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
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
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 – 1^st 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 1^st 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 1^st 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 1^st 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

Etiologies:

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, 6^th edition, 2000; Riikonen R Curr Op Neurol 2005; Shields, WDS, Current Review in Clinical Science, 2006.

KETOGENIC DIET

Pantea Sharifi, MD

BASIC Principles on diet:

-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

CHILD EATS FOOD WITH HIGH CARBOHYDRATE CONTENT: Continue on current ketogenic diet ratio. Never fast unless authorized by attending.

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