Seizures Flashcards
Seizures
Seizure – abnormal electrical discharge of neurons resulting in a
sudden involuntary change in function and behavior of an
individual
Acute symptomatic seizures – events occurring in close temporal
relationship with an acute CNS insult
- Metabolic, toxic, structural, infectious, due to
inflammation
- The ff criteria should be fulfilled to establish a causal
relationship between the insult and the occurrence of
seizure: temporal association, strength of association,
consistency, biological gradient, biological plausibility
- Varying interval from insult to sz:
o <24h: metabolic
o 1-7d: CVD, TBI, intracranial surgery, anoxic
encephalopathy, CNS infection
o >7d: subdural hematoma, CNS infections
Approach to a child with suspected seizure
What are the differentials for seizures?
Febrile seizures
metabolic and electrolyte imbalance
TBI
Toxic ingestions
Epilepsy
Status epilepticus
CNS infection
Brain tumor
What is febrile seizure?
Etio
- Most common sz disorder in childhood
- Age: 6-60mos
- Axillary T >38C
Patho
- Children have low seizure threshold. Possible role of
endogenous pyrogens (IL-1B) or activated cytokine
network causing inc neuronal excitability
What are the differences between simple febrile and complex febrile seizures?
SIMPLE FEBRILE
*few seconds to ≤15min
*Initially GTC, then a
brief period of post-ictal
drowsiness
*No focal neuro deficit
*no recurrence within 24 hr
COMPLEX FEBRILE
*≥15min
*focal seizure activity
*may have deficits
*may recur within 24hr
***Fulfillment of any one of the fx of complex febrile sz classifies
it as such.
What are the diagostics?
Dx
1. Lumbar puncture: indications:
- For all infants <6mos, with fever & sz
- Child ill-appearing
- Any child with s/sx of concern
- Febrile status epilepticus
- @6-12mos: optional if:
o Simple febrile sz and is deficient in HiB and
Strep vax/unknown vax status
o Pretreated with Abx
- PPS recommends LP for all <12 mos old (AAP) or <18
mos (PPS) with first febrile sz
o >18mos if with signs of meningitis:
meningeal signs, sensorial changes)
- When immunization status for Hib or strep pneumo is
incomplete or uncertain
- When patient has been given abx
- LP may be indicated for febrile sz >15 min
2. EEG – not done if first episode and otherwise
neurologically healthy
- Not predictive of future recurrence of febrile sz or
epilepsy
3. Serum studies – e’ and CBC not routinely
recommended for first simple sz
- Blood glc if with prolonged post-ictal obtundation or if
with poor oral intake (prolonged fasting)
4. Neuroimaging – not recommended after a first simple
febrile sz (no evidence)
- Workup for complex febrile sz need to be
individualized
- Considered for pxs with focal sz
- FSE – changes in the hippocampus
- Indications:
o <3yo, focal sz, abN neuro exam,
developmental delay, neurocutaneous d/o
What is the management of febrile seizures?
Mgt
1. Counselling and education on acute mgt and first-aid
2. Reassurance, emotional support, allaying fears of
parents
3. Antipyretics – decrease fever and discomfort
- Does not reduce risk of having recurrent febrile sz
4. Anticonvulsants – can reduce recurrence of febrile sz
- AE do not warrant routine use
- Prophylactic tx not recommended
- Phenobarbital 5mkdose LD q12hx2d then 10mkdose
q6-8h for 2 doses
- Phenytoin LD 15-20 mkdose then MD 5mkd IV/po
q8/12
- valproic acid LD 10-15 mkd q8-24 then MD 30-60 mkd
q8/12
a. Acute control of prolonged sz
- Diazepam 0.3 mkdose IV/IM, or 0.5 mkdose q8h per
rectum
- Midazolam IV/IM/buccal/intranasal 0.15-0.3 mg/kg
(<40kg=max 5mg, >40kg = max 10mg)
b. Intermittent prophylactic use for recurrent
prolonged febrile sz
- Diazepam po 0.3-0.5 mg/kg q8h for 24-48h during a
febrile illness
risk factors for recurrence of febrile sz
Risk factors for recurrence of febrile sz
Major risks: age <1yo, duration of fever <24h, fever 38-39C
Minor risks: FHx of febrile sz, FHx of epilepsy, complex febrile sz,
daycare, male, hyponatremia at presentation
No risk factor = 12%
1 RF = 25-50%
2 RF = 50-59%
>3 RF = 73-100%
risk for epilepsy after febrile sz
Risk for epilepsy after febrile sz:
- Neurodev abN (33%)
- Complex febrile sz (29%)
- Fhx of epilepsy (18%)
- Fever <1h before febrile sz (11%)
- Complex febrile sz (6%)
- Recurrent febrile sz (4%)
- Simple febrile sz (1%)
HYPOGLYCEMIA
HYPOGLYCEMIA
- Common in neonates, less common as age increases
- Most common cause: insulin-treated T1DM due to
mismatch in food, exercise and insulin
Etiology:
1. Hyperinsulinemia – maternal DM, insulin-producing
tumor, child abuse, perinatal stress (PT, SGA, hypoxia,
CS delivery)
2. Metabolic defects
3. Malnutrition, diets/fasting
4. Endo disorders – panhypopituitarism, GH deficiency,
cortisol def
5. Ethanol, salicylates, infection (malaria)
CM:
1. Neonate: jitteriness, brisk Moro, lethargy, poor
feeding, hypoT, irritability, RD, apnea, sz, coma, death
2. Child: dizziness, sweating, hunger, confusion, lethargy,
irritability, poor feeding, sz, coma, death
3. Tachychardia, bounding pulse (inc Epi secretion)
Dx:
1. CBG
a. NB: <30mg/dl
b. Infant: <40mg/dl
c. Child <2yoL <60mg/dl
d. Older child- adult: <75mg/dl
Mgt
1. Dextrose IV 10% 2.5ml/kg bolus then 5-8mg/kg/min
(infant) or 3-5mg/kg/min (older child)
2. Rapid (15g simple CHO= 4 oz juice/sweetened drink)
HYPERNATREMIA
HYPERNATREMIA
Etiopatho
- Mechanism:
o Excessive Na: improperly mixed milk
formula, iatrogenic
o Water deficit: DI, increased insensible
losses, inadequate intake
o Water and Na deficit: diarrhea, emesis,
osmotic diuresis, CKD, burns, ATN, osmotic
cathartics (lactulose), DM
CM
1. Dehydration
2. Doughy skin
3. CNS: irritability, restlessness, weakness, lethargy, sz,
coma
4. Fever
5. Hyperglycemia, hypocalcemia
6. Complication: brain hemorrhage – most dreaded
Dx:
1. Serum Na >145 mEq/L
Mgt
1. Address underlying cause
a. Mild/mod dehydration (AGE): ORS
b. Hypernatremic dehydration: isotonic bolus
10-20 ml/kg to restore intravascular volume
c. Central DI: desmopressin
d. Nephrogenic DI: thiazide diuretic
e. Iatrogenic hyperNa: decrease or stop Na
infusion
Goal: decrease Na by <12 mEq/L in 24h or at 0.5 mEq/L/h to avoid
cerebral edema
2. IVF – ½ NS, 0.3 NS, IMB, NM (Na<77 mEq/L) computed
at M rate plus 30-50 mL/kgx48h (subtract bolus from
TFR)
3. Dialysis – for severe hyperNa not responsive to fluid
mg
HYPONATREMIA
HYPONATREMIA
Etiopatho
- Infants at risk due to excess water ingestion from
lower GFR (water to infants <6mos old)
- Due to inc in intracellular water causing cell swelling
(brain swelling) à inc ICP, impaired cerebral BF
CM
1. Anorexia, nausea, emesis, malaise, lethargy, confusion,
agitation, headache, sz, coma, dec DTR
2. Cheyne-stokes respiration, muscle cramps, weakness,
rhabdomyolysis
3. Acute & severe à BS herniation, apnea
Dx:
1. Serum Na - <135 mEq/L
2. Serum osmolality
3. Spot Urine Na
Mgt
Hypovolemic hyponatremia – restore intravascular volume with
isotonic saline
Hypervolemic hyponatremia – water and Na retention
Euvolemic hyponatremia – eliminate excess water intake
- SIADH: fluid restriction
- Hypothyroidism and cortisol deficiency: hormone Tx
1. Sx’c px – goal: increase serum Na by 5-6 mEq/L in the
1st 1-2h
- Hypertonic saline (3% NaCl) 4-6 ml/kg over 1-2h
- Monitor serum Na, volume status, UO, acid base status
2. Asx’c px: goal: increase serum Na by <12 mEq/L in 24h
or 18 mEq/L in 48h to prevent central pontine
myelinosis
o confusion, agitation, flaccid or spastic
quadriparesis
- w/o fluid deficit: decrease drip rate to 50-80% of M
fluid requirement
- Na corrected slowly over 48h
- Freq monitoring of e’ and adjustment of IVF
HYPOCALCEMIA
HYPOCALCEMIA
- Ca exists in 3 forms in plasma: protein-bound (40%),
ionized (48%), complexed with anions like phosphate,
citrate and bicarbonate (12%)
Etiology:
1. Vitamin D deficiency – nutritional, VitD dependent
rickets, CKD
2. Hypoparathyroidism – DiGeorge syndrome, CHARGE
association, neck surgery, thalassemia, Wilson ds, I131
tx
3. Redistribution of plasma calcium – tumor lysis
syndrome, hyperphosphatemia, acute pancreatitis
4. Poor Ca intake – nutritional, dietary Ca chelators,
malabsorption
5. Septic shock, drugs (furosemide, CS, phenytoin,
rifampicin), massive BT
CM:
1. Often asx’c
2. Tetany, sz – most common
3. Acute: NM irritability, prolonged QT, heart block
4. Chronic: cataracts, basal ganglia calcifications,
extrapyramidal sx, enamel hypoplasia, papilledema,
rickets
5. Trousseau sign – carpopedal spasm
6. Chvostek sign – twitching of ipsilateral cheek/corner of
mouth “Chvostek = cheek”
Dx:
1. Serum Ca, PO4, Mg
Serum Ca <8.4 md/dL (<2.1 mmol/L)
Ionized Ca <4.3 mg/dL (<1.12 mmol/L)
2. Serum albumin
Mgt:
1. Sx’c
- Ca gluconate 10% at 100-200 mkdose + equal diluent
at <100mg/min. Give infusion over 1 h (max dose 1-
2g/dose or 10-20mL) then repeat q6-8h until asx’c
- Hook to cardiac monitor while on infusion WOF
arrhythmia
2. Asx’c
- Oral Ca supplements 50-100 mkd elemental Ca in 4 div
doses
HYPERCALCEMIA
HYPERCALCEMIA
Etiology
1. Hyperparathyroidism – adenoma, MEN, sec and
tertiary hyperparathyroidism from CKD
2. Excess Vit D – hypervitaminosis D, sarcoidosis, catscratch
ds, TB
3. Ca from bone – thyrotoxicosis, immobilization, CA, SLE
4. Idiopathic infantile hypercalcemia, PO4 depletion in PT,
Addison ds, Cushing ds
CM
1. Early: muscular weakness, fatigue, headache, anorexia,
nausea, vomiting, abd pain, constipation, polydipsia,
polyuria, weight loss, fever
2. Prolonged: nephrocalcinosis, progressively diminished
renal function, renal calculi, osseous changes, pain in
back or extremities, genu valgum, tumors, stunting
from vertebral compression, cognitive impairment, sz,
blindness, psychiatric sx (depression, confusion,
psychosis), stupor, coma
3. “Bones, stones, groans, thrones, psychic overtones”
Painful bones: bone-related complications
Renal stones
Abd groans: constipation, nausea, vomiting
Thrones: polyuria
Psychic overtones: fatigue, depression
Dx
1. Serum ca, iCa, serum PO4
Serum Ca >12 mg/dL (>3 mmol/L)
Severe: >15 mg/dL (>3.75 mmol/L)
2. Serum PTH
3. Plasma 25hydroxy vit D3
4. Urine Ca/crea ratio
5. Serum Crea
6. Thyroid function
7. Neck UTZ for parathyroid
Mgt
Goal: decrease intestinal Ca absorption, increase urinary Ca
excretion, decrease bone resorption, remove excess Ca
1. Hydration – isotonic saline 3000 mL/m2/d (N kidney
fxn)
2. Furosemide 1mkdose q6h
3. Hydrocortisone 1 mkdose q6h
- For vitamin D intoxication, granulomatous ds,
paraneoplastic syndrome
4. Bisphosphonates – Pamidronate
- Mild: 0.5-1 mkdose IV
- Severe: 1.5-2 mkdose
5. Calcitonin 4 IU/kg q12-24h IM or SC upto 8 IU/kg q6-
12h
6. Dialysis – for renal failure or recalcitrant hyperCa
7. Surgical subtotal parathyroidectomy – for primary or
tertiary hyperparathyroidism
HYPOMAGNESEMIA
HYPOMAGNESEMIA
Mg – necessary cofactor for enzymes, impt for mebrane
stabilization and nerve conduction
- Renal excretion – principal regulator of Mg balance
Etiology
1. GI and renal losses – major cause
2. Diarrhea (200mg/L), emesis (15mg/L), steatorrhea
(Mg-lipid salts)
3. Celiac ds, cystic fibrosis, small bowel resection
4. Drugs (loop diuretics, PPIs, aminogly, thiazides, insulin)
5. DM, CKD, hyperCa
6. Poor intake, marasmus
CM:
1. Sz, tetany, tremor, restlessness
2. Chvostek and Trosseau sign (due to concomitant
hypoCa)
3. Arrhythmia
Dx:
1. Serum Mg <1.5 mg/dL
2. Urine Mg, serum Crea (to compute fractional excretion
of Mg)
Mgt
1. MgSO4 25-50 mkdose slow IV infusion
2. Long term tx: Mg gluconate, Mg oxide, MgSO4 po
Another differential for seizure is traumatic brain injury
Etiopatho
- Most head trauma in childhood is minor
- The challenge for evaluating minor head trauma is to
identify clinically important traumatic brain injury
while limiting unnecessary imaging and radiation
exposure
Pathophysio
1. Immediate/primary brain injury
- focal injuries (contusions/hematoma) results from
linear forces when head is struck by a moving object
- inertial/angular forces due to accelerationdeceleration
leads to immediate physical shearing or
tearing of axons, “primary axotomy”
- delayed/secondary brain injury
- hypoxemia, hypotension, intracranial hypertension,
hypercarbia, hypo/hyperglycemia, e’ abN, enlarging
hematomas, coagulopathy, sz, hyperT
- endogenous cascade of cellular and biochemical events
in the brain occurs within minutes and continues for
months after the primary brain injury leading to
traumatic axonal injury and neuronal cell damage
(delayed)
clinical manifestations of TBI
CM
1. Minor head trauma
- < 2yo: hx of signs of blunt trauma to the scalp, skull,
brain. Infant or child is alert or awakens to voice or
light touch
- >2yo: GCS 14 or 15 at the initial exam. No abN findings
on neuro exam. No physical evidence of skull fracture.
2. Concussion – from a direct blow to the head, face, neck
or a blow elsewhere with an “impulsive” force
transmitted to the head
- Results in rapid onset of short-lived impairment of
neuro fxn that resolves spontaneously
- Sx: headache, confusion/disorientation, difficulties
with memory, blank stare, or “stunned” appearance,
inattentiveness, slow or incoherent speech, dizziness,
gait abN, vomiting, emotional lability (e.g
inappropriate laughing, crying)
3. Traumatic brain injury (TBI) – assoc with sx (brief loss
of consciousness, disorientation, vomiting)
- Severity:
o Mild TBI: GCS score 13-15
o Moderate TBI: 9-12
o Severe: <8 (3-8: hallmark). Coma, inc ICP
peak at 48-72h
- age-dependent injury patterns:
o infants and young children – inflicted or
non-accidental; repetitive injury
§ diffuse swelling (cerebral edema)
and subdural hematomas
common
o toddlers – accidental falls, abuse common
o school age – pedestrian vs vehicles;
passengers in MVA
o older child – bicycle
o teenager – MVA, sport-related and violence
4. Clinically important traumatic brain injury (ciTBI) –
presence of intracranial injury on CT scan assoc with >1
of the ff:
o Neurosx intervention: surg or invasive ICP
monitoring
o ET intubation for mgt of head injury
o Hospitalization directly related to the head
injury >48h
o death
- Depressed skull fracture warrants operative elevation
- Sx: LOC, vomiting, headache, sz
- Signs of basilar skull fracture: CSF rhinorrhea or
otorrhea, posterior auricular hematoma (Battle sign),
hemotympanum, periorbital hematoma (racoon eyes)
GLASGOW COMA SCALE
What are the diagnostics for TBI?
Dx
1. Plain Brain CT scan – highly sn for ID brain injury that
requires acute intervention
- Ideal for trauma
- Most children with minor head trauma do not need
head CT scan
- Decision to obtain head CT should be made using
clinical predictors to determine risk of ciTBI
- Include bone window and 3D imaging
2. Skull XR – little or no added value if a head CT is
performed. Used for <2 yo uncooperative px
3. Cervical spine XR
4. Fundoscopy – papilledema, retinal hemorrhages in
shaken infant syndrome
5. CBC, coagulation profile, BT, e’, BUN, crea, LFTs
What is the management of TBI
Mgt
1. ET intubation – for GCS<8, anisocoria, cervical spine
injury, herniation
2. IVF – isotonic fluids. Monitor SIADH and cerebral salt
wasting
3. Avoid hyperglycemia >200mg/dl
4. Early nutrition with enteral feedings
5. Sedation – avoid ketamine.
6. Prophylactic anti-sz meds
7. Head elevation
8. Mannitol – 0.25-1 g/kg/bolus. osmolar effect draws
water from intracellular to intravascular space.
Reduces cellular or cytotoxic edema. Onset in 15-30
min but lasts up to 6h. decrease cerebral blood volume
and ICP. Osmotic diuresis may cause hypotension
9. 3% hyperosmolar saline – for TBI with impending
herniation. Osmotic effect. Preserves intravascular
volume
10. Hyperventilation - PaCO2 30-35 mmHg. Fastest
method of reducing ICP in TBI with impending
herniation.
What is PECARN
Findings associated with very low risk of significant TBI in children
<2
normal mental status
normal behavior per routine caregiver
No LOC
no severe mechanism of injury
no nonfrontal scalp hematoma
no evidence of skull fracture
≥2 to 18
normal mental status
no LOC
no sever mechanism of injury
no vomiting
no severe headache
no signs of basilar skull fracture
Children <2yo
Neuroimaging warranted:
1. GCS <14
2. Palpable skull fracture
3. Altered sensorium (agitation, somnolence, slow
response)
4. Loss of consciousness
5. Severe mechanism of injury:
a. Motor vehicle collision with patient ejection
or death of another passenger
b. Rollover
c. Pedestrian or cyclist without helmet struck
by motorized vehicle
d. Head struck by high-impact object
Neuroimaging NOT warranted:
1. Normal mental status
2. No parietal, occipital, or temporal scalp hematoma
3. No LOC >5s
4. No evidence of skull fracture
5. N behavior according to the routine caregiver
6. No high-risk mechanism of injury
Skull XR – occasionally useful for 3-24mos old to screen for
fracture in asymptomatic pxs
Do not perform neuroimaging for children at very low risk of TBI.
Observation for 4-6h for GCS 15 and no altered mental status, but
with any of the ff:
1. Occipital, parietal, or temporal scalp hematoma
2. Hx of LOC >5s
3. Not acting normally according to parent
4. Vomiting that is self-limited
- CT scan for worsening S/Sx during observation period,
parent preference, <3 mos old, or unwitnessed trauma
of concern
B. Children >2 yo
Indications for neuroimaging:
1. GCS <14
2. Signs of basilar skull fracture
3. Altered mental status
4. Prolonged LOC
Neuroimaging not warranted
1. N neuro exam
2. No physical evidence suggesting skull fracture
3. No pre-existing condition that might increase risk of
intracranial hemorrhage (bleeding disorder)
4. N mental status
5. No LOC, vomiting, severe headache
6. No high-risk mechanism of injury
Skull XR indications:
1. Hx of trauma is uncertain (skeletal survey in the
evaluation of suspected abuse)
2. Rapidly evaluate location of radiopaque FB
3. Screen for fractures in asx’c px 3-24mos with
concerning scalp hematomas
- If Skull XR shows a fracture, a head CT scan should be
performed.
- If no fracture, risk of ciTBI is lower.
What are the discharge instructions?
Discharge instructions
1. Child should be taken to hospital in case of the ff:
a. Inability to awaken the child
b. Persistent or worsening headache
c. Vomiting that begins or continues 4-6h after
an injury
d. Change in mental status or behavior
e. Unsteady gait, clumsiness, incoordination
Differential for seizure
TOXIC INGESTIONS
sz in iron, isoniazid, kerosene, organophosphate
toxicity
Commonly encountered cases in toxicology
PARACETAMOL TOXICITY
Acute overdosage: ingestion occurring within a single-4 hour period; 150mg/kg in children: lowest dose capable of producing significant toxicity
STAGE 1 (0.5-24hrs): anorexia, vomiting, malaise; normal lab results except for acetaminophen levels
STAGE 2 (24-48 hours):
resolution of symptoms
elevated AST >1,000 IU/L
prolonged INR
STAGE 3 (3-5 days)
Peak AST >10,000 IU/L
onset of liver failure
STAGE 4 (4 days- 2 weeks)
Manifestations resolve
AST normalizes in a few weeks
INITIAL MANAGEMENT
*NAC should be started no later than 8 hours from the time of ingestion
*Insert NGT & do gastric lavage with activated charcoal (1g/kg to make a slurry)
*Manage specific complications: acute renal failure, bleeding tendencies, hepatic insufficiency, metabolic problems (hypoglycemia, acidosis, hypokalemia, hypocalcemia)