Neonatal Pharm Flashcards
Gestational Age
Definition
3 ways to determine GA
Estimated time since conception
- LMP
- Early ultrasound
- Dubowitz/Ballard – done within first 48 hour
Corrected Age
(actual age – weeks premature = Corrected age)
Helps anticipate complications and expectations
General Principles for Pharm (2)
Age – consider GA and PMA
Weight – update weekly (if not daily)
Normal weight gain
20-40grams/day in first 6 months
Enteral absorption
pH affects gastric absorption
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)
Enteral Absorption
Decreased Intestinal Motility
(3)
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
Enteral Absorption
Pancreatic Enzyme Activity (2)
- 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
Enteral Absorption
Preemies should be receiving ½ of total fluid intake enterally before PO meds are introduced (2) WHY?
- Indicates GI function = tolerating feeds
- Provides diluent and buffer for medications
Intramuscular absorption (5)
- 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)
Absorption
Increased topical absorption (5)
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
Absorption
Rectal (2)
o Useful for N/V, induction of anesthesia, status epilepticus
o Avoids first pass effect
Distribution
Volume of distribution (2)
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)
Distribution
Volume of distribution in neonates (7)
- 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
Distribution
Decreased protein binding (2)
o Decreased albumin and decreased affinity for drug binding
o Therefore – increased free drug
Albumin bound meds (4)
Phenytoin, phenobarbital, PCNs, morphine
High affinity for albumin – may displace drugs and increase free drug levels
Ex. Sulfonamides, ceftriaxone, may displace bilirubin = kernicterus
Distribution
Increased concentrations of (2)
Free fatty acids
Unconjugated (indirect) bilirubin
Metabolism (3)
Hepatic enzyme activity is…
- Hepatic enzyme activity is decreased
- Enzymatic microsomal systems responsible for drug metabolism are present at birth
- Their activities increase with advancing gestational age
Metabolism
Phase I hepatic reactions (3)
- Oxidation, reduction, hydroxylation develop rapidly during infancy
- Adult capacities by 6 months of life
- Ex.prolonged elimination for phenobarbital and cocaine
Metabolism
Phase II hepatic reactions (3)
- 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
Metabolism (4)
- 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
Elimination (4)
- 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
Normal CrCl = in newborns
newborns ~40-65ml/min
Elimination reaches 50% of adult GFR by 1 month of age
3
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
Decreased ability to concentrate urine
3
Normal urine output – 1-2 cc/kg/hour
Renal insufficiency - <1cc/kg/hr
Drugs dosing has to be adjusted with decreased urine output
Calculation of CrCl – Schwartz Method
CrCl (ml/min/1.73m2)= K x length (cm)
// SCr
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
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
Factors leading to ADRs in neonates
5
- Decreased plasma proteins- result in increased free (unbound) drug
- Immature renal function – decreased elimination of renally excreted drugs
- alteration in number of drug receptor sites
- immature hepatic metabolism
- increased permeability of skin
Common conditions Preterm Neonates (8)
Respiratory Distress Syndrome (RDS) Bronchopulmonary dysplasia (BPD) Patent Ductus Arteriosus (PDA) Apnea of Prematurity (AOP) Sepsis Necrotizing Enterocolitis (NEC) Seizures PPHN
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
Patho RDS (4)
- Surfactant deficiency is the primary cause of RDS
- Complicated by overly compliant chest wall
- Leads to progressive atelectasis – failure to develop effective FRC
- Surfactant is a surface active material produced by epithelial cells
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)
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
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
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!
Risk factors for RDS (5)
Prematurity Male sex C-section without labor Perinatal asphyxia Maternal diabetes
RDS Physical Exam (5)
Tachypnea Grunting Flaring Retractions Cyanosis in room air
Management RDS(4)
Administer surfactant
Reduces surface tension in lungs (anti-stick)
Improves gas exchange
? Decrease in BPD. LOS, or mechanical ventilation- ??
Surfactant Products
Synthetic (1)
Surfaxin
Surfactant Products
Natural (3)
Curosurf – porcine
Infasurf - bovine
Survanta – bovine
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
Surfactant Replacement Therapy
Early administration
Key to restore pulmonary function
Prevents tissue injury
Decreased mortality
Surfactant Replacement Therapy
Composition
Animal origin
All contain hydrophilic surfactant properties SpB and SpC
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
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
Surfactant Replacement Therapy Side effects (2)
Pulmonary hemorrhage (low) Air leak (pneumothorax) – change in tidal volume
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
Surfaxin (Lucinactant)
5.8 ml/kg – every 6 hours (up to 4 doses in 48 hours)
Curosurf (Poractant)
Initial 2.5ml/kg – may repeat with 1.25ml/kg every 12 hours up to 2 times
Infasurf (Calfactant)
3ml/kg – may repeat every 12 hours up to 3 times
Survanta (Beractant)
4ml/kg – may repeat every 6-8 hours up to 4 times
Surfactant Recommended prophylaxis (5)
- 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
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)
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
BPD
Risk factors
(4)
Prematurity
LBW
Aggressive mechanical ventilation (barotrauma)
High Fio2 – Oxygen is a drug!!
BPD
Manifestations (5)
airway hyper-reactivity (bronchospasms) Pulmonary edema Fibrosis Shifting atelectasis Airway hyperinflation (X-ray)
BPD Treatment (3)
- optimize nutrition(24 cal/oz formula or EBM)
- Fluid restrict (120ml/kg/day),
- Oxygen
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
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
ADE of Corticosteroids for BPD (10)
HTN, hyperglycemia, infection, intestinal perforation, GI bleed, growth restriction, adrenal insufficiency, decreased brain growth, PVL, CP
AAP- dexamethasone (4)
- 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.
- No routine use for preventing BPD,
- Recommend ONLY in exceptional circumstances
- Requirement of maximal ventilatory and oxygen support with parental informed consent
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
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
BPD Treatment
Furosemide (LASIX) (IV and po)
ADE
ADR- (the bad) low serum Na, K, Cl, Ca, nephrocalcinosis, bone demineralization, volume depletion, ototoxicity
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)
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!
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!
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
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
Xopenex- (levalbuterol)
nonracemic form of albuterol, limited experience in newborns- longer efficacy at lower doses..so less ADRs??
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
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
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
Diagnosis
PDA (2)
Echocardiogram – can visualize the ductus and direction of flow
Will also rule out additional cardiac diagnosis
Treatment
PDA (3)
- Ventilatory support as needed
- Fluid restriction- to decrease the PDA shunt as well as accumulation of fluid in the lungs.
- Increase HCT (40-45%)
may decrease the left-to-right shunting and increase oxygen carrying capacity
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
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
Indomethacin (Indocin) for PDA
Early symptomatic
(4)
- Dose (0.2 mg/kg/dose) IV over 20 minutes- 2nd and 3rd doses (0.1mg/kg/dose
- If < 1250grams and <7 days old) given 12 and 36 hours after 1st dose
- If > 1250grams and > 7days old 0.2mg/kg/dose
- TYPICALLY THIS IS DAYS 2-4 of life when symptoms appear!
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!!
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)
Indomethacin (Indocin) for PDA
Contraindications (4)
Thrombocytopenia
NEC
Sepis
Serum creatinine >1.7mg/dl
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.
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
Should we treat PDA?
2
Controversial
Risk vs.Benefit
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)
PDA – patho
AOP is a developmental disorder and reflects a physiological rather than pathological immature state of respiratory control
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.
Apnea
Central
Total cessation of inspiratory effort with no evidence of obstruction
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.
Side effects for treatment of apnea (5)
Tachycardia Jitteriness Feeding intolerance Emesis Restlessness
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.
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
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)
Neonatal sepsis Definition
is a clinical syndrome of systemic illness accompanied by bacteremia occurring in the first month of life
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%
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
Treatment for neonatal sepsis
EOS (3)
Ampicillin and Gentamicin- empirically until causative organism is identified
Covers most common microorganisms
GBS and Ecoli
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
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
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
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)
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)
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
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
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
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
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
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
NEC - Presentation (2)
Sick presenting newborn
Respiratory distress, apnea, lethargy, feeding intolerance, emesis, abdominal distention and bloody stool
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
GERD (3)
Zantac
Zantac- Ranitidine
Histamine receptor antagonist
Competitively inhibits the action of histamine on the gastric parietal cells inhibiting gastric acid secretion
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
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
