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بسم الله الرحمن الرحيم. Seizure due to Electrolytes Disturbances. Dr. Nasser Haidar MRCP (UK), ABM, KSUF, PCCMF, FRCPCH. Life Long Learning. Introduction. Body fluid and Electrolytes distrib . Electrolytes functions. General outlines in electrloytes disturb. Na. Ca. Mg. Summary.

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slide1

بسم الله الرحمن الرحيم

Seizure due to Electrolytes Disturbances

Dr. Nasser Haidar

MRCP (UK), ABM, KSUF, PCCMF, FRCPCH

Life Long Learning

slide2

Introduction

Body fluid and Electrolytes distrib.

Electrolytes functions

General outlines in electrloytes disturb.

Na

Ca

Mg

Summary

slide3

Body Composition and Fluid Compartments

5%

40%

15%

40% Solid

Fat

Proteins

CHO

60% of Body Weight Water

Minerals

slide4

Fluid Compartments and Electrolyte Balance

Na+ 142 K+ 5

Ca+ 5 Mg++ 2

K 100

Mg 123

Na 10

Ph – 149

Prot._ 55

HCO3 8

Cl 2

Cl 105 HCO3 24

Prot. 16 Phos 2

Sulfate 1 Total 154

slide5

Proteins

Osmotic Press.

Na and Cl

Fluid bal.

Osmotic pres.

K

Neuromusc.

Excitability

Acid-B balance

Functions

Mg++

Enzymes

Sulfate

Protein

Metabo.

Ca++

Bone

Blood clot.

Ph-

Energy storage

HCO3-

Acid-B

balance

slide7

Electrolytes Disturbances

Routine lab. findings

Clinical significance.

Serious complications

Neurologic

Seizures

Common in

Na, Ca and Mg

Acute and/or severe

Rapid identification

Prevent permanent brain damage

slide8

Electrolytes Disturbances

Regulation of ionic balance

Ion gradients across cell memb.

Critical process

Disturbed Homeostatic brain systems

Epileptiform activities

Consequences on brain metabolism and function

slide10

Effects of Electrolytes Disturbances

Functional  reversible

Seizure  Structural (Irreversible)

slide11

Effects of Electrolytes Disturbances

Low Ca

Low Mg

Na and osmolality

High Ca

High Mg

Neuronal

irritability

Neuronal depression, with encephalopathy

  • (Confusion and slight cognitive dist.)
slide12

Seizure in Electrolytes Disturbances

Generalized

tonic–clonic,

other seizure occur.

Not possible to assign absolute levels

slide14

Fast and Correct diagnosis of seizures

375 adult cases of status epil.(SE),

10% had a metabolic disorder as the primary etiology of their seizure

With first-time seizures

40%

Anticipate in certain conditions

slide15

Fast and Correct diagnosis of seizures

Treatment of the underlying cause

Anticonvulsant not necessary

slide16

The most prominent feature of the EEG slowing of the normal background

Mixtures of epileptiformdischarges, high incidence of triphasic waves (TWs), and (as a rule)

reversibility after treatment of underlying causes

slide18

Hyponatremia

<135 mEq/L.

The cause of seizures in 70% of infants who lacked findings suggesting another cause

slide19

Aetiology of Hyponatremia

Hypovolemic

Hypervolaemic

Euvolemic

Drugs

Adrena.

Renal loss

RTA

Salt wasting

Extrarenal loss

slide20

CNS

pathophysiology

slide21

Brain volume adaptation to Hyponatremia

Equilibrium

Rapid adaptation

3 hours

Might Be overcomed.

Fully adapted

If hyponat. continued

48 hours

slide22

Other factors influencing outcome

Hypoxia and ischemia

impair the brain adaptive mechanisms

Children

Menestruant women

Concurrent insults [e.g., alcoholism or severe liver dysfunction ].

slide23

Antiepileptic drugs can cause Seizure

CarbamazepineOxcarbazepine

Valproate

Lamotrigine

Induction of excessive water re-absorption in the collecting tubule

slide24

Clinical features

< 120 mEq/L usually around 110 mEq/L

Severe or rapid (within hours).

Ominous sign

High mortality

Stopped by rapid increases in Na only 3 to 7 mEq/L

slide25

Treatment

Prompt

3%

Quick decr. ICP

5 to 6 mmol/L.

Enough to stop sz

Maximum 5- 6 mL/kg of 3% saline bolus

Further treatment

with hypertonic saline may be unnecessary

slide26

Treatment

Acute

1 to 2 mmol/L/h

Chronic

0.5 mEq/L/h

120 - 125 mEq/L.

Target

slide27

Osmotic Demyelination Syndrome (ODS)

Rapid Correction of serum Na

+

Osmolytes goes back slowly into cells

Fluid loss from the neurons and glia

Osmotic Demyelination S. with pontine and extrapontinedemyelination

slide28

Complications

ODS

quadriplegia, pseudobul. palsy, seizures,

Coma, death.

Demyelinating lesions may occur despite a careful correction of hyponatremia

Additional risks to demyelination

Hypokalemia, hypophosphatemia, hypoxemia, and

malnutrition with vitamin B defic.

slide29

Hypernatremia

>145 mEq/L

slide30

Seizure

cause

Hypernatr.

?

Hypernatr.cause Seizure

?

slide31

Hypernatremia

Water deficit

High Na intake

Low intake

Loss

Confused

Insensible

Accidental salt intake

slide32

CNS Pathopysiology

Loss of water from brain cells

Intracellular accumulation of organic osmoly.

Moving electrolytes into cells.

Shrinkage of the brain

Within minutes

Few hours (rapid adap/)

(Slow adapta.) several days

Encephalopathy

slide33

Clinical presentation

Slowly increasing, to 170mEq/L, well tolerated.

Acute (within hours) elevation to >158–160 mEq/L

Rupture of cerebral veins, focal intracerebral and SAH

Values >180 mEq/L high MR,

Rapid correction may lead to convulsions, coma, and death

slide34

Treatment

Goal - replenish body water

Speed of correction depends on the speed of development

Chronic hypernatremia

0.5 mEq/L/h;

Developed over hours.

1 mEq/L/h

PO or NGT or IV

Normal saline in case of frank circulatory compromise, as volume expansion.

slide35

CNS Pathopysiology

Thus overly aggressive therapy carries the risk of serious neurologic impairment in chronic hypernatremia

slide36

Hypocalcemia

<8.5 mg/dl

or

Ionized <4.0 mg/dl.

slide37

Poor intake

Vita. D deff.

Low Calcitriol

CRF, HF

Low

Ca++

Drugs (antiepileptic)

Incr. calcidiolmetab.)

Calcitonin

Biphosphon.

PTH deff.

Postop, DiGeorg, idiopathic

Hypomagnesemia

Acute pancreatitis, citrated blood transf.

slide38

Clinical presentation

Generalized t/c,

focal motor,

atypical absence

akinetic seizures

May be

the sole presenting symptom

Nonconvulsive SE reported

Seizures may occur without tetany

slide39

Treatment

Emergency

IV calcium

100 - 300 mg of elemental calcium over 10 to 20 min

Calcium-infusion started at 0.5 mg/kg/h for several hours,

AEDs may abolish tetany, whereas hypocalcemic seizures may remain refractory

slide40

Hypercalcemia

≥10.5 mg/dl.

Seizures rare

slide41

Excess PTH

Primary

Tertiary

Ectopic PTH excr.

High

Ca++

Malignant disease

Renal,

Ovarain,

Squamous cell.

Multiple myeloma

Excess action of Vit. D

Self- adminstered

Sarcoidosis

Others:

Thyrotoxicosis, Addison disease,

renalfailure

Drugs:

Thiazides

slide42

Clinical presentation

Chronic severe hypercalcemia

(≥14 mg/dl)

only minimal neurologic symptoms

A rapid increase to

12–13.9 mg/dl marked neurologic dysfunction

Lethargy, confusion, seizure, coma

slide43

Clinical presentation

Hypercalcemia

Hypertensive encephalopathy

Seizures

rare

slide44

Treatment

Chronic or asymptomatic

Treatment of the underlying dis.

& hypocalcemicdiet.

Oral

bisphosphonates

Acute or symptomatic

vigorous rehydration

furesemide

Consider IV bisphosphonates:

Second line: glucocorticoids,

calcitonin,

slide46

HYPOMAGNESEMIA

<1.6 mEq/L

(<1.9 mg/dl).

Preeclampsia

Eclampsia

Mg Anticonvulsant

By inhibition of N-methyl-d-aspartate (NMDA) glutamate receptors and the increased production of vasodilator prostaglandins in the brain

slide47

Low Intake

Green vegitabl.,

Fruits, fish,

Meat, cereals

Decreased GIabsor.

Diaarhea,

Laxatives,

Malabsorpt.

Low

Mg++

Renal loss

Alcohol induced,

Drugs,

RTA

Others:

Cirrhosis

Hungry bone syndrome

slide48

Clinical presentation

Generalized T/C,

at levels <1 mEq/L

<1.2 mg/dl

slide49

Treatment

Mild asymptomatic

Seizures or severe

(<1.2 mg/dl, <1 mEq/L)

Mg gluconate,

divided

500 mg/d. PO

IV MgS over a 5-min ,

infusion few hours.

If seizures persist, the bolus may be repeated

Low K & Ca can't be alleviated until magnesium is replaced

slide52

Potassium

Rarely causes symptoms in the CNS, seizures do not occur.

Low

High

weakness

slide54

Summary

Seizures is important manifestation of electrolyte distur.

More in patients with Na, hypocal., and hypomag.

AEDs alone are generally ineffective

slide55

Summary

Electrolytes, should be part of the initial workup of sz.

Establishment of early and accurate diagnosis

Rapid and appropriate therapy

Prevent permanent

brain damage