بسم الله الرحمن الرحيم

1. بسم الله الرحمن الرحيم Seizure due to Electrolytes Disturbances Dr. Nasser Haidar MRCP (UK), ABM, KSUF, PCCMF, FRCPCH Life Long Learning

2. Introduction Body fluid and Electrolytes distrib. Electrolytes functions General outlines in electrloytes disturb. Na Ca Mg Summary

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

4. 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

5. 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

6. Daily Fluid Requirements In Out

7. 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

8. 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

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

11. 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.)

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

14. 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

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

16. 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

17. Hyponatremia

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

19. Aetiology of Hyponatremia Hypovolemic Hypervolaemic Euvolemic Drugs Adrena. Renal loss RTA Salt wasting Extrarenal loss

20. CNS pathophysiology

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

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

23. Antiepileptic drugs can cause Seizure CarbamazepineOxcarbazepine Valproate Lamotrigine Induction of excessive water re-absorption in the collecting tubule

24. 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

25. 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

26. Treatment Acute 1 to 2 mmol/L/h Chronic 0.5 mEq/L/h 120 - 125 mEq/L. Target

27. 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

28. 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.

29. Hypernatremia >145 mEq/L

30. Seizure cause Hypernatr. ? Hypernatr.cause Seizure ?

31. Hypernatremia Water deficit High Na intake Low intake Loss Confused Insensible Accidental salt intake

32. 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

33. 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

34. 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.

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

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

37. 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.

38. 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

39. 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

40. Hypercalcemia ≥10.5 mg/dl. Seizures rare

41. 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

42. 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

43. Clinical presentation Hypercalcemia Hypertensive encephalopathy Seizures rare

44. 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,

45. Hypomagnesemia

46. 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

47. 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

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

49. 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

50. OTHER ELECTROLYTE ABNORMALITIES