (10)
HTN, hyperglycemia, infection, intestinal perforation, GI bleed, growth restriction, adrenal insufficiency, decreased brain growth, PVL, CP
60
AAP- dexamethasone (4)
1. Dexamethasone decreases the incidence of BPD and extubation failure…BUT…does not decrease overall mortality, is associated with increased risks of short and longterm adverse effects.
2. No routine use for preventing BPD,
3. Recommend ONLY in exceptional circumstances
4. Requirement of maximal ventilatory and oxygen support with parental informed consent
61
BPD Treatment
5. Diuretics
Furosemide (LASIX) (IV and po)
Overview (2)
Acts in loop of Henle by inhibiting reabsorption of NA, K, Cl --- diuresis! (Potent diuretic for rapid diuresis.)
Also may decrease pulmonary capillary leak and decrease fluid filtration into the lungs
62
BPD Treatment
Furosemide (LASIX) (IV and po)
Onset of action
Duration
Onset of action --within hours po / within 5 minutes IV
| Duration – po = 6-8 hours/ IV = 2 hours
63
BPD Treatment
Furosemide (LASIX) (IV and po)
ADE
ADR- (the bad) low serum Na, K, Cl, Ca, nephrocalcinosis, bone demineralization, volume depletion, ototoxicity
64
BPD Treatment
Furosemide (LASIX) (IV and po)
DOSE
IV PO
IV- (0.5mg-1mg/kg/dose) – max 2mg/kg/dose Q24….can change to Q12.
or > 1month Q6-8 hours
PO- (1mg-2mg/kg/dose)- (double the IV dose- up to 6mg/kg/dose)
65
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BPD Treatment
Chlorothiazide (Diuril)
Onset of action
Dose
ADR
```
Thiazide diuretic
Onset of action 3-5 days
Dose- < 6months : (20-40mg/kg/day) po divided every 12 hours (max 375mg/day)
> 6 months: (20mg/kg/day) po divided every 12 hrs (max 1 gram)
ADR- same as furosemide!
66
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BPD Treatment
Spirolactone (aldactone)
MOA
Dose
ADR
```
Potassium sparing diuretic – increases Na and water excretion in the distal renal tubules
Primarily used in conjunction with Diuril
Dose (1-3mg/kg/day) po Q 24hours – 2mg/kg/d typical
ADR- hyperkalemia, dehydration, hyponatremia
CHECK ELECTROLYTES WITH DIURETICS!
67
BPD Treatment
| Bronchodilators (4)
- Increase pulmonary compliance
- Albuterol – Beta-2 agonist
~improve airway resistance- lung compliance- gas exchange- and decrease airway hyperactivity
~management of acute bronchoconstriction episodes
68
BPD Treatment
Bronchodilators
Dose, duration of action, ADE
DOSE- nebulizer – (2.5mg every 2-6 hours prn)
Duration of action is ~2-5 hours
ADRs- tachycardia, hyperglycemia, tremors
69
Xopenex- (levalbuterol)
nonracemic form of albuterol, limited experience in newborns- longer efficacy at lower doses..so less ADRs??
70
PDA
| Overview (6)
- The ductus arteriosus is a large vessel that connects the pulmonary artery and aorta
- During fetal life shunts the blood away from the pulmonary bed/lungs
- After birth – undergoes active constriction and finally obliteration
- Exposure to oxygen and Prostaglandin E
- Full term healthy newborns functional closure occurs rapidly after birth – Final functional closure occurs in 50% of fullterm infants by 24 hours of life
90% by 48 hours; and in all by 96 hours…
PDA refers to the failure of the closure process and continued patency of this fetal channel
71
PDA Factors (8)
Prematurity (inversely related to GA)
45% < 1750grams
80% < 1000grams
Increased risk of patency with RDS-after surfactant replacement clinical presentation may increase – earlier dx
Fluid administration- increased fluids in first few days of life =increased PDA
Asphyxia
High Altitude (decreased oxygen )
CHD (associated with coarctation, transposition of great vessels
72
PDA Clinical presentation
| 5
- Usually on days 1-4 of life (but may be at birth)
- Murmur – systolic, heard best at the left upper sternal border, continuous, best to disconnect from ventilator to appreciate
- Hyperactive pericordium – increased left ventricular stroke volume may cause this
- Bounding peripheral pulses- increased stroke volume with diastolic runoff through the PDA
- Respiratory distress – worsening even on vent – gradual increase in support needed over days – not acute like pneumothorax – left to right shunting may lead to heart failure and pulmonary edema if untreated
73
Diagnosis
| PDA (2)
Echocardiogram – can visualize the ductus and direction of flow
Will also rule out additional cardiac diagnosis
74
Treatment
| PDA (3)
1. Ventilatory support as needed
2. Fluid restriction- to decrease the PDA shunt as well as accumulation of fluid in the lungs.
3. Increase HCT (40-45%)
may decrease the left-to-right shunting and increase oxygen carrying capacity
75
Indomethacin (Indocin) for PDA
| Overview
A prostaglandin inhibitor – effective in promoting ductal closure. Effectiveness decreases with age –so the younger the better – 3 approaches to giving
76
Indomethacin (Indocin) for PDA
| Prophylactic (3)
Dose (0.1mg/kg/dose) IV over 20 minutes Q24 hours for the 1st 6 days of llife
All < 1250grams BW who have received surfactant for RDS
Controversial because 40% may not have had a problem PDA – has side effects
77
Indomethacin (Indocin) for PDA
Early symptomatic
(4)
1. Dose (0.2 mg/kg/dose) IV over 20 minutes- 2nd and 3rd doses (0.1mg/kg/dose
2. If < 1250grams and <7 days old) given 12 and 36 hours after 1st dose
3. If > 1250grams and > 7days old 0.2mg/kg/dose
4. TYPICALLY THIS IS DAYS 2-4 of life when symptoms appear!
78
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Indomethacin (Indocin) for PDA
Late symptomatic (2)
```
When signs of CHF – often fails to constrict significantly enough and surgery needed to close
IN ALL- FAILURE RATE IS 20-30% will reopen after 1st course…..2nd course is ok
NEC and infection are associated with ductus reopening so redose cautiously!!
79
Indomethacin (Indocin) for PDA
| Complications (5)
Renal – decrease in GFR and urine output
GI bleeding
Spontaneous intestinal perforation
Platelet function impairment – for 7to 9 days after dose regardless of platelet number - ?IVH risk
? CBC (if thrombocytopenia do not give)
80
Indomethacin (Indocin) for PDA
| Contraindications (4)
Thrombocytopenia
NEC
Sepis
Serum creatinine >1.7mg/dl
81
IBUPROFEN
For PDA
(8)
Nonselective cyclooxygenase inhibitor
Closes the ductus
Studies show as effective as Indocin for PDA
Advantage – does not reduce the mesenteric and renal artery blood flow….so fewer renal side effects
Higher urine output, lower serum creatinine
NEC and IVH rates the same
….so it is institutional preference…..
DOSE (10mg/kg/dose followed by 2doses of 5mg/kg) each after 24 and 48 hours within 1st week of life.
Do to change in pharmacokinetics…higher doses are used (18mg/kg and 9mg/kg) after the second week of life.
82
Feeding with a PDA?
| (4)
Given the physiologic effects of a PDA and the medications we treat it with (decreased blood flow to gut- ischemia from the decreased intestinal blood flow)…Data is lacking but risk if there?!
Closure rate can be up to 94% with conservative medication treatment
Closure rate ~ 72% sponteous if less than 30 weeks
Surgery/ligation is an option
83
Should we treat PDA?
| 2
Controversial
| Risk vs.Benefit
84
Apnea of Prematurity
| Definition (4)
- Is common in preterm neonates
- Unstable respiratory rhythm reflecting immaturity of the respiratory control system
- Apnea can be secondary to other conditions – therefore AOP is a diagnosis of exclusion
- Apnea is defined as cessation of breathing lasting at least 20 seconds and is accompanied by bradycardia, oxygen desaturation or cynanosis
(some may say 15 seconds)
85
PDA -- patho
AOP is a developmental disorder and reflects a physiological rather than pathological immature state of respiratory control
86
Apnea
Obstructive
(3)
Infant tries to breathe against an obstructed airway resulting in chest wall motion without air flow
MIXED- consists of obstructive resp efforts usually FOLLOWED by central apnea.
Periodic breathing – benign- normal breathing pattern followed by apnea for 5-10 seconds WITHOUT change in heart rate or color.
87
Apnea
| Central
Total cessation of inspiratory effort with no evidence of obstruction
88
Treatment for apnea (6)
Methylxanthine therapy
Caffeine, theophylline and aminophylline
Respiratory stimulants to decrease apnea
Caffeine most widely used today
Largely replace Theophylline
Increases minute ventilation-improve CO2 sensitivity – decrease hypoxic depression- and enhance diaphragmatic excursion.
89
Side effects for treatment of apnea (5)
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Tachycardia
Jitteriness
Feeding intolerance
Emesis
Restlessness
```
90
Caffeine for apnea has reported...
fewer side effects and is better tolerated – has a higher therapeutic index – a longer half-life which makes it convenient QD dosing –and monitoring of drug levels is rarely necessary unless a concern.
91
DOSE- Caffeine Citrate (CAFCIT)
loading dose – 20-25mg/kg IV or PO
Maintenance dose – 5-10 mg/kg/day IV or PO every 24 hours – to start 24 hours after the loading dose.
Therapeutic levels – (5-25mcg/ml trough) draw trough on day 5 of life if needed
92
Apnea Treatment FYI (4)
Treatment usually continues until > 35 weeks
Stop and observe until 5-7 days apnea free
Caffeine has weaker bronchodilator response so if BPD may put on Theophyliine
Theophylline has a narrower therapetuic range and caffeine has a wide range (Q24 hour dosing)
93
Neonatal sepsis Definition
is a clinical syndrome of systemic illness accompanied by bacteremia occurring in the first month of life
94
Incidence -- neonatal sepsis (5)
```
Primary sepsis is 1-5 per 1000 live births
Higher in VLBW infants
EOS – rate 2%
LOS – rate 36% (nosocomial)
Mortality rate – 13-25%
```
95
Patho -- neonatal sepsis (5)
- Classified into two distinct syndromes based on age of onset
- EOS- first week of life, multisystem fulminent
- GBS, Listeria, E-coli, Candida
- LOS- after 1st week of life- usually not fulminant- bacteremia and Meningitis
- GBS meningitis, Ecoli, Staphylococcus aureus, pseudomonas
96
Treatment for neonatal sepsis
| EOS (3)
Ampicillin and Gentamicin- empirically until causative organism is identified
Covers most common microorganisms
GBS and Ecoli
97
Treatment for neonatal sepsis
| LOS (4)
- Nosocomial add Vancomycin for Staphylococcal coverage
- Must consider flora of the unit
- Ampicillin and Gentamicin is also used for LOS neonates admitted from the community!
- Cefotaxime can be added if meningitis concerned – for better CSF coverage
98
Doses for sepsis
| Ampicillin
Ampicillin
Semisynthetic penicillinase –bactericidal- inhibits cell wall synthesis.
< 2kg=100mg/kg/day IV divided every 12 hours (meningitic dose but used most often in-house)
May see 50mg/kg/day IV divided every 12 hours
> 2 kg = divided every 8 hours (75-150mg/kg/day)
GBS meningitis- (200-300mg/kg/day divided every 8 hours IV
99
Gentamicin
| for neonatal sepsis (2)
Aminoglycoside with bactericidal activity against Gram negative bacteria
Pseudomonas, E-coli- some activity against Coagulase Negative Staph – but ineffective against Streptococci
100
Gentamicin for neonatal sepsis
Aged based dosing
= 29 weeks PMA
4-5mg/kg/dose every 36-48 hours (5mg and 48 hours if in first 7 days of life)
101
Gentamicin for neonatal sepsis
Aged based dosing
30-34 weeks PMA
4-4.5mg/kg/dose every 24-36 hours (4.5 and 36hrs if in first 7 days of life)
102
Gentamicin for neonatal sepsis
Aged based dosing
>/=35 weeks PMA
4mg/kg/dose IV every 24 hours
OTOTOXOCITY WITH HIGH LEVELS- RENAL EXCRETION SO WATCH URINE OUTPUT!
CHECK CREATININE LEVELS AND GENTAMICIN PEAK LEVELS (4-12 MCG/ML SERUM LEVEL)
Obtain sample 30 minutes after infusion complete
TROUGH- 0.5-2 mcg/ml (sample obtained 30 minutes to just before next dose)
Half life is 3-11 hours
IF PEAK HIGH ADJUST THE DOSE
IF TROUGH HIGH ADJUST THE INTERVAL
103
Vancomycin
| for neonatal sepsis (4)
Gram positive activity
Streptococci, Staph, MRSA, Listeria
15 mg/kg/day IV every 8 (> 2kg and > 7 days) – 24hours -based on age and weight
MRSA DOSING- 15mg/kg/dose every 6 hours for 2-6 weeks
104
Cefotaxime
| for neonatal sepsis (5)
- 3rd generation cephalosporin – bactericidal activity against Gram negative
- Pseudomonas, E-coli, Klebsiella, Serratia, Haemphilus Influenzae
- 100mg/kg/day divided every 12 hours (up to 1month of age) IV
- Half life – 1-4 hours
- Excreted in the urine
105
Clindamycin
| for neonatal sepsis (4)
(NEC)-anaerobic coverage for suspected perforation
Cleocin
Bacteriostaic against most aerobic Gram Positive Staph and Strep
10-15 mg/kg/day IV divided every 8-12 hours
Does not cross blood brain barrier so do not use to treat Meningitis
106
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Necrotizing Enterocolitis (NEC)
Overview (2)
```
An ischemic and inflammatory necrosis of the bowel primarily affecting premature neonates after the initiation of enteral feeds
6-10% infants weighing < 1500 grams
107
Multifactorial theory STILL
| NEC (3)
- Prematurity, feeding, ischemia, bacterial colonization all interact to initiate mucosal damage and invade the bowel walls with gas producing bacteria.
- May progress to gangrene of the bowel wall, perforation and death
- Anything that predisposes the ‘gut’ to lack of blood flow will increase the risk – both prenatally and post
108
NEC - Presentation (2)
Sick presenting newborn
Respiratory distress, apnea, lethargy, feeding intolerance, emesis, abdominal distention and bloody stool
109
NEC
| Abdominal X-ray (2)
SUSPICIOUS- shows abnormal gas pattern, ileus, fixes loop of bowel and or ?pneumatosis intestinalis (PI)
CONFIRMED- + PI, and intrahepatic air on left lateral decubitus film
110
GERD (3)
| Zantac
Zantac- Ranitidine
Histamine receptor antagonist
Competitively inhibits the action of histamine on the gastric parietal cells inhibiting gastric acid secretion
111
GERD DOSE
| Neonatal vs. infant
DOSE-
Neonatal- (2-4mg/kg/day) divided every 8-12 hours po (max is 6mg/kg/day)
Infants > 1 month –(5-10mg/kg/day) divided 2-3 times daily
112
GERD- Zantac
| ADE (3)
- Constipation, abdominal discomfort, sedation, brady or tachy, thrombocytopenia
- Late onset sepsis risk, fungal sepsis, increases serum creatinine- check renal function
- Adjust dose accordingly to weight and renal fx
