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. MgCa Na General outlines in electrloytes disturb. Electrolytes functions Summary

40%15% 5% 60% of Body Weight Water 40% Solid Fat Proteins CHO Minerals Body Composition and Fluid Compartments

K 100 Mg 123 Na 10 Na+ 142 K+ 5 Ca+ 5 Mg++ 2 Ph – 149 Prot._ 55 HCO3 8 Cl 2 Cl 105 HCO3 24 Prot. 16 Phos 2 Sulfate 1 Total 154 Fluid Compartments and Electrolyte Balance

K Neuromusc. Excitability Acid-B balance Mg++ Enzymes Na and Cl Fluid bal. Osmotic pres. Ca++ Bone Blood clot. HCO3- Acid-B balance Proteins Osmotic Press. Ph- Energy storage Sulfate Protein Metabo. Functions

Daily Fluid Requirements InOut

Routine lab. findingsClinical significance. Acute and/or severe Seizures Neurologic Serious complications Common in Na, Ca and Mg Rapid identification Prevent permanent brain damage Electrolytes Disturbances

Regulation of ionic balance Ion gradients across cell memb. Consequences on brain metabolism and function Electrolytes Disturbances Epileptiform activities Disturbed Homeostatic brain systems Critical process

Effects of Electrolytes Disturbances Functional  reversible Seizure  Structural (Irreversible)

Na and osmolality Neuronal depression, with encephalopathy Neuronal irritability High Ca High Mg Low Ca Low Mg (Confusion and slight cognitive dist. ) Effects of Electrolytes Disturbances

Generalized tonic–clonic, other seizure occur. Not possible to assign absolute levels Seizure in Electrolytes Disturbances

Electrolyte abnormality Frequency of seizures Hyponatremia ++ Hypernatremia++/+ Hypocalcemia++/+ Hypercalcemia+ Hypomagnesemia++/+ Hypokalemia − Hyperkalemia −

Fast and Correct diagnosis of seizures With first-time seizures 375 adult cases of status epil.(SE), 10% had a metabolic disorder as the primary etiology of their seizure Anticipate in certain conditions 40%

Treatment of the underlying cause Anticonvulsant not necessary Fast and Correct diagnosis of seizures

The most prominent feature of the EEG slowing of the normal background Mixtures of epileptiform discharges, high incidence of triphasic waves (TWs), and (as a rule) reversibility after treatment of underlying causes

Hyponatremia

The cause of seizures in 70% of infants who lacked findings suggesting another cause Hyponatremia <135 mEq/L.

Extrarenal loss Renal loss RTASalt wasting DrugsAdrena. Hypovolemic Hypervolaemic Euvolemic Aetiology of Hyponatremia

CNS pathophysiology

Brain volume adaptation to Hyponatremia Equilibrium Fully adapted If hyponat. continued 48 hours Rapid adaptation 3 hours Might Be overcomed.

Other factors influencing outcome Children Menestruant women Hypoxia and ischemia impair the brain adaptive mechanisms Concurrent insults [e.g., alcoholism or severe liver dysfunction ].

Carbamazepine Oxcarbazepine Valproate Lamotrigine Induction of excessive water re-absorption in the collecting tubule Antiepileptic drugs can cause Seizure

Clinical features Severe or rapid (within hours). < 120 mEq/L usually around 110 mEq/L Ominous sign High mortality Stopped by rapid increases in Na only 3 to 7 mEq/L

Further treatment with hypertonic saline may be unnecessary Further treatment with hypertonic saline may be unnecessary Maximum 5- 6 mL/kg of 3% saline bolus 5 to 6 mmol/L. Enough to stop sz Treatment Prompt 3% Quick decr. ICP

mEq/L. 1 to 2 mmol/L/h Treatment 0.5 mEq/L/h Acute Chronic Target

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 extrapontine demyelination +

ODS quadriplegia, pseudobul. palsy, seizures, Coma, death. Demyelinating lesions may occur despite a careful correction of hyponatremia Complications Hypokalemia, hypophosphatemia, hypoxemia, and malnutrition with vitamin B defic. Hypokalemia, hypophosphatemia, hypoxemia, and malnutrition with vitamin B defic. Additional risks to demyelination

Hypernatremia >145 mEq/L

Seizure cause Hypernatr. Hypernatr. cause Seizure ? ?

High Na intake Water deficit LossLow intake InsensibleAccidental salt intake Hypernatremia Confused

Loss of water from brain cells CNS Pathopysiology Shrinkage of the brain Within minutes Moving electrolytes into cells. Few hours (rapid adap/) Intracellular accumulation of organic osmoly. (Slow adapta.) several days Encephalopathy

Rupture of cerebral veins, focal intracerebral and SAH Values >180 mEq/L high MR, Acute (within hours) elevation to >158–160 mEq/L Slowly increasing, to 170 mEq/L, well tolerated. Clinical presentation Rapid correction may lead to convulsions, coma, and death

Normal saline in case of frank circulatory compromise, as volume expansion. Treatment Developed over hours. 1 mEq/L/h Chronic hypernatremia 0.5 mEq/L/h; Speed of correction depends on the speed of development Goal - replenish body water PO or NGT or IV

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

Hypocalcemia <8.5 mg/dl or Ionized <4.0 mg/dl. <8.5 mg/dl or Ionized <4.0 mg/dl.

Low Calcitriol CRF, HF Poor intake Acute pancreatitis, citrated blood transf. Drugs (antiepileptic) Incr. calcidiol metab.) Calcitonin Biphosphon. PTH deff. Postop, DiGeorg, idiopathic Hypomagnesemia Vita. D deff. Low Ca++

Generalized t/c, focal motor, atypical absence akinetic seizures Nonconvulsive SE reported Seizures may occur without tetany Clinical presentation May be the sole presenting symptom

Treatment Emergency AEDs may abolish tetany, whereas hypocalcemic seizures may remain refractory Calcium-infusion started at 0.5 mg/kg/h for several hours, mg of elemental calcium over 10 to 20 min IV calcium

Hypercalcemia ≥10.5 mg/dl. Seizures rare

Excess PTH Primary Tertiary Ectopic PTH excr. Malignant disease Renal, Ovarain, Squamous cell. Multiple myeloma Drugs: Thiazides Excess action of Vit. D Self- adminstered Sarcoidosis Others: Thyrotoxicosis, Addison disease, renal failure High Ca++

Clinical presentation A rapid increase to 12–13.9 mg/dl  marked neurologic dysfunction Chronic severe hypercalcemia (≥14 mg/dl) only minimal neurologic symptoms Lethargy, confusion, seizure, coma

Hypercalcemia Clinical presentation Hypertensive encephalopathy Seizures rare

Treatment Acute or symptomatic vigorous rehydration furesemide Consider IV bisphosphonates: Second line: glucocorticoids, calcitonin, Chronic or asymptomatic Treatment of the underlying dis. & hypocalcemic diet. Oral bisphosphonates

Hypomagnesemia

HYPOMAGNESEMIA <1.6 mEq/L (<1.9 mg/dl). Preeclampsia Eclampsia By inhibition of N-methyl-d-aspartate (NMDA) glutamate receptors and the increased production of vasodilator prostaglandins in the brain Mg Anticonvulsant

Low Intake Green vegitabl., Fruits, fish, Meat, cereals Decreased GI absor. Diaarhea, Laxatives, Malabsorpt. Renal loss Alcohol induced, Drugs, RTA Others: Cirrhosis Hungry bone syndrome Low Mg++

Clinical presentation <1.2 mg/dl Generalized T/C, at levels <1 mEq/L

IV MgS over a 5-min,  infusion few hours. If seizures persist, the bolus may be repeated Mg gluconate, divided 500 mg/d. PO Treatment Mild asymptomatic Seizures or severe (<1.2 mg/dl, <1 mEq/L) Low K & Ca can't be alleviated until magnesium is replaced

OTHER ELECTROLYTE ABNORMALITIES

Effects of Electrolytes Disturbances Rare K weakness

Potassium Rarely causes symptoms in the CNS, seizures do not occur. Low High weakness

Summary

Seizures is important manifestation of electrolyte distur. AEDs alone are generally ineffective More in patients with Na, hypocal., and hypomag.

Prevent permanent brain damage Establishment of early and accurate diagnosis Electrolytes, should be part of the initial workup of sz. Rapid and appropriate therapy Summary

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