PEDIATRIC MENINGITIS

INTRODUCTION

Mortality 20-40% in neonates

Mortaility 5-10% in infants and children

Pediatric incidence is highest in neonatal period

Next highest incidence is between 3-8months

90% of cases occur before 5 yo

INFECTIOUS MENINGITIS

BACTERIAL

Pneumococcus

Meningococcus

Listeria

Hflu

Staph aureus

E. coli

Borrelia (LYME)

Treponema (SYPHILUS)

Mycoplasma

VIRAL

Enteroviruses: coxsachi, echo, polio

Herpes virus: HSV, EBV, CMV, VZV

Arboviruses: WEE, EEE, Japaneses, St. Louis, WNV

Other: rabies, HIV, HTLV, measles, mumps

FUNGAL

Cryptococcus

Coccidiomyocosis

Candida

Histoplasma

Blastomyces

PARASITES

Toxoplasma

Cysticercosis

Amoeba

RICKESIA

RMSF
NON-INFECTIOUS MENINGITITS CDs

C
Cancer (carcinomatous meningitis)

D
Druges (Septra, isoniazid, NSAIDS) SIN

S
Serum sickness

S
Sarcoidosis

S
SLE, Bechets
NON-INFECTIOUS CAUSES UNCOMMON IN KIDS

PEDIATRIC BACTERIAL MENINGITIS

ETIOLOGIES

Neonatal Meningitis

Group B streptococcus: 50%

E. Coli: 25%

Others: other coliforms, Staph eip, Staph aureus, pneumococcus,

meningococcus, group D strep, ureaplasma, Heamophillus, , Listeria

Note that Listeria is actually fairly

Infants/Children

Pneumococcus: 45%

Meningococcus: 45%

H.flu: 5%

Other: salmonaella, camplylobacter, listeria, group B strep, anaerobes

PATHOPHYSIOLOGY

Neonates are immunologic immaturity = essentially immunosuppressed

Immunosuppression: AIDS, DM, sickle cell, corticosteroids

Other risks: poor living conditions, head trauma, neurosurgery, mastoiditis, recent AOM,
daycare, antibiotic use
CLINICAL FEATURES

General

Presentation depends on age: more nonspecific with younger kids

3/4 have subacute presentation over 2-5 days

Fever, malaise, lethargy, irritability, anorexia, N/V, diarrhhae

Symptoms are OFTEN nonspecific

1/4 have acute presentation within 24hrs

Look for locus of infection: AOM, mastoiditis, etc

Neonatal Period

Temperature is easiest clue

Temp > 38: 10% with SBI and 1-2% with bacterial meningitis

50% will be afebrile or hypothermic: absence of temp does not r/o

meningitis in a neonate

Other vital sign changes are a clue

May present with ALTE: apnea secondary to seizure or respiratory center

depression

Behavioural changes: irritable, lethargic

Irritability that is WORSE with consoling is a clue

Seizures: vacant stare, hypertonicity, trembling chin, bicycling motion of

extremities

Nuchal rigidity < 25%

Bulging fontanelle 15%

Rashes infrequent

Livedo reticularis: generalized pallor accompanied by indistinctly outlined

truncal pathces of blue discoloration

Infants (1mo-1yr)

Similar to newborns

Febrile illness, generally look toxic

Child 1-5yo

Nuchal rigidity again uncommon but specific if present

Headache + fever (90% but not 100%!)
Fever, headache, photophobia, neck stiffness
Neck stiffness becomes more reliable after the first year
Passive testing of neck stiffness: supine position, seated with legs
outstretched (better way of passive testing)
Active testing: distraction with an object and observe neck ROM with
tracking of object, also look for spontaneous ROM of neck
Sensitivity and specificity of Brudinskys and Kernigs are poor
Brudinskys sign: flexion of the Back of the neck produces involuntary hip
flexion
Kernigs sign: extension of the Knee causes involuntary contraction of the
hamstring :. inability to straighten knee; also described as extension of the
Knee causes pain in the neck

Must suspect meningitis in any infant with

fever.

Infants do not present with neck stiffness.

BUG NOTES

Meningococcus

Gram -ve intracellular diplococci

5 major serotypes: A, B, C, Y, W-135 (B,C,Y are now most prevalent)

Vaccine covers A,C,Y, W-135 (NOT B):

Vaccine is not 100% effective; even less effective < 2yo

Vaccine duration is not permanent

Adrenal hemorrhage more common than pneumococcus

Pneumococcus

Many serotypes

Vaccine covers most

50% have pneumonia on CXR

DIFFERENTIAL DIAGNOSIS

Infectious

Septicemia, encephalitis, subdural empyema, epidural abscess, brain

abscess, viral/fungal/TB meningitis, myocarditis, rickettsemia

Traumatic

Shaken baby, NAT, closed head injury

Metabolic

Hypoglycemia, DKA, hypo/hypernatremia, uremia, urea cycle defects

Miscellaneous

Intussuception, intoxication, toxic exposure, seizure disorder, brain tumor,

AVM, ruptured dermoid cysts

INVESTIGATIONS

General

CBC, etc

Blood culture a must

Indications for Lumbar Puncture

Suspected neonatal sepsis: fever, toxic appearing, seizure, ALTEs

Febrile illness between 1-2months: difficult to exclude meningitis by exam

Febrile illness after close contact to patients with a SBI

Nuchal signs

Toxic appearance

Febrile seizures: LP if < 1year, toxic (generally lower threshold)

Fever and petechiae: not all petechiae are meningitis related, LP if unwell

Immunocompromised

Dural penetration: craniofacial trauma; LP after CT

Acute hearing loss

Indications for CT scanning b/f LP

Focal neurological deficit

Focal seizure (vs ? all seizures)

Papilledema

Marked decreased LOC

Hx or evidence of head trauma (recent or remote)

Known intracranial mass

ALL immunocompromised patients

NORMAL CSF

WBC < 5 and PMNs < 1

NO esoinophils

May have occasional basophil

CSF CELL COUNT

Bacterial meningitis usually > 1000 cells/mm3

Normal CSF wbc counts vary widely

Normal wbc counts also vary with age

Age
Mean
Range
Treatment Threshold
Preterm
7
0-44
>9
Term
8
0-32
>22
0-4weeks
11
0-50
>35
4-8weeks
7
0-50
>10
>8weeks
2
0-8
>6

CSF DIFFERENTIAL

Bacterial usually higher wbc count; viral usually lower wbc count

Classical is neutrophils with bacterial and lymphs with viral, TB, fungal

Bacterial early can have diff with primarily lymphs

Viral early can have diff with primarily PMNs

Neonates: 60% of cells can be PMNs

> 1 month: maximum of 3 PMNs per mm3

Recent pediatric study: found NO predictive value of differential on initial

Gram Stain

Cultures

Glucose

LP and 24hr LP: early neutrophilia or abscence there of can predict or rule
out viral vs bacterial etiology
Powers et al 1984
10% of bacterial meningitis with early lymphocytic %
2/3 of viral had early neutrophil predominance
10% of bacterial had wbc count < 1000
Traumatic LP
No more than 1 wbc per 500 rbc are allowed
WBCcsf = Measured wbcin CSF [(rbccsf X wbcblood)]
RBC blood
60 - 90% sensitive depending on source
Gram stain sensitivity decreases 20% w/ abx on board
Clues on gram stain ....
Gram -ve intracellular diplococci
Meningococcus
Gram + diplococci
Pneumococcus
Gram + bacilli
Listeria
Gram -ve coccobacilli
H.flu
Gram -ve bacilli
Ecoli
85% sensitive with bacterial meningitis
Sensitivity < 50% with previous abx
Viral cultures detect 25%
Fungal cultures detect 75%
TB cultures detect 55% Opening pressure: normal 5-20 cm
Can do viral cultures: consider if you need to know the bug
Normal CSF/serum ratio is 0.6:1.0 unless serum hyperglycemia
Ration < 0.4 suggests bacterial, TB or fungal meningitis (only mild
decrease in glucose with viral meningitis)

Protein

Normal range = 0.2 - 0.4 g/L

Can increase with blood from traumatic tap

Viral: normal to mild increase (0.4 - 1.0)

Bacterial, fungal, TB: larger increased protein (0.4 - 5.0)

NOTE: can increase with SAH, vasculitis, cancer, MS

India Ink Staining

Budding microorganism = cryptococcus

NOTE: only 30% sensitive thus must do cryptococcal antigen testing

Antigen Detection

Counter Immuno Electrophoresis (CIE): not used as much

Latex Agglutination
More sensitive, faster, replacing CIE
Variable reports of sensitivity
Meningococcus: 50 - 90%
Pneumococcus: 50 - 100
Hflu 80%
Cryptococcal agglutination: 90%
Xanthochromia: takes 2hrs to devp after blood, can be due
to bloody tap
ETIOLOGY and EMPIRIC ANTIBIOTICS

ETIO

Note similarity to sepsis in peds

Ceftriaxone/Cefotaxime: excellent CSF penetration, good
pneumococcus/meningococcus coverage, make sure to give at CNS penetration doses
Add ampicillin for coverage of Listeria if > 50yo or < 3mo
Add vancomycin for coverage of penicillin resistant pneumococcus (20% here)
Resistant pneumococcus overall is 20%
Note: cefotaxime and ceftriaxone can cause biliary sludging < 1mo
Allergic to pencillins: cephalosporins OK unless anaphylactic
Allergic to cephalosporins: Meropenum
When to start acyclovir empirically?

Cold sores

Genital ulcers

Neonate with mom with ulcers

? any focal seizure (increased risk of HSV)

Special Circumstances

Closed head trauma: pneumococcus, meningo, GBS; ceftriaxone 2g iv

q12h

Open head trauma, neurosx, CSF shunt: staph aureus/epi; vancomycin +

ceftazidime
< 1 month

1 - 3 months

3 mo - 50 yrs

> 50yrs

Group B Strep
E. coli
Listeria
Consider HSV
encephalitis

E.coli
Listeria
Pneumococcus
Meningococcus
H.flu
Group B Strep
(uncommon 13mo)

Pneumococcus
Meningococcus
H.flu

Pneumococcus
40%
Meningococcus
25%
Listeria 5%
Other gram -ve 10%
(klebsiella,
ecoli,hflu)

Amp 50 mg/kg iv q6h

Cefotax 50 mg/kg
q6h

Ceftriaxone
50 mg/kg iv q 12h
(max 4g/d)
Vancomycin (pen
resistant
pneumococcus
20% here)

Ceftriaxone 2 g iv q12
+/Vancomycin 1gm iv
q12
+/Ampicillin 2g iv q4hr

-mom w/ HSV
-baby with vesicles
-focal sz
-focal neuro s/s

EMP
ABx

Amp 50 mg/kg iv
q12h
Gent 2.5 mg/kg iv
q12

Altern
Abx

Amp + cefotaxime

TREATMENT

General

Cefotaxime

Empiric antibiotics as above

Do not delay antibiotics: ie, order them up while doing LP; give before CT
Fluids: 20 ml/kg for shock X 2
Pressors: start norepinephrine if hypotensive after two boluses
Treat hypoglycemia if present (D10 for neonates, D25 for infants, D50 for

Steroids

kids)
Seizures: benzo > dilantin > phenobarb
Increased ICP: intubate, mild hyperventilation

Role of decadron in bacterial meningitis controversial

Animal studies: decreased CSF pressure, lactate, brain edema
Given before or at time of first antibiotic dose to decrease mortality
Adults: recent evidence from NEJM Nov 2002: dexamethasone 10 mg iv
q6hr

Children: data is in group with Hflu, shown to decrease hearing

complications; not generally used now as Hflu rates decreases due to
vaccine

Consider in kids who are > 2yo and unimmunized (higher risk of Hflu)

AAP recommendations: limit steroid use to those with presumptive Hflu

Dose: 0.15 mg/kg

Contact treatment

Inform public health

Pneumococcus
none

H.flu
prophylaxis required only if there is non-immunized siblings
or contacts > 25 hr/wk who are less than 4 years old
rifampin 20 mg/kg (max 600mg) od X 4 days
ALL daycare contacts if > 1 case
F is for HFlu for four days

Meningococcus
prophylaxis required for all close contacts such as
household members, daycare, including adults; medical
personel only necessary if in contact with mucosal
secretions
only eradicates nasopharyngeal colonization
rifampin 10 mg/kg (max 600mg) bid X 2 days
ceftriaxone im, or cipro are alternatives

COMPLICATIONS

Acute/Subacute

Sepsis: DIC, ARDS, ARF, hepatobiliary

Dehydrataion

Pericardial effusion

Adrenal hemorrhage

Abcess

SIADH and hyponatremic seizures

Seizures: ativan > phenytoin > phenobarb

Cerebral edema: thus only give 70% maintenance fluids to prevent this

Subdural effusions: liquidification of pus

Hydrocephalus: results from pus in arachnoid villi preventing drainage

Increased ICP: treat w/ ETT and hyperventilation, mannitol 1 g/kg iv

Chronic

Deaf: sensorineural deafness in 5%

Blind: uncommon
Dumb: MR or devtal delay, learning disabilities
Ataxia
Seizure disorder
Focal paralysis
Hydrocephalus

PEDIATRIC SEIZURES
CLASSIFICATION OF SEIZURES
GENERALIZED (Loss of consciousness)

Tonic

Clonic

Tonic - Clonic (GrandMal)

Absence (PetitMal)

Myoclonic

Atonic
FOCAL/PARTIAL (NO loss of consciousness)

Simple (consciousness/mentation NOT affected)

Sensory: auditory, visual, olfactory, gustatory, vertiginous

Motor: tonic, clonic, tonic-clonic, jacksonian

Automomic

Psychic

Complex (consciouness/mentation affected but NO loss of consciousness)

Visceral symptoms

Hallucinations

Memory disturbance

Dream - like state

Affective disorder

Automatisms

Secondarily Generalized
MODIFIED CLASSIFICATION OF EPILEPTIC SYNDROMES

Idiopathic

Benign neonatal covulsions

Benign childhood epilepsy (includes Benign Rolandic Epilepsy)

Childhood/juvenile absense epilepsy

Jeuvenile myoclonic epilepsy

Idiopathic epilepsy - otherwise unspecified

Symptomatic Epilepsy Syndromes

West synrome(Infantile Spasms)

Lennox - Gaustaux

Early Myoclonic encephalopathy

Temporal Lobe epilepsy

Epilepsia Partialis continua

Frontal Lobe epilepsy

Post traumatic epilepsy

Mixed or Uncertain Classification

Neonatal seizures

Febrile seizures

Reflex epilepsy

PATHOPHYSIOLOGY

Any disturbance of excitatory or inhibatory mechanisms

Spread of seizure activity limited by active synapse inhibition

Young, immature nervous system MORE prone to seizures because excitatory systems
are relatively over - developed compared to the inhibatory systems (period of
vulnerability)

Seizures do affect long term behaviour and cognition: the longer and the more frequent
the seizures the more likely that development will be abnormal

INFANTS have different seizures

Poor white matter connections b/w hemispheres thus more likely to be

focal and thus generalized tonic-clonic seizures uncommon

Blinking, lip-smacking, hand twitching, pill rolling, ALTEs (parents miss the
short seizure activity but notice the apnea)
NOTES ON GENERALIZED SEIZURES

Begin with abrupt loss of consciousness with NO aura

Motor activity when present involves all four extremities and is usu symmetrical

May have prodrome of irritability, tension, isolated myoclonic jerks but NO true aura

Hx of aura implies focal onset with secondary generalization

Post-ictal phase of variable duration is universal

Convulsive Generalized Seizures

Tonic/Clonic (GrandMal)
abrupt loss of consciousness w/o warning and no true aura
b/cms tonic: rigid, trunk extended
falls to ground, may b/cm apneic, vomit, incontinent,
cyanotic
b/cms clonic: rhythmic jerking

Clonic
rhythmic flexor mvmts of muscles which gradually slow

Non-Convulsive Generalized Seizures

Absence (PetitMal)
sudden interuption of consciousness; stairs, stops talking,
not responsive, doesnt fall, lasts seconds +/- automatisms,
NO post ictal phase , no incontinence
school age children; rare in adult (temp lobe sz mc)
ppt by hyperventilation - good office test
3 Hz spike and wave on EEG

Atonic (Akinetic):
sudden loss of postural tone; drops to ground abruptly w/
no postural reflexes. Often confused w/ syncope

Myoclonic
sudden, brief muscle group contraction without LOC
drop-attack occurs when the entire body is involved
shock-like contraction of groups of muscles, often irregular

in rhythm and amplitude, and may not be repetitive

Tonic
-

trunk flexion, open eyes and mouth, upward eye deviation,

neck extension

NOTES ON PARTIAL/FOCAL

Local electrical discharges which may spread

More often secondary seizures

Can figure out location from symptoms

Aura is characteristic of focal sz

Sensory hallucination: sensory cortex

Focal motor mvmt: motor cortex

Tonic deviation of head and eyes away from side of discharge: frontal cortex

Bizzare olfactory/gustatory hallucination: medial-temporal cortex

Types .....

Simple
localized, consciousness not affected
generally NO post-ictal phase
motor: focal, jacksonian spread, todds paralysis (a/f up to
hrs),march may occur
motor autmatisms: lipsmaking, fiddling, repeating words
sensory: hallucinations, smells, tastes
autonomic: pupil dilation, salivation, lacrimation, visceral
symptoms (butterflies in stomach)
psychic: fear, deja vu, dream-like states, paranoia, elation

Complex
locaized with altered level of consciousness but not
unconscious
usually amnestic to event but may be responsive during
event
post-ictal state is common
motor, sensory, autonomic, psychic
often caused by focal d/c in temporal lobe :. has been
called temporal lobe szs (poorly); also often affect thinking
and behaviour :. has been called psyhomotor szs (poorly)
commonly misdiagnosed as psychiatric disorder
aura for seconds - min then pt appears distant and
unresponsive, sutomatisms occur in 90% (chewing,
swallowing, lipsmaking, scratching, fumbling, disrobing)

Secondarily Generalized
begins focally then spreads
hx will differentiate this
starts w/ aura, lip-smaking, etc
important b/c focal sz implies underlying structural lesion

NOTES ON EPILEPTIC SYNDROMES

Infantile Spasms (West Syndrome)

Presents in first year

Rapid, jackknife flexor or extensor spasms in clusters

Misdiagnosis of colic common as they tend to cry and draw legs up

West syndrome = infantile spasms + abnormal psychomotor development

+ hypsarrhythmia on EEG

2/3 have underlying CNS anomaly: brain malformation, tuberous sclerosis

LOOK for ash leaf spots, adenoma sebaceum, periungual fibromas (T.S.)

95% mentally retarded

Seizures well controlled in < 50%

Tx: ACTH, prednisone, bigabatrin

Lennox - Gastaut syndrome

Mental retardation, multiple seizure types, classic EEG pattern (spike and
wave)

Onset b/w 1-6yrs and may evolve from infantile spasms

Frequent seizures of various types

Valproic acid usually first line tx but usually end up on several meds

Jeuvenile Absence Epilepsy

Begins at 4-12 yo in most

Spike and wave on EEG co-incides with absence spell

Generalized convulsions occur in 50%

Hyperventilation can trigger

Prognosis excellent

Valproate or ethosuximide for those with generalized seizures

Benign Rolandic Epilepsy

Partial epilepsy, 3-13yo

Classically seizures occur while sleeping (twisting of mouth)

Rolandic region spikes on EEG

Treatment controversial

FEBRILE SEIZURE

Introduction

Definition = seizure in presense of a fever w/o evidence of CNS infection

or other caused cause

Common: 5% of children

Occurs b/w 5mo - 5yo; peak at 9-20 months

Note age range: most will say < 5 monthers do not get febrile seizures
thus they all require abx pending septic workup

Various types: clonic, tonic, tonic - clonic

Very low mortality

Classification

Simple febrile seizure (97%): non of criterion for complex/complicated

Complex febrile seizure (3%)

duration > 15 min

multiple seizures within the same illness
partial/focal features
neurologically abnormal child (devt, sz, structural)

Features

Why did it happen? Thought to occur while temperature rising; 50% have
temp > 39 degrees on first examination; EEG does NOT reveal
paroxysmal epileptic activity; ? related to bug and not temperature

What is the rate of recurrence of febrile sz?

30% have 2nd seizure
50% of those have 3rd seizure

Is it genetic? Fhx positive in 30%

Will the child get epilepsy?

General population incidence is 0.5-1%
Incidence after SIMPLE febrile seizure is 3%
Incidence after COMPLEX febrile seizure is 10%
Risk increased with fhx of epilepsy

Do febrile seizures have a post-ictal phase: some texts say NO post-ictal

phase; it is commonly seen; length of post-ictal phase not predictive of
pathology

Will giving the child tylenol prevent the next febrile seizure: NO (Multiple
studies including a cochrane review)
General approach

Stop the seizure

Examine for a source of infection

Examine for a neurologic abnormality

Decide simple vs complex seizure

Decide source vs no source for infection; normal vs abnormal neuro exam

Decide well vs unwell child

Approach to Investigations and Management

Stop the seizure

Ativan
Dilantin
Phenobarb

Complex febrile seizure

Labs: CBC, lytes, Ca, Mg, PO4, ? cap gas, ammonia
Draw blood cultures, do LP and full septic work up
Give antibiotics ASAP (before LP if there will be a delay)
CT head (may need to do before LP if there is decreased
LOC but dont delay abx for CT or LP
EEG if CT and LP normal

Simple febrile seizure

Looks unwell: full septic workup, antibiotics after cultures,
Looks well + source of infection: treat source
Looks well and no source of infection

Treatment

Approach as per any febrile kid

Febrile seizures < 5 months uncommon thus
lower threshold for cultures, abx, admit

Febrile seizure > 5 months approached as

any other febrile kid (r/o UTI)
AAP guideline 1996 for Febrile seizures: strongly
consider LP in infants < 1yo; NO routine CT/MRI/EEG for
febrile sz
Complete hx, PE looking for causes of fever and focal
neurological signs

Tx cause of fever
Admission criteria: complex febrile seizure, social reasons, cause of fever
Prophylaxis: AAP recommendation -> NO routine febrile seizure
prophylaxis
Febrile seizure prophylaxis is occasionally used for very frequent
recurrences
Do NOT start in ED without neuro consultation
NNT 4-8 to prevent one seizure
High side effects
Discharge instructions
Seizure instructions: turn on side, nothing in mouth, safe
env
When to bring back: as per febrile illness
Follow up: GP or peds
Tylenol prn for fever symptoms

NEONATAL SEIZURES

Present DIFFERENTLY than older children and adults --------------------------> Subtle physical
findings are common: lip smacking, staring spells, tongue thrusting, bicycling, apnea, prolonged
eye deviation, rhythmic movement, bicycling, peddling, posturing of limbs (sustained)

Generalized tonic - clonic less common (connections between sides are not well developed corpus callosum - thus harder for seizure activity to become generalized)

Structural Etiologies:

CNS bleed: IVH, SAH

CNS infarct: hypoxemic ischemic encephalopathy

CNS tumor

Cerebral dysgenesis

Metabolic Etiologies:

Meningitis

Sepsis

Hypoglycemia

Investigations

Managment

Hypocalcemia
Hyponatremia
Hypernatremia
Pyridoxine deficiency
Narcotic (etc) withdrawl
Septic work up
Gluc, Ca, lytes
Metabolic d/o screen: lytes, cap gas, ammonia, lactate, serum amino acids, urine
organic acids
Urine drug tox screen prn
CT head
EEG
Phenobarbital is first line in neonates 20 mg/kg iv
Dilantin, lorazepam second lines
Hypoglycemia: 6 ml/kg of D10
Hypocalcemia: 0.2 ml/kg of Calcium Chloride
Pyridoxine: 50 mg iv
Admit to PICU

DIFFERENTIAL DIAGNOSIS OF PEDIATRIC SEIZURES

(similar to altered LOC)
STRUCTURAL

Trauma

Bleed

Infarct

Tumor

Abscess

AVM

Hydrocephalus

Increased ICP
METABOLIC

Major organ failure

Heart: arrrythmia

Lungs: hypoxia, hypercarbia

Kidneys: uremia

Liver: hepatic encephalopathy

Brain: hypertensive encephalopathy

Endocrine

Hypoglycemia

Thyroid storm

Myxedemic coma

Addisonian crisis

Electrolytes

Na: up or down

Ca: up or down

Mg

P04
Toxicologic

EtOH withdrawl

Glucose related:Insulin, Oral hypoglycemics

Cardiotoxic: BB, CCB

TCA, Lithium, Seritonin syndrome, ASA, INH, anticholinergics

Anticonvulsants

Toxic alcohols
Acidosis: Congenital inborn errors of metabolism causing acidosis
Base excess
Other

PREGNANCY (ECLAMPSIA)

Neurocutanous disorders: sturg weber, neurofibromatosis, tuberous

sclerosis
Lytes
Infectious

Meningitis, Encephalitis

Sepsis

TORCH infections
Conversion disorder/psychogeni

NOTES OF VARIOUS ETIOLOGIES

Hypoglycemia: common cause, must check chemstrip, can be focal or generalized

Ketotic hypoglycemia

MCC of childhood hypoglycemia, presents with new-onset seizure

Episodes of symptomatic hypoglycemia associated with periods of calorie

deprivation

Onset usually 6 - 18 months

Symptoms commonly in morning

Seizure often ppt by vomiting/diarrhea

Chemstrip normal b/w attacks but low during episode

ED dx = hypoglycemia + ketonuria

Can be provocated by ketogenic diet

Avoid ketogenic diets effective

Cataracts are complication: refer to optho (recurrent lens swelling)

Electrolytes

Hypernatremia > 160

Hyponatremia < 120 although rate of devt important

Hypercalcemia: rarely can cause seizure

Hypocalcemia: rarely

Hypomagnesemia: rarely

Drugs and Toxins

Extensive list of drugs/toxins: see box 168-7

Plants, insecticides, hydrocoarbons, rodenticides also

Common: amphetemines, cocaine, PCPs, TCAs, EtOH w/drawl, BZD

withdrawl

Less common: ASA, theophylline, isoniazid, lithium, phenytoin,

carbemezepine,

Post Traumatic Seizures

Up to 10% after head injuries

Impact seizures within 1-2 min not associated with severe injury or
epilepsy

Severe injuries more likely to go on to epilepsy

Neurofibromatosis

Caf-au-lait lesions

Axillary freckling

Subcutaneous nodules

Seizures and mental retardation are common

Optic gliomas, CNS tumors also common

Tuberous Sclerosis

Ash leaf spots

Adenoma sebaceum

Mixed seizure disorder of infantile spasms, severe MR

Brain stones: calcified intracranial tumors

Sturge - Weber

Port-wine stain, hemiplegia, seizures

CLINICAL APPROACH TO Szs

HISTORY

Was it really a seizure? Consider paroxysmal events.

Automatisms = coordinated activity which occurs during the state of clouding of

consciousness and for which the patient is amnesic

Occur most often complex partial sz but may be seen in absence sz

Ex: eating, mimicry (anger, fear), perseverative

Key points in hx

Onset: when, where, what doing, rapid, slow, breathholding, grey over
eyes, sweating, lipsmaking, blinking, staring, aura

During: mvmts, symmetrical, purposeful, rhythmic

Duration: how long

After: post-ictal confusion, lethargy, memory of attack

No previous SZ hx

vmts)

Shx: EtOH, drugs

Fhx: szs, neuro disorders

ROS: systemic features, fever, any other neurological s/s

Previous SZ hx

As above but less detailed

Look for change in dose, changed medication, missed dose, change from
brand name to generic medication, noncompliance, drug interactions, new
Rx

Look for precipitants: substances, sleep deprivation, stress, infections,

strobe light, dehydration, blood sugar, endocrine

Progression of underlying dz

Superimposed head trauma

Complications of Mx: toxic level of Rx; phenytoin may inc myoclonic sz;

valproate in complex partial sz may inc focal sz; anticonvulsant induced

osteomalacia :. hypocalcemic :. inc sz (7 yrs of Rx)
PHYSICAL EXAMINATION

Gen: level of consciousness, confusion

Vit: fever

Derm: lesions of neurocut syndromes (neurofibromatosis, tuberous sclerosis,

sturge/weber

H/N: tongue lacerations, broken teeth, auscultate for bruits (AVMs) orbital/cranial/carotid

Resp: aspiration

MSK: #s, posterior shoulder dislocation

Neuro: full exam important - look for focal finding, papilledema

INVESTIGATIONS

First SZ

Previous SZ

See AAN guidelines

Routine blood work has extremely low yield
Short seizure, neurologically normal child: no investigations neccessary
Persistent altered LOC: CBC, urea, Cr, lytes, Mg, Ca, PO4, toxicology
Emergent CT head for suspected serious structural lesion: focal deficit,
persistent altered LOC, persistent h/a, cancer hx, anticoagulant use,
partial seizure at onset
AAN recomendation: imaging not routinely indicated for first nonfebrile sz
MRI actually better than CT
LP in child > 18 months: normal neuro and general examination, no
suspicion for meningitis; does not need LP and can be diagnosed with
febrile seizure
LP in child < 12 months: strongly consider LP in all presumed febrile
seizures as meningeal signs are unreliable (AAP recommendation)
EEG is recommended for all (AAP recommendation)
CT for change in seizure pattern, prolonged postictal state, persistent
abnormal mental status, fever, or other suspicion for new structural lesion
Anticonvulsant level: interpret w/ caution (MCC is Rx noncompliance)
May do full w/u depending on presentation

PROBLEMS W/ ANTICONVULSANTS

Side-effects: lethargy, irritability, rash

Remember serious side-effects: Stevens - Johnson syndrome, hepatic failure

(valproate)

Phenytoin toxicity: Nausea, dysarthria, dipolpia, ataxia, impaired LOC

---->
Chronic use: neurtopenia, osteopmalacia, anemia, lupu-like syn, myasthenia, etc

Thrombocytopenia

Drug interactions can be very important

Mvmt disorders

NON-EPILEPTIC PAROXYSMAL EVENTS

PSEUDOSEIZURES

Difficult dx that may occur in pts that do have epilepsy (commonly)

Ddx w/ EEG monitor: may induce by hyperventilation, tuning forks or IV saline

Trick: insert NG tube, the pseudosz pt will b/cm immediately responsive

Consider dx when .....

Long hx with no modification by medications

Exacerbated by stress or emotional upset

Highly suggestible

Sz only occur when witnesses present

Lack of incontinence, injury, post-ictal phase

SYNCOPE

History is the key to distinguish; what happened right b/f you went out

Presyncope: lightheadedness, faint, vertigo, greying of vision, pallor, nausea,

diaphoresis

Tone decreased vs increased

Lack of prolonged post-event confusion

Incontinence, injury, fhx, previous sz hx less common

BREATH-HOLDING SPELLS

Multiple names: infantile syncope, anoxic convulsion, anoxic seizures, white reflex
syncope

MCC of non-ictal paroxysmal events in children

Onset in infancy and toddler age and usu resolves by 5 yo

5% of children; fhx in 25%;

Simple is only color change; complex if there is loss of tone

Breath-holding is a misnomer: involuntary and reflexive and occurs during active or full
expiraiton

Commonly initiated by emotional or provocative stimuli

Starts by becoming quiet, mouth is wide open in full expiration as the face and trunk
changes color; returns to normal breathing before LOC if simple; complex spells have
deepening of the color change then loss of consciousness; tone then changes from limp
to opisthotonos and there is occasionally body jerking and urinary incontinence (anoxic
seizure); inspiratory gasp then normal breathing; event lasts about 40 seconds; may be
hypotonic for few minutes after

Two types: cyanotic (Blue): 60%; palid (white) in 20% or mixed in 20%

Ocular compression test: bilateral ocular compression for 10 seconds leads to

bradycardia, asystole > 2 sec, precipitates breath-holding spell

Frequently misdiagnosed as seizures:

Seizure: loss of muscle tone and posture BEFORE color change, post
ictal, no crying before episode, precipitating event, no opisthotonos

Breath-hold: loss of tone/posture AFTER color change, no post ictal,

crying before episode, precipitating event, opisthotonus

EEG useful to help distinguish

Other ddx: anemia, brain stem event, syncope, apneas

Mangement: generally conservative, atropine orally and scopolamine patches have been
used

OTHER

Migraine variant: motor, sensory, autonomic deficits

Sleep disorders: nightmares, night terrors

Tics: Intermittent, non-rythmic mvmts or utterances

Shuddering attacks: shuddering infants, fhx of same or tremors

Daydreaming spells: mimics absence sz

Panic attacks/hyperventilation

Sandifers syndrome: abnormal arching of back and torticollis seen in infants w/ GE

STATUS EPILEPTICUS IN CHILDREN

General

See Canadian Pediatric Society Guidelines (cps.ca)

Protect from injury, recovery position

Airway: push mandible forward, nasopharyngeal airway, intubate if any

concern re airway protection or for need to ventilate, suction airway

When to intubate? 45 min and failure to respond to bzd/dilantin (CPS

recmdtn)

Breathing: ventilate, pulsox, give oxygen by face mask or np

Circulation: establish large bore iv and give NS

Emergency tx: chemstrip and glucose 2 ml/kg of DW50 iv + thiamine

100mg iv/im

Adjuncts: NG tube to dec aspiration risk, cardiac monitor, pulsox, BP

monitor

History: ask parents hpi, pmhx, meds, what controlled previous seizures,
etc

Physical: trauma, fever, rash, locus of infection

Investigations: CBC, Urea, Cr, lytes, Ca, Mg, P04, glucose, toxicology
screen, myoglobinuria, CK, blood culture

Anticonvulsant hierarchy

Lorazepam 0.1 mg/kg iv/sl/pr over 2 min repeat in 15 & 30 min if necc.
[or Diazepam 0.2 mg/kg and repeat up to max 2.6 mg/kg or resp
depression]
+
Phenytoin 20 mg/kg iv at maximum of 50 mg/min or Fosphenytoin

Phenobarbital iv 20 mg/kg iv at rate of 1mg/kg/min

Barbituate coma (pentobarbitol 2 mg/kg bolus then 1 mg/kg/hr), general

anesthesia, diazepam drip, propofol drip

Specifics

Benzodiazepines
respiratory depression and hypotension may occur esp if
coningested alcohol, barbituates, narcotics, or other
sedatives
lorazepam has slower onset of action but longer duration
than diazepam :. theoretically preferred over diazepam
rectal lorazepam: same does; syringe in 2 inch, squeeze
buts
can be injected sublingual

Other Mx

Phenytoin
Fosphenytoin
-

most imp drug

do NOT give w/ glucos (precipitates), do NOT give im
mixed in propylene glycol: hypotension, tissue toxicity
hypotension, decreased contractility, AV block
contraindications: 2nd or 3rd degree AV block
watch closesly, stop if s/e devp
Produrg, water-soluble, rapidly converted to phenytoin
Can be given im or iv; can be given with dextrose solutions
Can be given faster (150 mg PE/min)
Doesnt contain propylene glycol thus less hyptotension
and tissue/vascular toxicity
Dose: 20 mg PE/kg iv given at rate of 150 mg PE/min
Phenobarbital
respiratory depression common; watch for
ventilator support commonly reqd
may result in prolonged obtundation or coma

Phenobarbitol
Generally third line
Usually first-line in infants < 1yo (dilantin is erratically
absorbed and difficult to maintain appropriate levels)
Paraldehyde
Must be rectal
Must be glass syringe (eats plastic)
Hyponatremia: 4 ml/kg of 3% NS over 30 minutes
Hypocalcemia: 0.1 ml/kg of 10% calcium chloride
Isoniazid: pyridoxime 1 mg per mg of INH (or 5 mg on spec)

DISPOSITION

Indications for admission

Prolonged seizure

Abnormal neurological examination

Prolonged post-ictal phase

Social factors

Significant underlying medical conditions

Anticonvulsant Therapy with first unprovoked seizure

1/3 will have recurrence and 75% of those will have third seizure

Risk of recurrence increases with +ve fhx, abnormal EEG, seizure during
sleep

General recommendation is NOT to treat after first seizure

No evidence that early treatment with anticonvulsant effects rates of

further seizures

DONT start in ED

Problems with Anticonvulsants

Side-effects common problem

Sedation, dizziness, blurry vision, ataxia, GI upset

Hepatoxocity, aplastic anemias, agranulocytosis, serum sickness
STEVENS - JOHNSON SYNDROME: rash + anticonvulsant, must think
of this, stop anticonvulsant, consult
Discharge education

Educate pt and family: can drive a/f sz free for one year whether on or off
Rx, take drug at same time, dont miss doses, avoid alcohol, refill
prescriptions regularly, wear medi-alert bracelet

Advise about swimming, ladders, dangerous equipment, driving, boating,

climbing, gum

Pregnancy: tertaogens, monitorin

Inform govt about driving

Support groups

F/U

NEUROCUTANEOUS DISORDERS
NEUROFIBROMATOSIS

Neural crest cells proliferate in multiple foci

Diagnostic criteria exist

NF1 and NF2 are very different (NF1 is much more common)

NF1 Features

Caf-au-lait spots: seen in essentially all; appear by age 1

Neurofibromas: usually appear by teens

Lisch nodules of the eye

Optic nerve gliomas

Astrocytomas

Intraspinal tumors: back pain, scoliosis, neuro deficits

Hypertension, pheochromocytoma

Vascular anomalies

Wilms tumor, sarcomas

TUBEROUS SCLEROSIS

Disorder of cellular differentiation

Ash leaf spots: seen better with woods light

Adenoma sebaceum (looks like acne)

Peri/subungual fibromas

Seizures, infantile spasms

Developmental delay

Renal angiomas
OTHER

Sturge Weber: portwine stain of V1: seizures, intracranial angiomas

Ataxia Telangiectasia: progressive ataxia

Von Hippel-Lindau: cerebellar or spinal hemangiomas :. present with CB or SC findings

PEDIATRIC HEADACHES
INTRODUCTION

Common problem, usually benign but not always

Migraines occur in 1% by age 7, 5% by age 15

Vascular theory: vasodilation of cranial arteries causes headache

Neuronal theory: wave of neuronal depression and decreased cerebral blood flow

Trigeminal theory: headache is an expression of the nerve-blood vessel interaction

CLINICAL FEATURES

Acute, chronic progressive or non-progressive

History is the key (as per adults): onset, associations, description, pattern, prior headaches,
therapies used, trauma, red flags for tumors

Physical: look for HTN, neurocutaneous disorders, neuro findings, fundoscopy

DIFFERENTIAL DIAGNOSIS

Benign

Tension

Migraine

Cluster:

Malignant

Infectious: any viral illness with fever, meningitis, encephalitis, sinusitis, otitis
media, mastoiditis, dental absess

Traumatic: recall leptomeningeal cysts with recent skull #

Hypertension

Toxic: sympathomimetics, analgesia rebound, CO

CNS tumor

AVMs

SAH

Hydrocephalus

Pseudotumor cerebri

Congenital Malformations
ACUTE HEADACHES

Viral illness with fever is MC diagnosis

SAHs due to cerebral aneurysms does occur

Same approach as for adults

Pediatric Migraines common

CHRONIC NON-PROGRESSIVE HEADACHES

Tension

Migraine

Depression

Conversion

CHRONIC - PROGRESSIVE HEADACHES

Main concern is increased ICP: tumors, abscess, hydrocephalus, bleeding

Signs of increased ICP

Headaches that awaken child or are present first thing in the am

Postural changes

Noctural or morning emesis

Papilledema

Pseudotumor Cerebri

Benign intracranial hypertension

Normal CT head; normal CSF, high opening pressure on LP

Females, younger

Obesity, tetracycline, OCP, vitamin A, steroids

Tx: diuretics and repeat LPs

DIAGNOSIS

History and physical are key

CT head prn

LP prn

MRI
PEDIATRIC MIGRAINES

Classification

Classic migraine = migraine with aura

Common migraine = migraine without aura

Complicated migraine = migraine with hemiplegia, opthalmoplegia, basilar artery,

acute confusion, alice-in-wonderland syndrome

Migraine variants: abdominal migraine, BPV, torticollis, ocular migraine

Pediatric Criteria for Migraine without aura (box 168-12)

Hemiplegic migraine: sudden onset of hemiparesis or hemisensory loss followed by headache,

more frequent in kids than adults

Opthalmopleic migraine: severe unilateral eye pain and headach followed by 3rd nerve palsy

Basilar artery: common in kids, visual symptoms, vertigo, ataxia, LOC, drop attacks

Acute confusional state: change of personality or behavior with migraine

Alice-in-wonderland syndrome: distortions in body images and shapes; objects appear larger or
smaller before, during, or after a headache

PEDIATRIC ATAXIA
DIFFERENTIAL DX

Toxic ingestions: EtOH, bzd, lithium, dilantin, carbon monoxide, antiHT, anticonvulsants

Posterior fossa structural lesion: tumor, AVM, abscess, infarct, MS, dandy walker cysts

Elevated ICP any reason: tumor, hydrocephalus, etc

Trauma, non-accidental truma

Post infectious cerebellitis

Acute Disseminated EncephaloMyelitis

Non-convulsive status
Vertebrobasillar migraine
Inborn errors of metabolism
Peripheral vertigo
Peripheral neuropathy: GBS, botulism, Millar fishcer

ACUTE POST-INFECTIOUS CEREBELLITIS

Demyelination post viral infection

Fairly common

Can be any virus but common with VARICELLA, EBV, coxsachie (and mycoplasma)

Afebrile, nystagumus, ataxic

Investigations

CT head normal

LP normal or mild increased wbc

MRI with diffuse uptake if MR is done

EEG if there is concern for non-convulsive status

Nhx: most resolve over 10 days but occasionally persist for months (worst at onset)

Has been treated with steroids

Disposition

Do CT and LP

Discuss with ped neurology: ? MR, ? EEG, ? d/c home if well

ACUTE DISSEMINATED ENCEPHALOMYELITIS = ADEM

Similar to post infectious cerebellitits except has BRAIN STEM findings

Brain stem findings = altered LOC, facial palsy, nystagmus, EOM abnormality, other CN palsy

May have meningismus

CT may be normal

LP may be normal or mild incr wbc

MRI = multifocal lesions

Tx = steroids + IVIG

ADEM vs HSV encephalitis may be difficult to distinguish

Send PCR for HSV and treat with acyclovir until pending