neurological manifestations of electrolyte disturbances

1. Neurological manifestations of
Electrolytes disorders
By
Dr. Mohamed elshafei
Dr.link147@yahoo.com

2. Metabolic encephalopathy
 It encompasses a diverse array of systemic
conditions that cause global cerebral dysfunction
in absence of structural brain injury.
 Rapid metabolic disturbanes are more likely to
be symptomatic than gradual disturbances.

3.  Characters :
1. Fluctuating conscious level
2. Concordant with organ system dysfunction
3. Preservation of pupillary function is a hallmark
4. No focal neurological deficit
5. More commonly neuromuscular disorders
(cramps, weakness, fasciculations,….)
6. Often reversible.

4.  Both hypoglycemia and hyperglycemia can cause
focal neurological deficit.
 Metabolic dysarray can unmask or worsen old or
subclinical focal neurological deficits from an old
stroke .. Referred to as ``peeling the onion``.

6. Regulation of body fluids
 Water is the main component of the body and is
distributed between intracellular and extracellular
spaces
 Balance is maintained through osmosis which is a
passage of water through the cell membrane to
equalize concentrations of the two components

8.  Osmolality is the concentration of a solute
(Na,K,CL,Glucose) to a solvent.
 Normal serum osmolality is 280-295.
 There are neuro-hormonal and renal mechanisms
that control H2O balance.

14. Neurological manifestations
of electrolytes disturbances

15. Sodium
(135-145
mEq/L)

16. Hypernatremia
 Causes :
1. Increase water loss e.g diarrhea,vomiting,or
insensible loss
2. Decrease water intake
3. Overcorrection of hyponatremia with hypertonic
saline
4. Primary aldosteronism : suspect if BP↑ , K ↓,
alkalosis (HCO3 ↑).

17. Hypernatremia
 Clinical picture :
1. Progressive encephalopathy from drowsiness to
coma.
2. In rare cases : subdural hge from tearing of
venous sinuses due to shrinkage of brain cells.
3. Signs of dehydration.

18.  Correction :
1. Give water orally if possible .
2. Give dextrose 5% IV slowly (1L/6h) guided by
urine output and plasma Na.
3. Use 0.9% saline if hypovolemic.

19. Hyponatremia
 Causes :
1. Hypovolemic hyponatremia  Na loss from kidney,
gut, or excessive sweating
2. Euvolemic hyponatremia  SIADH, Hypocorticalism,
Hypothyroidism
3. Hypervolemic hyponatremia  fluid iverload states e.g
heart failure, liver cirrhosis, renal disease
4. Postoperative hyponatremia
5. Hyponatremia in severe exercise

21. Hyponatremia
 Clinical picture :
1. Confusion , headache, vomiting, cramps and
confusion
2. May be brain edema and seizures
3. Central pontine myelinolysis  from rapid or
overcorrection of hyponatremia ; Locked-Like
state or coma with quadriparesis.

22.  Correction :
 Correct the underlying cause
 never base treatment on Na concentration
alone.
 Replace Na and water at the same rate they were
lost.

23.  Hypervolemic hyponatremia :
 Fluid restriction
 Demeclocycline (ADH antagonist)
 Hypovolemic hyponatremia:
 Catious rehydration
 Avoid CPM
 Max rise in serum Na 15mmol/L perday if chronic or 1mmol/L/hr if
acute.
 Euvolemic hyponatremia :
 Vasopressor receptor antagonist (vaptans e.g conivaptan, tolvaptan,..)

24. Hyponatremia
Is the patient dehydrated?
Is urinary Na > 20mmol/L? Is the patient oedematous?
•Nephro
tic $
•Cirrhoti
c liver
•Renal
failure
•Heart
failure
Is the urine osm.
> 500 mmol / kg?
SIADH •Water
overload
•Severe
hypothyroidi
sm
•Glucocortic
oid
insufficiency
Na and H2O
are lost via
kidneys :
•Addison`s dis.
•Renal failure
e.g diuritic
phase
•Diuretic excess
•Osmolar
diuresis
(increase
glucose or urea)
Na and H2O are lost
other than via kidneys :
•Diarhae
•Vomiting
•Fistulae
•Burns
•Rectal villous adenoma
•Small bowel obstruction
•Trauma
•Cystic fibrosis
•Heat exposure

25. Potassium
(3.5-5 mEq/L)

26. Hyperkalemia
 Causes :
1. Renal insufficiency
2. Hypocortisolism
3. K shift extracellularly

27. Hyperkalemia
 Clinical picture :
1. Predominant symptom is muscle weakness
2. Cerebral symptoms are rare
3. Fatal complication : malignant cardia
dysrythmia (VF/VT)

29.  Correction :
1. Monitor ECG
2. 10 mL calcium gluconate (10%) IV over 2 min.,
repeated as necessary if severe ECG changes
3. Insulin + glucose (50mL of 50% glucose with 10U
rapidly acting insulin via large vein over 30 min **
monitor for hypoglycemia
4. Nebulized salbutamol (2.5mg)
5. Polystyrene sulfonate resin (eg. Calcium resonium
15g/6-8hrs in water )orally or if vomiting ,, as 30g
enema followed by colonic irrigation after 9 hrs)
6. dialysis

30. Hypokalemia
 Causes :
1. Renal loss  with diuretics or
mineralocorticoid excess
2. GIT loss  diarrhae and vomiting
3. Inadequate intake
4. K shift intracellularly

31. Hypokalemia
 Clinical picture :
1. Muscle weakness  may cause rhabdomyolysis
2. Cerebral symptoms are rare
3. Severe hypokalemia  metabolic alkalosis 
tetany

32.  Correction :
1. Mild : 2.5-3 , asymptomatic : give oral supplement ≥
80mmol/24h e.g slow k 2tab /8h . review K after 3
days.
2. Severe : < 2.5 mmol and/or symptomatic give IV K
cautiously, not more than 20mmol/h, and not more
concentrated than 40mmol/L
 Rapid K infusion  arrythmia
 Concentrated K infusion  thrombophlebitis
 Don`t give potassium if oliguric.

33. Calcium
(8.5-10.5
mg/dL)

34. Hypercalcemia
 Causes :
1. Primary hyperparathyroidism
2. Malignancy  tumors lysis syndrome (cofusion
in pt with malignancy !! Hypercalemia)
3. Drugs : thiazide diuretics, vitamin D

35. Hypercalcemia
 Clinical picture :
1. Mild : personality changes or memory
impairement
2. Moderate : neuromuscular symptoms as
cramps, proximal wasting, or weakness, normal
CK, EMG shows myopathic changes
3. Severe :lethergy and coma

36.  Correction of acute hypercalcemia :
 Diagnose and treat the cause
 If ca > 3.5mmol/L and symptomatic :
1- correct dehydration if present with IV 0.9% saline
2- Bisphosphonates :
- pamidronate 30mg in 300mL 0.9% saline over 3 hrs
(Max 90mg) lowers ca over 2-3 days max effect at 1
weak.
- zolidronic acid (more effective) 4mg IVI over 2 hrs will
normalize plasma ca over 1 weak
3- steroid may be useful in sarcoidosis
4- chemotherapy in malignancy

37. Hypercalcemia
Albumin raised Albumin normal or low
Urea raised
* dehydration
Urea normal
*cuffed specimen
Phosphate
↓ or ++
Urea normal
* 1ry or 3ry
hyperparathy
roidism
Phosphate
↑ or ++
Alk. Phosphatase
high (↑ bone turn
over )
-Bone mets
-Sarcoidosis
-Thyrotoxicosis
-lithium
Alk. Phosphatase
normal
-Myeloma (plasma
ptn ↑ )
-Vit. D excess
-Sarcoidosis
-With HCO3 (milk
alkali $)

38. Hypocalcemia
 Causes :
1. Hypoparathyroidism  thyroid or parathyroid surgery
2. Severe renal failure
3. Vitamin D deficiency
4. Massive transfusion
5. Pancreatitis
 Apparent hypocalcemia may be an artefact of hypo-
albuminemia

39. Hypocalcemia
 Clinical picture :
1. Irritability, anxiety, delirium, …
2. Seizures (may be nonconvulsive status)
3. Tetany

41.  Longstanding hypoparathyroidism :
 Manifests on CT-Brain as calcification of basal
gangliaand may be cerebellum, brainstem and
cortex
 May cause chorea, regidity, or other
extrapyramidal manifestations and may be
asymptomatic
 Most basal gang. Calcifications in CT-Brain are
idiopathic

42. Tetany
 Manifest tetany : ( s. ca < 9)
- Mild (s. ca = 9-8) : circum oral numbness
- Moderate (s. ca = 8-7) : 1+ carpopedal spasm
- Severe (s. ca < 7) : 2+ laryngospasm
 Latent tetany : (s. ca = 9-10)
- Trousseau`s sign
- Chvostek`s sign

43.  Correction :
 Mild : give calcium 5mmol/6h PO with daily plasma
Ca level
 In CRF :may require alfacalcidol 0.5-1μg/24h PO
 Severe symptoms: give 10mL of 10% calcium
gluconate IV over 30 minutes and repeat if
necessary
 If due to respiratory alkalosis : correct alkalosis

44. Magnesium
(1.5-2.5 mg/dL)

45. Hypermagnesemia
 Causes :
1. IV Mg Sulfate in pre-eclampsia and eclampsia
2. Excessive Mg intake in patient with renal failure
e.g antacids and laxatives

46. Hypermagnesemia
 Clinical picture :
1. Neuromuscular dysfunction
2. Alarming sign  depressed deep tendon
reflexes >>>> Impending paralysis
3. Lethergy due to hypoxia and hypercapnia that
occur due to respiratory muscle affection not
due to cerebral affection

47.  Correction :
1. Rarely require ttt unless severe > 7.5
mmol/L
2. Ttt of the cause

48. Hypomagnesemia
 Causes :
1. Decrease intake
2. Decrease absorbtion
3. Increase renal loss with diuretics

49. Hypomagnesemia
 Clinical picture :
1. e.g hypocalcemia
2. Hypomag. Decreases activity and levels of
parathyormone and should be suspected in
symptomatic hypocalcemia that`s not
responding to calcium repletion

50.  Correction:
1. Mg salts PO or IV as 8 mmol MgSO4 IV
over 3min-2hr acc to severity
2. Frequent measuring of Mg levels

51. Phosphorus

52. Hyperphosphatemia
 Causes :
1. Acute or chronic renal failure

53. Hyperphosphatemia
 Clinical picture :
1. Symptomatic hypercalcemia from binding with
calcium

54.  Correction :
1. Use phophate binder as sevelamer 800
mg/8h PO during meal

55. Hypophosphatemia
 Causes :
1. Malnutrition
2. Increased renal losses

56. Hypophosphatemia
 Clinical picture :
1. Weakness of cranial and limb muscles esp. if
blood level < 1mg/dl
2. Can manifest as respiratory failure or inability
to wean from ventilator

57.  Correction :
1. Oral or parentral phosphate
supplementation e.g phosphate polyfusor
IVI (100mmol PO4 in 500mL)
2. Never give phosphate to hypercalcemic or
oliguric patient

63. Electrolytes disturbances
due to neurological disorders

64. 1. Diabetes insipidus.
2. Syndrome of inappropriate ADH
(SIADH).
3. Cerebral salt wasting.

65. Diabetes insipidus
 High and Dry
 Decrease secretion of ADH  increase urine
output
 Two types :
 Central (neurogenic) : ↓ ADH secretion
 Peripheral (nephrogenic) : ↓ ADH renal response

66.  Neurogenic causes :
1. Brain tumours
2. Head trauma-basilar skull fractures
3. Neurosurgery
4. Anterior communicating artery aneurisms
5. CNS infection- maningitis
6. Ischemia/hypoxic events
7. Brain death

67.  Clinical picture :
1. Polyurea ( > 200 cc/hr )
2. Polydypsia d.t thirst
3. Signs of dehydration
4. Decreased weight

68.  Labs :
1. Serum osm. > 300
2. Serum Na > 145
3. Urine osm. And Na < 10
4. Urine specific gravity < 1,005

69.  Tratment :
1. Fluid replacement : replace output + 10% ( if
patient is tachypnic or feverish may need more)
2. ADH replacement :vasopressin or DDAVP may
be given IV, SC or intranasal 2-4 mcg/day IV in
two doses common

70. Syndrome of inappropriate ADH
(SIADH)
 Low and wet.
 A syndrome of exessive secretion of ADH

71.  Nerological causes :
1. Hydrocephalus
2. Meningitis
3. Stroke
4. Brain tumours
5. SAH
6. oat call carcinoma
7. Bronchial pneumonia

72.  Clinical picture :
1. Small amounts of concentrated urine
2. Weight gain/pitting oedema
3. Hypertension (increased volume)
4. Signs of water intoxication
(nausea,vomiting,headache,irritability,..)

73.  Labs :
1. Serum osm. < 275
2. Serum Na < 130
3. Urine Na : 70-140
4. Urine osm. And specific gravity are high
5. Dilutional hemoglobin

74.  Treatment :
1. Strict fluid restriction 500-1000 cc/day
2. Administer diuretics
3. IV fluids should be isotonic
4. Replace Na slowly with 3% saline over 3-6 days
if severe hyponatremia present
5. Consider tube feedings and vasopressors part of
I&O

75. Cerebral salt wasting
 A condition of true hyponatremia without
increases in ECF volume

76.  Causes :
 Unknown but seen in 30% of SAH patients

77.  Clinical picture :
1. Hyponatremia
2. Hypo-osmolality
3. Decreased ECF
4. Increased BUN
5. Negative salt balance
6. Decreased ADH levels
7. Large urine outputs
8. Increased Na in urine

78.  Treatment :
1. Sodium replacement
2. Fluid replacement
3. Monitor and treat the same as a combination of
the other two dysfunctions
4. Pt may show signs and symptoms of both
disorders which make it difficult to treat.

79. Parameter DI SIADH CSW
Serum Na high Low low
Urine Large and
diluted
Small and
concentrated
Large and
normal
osmolarity
Skin dry Pitting odema -
ADH low Too much low
ECF volume Down (dry) Fluid up
(wet)
Normal to
low