PEDIATRIC NEUROLOGIC EXAMINATION
Christopher Giza, MD. Adapted by Jeffrey Ekstrand, MD PhD and Melissa Przeklasa Auth, MD
GENERAL PHYSICAL EXAM: These are parts of the general physical examination that are of particular interest to Pediatric Neurologists.
General: Level of activity, vitals, ht, wt, overall appearance, unusual odors
Head Circumference: General guideline is 3-9 rule:
35cm @ birth; 40cm @ 3mo; 45cm @ 9mo; 50cm @ 3yr; 55cm @ 9 yr.
Fontanelle: Sunken, soft, full, bulging
Sutures: Split, overriding, fused
Fundoscopic: Papilledema, retinal hemorrhages, cherry red spot, chorioretinitis
Dysmorphic features: Down’s facies, low set ears, clefts, webbed neck,
wide-spaced nipples, simian creases
Neck: Meningismus
Cardiac: Murmurs
Abdomen: Organomegaly
Back: Sacral dimple/hair/tract/hemangioma
Genitalia: Normal/abnormal
Extremities: # digits, arthrogryposis, contractures, nailbed size
Skin: Café-au-lait, ash leaf, hemangiomas/telangiectasias, neurofibromas,
Shagreen, adenoma sebaceum, port wine stain
NEUROLOGICAL EXAMINATION: This differs quite a bit for children of different ages, but it is always sensible to examine 5 major areas (usually presented in this order, often examined out of order based on pt. cooperation).
Mental Status:
Arousal: spontaneous, to voice, to pain, unarousable. Able to maintain arousal.
Behavior: level of attention, impulsiveness, hyperactivity, self-injurious behavior, repetitive behavior
Orientation: aware of surroundings, knows name, knows location/date.
Language: 1st words @ 1yr, combine words/name body parts @ 18-24mo,
3-4 colors @ 3-4yr, count to 5 @ 5yr. Fluency, comprehension/follows commands.
Social: social smile @ 2m, wave bye/pat-a-cake @ 9-10m, plays ball 11-14m, removes garment @ 16-20m, puts on clothing 2-3yr, dresses self w/o help @ 3.5-4.5yr.
Cranial Nerves:
II – blinks to visual threat, counts fingers, visual fields.
III, IV, VI – pupil reactivity (II, III), extraocular movements/fix & follow, ptosis (III, IV, VI), “doll’s eyes”
V – facial sensation, corneal reflex
VII – facial expression (central spares forehead), corneal reflex, muscles of mastication
VIII – hearing (whisper, finger rub, bell ringing/clap)
IX, X – suck/swallow, palate elevation, dysarthria, gag reflex
XI – shoulder shrug, sternocleidomastoid
XII – tongue protrusion and side-to-side movement
Motor:
Tone: traction response/head lag, horizontal and vertical suspension, scarf sign, hypotonia, spasticity
Bulk: atrophy, fasciculations
Power: symmetric movement, strength grading scale 0-5
Reflexes: symmetry most important for DTRs, reflex grading 0-4
Fine motor: hands midline @ 2-3m, reaches @ 4m, pincer grasp @ 8-12m, scribbles @14-16m, draw vertical line @ 2yr, copy circle @ 2-3yr, copy square @ 4-5.5yr
Gross motor: roll over @3-4m, sit, no support @ 6m, walk @ 1yr, walk up steps @16-20m, throws overhand @ 20-24m, balance 1 foot 1 sec @ 2-3yr, hop on 1 foot @ 3-4yr, heel-toe walk @ 4.5yr
Tests of function: stand up from floor/chair, knee bend, pronator drift, tip toe, skip.
Sensory:
Light touch/tickle, pin prick, temperature, and vibration/proprioception;
withdraw to touch/pinch; Romberg.
Coordination/cerebellar:
Dysmetria (past-pointing/tremor) when reaching for objects as opposed to formal finger to nose, fine finger movements, etc.
Gait: casual, tiptoe, heel walk, tandem gait, running.
NEONATAL REFLEXES:
(+) Present (-) Disappears
PEDIATRIC ANTIEPILEPTIC MEDICATIONS
Pantea Sharifi, MD, Melissa Przeklasa Auth, MD, Lekha M. Rao, MD, Neal Rao, MD
Name/Mech |
Forms |
Starting dose |
Maintenance /Adult Dose |
Therap Range/ Toxic |
Metab |
Carbamazepine (Tegretol) Na ch inh |
chew:100 elixir 100/5 tabs:100,200,400 XR/Oxcarb conversion: 250mg oxcarb:200mg carbam |
5-10 mg/kg/d div BID (take w/ food) Incr by 5mg Q5-7d |
20-30 mg/kg/day div TID 600-2400mg/day |
4-12 mg/ml Rashes, hepatitis, neutropenia, aplastic anemia, hyponatremia, diplopia, ataxia, GI upset, sedation, hyponatremia |
Liver inducer 70% Renal excr |
Carbatrol (XR) |
Tabs: 100,200, 300 |
Max 35mg/kg/day |
|||
Clonazepam (Klonopin) GABA agonist |
tabs: 0.5, 1, 2 mg wafers: 0.125,0.25,0.5,1,2mg |
0.025 mg/kg |
0.01-0.03 mg/kg/d div BID-TID Max 0.1-0.2mg/kg/d |
N/A Sedation, behavioral, inc secretions, GI upset |
Liver, Renal excr |
Clorazepate (Tranxene) GABA agonist |
tabs: 3.75, 7.5, 15 mg |
0.3 mg/kg |
0.3-1.0 mg/kg/dy QD-TID |
N/A sedation, ataxia, hyperkinesia, rash, dizziness, headache, rhinitis, asthma |
Liver, Renal excr |
Diazepam (Diastat) GABA agnonist |
PR: 2.5,5, 10, 15,20 mg |
2-5 y/o= 0.5 mg/kg 6-11y/o= 0.3 mg/kg |
12+ : 0.2-0.5 mg/kg 15-20mg |
N/A Sedation |
Liver |
(Valium) |
Tab: 2, 5, 10mg Soln: 5mg/5ml |
0.2-0.5mg/kg/dose IV ESES: 1-2mg/kg QHS, max 30mg |
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Ethosuximide (Zarontin) Thalamic T-type Ca channel antagonist |
syrup: 250 mg/5 ml Caps: 250 mg |
< 6 yo:10 mg/kg/dy > 6 yo: 250 mg/ dy |
12-40 mg/kg/dy TID (usually 15-20 /dy) |
40-100 mg/ml rash, neutropenia, SLE, pancytopenia,sedation, psychosis, worsens GTCs |
Liver, Renal excr |
Felbamate (Felbatol) GABA agonist NMDA antagonist |
susp: 600 mg/5ml tabs: 400, 600 mg |
15 mg/kg/dy- in 10 mg/kg increments Q3-7 days (blood tests q2wks) |
60-100 mg/kg/dy TID |
N/A Aplastic anemia, hepatotoxicity, N/V, ataxia, anorexia, insomnia |
Liver, Renal excr |
Gabapentin (Neurontin) Inc postsynaptic GABA vs unknown |
caps: 100, 300, 400, 600,800 susp: 250mg/5cc |
10 mg/kg/dy- incr in 5 mg/kg increments |
30-60 mg/kg/dy TID |
N/A rash, behav changes, sedation, dizziness, ataxia, constipation, pruritis, hostility, hyperkinesia, dry mouth |
Renal |
Lacosamide (Vimpat) Enhances slow inactivating Na ch |
Tabs: 50, 100, 200 |
No official peds dosing Generally start 50 Qday, incr by 50mg Qwk to 200/day dv BID |
100-200/day div BID Adults: 200-400/day |
N/A Sedation, dizziness, headache, nausea, diplopia |
Renal |
Lamotrigine (Lamictal) Na ch inhibitor Inhibits Glutamate release |
chew: 2mg, 5 mg, 25 mg tabs: 25, 100, 150, 200 |
Mono: 0.5-0.8 mg/kg/dy + EIAED: 1-1.5 mg/kg/dy + VPA: 0.15 mg/kg/dy incr q1-2wks! |
monotx: 10 mg/kg/dy if on VPA: 5 mg/kg/dy if on enzyme inducer: 15 mg/kg/dy BID |
N/A rash (esp with VPA), SJS, ,hepatotox, diplopia, tremor, flu like sx, N/V, sedation, headache, GI upset, irritable |
Liver, Renal excr |
Levetiracetam(Keppra) Unknown, inhibits burst firing |
Tabs: 250, 500, 750 Susp: 100mg/cc |
10-20 mg/kg/dy Incr q3-7d by 10/kg IV Load: 30mg/kg |
50-60 mg/kg/dy BID |
N/A somnolence, ataxia, behav changes/irritability, hyperactivity, |
Renal |
Oxcarbazepine (Trileptal) Na channel antag |
Tabs: 150, 300, 600 Susp: 300 mg/5 ml |
10 – 20 mg/kg/dy |
50 mg/kg/dy BID |
N/A hyponatremia, sedation, abnormal vision, rash, H/A |
Liver, Renal excr |
Phenobarbital GABA agonist Na channel antag T-type Ca ch antag Glutamate Antag |
elixir: 20 mg/5 ml tabs: 15, 30, 60, 100 |
IV Load: 10-20 mg/kg |
<1 yo: 3-5 mg/kg/dy div bid >1yo: 5-8 mg/kg/d adult 2-3mg QD-BID |
15-40 mg/ml rash, hyper, behavior, irritable, lethargy |
Liver |
Phenytoin (Dilantin) Na Channel inhibitor |
chew: 50 mg (infatab) caps: 30, 100, 200, 300 mg susp: 125mg/5ml |
Load: Fosphenytoin 20 mg/kg |
5 - 10 mg/kg/dy BID (may need higher in kids < 6 yo) |
10-20mg/ml rash, LFTs, ataxia, aplasic anemia, lethargy, coarse facial, gingival hyper, serum sickness, lupus like syndrome, neuropathy, hepatitis, sz, cardiac suppression |
Liver, 85-90% protein bound |
Primidone (Mysoline) Na channel antag GABA agonist Glutamate antagonist |
susp: 250 mg/5 ml tabs: 50, 250 mg |
2-5 mg/kg/dy |
12-25 mg/kg/dy TID |
5-12 mg/ml (+ PB) Same as PB |
750-2000 |
Rufinamide (Banzel) Unk. Prolong inactive state Na ch |
Tabs: 200, 400mg |
5mg/kg BID Incr by 10mg/kg Qweek |
45mg/kg/day div BID Max 3200mg/day |
Sedation,, decreased appetite, rare:rash, worsening szs |
Renal |
Topiramate (Topamax) Na channel inhibitor GABA agonist NMDA antagonist |
sprinkles: 15, 25 mg tabs: 25, 100, 200 |
1-3 mg/kg/dy; incr q3-5d by 1 mg/kg/dy |
5-10 mg/kg/dy BID IS or neonatal status: 15-25 mg/kg/dy |
N/A wt loss, hyper, mental dullness, irritable, anhydriasis, hyperthermia, sedation, renal stones, diplopia, parasthesias |
Renal |
Valproic Acid (Depakote) Na channel antag GABA agonist T-type Ca chan antag |
syrup (depakene)250/5 sprinkles: 125 mg Caps: 125, 250, 500 IV Depacon 15mg/kg load, max 60mg/kg/d ER: 250, 500mg bid |
15 mg/kg/dy; increase by 10-15 mg/kg q 3-5 days |
30-80 mg/kg/dy TID or BID if ER |
50-150 mg/ml rash, LFTs, anemia, low PLT, wt gain, tremor, pancreatitis, abd pain, N/V, sedation, osteopenia, PCO, hair loss, hyperammenemia, Fanconi’s syn, SJS |
Liver |
Vigabatrin (Sabril) Inhibits GABA breakdown |
Tabs: 500 mg Sachet: 500 mg |
25-50 mg/kg Increase q 3 d |
Max 200 mg/kg BID |
N/A Visual Field Loss/retinal toxicity, white matter changes, mood changes, sedation, psychosis |
N/A |
Zonisamide (Zonegran) Na channel inhibitor T-type Ca chan inh GABA agonist |
Caps: 25,50,100mg Liquid: 100 mg cap/10ml |
2 – 4 mg/kg/dy Incr qwk by 1/kg |
8-12 mg/kg/dy BID (10-20mg/kg in IS) |
N/A somnolence, ataxia, behav changes, kidney stones, rash, hyperthermia/anhydriasis, diarrhea, insomnia, depression |
Renal |
PEDIATRIC DEVELOPMENTAL MILESTONES
Pantea Sharifi, MD
AGE |
Gross Motor |
Visual & Fine Motor |
Language & Comprehension |
Social |
Reflexes |
0-1 mo |
Elevates head slightly Tight grasp |
Follows 22.5` past midline in each direction. By 2wks age, moves eyes to light and fixes and conjugate gaze. “Setting sun” sign is seen w/ sudden change in position of head |
Alerts to sound by blinking or startling |
Regards face |
Grasp, Moro, Stepping, Clonus ATNR |
2 mos |
Holds head in midline Opens hand at times |
Follows 45’ past midline Turns eyes to direction of sound |
Recognizes parents Smiles |
||
3 mos |
Holds head up past midline Holds hand open at rest |
Follows 90’ past midline Reaches for objects |
Coos |
Recognizes bottle Smiles spontaneously |
Lose Stepping Lose ATNR Blink reflex |
4-5 mos |
Rolls front to back Good head control Hands come together Initiates foot play Extends arms when placed on tummy |
Consistent conjugate gaze Looks around Turns eyes and head to direction of sound |
Coos Chuckles |
Laughs aloud Smiles at image in mirror |
Loses palmar grasp No ATNR No Stepping |
6 mos |
Rolls back to front Sits with support Transfers objects from hands Grasps cube (coarse) Chews |
Looks after dropped objects |
Babbles vowels |
Recognizes strangers Plays with toes/feet (toe in mouth) |
Loses Moro Parachute |
7-8 mos |
Sits with no support Begins to pull to stand |
Developing perception |
Babbles consonants |
Stranger/separation anxiety |
Parachute |
9 mos |
Pulls to stand Cruises (walks with help) Crawls |
Uses pincer grasp (finger-thumb opposition) Finger feeds Holds bottle |
Understands ‘no’ Imitates sounds Says “mama/dada” non-specifically Vocab: 5 words |
Waves ‘bye-bye’ Plays ‘patty cake’ Plays ‘peek a boo’ Explores environment |
Parachute |
10-11 mos |
Cruises Voluntary release of objects Casts objects |
Pincer grasp maturing |
Naming period (colors, body parts) |
Same as above |
Parachute |
12 mos |
Walks with only one hand held Rolls balls Throws objects more accurately |
Mature pincer grasp Object permanence |
Specific “mama/dada” Knows 2 words other than “mama/dada” Begins to follows 1 step commands (w/ gestures) |
Responds to name Imitates actions Responds to music and rhythm |
|
13-14 mos |
Walks alone (unsteady) Creeps up stairs |
Builds tower of 2 cubes |
Able to follow 1 step commands (w/o gestures) Uses 4-6 words |
Cooperates with dressing |
|
15 mos |
Walks alone well Walks backwards |
Begins using spoon (tries to feeds self) Drinks with cup Scribbles |
Uses 4-6 words |
||
16-17 mos |
Scribbles |
Points to 5 body parts Uses 7-20 words |
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18 mos |
Runs Throws from standing |
Feeds self Tower of 4 cubes Turns 2-3pgs of book together Shows hand preference |
Knows 8 body parts Uses 10-50 words |
Copies parent in tasks (vacuuming, dusting) Plays in company of other kids |
|
21 mos |
Begins to climb up stairs Creeps downstairs Squats in play |
Drinks well from cup Builds tower of 5 cubes |
Starts 2 word combos Uses 50-75 words |
Pretend play Magical thinking Autonomy and independent issues begin (“terrible twos”) |
|
24 mos |
Walks up and down stairs (using 2 feet together) Runs well |
Builds tower of 6-7 cubes Turns 1 page at a time Removes clothes Unzips zipper Puts shoes on partway |
Puts together 2 words (asks for food, toilet) Follows 2 step commands 50% perfect articulation of lang |
Parallel play |
|
30 mos |
Jumps with both feet off floor Throws ball overhead |
Unbuttons Holds pen correctly Develops handedness |
Repeats 2 digits forward Understands “I” |
Tells first and last name |
|
36 mos |
Walks downstairs (one foot at a time) Walks upstairs (2 feet together still) Balances on each foot (2-3sec) Pedals tricycle |
Builds tower of 10 cubes Dresses self Draws circle |
Vocabulary- 250 words Puts together 3+ words 75% perfect articulation of lang Knows age and sex |
Begins cooperative play Shares toys |
|
4 yrs |
Hops on one foot at a time Balances on each foot (6-10sec) Walks up and down stairs one foot at a time |
Dresses self |
Puts together 4+ words Sings from memory Knows colors 100% articulation |
Tells “tall” tails |
|
5 yrs |
Skips Jumps over things Rides bicycle |
Ties shoe laces Spreads w/ knife |
Puts together 5+ words Prints 1st name |
Can distinguish from fantasy and reality Abides rules Plays competitive games Helps in house chores |
DEVELOPMENTAL DELAY
Christopher Giza, MD and Jeffrey Ekstrand, MD, PhD
Definitions: Static, nonprogressive, significant delay in ≥2 of the following: gross/fine motor, speech/language, cognition, social/personal, ADLs. Called mental retardation in kids >5ys. Epidem: 5-10% of children have specific dev disabilities; 1-3% of all children have global dev delay.
DDx: (Listed below is only partial differential)
A. PREDOMINANTLY LANGUAGE DELAY
1. Hearing impairment - #1 cause of isolated language delay.
2. Autism – presents as apparent regression or delay of language, impaired
social interactions, stereotyped behavior, pain insensitivity.
Current AAP guideline to screen at 16 mos well-child check
B. PREDOMINANTLY MOTOR DELAY
1. Ataxia – cerebellar malformation, metabolic disorders, etc.
2. Hemiparesis/plegia – cerebral palsy, infarction, cerebral dysgenesis, etc.
3. Hypotonia/neuromuscular – neuropathy, metabolic disorders, muscular
dystrophy, etc.
4. Paraparesis/plegia – spinal lesions/malformations, spastic diplegia, etc.
C. GLOBAL DEVELOPMENTAL DELAY
1. Perinatal insult/disorder
2. Cerebral malformation
3. Chromosomal abnormality
4. Intrauterine infection
5. Lead encephalopathy
6. Fragile X syndrome (more boys) – FMR1
7. Rett syndrome (females) – MECP2. Sm head, wringing hands, regression
8. Progressive encephalopathy/developmental regression
Studies:
Hearing test / audiometry – for primary language delay
Chromosome testing – 3.7% yield, ≥2 dysmorph feat increases yield to 20%.
Fragile X testing – FHx of MR, long jaw/high forehead, large ears, hyperext
joints, redund dorsal hand skin, enlarged testes in male incr yield to 7.6%.
MRI – r/o structural lesions
EEG – only to r/o epilepsy/seizures
Serum lead levels – in children with identifiable risk factors/exposure
TORCH titers – r/o congenital infection
Metabolic screen (urine OA & serum AA) – <1% yield, NOT recommended
initially; stepwise screening increases yield to 14%.
Thyroid functions – NOT recommended routinely if newborn screen was done.
Tx:
1. Treat underlying cause, if identified.
2. Assessment at regional center for therapy (PT, OT, speech, etc.).
3. May require pharmacological management of behavior.
4. Family may benefit from genetic counseling in appropriate circumstances.
Prog: Dependent upon etiology. In most cases, developmental delay is a chronic problem, and serial evaluation will determine the rate at which an individual is achieving milestones. From these serial evaluations, one can then determine an approximate developmental trajectory for that child.
DEVELOPMENTAL REGRESSION
Christopher Giza, MD and Jeffrey Ekstrand, MD, PhD. Updated by Lekha M. Rao, MD
Definitions: a clear loss of previously acquired milestones. Important to distinguish from developmental delay.
Clinical: Approach to diagnosis requires consideration of time course, predominant localization of symptoms (gray matter –GM, white matter – WM, or peripheral nervous system) and other organ involvement. Symptoms can present with insidious regression (autism, AIDS, hypothyroidism), intermittent acute events with stepwise deterioration (aminoacidopathies, organic acidopathies, mito) or relentlessly progressive impairments (lysosomal d/o, peroxisomal d/o).
Primarily Gray Matter Primarily White Matter
Dementia Spasticity
Visual loss/impairment Visual loss/impairment
Seizures Focal neurological deficits
Personality change
Peripheral nervous system involvement: Peripheral nerve distribution of sensorimotor deficits, palpable nerves, flaccid weakness, pain, insensitivity to pain, diminished DTRs (Krabbe, MLD, multiple sulfatase def)
Other organ system involvement: Coarsened facies (MPS), dysmorphic features (peroxisomal), cataracts (homocystinuria), retinopathy/retinitis (mito, NCL), cherry-red spot (GM1, GM2, Niemann-Pick A, MLD, sialidosis), cardiomyopathy (mito, homocystinuria), hepatosplenomegaly (Gaucher, MPS, Niemann-Pick A>C), skin (neurocutaneous, XP), hair (Menkes).
DDx:
1. Primarily gray matter disorders: Usually slow progressive deterioration. Examples include : autism, Rett, infantile NCL, Menkes, neuroaxonal dystrophy, Lesch Nyhan, Huntington, XP
2. Progressive hydrocephalus: Macrocephaly, full/open fontanelle, lethargy, vomiting, ‘sunset sign’
3. Aminoacidopathy / organic acidopathy: May present with acute encephalopathy, vomiting, seizures or intermittent attacks with stepwise decline. Examples include: homocystinuria, MSUD, PKU, urea cycle disturbances, organic acidurias, Lowe syndrome, NKH, acidemias: propionic, isovaleric, methylmalonic
4. Hypothyroidism: Big posterior fontanelle, constipation, umbilical hernia, macroglossia, delayed dentition
5. Lysosomal disorders: Coarse facies, Hurler phenotype, organomegaly. Examples include: GM1, GM2 gangliosidoses, mucopolysaccharidoses, Niemann-Pick
6. Mitochondrial disorders: Myriad presentations; think about when faced with intermittent encephalopathy, seizures, myopathy, other organ system involvement. Examples include: MELAS, Leigh, Alpers, MERRF, Kearns-Sayre
7. Primarily white matter disorders: Worsening spasticity, visual impairment. Examples include: galactosemia, Canavan, Alexander, Krabbe, neonatal ALD, XL-ALD, Pelizaeus-Merzbacher, MLD, cerebrotendinous xanthomatosis
8. Peroxisomal disorders: Zellweger, infantile Refsum
9. Infectious disorders: AIDS encephalopathy, SSPE
10. Neurocutaneous syndromes: Café-au-lait, ash-leaf, Shagreen patch, facial angiofibroma, seizures.
11. Landau-Kleffner syndrome– associated with language regression, seizures.
Studies:
CT / MRI – (hydrocephalus), leukodystrophy (WM d/o, Krabbe), atrophy, dysplasia (NF, TS)
Labs – glucose, ketones, lytes, ammonia (urea cycle d/o), CBC with platelets,lactate (mito), pyruvate (mito), ¯ceruloplasmin/copper (Menkes), uric acid (Lesch-Nyhan), TSH, (hypothyroidism)Serum amino acids / Urine organic acids – (aminoacidopathies, organic acidopathies)
Ophtho eval – DFE helpful to look for cherry red spot, retinopathy/retinitis pigmentosa, or other abnormalities – specify that you are looking for a genetic disorder on your consult request
Urine mucopolysaccharides – (MPS)
Skin / conjunctival biopsy – (MPS, neuroaxonal dystrophy, NCL)
Enzyme assay – (lysosomal d/o, MLD, Lesch-Nyhan, Niemann-Pick A&C)
EEG – for associated epilepsy (GM d/o, aminoacidopathies, mito, neurocutaneous), 5-7Hz (SSPE), ESES (for language regression)
VEPs, SSEPs – (WM d/o)
LP – elevated protein (Krabbe), elevated glycine (NKH), measles titer (SSPE)
Muscle bx – (mito)
Genetic test – (Rett, Menkes, mito)
Tx:
Disease specific:
1. Enzyme replacement (some enzyme deficiencies, Gaucher)
2. Bone marrow transplantation (MPS, Krabbe).
3. Special diets / dietary restriction (MSUD, PKU, other organic
acidopathies, urea cycle disturbances)
4. Vitamin supplementation – thiamine (MSUD), B6 (homocystinuria),
folate (homocystinuria)
5. Carnitine – maybe helpful (NKH, organic acidopathies)
6. Benzoate – (aminoacidopathies especially urea cycle d/o, NKH)
7. Hydration, dialysis – (aminoacidopathies, organic acidopathies)
8. Levothyroxine (hypothyroidism)
9. Antiretrovirals (AIDS)
Nonspecific treatments:
1. Anticonvulsants – for associated epilepsy
2. VP shunt – for hydrocephalus
3. Infant stimulation therapy, PT, OT – Regional Center early intervention
Prog: Depends upon specific diagnosis, but usually either progressive or occasionally stabilized with appropriate therapy.
CONCUSSION / MILD TRAUMATIC BRAIN INJURY: PEDS
Chris Giza, MD 4/19/09
Definition: Any transient disturbance of neurological function induced by biomechanical forces. LOC not required.
Classification: No well-validated system; no pediatric specific grading. In general PTA more important than LOC.
Epidem: Male>>female; Common etiologies – contact sports, falls, MVAs (with whiplash)
Sports concussion - after one, 3x risk for second concussion during same season.
Initial Assessment:
1. ABCs, resuscitation if necessary.
2. Initial assessment/Glasgow Coma Scale: Mild 13-15; Moderate 9-12; Severe 3-8; concussion patients will be GCS 13-15.
3. Symptoms Signs
Headache Dazed appearance, AMS
Dizziness, Nausea Disorientation, slow to respond
Visual disturbance Amnesia
Hearing disturbance (tinnitis, etc) Vomiting
Irritability Emotional lability
Fatigue, feeling of grogginess Slurred speech, dysarthria
Increased effort required for simple things Ataxia, unsteadiness
4. Sports concussion assessment tool (SCAT2) (Mc Crory 2005, updated 2009)
a. Signs: LOC/unresponsive Y/N; Seizure Y/N; Balance problem/unsteadiness Y/N.
b. Memory (orientation/amnesia): What venue? Which half? Who scored last? Who is opponent?
c. Post-concussion symptom checklist.
d. Word recall (5 words) – immediate, delayed
e. Months in reverse
f. Reverse digit span (up to 6)
g. Neurological screening exam (Normal/abnormal = N/A): Speech N/A; Eye motion and pupils N/A; Pronator Drift N/A; Gait assessment N/A.
Dx: Head CT scan (noncontrast) – definite indications – GCS<15, altered mentation, seizure, focal neuro deficit, pupillary asymmetry.
For mild TBI GCS 14-15, the following rules also apply:
< 2years: skull fracture; relative indications - nonfrontal scalp hematoma, LOC >5s, severe mechanism, ‘not behaving normally’
> 2years: basilar skull fracture; relative indications - LOC, vomiting, severe mechanism, severe headache
Skull XR – rarely indicated. Not sensitive for operative process and some difficulties in interpretation.
Labs – rarely needed - CBC, lytes, glucose, (particularly if AMS) type and cross (if needed).
Urine/blood toxicology screen (if AMS)
Dispo: 1. Criteria for admission
a. absolute - 1. coma/ persistent AMS/ significant LOC, 2. prolonged memory deficit/ amnesia, 3. possibility of child abuse, 4. focal neurological deficits, 5. lack of reliable observation at home
b. relative - 1. skull fracture, 2. seizures, 3. persistent vomiting or headache.
2. If discharged, need head injury precautions – periodically check child at night, observe for increased lethargy/confusion, nausea, vomiting, seizures, new focal deficits.
3. Return to play guidelines: Graded, symptom-limited return to activity. (Mc Crory 2005; 2009).
a. Rest until asymptomatic
b. Light aerobic exercise (e.g. stationary cycle)
c. Sport-specific exercise
d. Non-contact training drills (light resistance training)
e. Full contact training after medical clearance
f. Return to competition (game play)
Tx: 1. Graded return to activity – see above.
2. Return to normalcy is important in terms of returning to school promptly. Counsel regarding injury prevention.
3. Reassurance rather than medication for most symptom management.
4. For chronic symptoms – treat specifics – chronic daily headache (amitriptyline, gabapentin, etc); migraines (abortive-midrin, triptans; preventive-like CDH); seizures (AEDs); attention deficit (methylphenidate, dexedrin, etc), cognitive impairments (consider neuropsychological testing); behavior disorders (psychiatric consultation).
Prog: ♦ Kids can have longer cognitive recovery than adults & may have cognitive impairments when asymptomatic (Field, 2003).
¨ Post-concussive syndrome has been described in kids.
¨ Following mild TBI, few long-term deficits have been rigorously described after a single injury.
¨ Following repetitive mild TBI, persistent neurocognitive deficits are seen (Collins, 1999). Furthermore, kids with pre-existing learning disabilities may be more vulnerable.
FEBRILE SEIZURES
Christopher Giza, MD, and Sarah Copeland, MD. Reviewed by Donald Shields, MD.
Definitions: a (probably) genetic age-limited epilepsy in which seizures occur only with fever. Not associated with CNS infection, though this may need to be ruled out.
Epidemiology:
Incidence – Very common. about 4/100 of all children will have a febrile seizure
Age of onset – 1st febrile sz between age 6m-3y in 93% of cases. Seizures generally stop by 5-6 years of age.
Genetics:
Probably autosomal dominant with incomplete penetrance. Positive family history in 10-22% in studies.
Genes – linkage to 19p3, 19q13, 8q13-21, 5q14-15, 2q21-33. Linkage to 19q is sodium channel beta 1 subunit (SCN1B). Linkage to 2q is sodium channel alpha 1 subunit (SCN1A, also seen in Dravet)
Clinical:
Simple: a) single, b) brief, c) generalized, d) occur with fever (generally >37.8º) – 97% of total
Complex: a) multiple within 24 hours, b) prolonged (generally >15 minutes), c) focal – 3% of total
Pre-existing neurological abnormality, developmental delay
Seizure may be the first manifestation of a febrile illness in children. In one study, 44% of infants had fever <1 hour prior to seizure.
HHV-6 (cause of roseola or exanthem subitum) may cause up to 1/3 of febrile seizures. In other cases, precipitant is usually an upper respiratory or GI infection.
DDx:
Febrile seizure
Epileptic seizure during fever
Meningoencephalitis
Diagnosis:
· LP – if suspected meningitis. Any child <6-15m of age, or with altered mental status that persists after sz, or with other s/sx of meningitis.
· EEG – in children with pre-existing neurological abnormalities, with complex sz, with family hx of epilepsy. Generally not necessary in other cases.
· CT/MRI – in children with prolonged focal febrile sz, focal exam, focal EEG.
· Labs – determined on an individual basis as needed to determine cause of fever; consider CBC, lytes, UA, but not necessary in all cases.
· No neurodiagnostic testing – is ok in neurologically normal children with 1st simple febrile sz.
Treatment:
In general, treat fever, ongoing seizure >5 minutes, and look for source of infection if none evident.
-Simple febrile sz, single – treatment not indicated unless seizure ongoing, then treat as for any status epilepticus
-Complex febrile sz, single – treatment not indicated (unless family hx + for epilepsy).
-Family hx + for simple febrile sz – treatment generally not indicated
-Previous neuro abnormalities / developmental delay – consider treatment
Choose drug based on presumed diagnosis
-Frequent or prolonged febrile sz – consider abortive for history of szs > 5 mins, AEDs can be used though may not prevent a recurrence of the febrile seizures
diazepam pr (0.5 mg/kg/d) at onset of febrile illness.
Lamictal safest but no RCT, does not necessarily prevent
Prognosis:
Simple febrile sz – risk of recurrent febrile sz:
· 33% of first febrile sz will have a second. 17% (half of seconds) will have a third febrile sz.
· Highest risk of recurrence (>50%) in the first year, 90% first 2 years
· Increased risk of recurrence
Ø If first febrile sz occurs at <12m old.
Ø If first febrile sz occurs at <40°C.
Ø If complex febrile sz or multiple febrile sz
Ø With a positive family history of febrile or nonfebrile sz in 1st degree relative
Ø With prior neurologic or developmental abnormalities
Risk factors for later epilepsy/nonfebrile sz: (in order of importance)
· Pre-existing neurological or developmental abnormalities.
· Epilepsy in 1st degree relative
· Complex febrile sz
· Onset of febrile sz < 12m
· >3 febrile sz suggests child may later develop epilepsy/nonfebrile sz
Overall, 1-2% of children without these risk factors develop later epilepsy (by age 7), compared with 0.5 - 1% of the general population.
No evidence that developmentally normal children with only febrile seizures have lower IQs than other children.
HYPOTONIC INFANT
Christopher Giza, MD. Adapted by Sarah Copeland, MD, PhD.
Definitions: Reduction in muscle tone. May be due to central or peripheral causes (or both).
Clinical: most concerning = respiratory insufficiency and aspiration! Beware of progressive disorders! Head lag, poor suck, frog leg posture, poor traction response, poor posture in horizontal and/or vertical suspension, drooling/ bulbar involvement, diminished movements or loss of motor milestones. General exam findings include flattened occiput, occipital hair loss, arthrogryposis, congenital hip dislocation, pectus excavatum.
Atrophy, fasciculations, loss of DTRs suggest PNS involvement. Axial hypotonia, cortical thumbing/fisting, scissoring, dysmorphology, concomitant seizures, global developmental delay suggest CNS involvement.
The timing of infantile hypotonia may be congenital, new onset or slowly progressive.
Congenital – poor suck/feeding, head lag, frog leg posture, respiratory insufficiency, arthrogryposis, reduced movements (even in utero).
New onset – acute onset rare except after spinal cord or nerve root/plexus injury. Subacute may present with progressive weakness, ascending paralysis, cranial nerve involvement, drooling. Look for associated symptoms- constipation, insect bites, febrile illness, recent vaccination.
Slowly progressive – insidiously progressive weakness, loss of motor milestones, other developmental delay and/or regression.
DDx:
Cerebral hypotonia:
Nonprogressive encephalopathies – cerebral malformation, perinatalasphyxia, other acquired cerebral injury (infection, hemorrhage, trauma, etc.).
Chromosomal disorders – Prader-Willi, Down syndrome
Benign congenital hypotonia – resolves as infant matures.
Metabolic disorders – Zellweger, Neonatal ALD, Lowe (oculocerebrorenal), Riley-Day (familial dysautonomia), infantile GM1 gangliosidosis, acid maltase deficiency.
Spinal hypotonia:
Traumatic birth injury (cord or plexus) – beware high cord/root injury – phrenic nerve
Perinatal asphyxia with hypoxic-ischemic myelopathy.
Spinal muscular atrophy:
Acute infantile (SMA I) – onset <6m, reduced fetal movement.
Chronic infantile (SMA II) – onset 3-18m, normal at birth.
Polyneuropathies:
Guillain Barre syndrome– rare in infants but can occur.
Congenital hypomyelinating neuropathy
Hereditary motor-sensory neuropathies (HMSN III)
Neuromuscular junction disorders:
Congenital myasthenia – non-myasthenic mom, genetic defect in neurotransmission, decremental repetitive stim.
Neonatal myasthenia– myasthenic mom, passive transfer of AChR autoantibodies.
Infantile botulism– constipation, ocular involvement/sluggish pupils, dysphagia, incremental rep stim.
Muscle disorders:
Congenital myotonic dystrophy – maternal myotonia, facial diplegia, cardiomyopathy
Congenital myopathy – central core, congenital fiber-type disproportion, myotubular, nemaline rod.
Congenital muscular dystrophy
Metabolic myopathies – acid maltase deficiency, cytochrome C deficiency, phosphofructokinase deficiency, phosphorylase deficiency (McArdle disease), mitochondrial encephalomyopathy.
Dx:
Vital capacity (or other surrogate for respiratory function) – for older kids; count out loud on a single breath.
CT/MRI – cerebral malformation, perinatal asphyxia, some metabolic disorders, spinal cord injury/lesion
Chromosomal testing – Prader Willi, Down syndrome; other genetic testing – SMA, mitochondrial disorders, myotonic dystrophy
EMG/NCV – myopathies, especially congenital; neuromuscular junction disorders; some neuropathies
LP – Guillain-Barre assoc w/cytoalbuminologic dissociation.
Botulism toxin assay – infantile botulism
Biopsy – nerve and/or muscle
Serum lactate, pyruvate, CPK, aldolase
Tx: Etiology dependent!!
· Respiratory support – for any cases with progressive weakness, hypoventilation, aspiration risk, etc.
· Guilllain-Barre – plasmapheresis, IVIg
· Infantile botulism – botulinum antitoxin
· Myasthenia – pyridostigmine, neostigmine, 4-aminopyridine, plasmapheresis, prednisone?
· Supportive care – Foley, aspiration precautions, decub prophylaxis, PT/OT, nutritional support
Prognosis:
· Improve with time – benign congenital hypotonia, neonatal myasthenia
· Acute/subacute worsening – traumatic, asphyxia, Guillain-Barre, congenital/neonatal myasthenia, infantile botulism, myotonic dystrophy, mitochondrial encephalomyopathy
· Chronic progression – spinal muscular atrophy, polyneuropathy, congenital myopathy/dystrophy
· Nonprogressive – cerebral malformation, chromosomal disorders, traumatic injury
PEDIATRIC EPILEPSY DIFFERENTIAL DIAGNOSIS
Dan Arndt, MD 2/07
NONEPILEPTIC NEONATAL MOVEMENTS:
? Benign Nocturnal Myoclonus: During sleep, primarily @ sleep onset
? Benign Myoclonus: ↑ Freqquency/intensity & clusters over wks, ↓ > Age 3mos, none > 2yo, neuro exam normal, work-up normal
? Jitteriness/Tremulousness: ↓ Freq, ↑ Amp, shaking of limbs/jaw in resp to stim. ? Perinatal asphyxia
? Nonconvulsive Apnea: 1º Premies. Immature Resp center. Resolves by 43-44wks PCA
? Opisthotonos: Prolonged arching of back, probable meningeal irritation, e.g. infantile Gaucher’s, kernicterus
? Sandifer’s Syndrome: GERD, nystagmus, arching/Moro, head version, +/- torticollis, no LOC
? Hyperekplexia: Familial, AD, exaggerated startle reflex, DDx: Stiff Man’s, stimulus induced myoclonus, startle epilepsy
NEONATAL SZ BY TIME OF ONSET:
1st 24hrs: (In order of frequency, esp during 1st 12hrs): |
1. HIE, 2. Sepsis/bacterial meningitis, 3. SAH, 4. Intrauterine infections, 5. Trauma from tentorium or falx laceration, 6. Direct drug effect, 7. IVH @ term, 8. Pyridoxine dependency |
24-72hrs: (In order of frequency & importance): |
1. IVH in premies, 2. SAH, 3. Cerebral Contusion + SDH, 4. Sepsis/bact meningitis, 5. Cerebral infarction or intracerebral hemorrhage, 6. Cerebral dysgenesis, 7. Drug withdrawal, 8. Metabolic disorders including glycine encephalopathy, glycogen synthetase deficiency, hypoparathyroidism with hypocalcemia, pyridoxine encephalopathy, and Urea cycle disturbances |
72hrs-1wk: (In order of frequency & importance): |
1. Inborn Errors of metabolism → Esp organic acidemia: ? Hypoglycemia: Fructose dysmetabolism, maple syrup urine disease ? Hypocalcemia: Hypoparathyroidism ? Hyperammonemia: Propionic academia, methylmalonic Acidemia ? Hyperlactacidemia: Glycogen storage disease, mitochondrial disease ? Metabolic Acidosis: Maple syrup urine disease, fructose dysmetabolism, multiple carboxylase deficiency ? No Rapid Screening Test: Neonatal adrenoleukodystrophy, glycine encephalopathy, infantile gangliosidosis GM, Gaucher Type 2 2. Cerebral dysgenesis, 3. Cerebral infarction, 4. Intracerebral hemorrhage, 5. Familial neonatal seizures, 6. Kernicterus, 7. Tuberous sclerosis |
1-4wks: |
1. Inborn Errors of metabolism → Esp organic acidemia: Same as for 72hrs – 1wk. 2. Herpes encephalitis, 3. cerebral dysgenesis, 4. Familial neonatal seizures, 5. Tuberous sclerosis |
INFANTILE SPASMS
Sarah Copeland, MD, PhD and Christopher Giza, MD. Updated by Lekha M. Rao, MD 2010.
Definition: Catastrophic epilepsy syndrome of infancy associated with clusters of sudden extensor or flexor muscular contractions. Multiple etiologies.
Epidemiology: Age of onset usually 3-8 months. 85% <1yr; 93% <2yrs. Males slightly > females. Incidence 20-25/100,000.
Clinical:
Sudden brief flexor or extensor contractions, head/neck may flex, legs may be drawn up. Often occur in clusters, usually during sleep transitions. Child often cries or irritable following cluster
Other seizure types may present concurrently or may evolve later.
CRYPTOGENIC (30%)– previously normal infant, no obvious cause
SYMPTOMATIC (70%) - known etiology, often with dev.delay.
DDx:
Benign myoclonus of infancy, Benign nocturnal myoclonus – normal EEG.
Severe myoclonic epilepsy of infancy
Sandifer syndrome – gastroesophageal reflux
Hyperactive Moro response – normally gone by 5 months
Colic
Cortical dysplasia / dysgenesis [overall 30%+](focal cortical dysplasia [up to 25-30%], hemimegalencephaly, lissencephaly, schizencephaly, polymicrogyria, Aicardi syndrome
Pre- or perinatal insults [up to 25%] – maternal or fetal/neonatal infection , hypoxic ischemic encephalopthy, perinatal hypoglycemia, prematurity, perinatal stroke (often focal).
Neurocutaneous syndromes (tuberous sclerosis [up to 20%], neurofibromatosis, Sturge-Weber syndrome, incontinentia pigmenti)
Pyridoxine deficiency / dependency
Metabolic disorders (PKU, MSUD, mitochondrial encephalomyopathy, hyperammonemia)
Traumatic brain injury / nonaccidental trauma / birth trauma
Congenital infection (CMV, toxo, rubella, syphilis),
Chromosomal disorders (Trisomy 21, Duplication of 15q)
Other focal lesion - Brain tumor, AVM
If neonatal onset, more likely to be due to cortical dysplasia. If onset is later than 1 year, more likely due to cortical dysplasia, HIE, or genetic anomaly.
Diagnosis:
EEG – Hypsarrhythmia – chaotic, >200mV multifocal spike and slow-wave pattern. Usually becomes apparent at 3-4 months of age, sometimes more evident in nonREM sleep. This or modified (less chaotic) pattern seen in 2/3, other patterns (i.e. MISD) in remainder. EEG pattern includes electrodecremental response (EDR) associated with clinical spasm, paroxysmal fast activity (PFA) .
Brain MRI – may show underlying abnormality such as cortical dysplasia, tuberous sclerosis, HIE, trauma, infarction, etc.
PET – brainstem/diencephalon hypermetabolism (nonspecific finding); may show hypometabolism in region of cortical dysplasia; obtain only if considering surgery.
Metabolic workup: Obtain if prior studies are unrevealing, as metabolic abnormalities are a rare cause of IS
Labs – Lytes, serum amino acids & urine organic acids, NH4, lactate, pyruvate, acidosis – rarely associated with inborn metabolic error (MSUD, PKU, NKH, hyperammonemia, mitochondrial). Metabolic w/u if Hx/PE/MRI unrevealing.
CSF – Glucose – low (glucose transporter deficiency); amino acids/glycine – elevated (hyperglycinemia); infectious labs
Treatment: Complete control may significantly improve development
1. ACTH - 150 IU/m2/day IM.div BID In general, drug of choice especially if cryptogenic. Side effects include hyperglycemia, hypertension, hypokalemia, behavior change/irritability, weight gain/cushingoid features, gastric ulcer, insomnia, infection. Response rate is from 50-90%. Must be tapered off over 1-4 months to avoid adrenal insufficiency. Must give GI prophylaxis (PPI) while on ACTH, and monitor lytes and BP regularly. Very costly (>$10,000/vial). Obtain through ACTHAR
2. Vigabatrin – 50-200mg/kg/d bid; drug of choice tuberous sclerosis; 70-90% response rate. Side effects include somnolence, hypotonia, insomnia, white matter changes, retinal toxicity/visual field constriction. Patients must have initial formal ophtho exam within 6 weeks of starting med and every 6 months thereafter. Taper off if no response in 1-2 months. Obtain through SHARE.
3. Prednisone – 2mg/kg/d; perhaps less effective than ACTH.
4. Vitamin B6 (pyridoxine) – always worth a trial, though pyridoxine dependence is a rare cause of IS. 100mg IV while on EEG if etiology is not apparent. EEG should normalize Even if response is not apparent, may give a trial of 100-400 mg/day as some patients will respond.
5. Other AEDs: Topiramate – up to 45% response rate in pilot studies, 10-20/kg/day. Zonegran – some studies suggest up to 30% efficacy, no controlled trials, 10-20/kg/day. Felbamate – may be tried when other meds fail.
6. Clonazepam – can be used PRN for clusters
7. Epilepsy surgery – may be useful in patients with focal etiologies
8. Ketogenic diet – may be effective in 20-35% of patients; side effects include kidney stones, hyperlipidemia. GER.
9. IVIG – may be effective in cryptogenic cases unresponsive to other treatments, but no controlled trials.
Prognosis:
Variable, but symptomatic group does poorly; only 5% are normal or with mild delay. Cryptogenic/idiopathic group does better; up to 40% are normal or with mild delay only. High morbidity/mortality.
Poor prognostic factors: pre-spasms developmental or neurological abnormality, onset <5m, post-spasms regression, focal EEG/MRI findings, poor response to medications, recurrence after initial medical response.
Good prognostic factors: normal pre-spasms development, no focal abnormality, good response to treatment.
References: Carmant L, Infantile Spasms in Current Management in Child Neurology, Maria BL, 2002;Fenichel, GM Clinical Pediatric Neurology 2001; Menkes JH & Sarnat HB, Child Neurology, 6th edition, 2000; Riikonen R Curr Op Neurol 2005; Shields, WDS, Current Review in Clinical Science, 2006.
KETOGENIC DIET
Pantea Sharifi, MD
-Average serum bicarb is 18-23, Average Blood Sugars are 60-80
-Children taking Zonegran and/or Topamax may have lower Bicarb levels
-Must eat all meals, even when ill, to maintain ketosis and avoid hypoglycemia
-Must drink assigned quantity of fluids to prevent kidney stones and dehydration (zero calorie, zero caffeine except fluids used in meal/snack plans)
-Must drink same quantity of fluids when ill
-Parent has liquid replacement meal/snack recipe which is equivalent of a full meal/snack if child unable to eat solid foods.
-Clear liquid replacement liquids replace carbohydrates only: usually around 1 ½ -2 oz regular soda or juice or larger quantity of pedialyte for small children
GOALS: Maintain ketosis; Avoid all but minimal carbohydrates in foods
Illness and/or refusal to eat and/or significant decrease of ketones in urine:
1. If vomited or won’t eat, give double the number of meals at ½ portion each.
a. If vomiting or refusal to eat reoccurs, try the liquid ketogenic replacement meal. The child can sip small amounts continuously throughout day as each sip contains proper ketogenic diet ratio.
b. Try the carbohydrate replacement liquids if child is refusing to take anything or continues to vomit. This is usually 1.5- 2 oz of regular soda, oj, apple juice. Pedialyte okay also for small children especially if vomiting or diarrhea, but has less CHO/oz. and will require more.
c. Encourage intake of prescribed quantities of 0 calorie, 0 caffeinated fluids; try small amounts frequently if child refusing fluids.
2. If child is becoming dehydrated
a. Increase fluid intake to 1 ½ times maintenance
b. If still concerned about dehydration, refer to pediatrician/PCC/ER
i. Advise to bring paramedic/ER letter regarding ketogenic diet with them
ii. If needs continuous IV, no continuous dextrose in IV: Normal saline only for boluses
iii. If blood sugar < 50, give 4-5 grams dextrose; repeat BS prn and give boluses of dextrose to keep BS >50<80.
1. In D5W, there are 5 grams of dextrose per 100 cc intravenous fluid.
2. In D10W, there are 10 grams of dextrose per 100 cc intravenous fluid.
3. Concentrations greater than 10% Dextrose per peripheral vein are discouraged as they can lead to complications such as thrombosis.
3. Ketones will return to pre-illness levels after recovery
4. If child c/o back/abdominal pain with/without dark/bloody urine or crying inconsolably without known cause, suspect kidney stone. If found or suspected, increase fluids to 130-150% maintenanceand consider tx with CitraK.
GENERAL PEDIATRICS/CROSS-COVER
Compiled by Susan Shaw, MD, revised by Lekha M. Rao, MD
Fluids
4:2:1 rule
For first 10 kg à 4 cc/hr/kg
For next 10 kg à add 2 cc/hr/kg
Above 20 kg à add 1 cc/hr/kg
If < 6 months old, use D10 1/4 NS, if <10kg D5 1/4NS
If > 6 months old, use D5 1/2 NS + 20 mEq KCl
Pre-PET: NS + 20meq KCl
Bolus: NS 20mg/kg
NO WATER for babies less than 6 months old or until taking solids
Conversions :
1 teaspoon = 5ml
1 oz = 30ml
Pain Medications
Tylenol 15 mg/kg PO/PR Q4 PRN
Motrin 10 mg/kg PO Q6 PRN
Premedications/Allergies:
Benadryl 1mg/kg/dose PO/IV/IM Q6
Gastroenterology
GI prophylaxis:
Famotidine 0.5-1 mg/kg/day PO/IV bid
Ranitidine 1-2mg/kg/dose PO BID
Motility agents:
Reglan 0.1 mg/kg/dose PO/IV/IM q6
Constipation:
Lactulose 7.5ml PO QAM
Colace 10 mg/yr/dose PO qday-qid (max 500 mg/dose)
Dulcolax 5 mg if <2 yrs, 10 mg if >2 yrs PR prn.
Miralax 17g (1 packet or 1 capful) PO BID if >
Gas:
Simethicone
Nausea:
Compazine 0.1 mg/kg/dose q6 PO/PR
Phenergan 0.5 mg/kg/dose q6h PO/PR/IM
Zofran 0.15 mg/kg IV q4 (comes in 4 or 8mg)
If a patient vomits within 20-30 minutes of giving AED, give back half the dose. If it has been longer than 20-30 minutes, no need to repeat dose.
Wait 20 minutes after vomiting to resume PO
Antibiotics (meningitic dosing)
Ampicillin 100mg/kg/dose IV/IM Q6-8
For neonates (<7d) 50mg/kg/dose IV Q8
Acyclovir 500 mg/kg/dose IV Q8 over 1 hour with IVF.
For neonates 20/kg/dose IV q8
Cefotaxime 50 mg/kg/dose IV Q8
For neonates (<7d) 50 mg/kg/dose q12 IV/IM
Ceftazidime 50 mg/kg/dose q8 IV
Ceftriaxone 50 mg/kg/dose qday IM
Gentamicin 2.5mg/kg/dose IV Q8 check peak/trough with third dose
Vancomycin 15-20 mg/kg/dose q8 IV check trough with third dose
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