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Metabolic & Toxic Causes Of

Seizures & their Management

DR. RAZA AHMAD


PGR, MEDICAL UNIT-I,
SHL.
Causes

Electrolytes:
Hyponatremia/Hypernatremia
Hypocalcemia
Hypomagnsemia
Metabolic:
Hypoglycemia/ Hyperglycemia
Uremia
Bilirubin encephalopathy
Inborn errors of metabolism
Pyridoxine dependency
Drugs/ Toxins:
Cocaine, Alcohol withdrawl, INH, Theophylline, SSRIs
Mechanisms

Metabolic disorders cause seizures in three ways:


Alteration of intracellular Osmolality
Depletion of substrates essential for
cellular metabolism or membrane function
Intracellular accumulation of toxic substances
Table 1. Different degrees of the electrolyte
disturbances that most frequently cause seizures

Electrolyte
Disturbance Mild Moderate Severe
• Hyponatremia 130–134 mEq/L 125–129 mEq/L <125 mEq/L
• Hypernatremia 145–149 mEq/L 150–169 mEq/L ≥170 mEq/L
• Hypocalcemia 1.9–2.2 mEq/L <1.9 mEq/L
• Hypercalcemia 2.5–3 mEq/L 3–3.5 mEq/L 3.5–4 mEq/L
• Hypomgnesemia 0.8–1.6 mEq/L <0.8 mEq/L
HYPONATREMIA
Clinical Features

Cerebral symptoms in hyponatraemia:


Severe symptoms
Decreased consciousness
Seizures
Muscle rigidity
Other symptoms
Nausea and vomiting
Headache
Bloating, 'puffiness'
Muscle weakness, cramps or spasms
TREATMENT

Sodium deficit
Total body water % × weight in kg × (desired sodium −
actual sodium)
For total body water %, use 0.6 for men and 0.5 for
women
Example: for a 70-kg man with a serum sodium level
of 120 mEq per L and a desired serum sodium level
of 140 mEq per L, the calculation is 0.6 × 70 (140 −
120) = 42 × 20 = 840 mEq
Rate of Na Correction

Serum sodium correction should generally not


proceed faster than 0.5 mEq/L/h for the first 24 to
48 hours; however, in severely symptomatic
patients, the rate can be 1.0 to 2.0 mEq/L/h; these
situations typically require use of 3% saline
The goal is to raise the serum sodium level not to
exceed 10 to 12 mEq per L in the first 24 hours and
18 mEq per L in the first 48 hours
Sodium Concentration of Intravenous Fluids
FLUIDS CONCENTRATION (MEQ/L)
Dextrose 5% 0
Dextrose 5% with sodium chloride 0.2% 34
Sodium chloride 0.45% 77
Lactated Ringer solution 130
Sodium chloride 0.9% 154
Sodium Chloride 3% 513
HYPERNATREMIA
Clinical Presentation
Water Deficit

 CBW refers to estimated current body water. The total body water
is normally about 60 and 50 percent of lean body weight in
younger men and women, respectively. However, it is probably
reasonable to use values about 10 percent lower (50 and 40
percent) in hypernatremic patients who are water-depleted.
 Thus, in a 60 kg woman with a plasma sodium concentration of
168 mEq/L, total body water is about 40 percent of body weight
and the water deficit can be approximated from :
Water deficit=0.4×60 ([168/140]-1) = 4.8 liters
Treatment

Hypovolmic hypernatremia: Initially Normal saline


then switch to 0.45% Saline or 5% D/W sol.
Euvolemic: Oral free water or 5% D/W.
Hypervolemic: Oral free water replacement
Rate of Correction

Hypernatremia that has developed over a period of


hours, rapid correction of plasma sodium (falling by
1 mmol/L per hour) improves the prognosis
Maximum safe rate at which the plasma sodium
concentration should be lowered is by 0.5 mEq/L per
hour and no more than by 12 mEq/L per day.
HYPOCALCEMIA
Clinical features

The typical CNS manifestations of acute


hypocalcemia are mental status changes and
seizures.Generalized tonic-clonic, focal motor, and
(less frequently) atypical absence or even akinetic
seizures may occur in patients with hypocalcemia
even without muscular tetany
Seizures are noted in 20–25% of patients with acute
hypocalcemia, and in 30–70% of patients with
idiopathic hypoparathyroidism
Treament

Intravenous calcium is the most appropriate


therapy. Doses of 100 mg to 300 mg of elemental
calcium should be infused intravenously over a
period of 10 min to 20 min.
Calcium-infusion drips should be started at 0.5
mg/kg/h and continued for several hours, with close
monitoring
AEDs are typically not needed
HYPOMAGNESEMIA
Clinical Features

Neuromuscular irritability, CNS hyperexcitability,


and cardiac arrhythmias. Seizures (usually
generalized tonic-clonic) can occur in neonates and
adults in association with severe hypomagnesemia,
usually at levels <1 mEq/L
HIV positive adults are at particular risk.
Hypomagnesemia has recently been recognized as an
important side effect of PPIs, and also several cases
of hypomagnesemia-induced seizures in subjects
taking PPIs have been reported
Treatment

Mild (magnesium levels between 0.8 mEq/L and 1.6


mEq/L) and/or asymptomatic hypomagnesemia can
be treated with oral administration of magnesium
(e.g., magnesium gluconate), usually given in divided
doses (total daily dose of 500 mg).
Symptomatic or severe (<1.2 mg/dL, <1 mEq/L)
hypomagnesemia, especially if seizures are present,
requires an injection of 1 to 2 g of magnesium sulfate
over a 5-min period, followed by an infusion of 1 to 2
g per hour for the next few hours, which may be
repeated if seizures persist
In women with eclampsia/preeclampsia, magnesium
sulfate 4-g to 6-g loading dose diluted in 100 mL
fluid should be given intravenously over 15 minutes,
followed by continuous intravenous infusion at 1 to 2
g per hour, which can be discontinued 24 hours after
delivery or last seizure.
HYPOGLYCEMIA
Neurogenic (adrenergic) (sympathoadrenal
activation) symptoms: Sweating, shakiness,
tachycardia, anxiety, and a sensation of hunger
Neuroglycopenic symptoms: Weakness, tiredness, or
dizziness; inappropriate behavior (sometimes
mistaken for inebriation), difficulty with
concentration; confusion; blurred vision; and, in
extreme cases, coma and death
TREATMENT

eat or drink 15 grams of easily digestible


carbohydrates, such as:
half a cup of juice or regular soda
1 tablespoon of honey
4 or 5 saltine crackers
3 or 4 pieces of hard candy or glucose tablets
1 tablespoon of sugar
Drugs

Glucose supplement: Dextrose


Glucagon
Inhibitors of Insulin Secretion: Diazoxide,
Octreotide
Thank You

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