ELECTROLYTE DISTURBANCES

SYAFRI K.ARIF

Dept.of Anesthesiology ,Intensive

Care & Pain Management
Faculty of Medicine Hasanuddin
University
®
 Objectives
 Reviewcauses and clinical manifestations of
severe electrolyte disturbances
 Outlineemergent management of electrolyte
disturbances
 Recognizeacute adrenal insufficiency and
appropriate treatment
 Describe
management of severe hyperglycemic
syndromes
Principles of Electrolyte Disturbances

 Implies an underlying disease process

 Treat the electrolyte change, but seek the cause
 Clinical manifestations usually not specific to a
particular electrolyte change, e.g., seizures,
arrhythmias
Principles of Electrolyte Disturbances

 Clinical
manifestations determine urgency of
treatment, not laboratory values
 Speed and magnitude of correction
dependent
on clinical circumstances
 Frequent reassessment of electrolytes
required
Hyponatremia
 A low serum Na does not tell us whether total
extracellular Na is increased, decreased,or normal
 It only tells us that there is excess water relative to
Na
 Most cases of hyponatremia are caused by
impaired water excretion in the presence of
continued water intake.
Hyponatremia
 Impaired water excretion
 impaired GFR (renal failure)
 ECFV depletion
 edematous states
 thiazide diuretics
 syndrome of inappropriate ADH (SIADH)
 endocrine (hypothyroid/adrenal insufficiency
 markedly decreased solute intake combined with high water
intake
Hyponatremia
 History
 Causes of ECFV depletion (vomiting, diarrhea)
 ?edematous states
 Medications
 Other underlying systemic diseases (SIADH)
 CNS diseases, pulmonary diseases, malignancy, drugs
Hyponatremia
 Physical exam
 Signs of ECFV depletion (skin turgor, mucus
membranes, orthostatic vitals)
 Signs of ECFV overload (JVD, rales, pleural
effusion, ascites, edema)
 Physical signs of adrenal insufficiency or
hypothyroidism
Hyponatremia
 Laboratory studies
 Serum osmolality (a low level excludes
pseudohyponatremia and hypertonicity)
 Spot urine Na
Hyponatremia
 Treatment
 Carefully correct the Na toward normal and correct any
coexisting ECFV alterations
 Symptoms dictate the urgency and the rapidity of
correction
 Acute decrease in osmolality leads to a shift of water
from the ECF to ICF compartments, leading to cerebral
edema, lethargy, stupor, coma, seizures, death
Hyponatremia
 Acute, symptomatic hyponatremia
 Correct no faster than 1 mEq/L per hour for the first
6-8 mEq/L
 No more than 10-12 mEq/L in first 24 hours
 5% saline is almost never needed
 Calculate the Na deficit
 Na mEq = ([Na desired] - [Na measured]) X TBW
 TBW = .5 or .6 X weight in KG
Hypernatremia
 Results from a deficit of water
 Loss of water
 Failure to adequately replace the water loss
 Look thoroughly for alterations in neurological status that
are causing inadequate water intake
 Water loss is extra-renal or renal
 Rarely iatrogenic (administration of hypertonic saline
or NaHCO3)
Hypernatremia
 Extra-renal water loss
 fever, profuse sweating, hyperventilation, diarrhea
 Renal water loss (key is to look for polyuria)
 Key to evaluating renal water loss is to measure
urine osmolality
Hypernatremia
 Osmotic diuresis (urine Osm > 300)
 the excretion of the osmotic load obligates a certain water
loss
 poorly controlled diabetes, mannitol administration, protein
catabolism with urea
 Diabetes Insipidus (urine Osm < 150)
 inability
of the kidney to concentrate urine due to absence of
ADH (central) or unresponsiveness to ADH (nephrogenic)
Hypernatremia
 Diagnosis
 Reason for water loss or sodium gain?
 Reason for inadequate water intake?
 Is polyuria present? (urine volume > 3L/24hrs)
 What is the spot urine Osm?
 Response to vasopressin?
Hypernatremia
 Treatment
 Severe ECFV depletion is the priority and should be
corrected with NS first. Subsequent fluid
replacement can be hypotonic
 Major complication of overly rapid correction is
cerebral edema
 Safe rate is no more than .5- 1 mEq/L per hour
 Should take 36-72 to hours to completely correct
Hypernatremia
 Treatment
 Calculate the water deficit
 H2O deficit = TBW X ([Na meas]- [Na des])/[Na des]
 Important to take into account ongoing losses
 insensible losses .5 - 1 liter/24 hours
 with fever, these losses increase by 60-80ml/24 hrs for

each degree Farenheit

Hypokalemia
 Neuromuscular manifestations (weakness,
fatigue, paralysis, respiratory dysfunction)
 GI (constipation, ileus)
 Nephrogenic DI
 ECG changes (U waves, flattened T waves)
 Arrhythmias
Hypokalemia
 Spurious hypokalemia
 Marked leukocytosis
 A dose of insulin right before the blood draw
 Redistribution hypokalemia
 Alkalosis(K decreases .3 for every .1 increase in pH)
 Increased Beta2 adrenergic activity
 Theophylline toxicity
 Familial
Hypokalemia
 Extrarenal depletion
 diarrhea
 laxative abuse
 sweat losses
 fasting or inadequate intake
Hypokalemia
 Renal potassium depletion
 urine potassium > 20 mEq/24 hrs
 spot urine with > 20 mEq K/gram creatinine
 classified whether they occur with a metabolic
alkalosis
 vomiting/NG suction
 diuretic tx

 Mineralocorticoid excess syndromes

Hypokalemia
 Renal losses
 metabolic acidosis
 RTA Type I and II
 DKA

 Carbonic anhydrase inhibitor therapy

 Ureterosigmoidostomy

 No acid-base disorder
 Mg deficiency
 Drugs
Hyperkalemia
 Severe hyperkalemia is a medical emergency
 Neuromuscular signs (weakness, ascending
paralysis, respiratory failure)
 Progressive ECG changes (peaked T waves,
flattened P waves, prolonged PR interval,
idioventricular rhythm and widened QRS
complex, “sine wave” pattern, V fib)
Hyperkalemia

 Etiology – renal failure,

transcellular shifts, cell
death, drugs,
pseudohyperkalemia
 Manifestations –
cardiac, neuromuscular
Hyperkalemia
 Impaired potassium secretion
 Aldosterone deficiency
 adrenal failure
 Syndrome of hyporeninemic hypoaldosteronism (SHH)

 tubular unresponsiveness

 Renal failure
 GFR < 10 -20% of normal
Hyperkalemia
 Treatment
 Stop potassium!
 Get and ECG
 Hyperkalemia with ECG changes is a medical
emergency
Hyperkalemia
 Treatment
 Firstphase is emergency treatment to counteract the
effects of hyperkalemia
 IV Calcium
 Temporizing treatment to drive the potassium into the cells
 glucose plus insulin
 Beta2 agonist

 NaHCO3
Hyperkalemia
 Treatment
 Therapy directed at actual removal of potassium
from the body
 sodium polystyrene sulfonate (Kayexalate)
 dialysis

 Determine and correct the underlying cause

 Pediatric Considerations –Potassium
 Replace at maximum iv rate <1.0–
mmol/kg/hr; monitor ECG
 Hyperkalemia
 ECG abnormality: calcium
gluconate or chloride
 Shift: NaHCO33, glucose + insulin,
inhaled -agonists
 Removal: diuretic, sodium
polystyrene sulfonate, dialysis
MET 29 ®
 Pediatric Considerations – Sodium
 Hyponatremia – seizures:
titrate 3% NaCl; usual dose
1.5-2.5 mmol/kg
 Hypernatremia – calculate H22O
deficit as 4 mL/kg for each 1
mmol/L serum Na >145
mmol/L
 Decrease serum Na no faster
than 0.5 mmol/L/hr
MET 30 ®
Other Electrolyte Deficits
Ca, PO4, Mg
 May produce serious but nonspecific cardiac,
neuromuscular, respiratory, and other effects
 All are primarily intracellular ions, so deficits
difficult to estimate
 Titrate replacement against clinical findings
Other Electrolyte Disorders

 Hypocalcemia
Calcium chloride or gluconate
Bolus + continuous infusion
 Hypercalcemia
Rehydration with normal saline
Loop diuretics
Other Electrolyte Disorders
 Hypophosphatemia

Replacement iv for level < 1 mg/dL (0.32
mmol/L)
 Hypomagnesemia

Emergent administration over
5–10 mins
Less urgent administration over
10–60 mins
 Please complete reading of
metabolic and electrolyte
disturbances covered
in the FCCS textbook.

MET 34 ®
Key Points
Important Concepts
 Concentrations
 Compartments
 Contents
 Volumes
 Rates of gain & loss

All five concepts are interconnected!

In the main the laboratory measures concentrations.

The other factors are deduced
Concepts
ECF
Plasma + Interstitial
14L

Intake Excretion
ICF
28L

Normally the system is maintained in equilibrium

Changing any factor causes a new steady state to be reached
Decreasing the volume -4L
ECF
Plasma + Interstitial
10L

Intake Excretion
ICF
26L

This will raise the concentration of any solute

Increasing the excretion of a solute
ECF
Plasma + Interstitial
14L

Intake Excretion
ICF
28L

This will decrease the solute concentration

Body Fluid Distribution
Water [Na] [K]
(L) (mmol/L) (mmol/L)
ECF
Vascular 3 140 5
Interstitial 16 140 5
ICF
Intracellular 23 10 150

TOTAL 42
Loss of 2L of isotonic fluid,
e.g. blood, fistula fluid
ECF ECF
14L 12L
- 2L of isotonic fluid

ICF ICF
28L 28L
Note :
Loss is from ECF
No change in [Na]
No fluid redistribution
 Loss of 3L of hypotonic fluid,
e.g. insensible loss
- 3L of hypotonic fluid
ECF
ECF ECF
14L
11L 13L

ICF ICF ICF

28L 28L 26L

Note :
Greater loss from ICF than ECF
Small increase in [Na]
Fluid redistribution between ECF & ICF
 Gain of 2L of isotonic fluid,
e.g. saline drip
ECF ECF
14L 16L
+ 2L of isotonic fluid

ICF ICF
28L 28L
Note :
Gain is to ECF
No change in [Na]
No fluid redistribution
 Gain of 3L of hypotonic fluid,
e.g. water, dextrose
+ 3L of hypotonic fluid

ECF ECF
ECF
14L 17L
15L

ICF ICF
ICF
28L 30L
28L

Note :
Greater gain to ICF than ECF
Small decrease in [Na]
Fluid redistribution between ECF & ICF
Summary
 Water & electrolyte metabolism central to much acute clinical care
 Multitude of causes of disturbances & many important effects
 Most clinical problems can be solved using a common sense
approach to the concepts of
 volumes
 compartments
 contents
 concentrations
 input /output