Electrolyte imbalances and

their management.
By NABAWANDA SALUWA
FACILITATOR: DR.SSEBULIBA MOSES
Introduction
• Electrolytes are positively and negatively charged ions which are in
solution in all body fluids. Sodium is the principal extracellular cation
and potassium is the main intracellular cation.
• Inside the cell the main anions are proteins and phosphate and in ECF
chloride and bicarbonates are the main anions.
• Sodium determine the serum osmolality since they are the main
cations in the ECF space.
Introduction
• The kidney controls the homeostasis of a number of serum
electrolytes i.e. sodium, potassium, calcium and phosphate and also
Acid base balance via the RAAS
• It also produces erythropoietin, renin and activation of vitamin D.
• Also levels of electrolytes are determined by some hormones like
insulin for potassium, parathyroid hormone for calcium and
phosphate.
Renin-angiotensin aldosterone system
SODIUM DISORDERS
Hyponatremia is defined as serum sodium levels <135mmol/L. this is
the most common electrolyte abnormality encountered in the
hospitalized patients. And patient may manifest as anorexia, nausea,
vomiting, confusion, lethargy, seizures and coma
This can be divided into;
• Hypovolemic hyponatremia: decrease in both Na and water
• Hypervolemic hyponatremia: normal Na and increase in total water
• Normovolemic hyponatremia: increase in Na but greater increase in
water
Hypovolemic hyponatremia

Urine sodium >20 Urine sodium<20

Renal loses Extrarenal loses
• Diuretic excess • Vomiting
• Primary adrenal insufficiency • Diarrhea
• Ketonuria • Burns
• Osmotic diuresis • Pancreatitis
• Cerebral salt wasting syndrome • Trauma
• hypoaldosteronism
Hypovolemic hyponatremia
• Hypovolemia causes profound neurohumoral activation including
systems that preserve effective circulating volume i.e. renin-
angiotensin-aldosterone axis, the sympathetic nervous system and
AVP.
• The circulating AVP serves to increase the retention of ingested free
water leading to hyponatremia
Treatment
• Use isotonic crystalloid i.e. 0.9% normal saline
Hypervolemic hyponatremia

Urine sodium >20 Urine sodium<20

• Acute or chronic renal failure • Nephrotic syndrome
• Cirrhosis
• Cardiac failure
Hypervolemic hyponatremia
• These disorders are often associated with mild to moderate degrees of hyponatremia.
• Here there is effective circulating volume is decreased due to specific etiologic factors
i.e. cardiac dysfunction, peripheral vasodilation and hypoalbuminemia in nephrotic
syndrome.
Treatment
• Treatment of the underlying disorder
• Sodium restriction
• Diuretic therapy
• Water restriction
• Vasopressin antagonist e.g. tolvaptan and conivaptan are effective in normalizing
hyponatremia associated with both cirrhosis and CHF
Normovolemic hyponatremia
• Inappropriate ADH secretion (SIADH)
• Hypothyroidism
• Secondary adrenal insufficiency
• Stress
• Glucocorticoid deficiency
Treatment of normovolemic hyponatremia
• Treatment of underlying disease
• Water restriction to <1l/day
• Vasopressin antagonist in SIADH
• Coadministration of loop diuretics to inhibit the countercurrent
mechanism and reduce urinary concentration, combined with oral salt
tablets to correct diuretic induced salt loss and attendant
hypovolemia.
Acute symptomatic hyponatremia
• This is a medical emergency due to sudden drop in serum sodium which
can overwhelm the capacity of the brain to regulate cell volume, leading
to cerebral edema, seizures and death.
• Many of these patients hyponatremia is from iatrogenic cause i.e.
hypotonic fluids, postoperative period, thiazide therapy, colonoscopy
Presentation
• Nausea and vomiting
• Respiratory failure causing hypercapnia due to CNS depression or
normocapnic due to neurogenic
• Hypoxia due to hyponatremic encephalopathy
Hypernatremia
• This is defined as serum sodium >150meq/L and usually present with
reduced brain function, dizziness, confusion, weakness, coma. And
usually due to water reduction( impaired thirst and fluid loss) but not
necessary the sodium increase
Acute symptomatic hypernatremia: occurs within 24hrs and should be
corrected rapidly
Chronic hypernatremia: >48hrs should be corrected more slowly due to
the risk of cerebral edema during treatment
Treatment
Give hypotonic saline
Causes of hypernatremia
Potassium regulation
Potassium disorders
• Potassium is mainly an intracellular electrolyte
Hypokalemia is defined as serum potassium <3.5mmol/L.
Factors affecting distribution of potassium
• Extracellular alkalosis can cause potassium influx
• Insulin
• Catecholamines
• Aldosterone
Causes of hypokalemia
Management of hypokalemia
Presentation include; ventricular ectopics, muscular weakness, typical
ECG changes affecting the T waves, functional paralytic ileus, long
standing hypokalemia damages renal tubular structures and interferes
with the tubular response to ADH
Management
• Management of the underlying cause
• Withdrawal of the offending medication e.g. loop or thiazide diuretics
• Oral KCL Supplementation
• Iv fluids with high potassium intake
Hyperkalemia
• This is defined as the increased serum potassium levels.
• The first priority in the management of hyperkalemia is to assess the
need for emergency treatment (ECG changes and/or potassium
greater than 6mmol.
• This should be followed by comprehensive workup to determine the
cause of hyperkalemia.
• History and physical examination should focus on medications (e.g.
ACE inhibitors, NSAIDs), diet supplements, risk factors for acute
kidney failure, reduction in urine output, blood pressure and volume
status.
ECG for hyperkalemia
Causes of hyperkalemia
Pseudo hyperkalemia Drugs i.e. ACEI, potassium sparing
• Cellular efflux: thrombocytosis, diuretics., ARBs .
erythrocytosis, leukocytosis, hemolysis
Primary adrenal insufficiency
• Hereditary defects in RBC membrane
transport Advanced renal insufficiency
Intra to extracellular shift Diabetes, diabetic nephropathy
• Acidosis
Decreased distal delivery
• Hyperosmolality i.e. hypertonic
dextrose, mannitol • Congestive heart failure
• Tumor lysis syndrome • Volume depletion
• succinylcholine
Investigations for hyperkalemia
• ECG
• Urine potassium, sodium and osmolality
• Glucose levels
• Digoxin
• Arterial blood gas
• Serum cortisol and aldosterone levels
• Serum uric acid and phosphorus levels
• RFT
Management of hyperkalemia
• Hyperkalemia causes altered cardiac conduction with the risk of
bradycardic arrest.
• Urgent management of hyperkalemia constitutes a 12-lead ECG,
admission to the hospital, continuous cardiac monitoring and
immediate treatment.
Treatment of hyperkalemia is divided into 3 categories;
Antagonism of the cardiac effects of hyperkalemia
Rapid reduction in potassium by redistribution into cells
Removal of potassium from the body
management
Patients with moderate elevation in potassium level and no ECG abnormalities
treat as follows
Increase k+ excretion using a cation exchange resin or diuretics
Correct the source of excess k+
Patients with severe hyperkalemia treat as follows
IV calcium to ameliorate cardiac toxicity if present
Identify and remove sources of potassium intake
IV glucose and insulin infusion to enhance potassium uptake by cells
Correct severe metabolic acidosis with sodium bicarbonate
Emergency dialysis for patients with potentially lethal hyperkalemia
Management
Potassium binders
Cation exchange resins i.e. sodium polystyrene sulfonate, sodium
zirconium cyclosilicate
Aldosterone
Beta adrenergic agents i.e. salbutamol
Calcium metabolism
Hypercalcemia
• This is defined as increase in serum calcium levels.
• CNS and GI symptoms can occur at levels of serum calcium >
2.9mmol/L (>11.5mg/dl)
• In nephrocalcinosis and impairment of renal function occur when
serum calcium is >3.2mmol/L(13mg/dl).
• Severe hypercalcemia is defined as >3.7mmol/L and can be a medical
emergency leading to coma and cardiac arrest.
Calcium metabolism
Causes of hypercalcemia
Parathyroid related Vitamin D intoxication
• Primary hyperparathyroidism • Idiopathic hypercalcemia of
• Lithium therapy infancy
Malignancy related Associated with renal failure
• Solid tumors with humoral • Severe secondary or tertiary
mediation of hypercalcemia i.e. hyperparathyroidism
lung, kidney, SCC
• Aluminum intoxication
• Solid tumors with Mets
• Hematologic malignancies i.e. MM,
lymphoma, leukemia
Clinical features of hypercalcemia
• Hypercalciuria
• Polyuria
• Calcium oxalate stones
• Osteoporosis
• Cardiac arrhythmias
• CNS i.e. lethargy, confusion, irritability and depression
• GIT i.e. anorexia, abdominal pain, nausea, vomiting and constipation
Diagnosis
• High levels if PTH
• Hypercalciuria helps to distinguish this disorder from FHH in which PTH levels are usually in the
normal range and urine calcium level is low.
• Calcium levels
Treatment of hypercalcemia
Hydration with IV fluids normal saline
Treat the cause
Patients with severe primary hyperparathyroidism, surgical parathyroidectomy
Dialysis
Glucocorticoids
Calcitonin
bisphosphonates
Hypocalcemia
• Normally half of calcium is bound to protein esp to albumin.
• Binding is PH dependent and is decreased in acidosis because of
amino acid side chain on albumin become more positively charged.
• Binding is increased if an alkalosis is present. Hence the percentage of
unbound calcium is increased in acidosis and decreases in alkalosis.
• Hence if albumin is decreased total serum calcium is low because the
bound fraction is decreased.
• Hemostatic mechanism for regulating plasma calcium respond to the
unbound fraction not to total calcium.
Clinical features
• Tetany
• Papilledema
• Prolongation of the ECG QT interval
• Epilepsy
• Rickets
Calicum and albumin
Causes of hypocalcemia
• Critically ill patients with burns, sepsis • Absent PTH
and acute renal failure
• Hypoparathyroidism
• Drugs i.e. protamine and heparin
• Hypoalbuminemia • Hypomagnesemia
• Overwhelmed PTH • Ineffective PTH
• Severe, acute hyperphosphatemia in • Chronic renal failure
TLS
• Acute renal failure
• Vitamin D deficiency
• Rhabdomyolysis • Intestinal malabsorption
• Hungry bone syndrome following • pseudohypoparathyroidism
parathroidectomy
Management of hypocalcemia
• Symptomatic hypocalcemia
• Control the tetany, alkalosis
• IV calcium gluconate 1-2g over 10-20min followed by infusion of
10ampoules of 10% calcium gluconate diluted in 1L D5W it often
relieves the spams
• Chronic hypocalcemia requires high oral calcium intake
• Vitamin D supplementation
• Hypoparathyroidism requires administration of calcium and calcitriol
• Restoration of magnesium stores
Hypophosphatemia
• This occurs when phosphate levels< 0.3mmo/L.
• Mild hypophosphatemia is not usually associated with clinical
symptoms
• In severe cases patients may have muscle weakness, numbness,
paresthesia and confusion, respiratory insufficiency.
• Rhabdomyolysis may develop during rapidly progressive
hypophosphatemia
Causes of hypophosphatemia
Decreased intestinal absorption Shift from ECF to ICF
• Vitamin D deficiency • Administration of insulin
• Phosphorus binding antacids Syndromes of severe primary
• Malabsorption renal phosphate wasting
Urinary losses • X-linked hypophosphatemic
rickets
• Hyperparathyroidism
• Autosomal dominant
• Alcoholism hypophosphatemic rickets
• Oncogenic osteomalacia
Management of hypophosphatemia
Mild
• Increase milk intake
• Carbonated beverages
• Neutra-phosphorus or potassium phosphorus
Severe
• IV phosphate 0.2-0.8mmol/kg
• Ensure to measure serum calcium and phosphate levels during therapy
• Hypocalcemia should be corrected first and the dose reduced 50% in
hypercalcemia
Hyperphosphatemia
• In adults its defined as a level >1.8mmol/L(>5.5mg/dL)
Causes of hyperphosphatemia
 Acute and chronic renal failure
 Hypoparathyroidism
 Vitamin D intoxication
 Acidosis
 Rhabdomyolysis
 Hemolysis
Continuation
• Consequences of severe hyperphosphatemia are hypocalcemia and
calcium phosphate deposition in tissues
• Depending on the location of tissue calcifications serious chronic or
acute complications .
Treatment
 Treat the underlying causes
 Limiting dietary phosphorus intake and absorption
 Oral aluminum phosphate binders
 Hemodialysis in severe cases
Hypermagnesemia
• This is rare but can be seen in renal failure when patients are taking
magnesium containing antacids, laxatives, enemas or infusions or in
acute rhabdomyolysis
• Clinical features include; loss of deep tendon reflexes, but
hypocalcemia, hypotension, paralysis of respiratory muscles,
complete heart block and cardiac arrest
Treatment
• Stop the offending drugs
• In life threatening complications, 100-200mg of IV calcium over 1-2hr
Hypomagnesemia
• Decrease in magnesium levels <0.7mmo/l
• Clinical features include muscle weakness, prolonged PR and QT
intervals and cardiac arrhythmias
• Causes include; derangement in renal or intestinal, hereditary causes
include both disorders of absorption and those of renal loss (e.g.
barter’s and gitelman syndrome), drugs, vomiting and diarrhea.
Treatment
• Magnesium supplements.