Seizures

Question 1

Seizures

Answer 1

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

Question 2

Approach to a child with suspected seizure

Question 3

What are the differentials for seizures?

Answer 3

Febrile seizures
metabolic and electrolyte imbalance
TBI
Toxic ingestions
Epilepsy
Status epilepticus
CNS infection
Brain tumor

Question 4

What is febrile seizure?

Answer 4

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

Question 5

What are the differences between simple febrile and complex febrile seizures?

Answer 5

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.

Question 6

What are the diagostics?

Answer 6

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

Question 7

What is the management of febrile seizures?

Answer 7

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

Question 8

risk factors for recurrence of febrile sz

Answer 8

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%

Question 9

risk for epilepsy after febrile sz

Answer 9

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%)

Question 10

HYPOGLYCEMIA

Answer 10

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)

Question 11

HYPERNATREMIA

Answer 11

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

Question 12

HYPONATREMIA

Answer 12

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

Question 13

HYPOCALCEMIA

Answer 13

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

Question 14

HYPERCALCEMIA

Answer 14

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

Question 15

HYPOMAGNESEMIA

Answer 15

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

Question 16

Another differential for seizure is traumatic brain injury

Answer 16

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”

2. 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)

Question 17

clinical manifestations of TBI

Answer 17

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)

Question 18

GLASGOW COMA SCALE

Question 19

What are the diagnostics for TBI?

Answer 19

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

Question 20

What is the management of TBI

Answer 20

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.

Question 21

What is PECARN

Answer 21

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.

Question 22

What are the discharge instructions?

Answer 22

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

Question 23

Differential for seizure

Answer 23

TOXIC INGESTIONS
sz in iron, isoniazid, kerosene, organophosphate
toxicity

Question 24

Commonly encountered cases in toxicology

Answer 24

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)

Question 25

IRON TOXICITY

Answer 25

IRON TOXICITY

-due to direct corrosive effects on mucosal tissue and cellular dysfunction
-an elemental iron dose of:
20mg/kg: abdominal pain, diarrhea, vomiting
60mg/kg may be fatal

INITIAL PERIOD (0-6hours):
severe gastritis, vomiting
tachycardia, hypotension

QUIESCENT PERIOD (up to 12hours)
deceptive improvement, patient may appear stabilized
subtle signs of hypotension

RECURRENT PERIOD (12-48 hrs)
multiorgan failure, GI bleeding, lethargy, vasomotor collapse, pulmonary edema, hepatorenal failure, hypoglycemia and acidosis

LATE PERIOD (2-6 weeks)

INITIAL MANAGEMENT
*Ask for amount of elemental iron ingested, time ingested and other substances ingested
*collect 10ml blood for total serum iron (TSI) 3-5 hours post ingestion and send sample of gastric aspirate
*May request for stool exam with occult blood and plain abdominal radiograph
*manage specific problems: cerebral edema, decreased PT, hypovolemic shock, metabolic derangements, renal failure, seizures

Question 26

ISONIAZID TOXICITY

Answer 26

ISONIAZID TOXICITY

-Clinical effects occur 30mins to 2hrs
seizure dose: 80-120 mg/kg

Triad of toxicity: seizure, coma, metabolic acidosis

Severe overdose: seizures and LOC

Signs: hyperpyrexia, tachycardia, dilated pupils, dysarthria, hyperreflexia, hypotension, coma

MANAGEMENT:
*Insert NGT and do gastric lavage with activated charcoal (1g/kg) to make a slurry
*To enhance excretion, five alkalinization therapy with NaHCO3 at 1meq/kg IV every 6 hours until urine PH ≥7.5

Question 27

KEROSENE TOXICITY

Answer 27

KEROSENE TOXICITY

-leading cause of accidental ingestion in children ≤6yo
-may be absorbed in the GIT (optimal), through inhalation or via skin
-can depress the CNS and lead to hypoxia

Nausea, vomiting, diarreah, cough, mucous membrane irritation, DOB
CNS symptoms: initially may be excited but seizures may follow
Signs: respi distress, cyanosis, tachycardia, abdominal tenderness, perianal burns, altered sensorium

MANAGEMENT
*remove clothes and do decontamination procedures
*Give O2 via nasal cannula
*do not induce emesis
*no benefit with using activated charcoal
*specific problems: gastritis, seizures, aspiration pneumonia

Question 28

ORGANOPHOSPHATE TOXICITY

Answer 28

ORGANOPHOSPHATE TOXICITY
-Organophosphates inhibit the action of cholinesterase, the enzyme that breaks down acetylcholine to acetic acid and choline
-can be absorbed through inhalation, ingestion and dermal contact
-its toxic effects may appear as early as 10 minutes to as late as 2 hours post-exposure

MUSCARINIC (MILD): malaise, vomiting, diarrhea, sweating, pain, salivation, miosis

MUSCARINIC AND NICOTINIC (MODERATE): mild symptoms plus:
dyspnea, decreased muscle strength, bronchospasm, muscle fasciculations, motor incoordination, impairment of speech, bradycardia, involuntary defacation/urination

MUSCARINIC, NICOTINIC and CNS (severe):
moderate symptoms plus:
Respiratory paralysis, extreme hyper secretion, coma, cyanosis, hypotension, paralysis, behavioral changes, seizures

MANAGEMENT:
*If poison absorbed dermally, inhaled or ingested then vomited, provide O2, remove clothing and do sponge bath using alkaline soap
*If poison ingested: insert NGT and do gastric lavage with activated charcoal (1g/kg to make a slurry)
*Phenytoin for cases of malathion, parathion, or dichlorvos poisoining
*Pralidoxime chloride
*Atropine
*Manage other problems: acidosis, pulmonary congestion and seizures

Question 29

BENZODIAZEPINE TOXICITY

Answer 29

BENZODIAZEPINE TOXICITY

-effects are mediated mainly by binding with GABA receptors
-most significant finding of overdose: CNS depression
-other findings: slurred speech, incoordination and ataxia

Symptoms:
Slurred speech, dizziness, increased sleepiness

Signs: changes in sensorium (may be intermittent), hypothermia, bronchial hypersecretion, ataxia,nystagmus, dysarthria, weakness, aggressive behavior

MANAGEMENT:
*If within 1 hr of ingestion, insert NGT and do gastric lavage with activated charcoal at 1g/kg to make a slurry
*Flumazenil (0.01mg/kg) if with respiratory depression (may be repeated at 1-2 minute intervals up to a total dose of 1mg)
*specific problems: hypoxia, hypotension, respiratory acidosis

Question 30

ORGANOPHOSPHATE POISONING

Answer 30

Cholinergic syndrome

• “SLUDGE”
  o Salivation, Lacrimation, Urination, Diarrhea
  + Diaphoresis, GI upset, Emesis
• “DUMBBELLS”
  o Diarrhea, Urination, Miosis, Bradycardia,
  Bronchospasm, Emesis, Lacrimation, Limp,
  Salivation/Sweating

Question 31

What is epilepsy?

Answer 31

• Enduring predisposition to generate seizures
• > 2 uprovoked seizures occurring in a time frame of
  24h
• 2 or more independent sz that are unprovoked
  Breakthrough seizure – already treated with antiepileptic drugs
  but has achieved low drug levels. Sz recurrence in a person with
  epilepsy who has had a sustained period of sz freedom.
• Causes: noncompliance to AED, sleep deprivation,
  severe emotional stress, menstrual-related, infection,
  metabolic
• Tx: load with appropriate antiepileptic medication
  Seizure type – primary determinant of type of Rx px is likely to
  respond to
  Epilepsy syndrome – determines prognosis

Question 32

Pathophysiology of epilesy

Answer 32

Pathophysiology
Etiology – any pathology that disrupts neural function and
connectivity. Often leads to epileptogenesis
Epileptogenesis – ID which part of the brain turns epileptic
- Kindling: repeated electrical stimulation of selected
areas initially causes no apparent changes but with
repeated stimulation cause epilepsy
Epileptic state of increased excitability – seen in all pxs regardless
of etiology
- In a sz focus, neurons develop a stereotypic
synchronized response called paroxysmal
depolarization shift
- When after hyper-polarization is disrupted, the
inhibitory surrounding is lost, and neurons fire at the
same rate and time resulting in a sz focus
Seizure related neuronal injury – neuronal injury on MRI
- May be transient/permanent
- May include apoptosis and necrosis of neurons

Question 33

Clinical manifestations of Epilepsy

Answer 33

CM
Common Epilepsy syndromes

1. Benign Rolandic epilepsy – benign childhood epilepsy
   with centrotemporal spikes
   - Usually begins 3-13yo
   - Single nocturnal sz with clonic movt of the mouth and
   gurgling, inability to speak, preserved consciousness
   and comprehension
   - Sz resolve by 16yo
   - Altered consciousness, postictal confusion, and aura
   rare
   - EEG: typical broad-based centrotemporal spikes that
   are markedly inc in freq in drowsiness and sleep
   - MRI normal
2. Temporal lobe epilepsy – 70% of partial sz
   - Many w/ prior febrile sz or head trauma
   - Prodrome: lethargy
   - Oral or motor automatisms, altered consciousness,
   head and eye deviation, contralateral twitching, or
   tonic-clonic movts, posturing
3. Absence seizures – sudden cessation of motor activity
   or speech with a blank facial expression and flickering
   of the eyelids
   - Uncommon <5yo. Usually starts at 5-8yo
   - Never associated with an aura, rarely persists for
   >30sec
   - Not assoc with postictal state
   - Patients do not lose body tone and usually resume
   activity after sz
   - Hyperventilation of 3-5min can precipitate sz
   - EEG: 3 Hz spike-and-slow-wave discharges
4. Generalized tonic-clonic – most common generalized
   motor sz
   - Can be primary (bilateral) or secondarily generalized
   - Starts with LOC or sudden cry
   - Tonic phase: jaw snaps ff by 10-15s or longer of tonic
   spasms, apnea, cyanosis
   - Clonic phase: 1-2 min of rhythmic gen contractions
   - Postictal state: vomiting, confusion, somnolence,
   intense headache
5. Myoclonic – repetitive sz of brief, often symmetric
   muscular contractions with loss of body tone and
   falling or slumping forward
6. Infantile spasms – West syndrome
   - Begins at 4-8 mos
   - Brief symmetric contractions of neck, trunk,
   extremities
   - EEG: hypsarrhythmia

Question 34

Diagnostics

Answer 34

Dx:
1. EEG
2. CT/MRI

Question 35

What is the management of epilesy?

Answer 35

Mgt
Refer to Neurology
1. Benign Rolandic epilepsy - Oxcarbazepine,
carbamazepine, levetiracetam, valproic acid
2. Focal sz – oxcarbazepine, carbamazepine
3. Absence – ethosuximide: as effective as valproic acid
but less toxic (most common initial drug)
- Valproic acid, lamotrigine (less effective)
4. Juvenile myoclonic epilepsy – levetiracetam,
topiramate, valproic acid
5. Infantile spasms – ACTH, CS, vigabatrin
6. Epilepsy with GTC sz only – levetiracetam, lamotrigine,
topiramate, valproic acid

Question 36

What is status epilepticus?

Answer 36

• Continuous sz lasting for at least 30min, or a series of
  sz with no regaining of consciousness between sz
• Medical emergency!
  International League Against Epilepsy (ILAE) definition (2015):
• Condition resulting from:
  1. The failure of the mechanisms responsible for sz
  termination OR
  2. Initiation of mechanisms w/c lead to abnormally
  prolonged sz (after time point t1)
• Long term consequences (after time point t2):
  neuronal death, neuronal injury, alteration of neuronal
  networks, depending on type and duration of sz
  Mechanism
• Failure of desensitization of AMPA glutamate receptors
  leading to increased excitability
• Reduction of GABA-mediated inhibition –> BZDs are less effective the longer the sz episode

Question 37

What are the types of status epilepticus?

Answer 37

Type of SE

Operational
Dimension 1
Time (t1) when a sz
is likely to be
prolonged

Operational
dimension 2
Time (t2) when a
sz may cause
long-term
consequences

Tonic-clonic SE
Operational
Dimension 1
Time (t1) when a sz
is likely to be
prolonged: 5 min 30 min

Focal SE with
impaired
consciousness
Operational
Dimension 1
Time (t1) when a sz
is likely to be
prolonged10 min

Operational
dimension 2
Time (t2) when a
sz may cause
long-term
consequences>60 min

Absence SE
Operational
Dimension 1
Time (t1) when a sz
is likely to be
prolonged10-15min

Operational
dimension 2
Time (t2) when a
sz may cause
long-term
consequences
unknown

Question 38

diagnostics

Answer 38

Dx
1. Serum glu, Na, Ca, Mg
2. CBC
3. Basic metabolic panel
4. CT scan – r/o organic pathology
5. Continuous EEG – ID type (gen/focal), monitor tx
6. BCS, spinal CSF C/S
7. Toxic screen
8. Tests for inborn errors of metabolism

Question 39

Management

Answer 39

Mgt
Goal of tx is to stop EEG sz activity before reducing tx (complete
flattening of EEG).
Long term consequences start to ensue after 30 min of
generalized convulsive status epilepticus
And after 60 minutes of focal motor status epilepticus with
impaired awareness.