SEMINAR 2

ELECTROLYTE IMBALANCE
 LEARNING OUTCOMES
• Describe the aetiology, clinical features, complications, investigations
and management of
 Hyponatremia
 Hypernatremia
 Hypokalaemia
 Hyperkalaemia
 Hypercalcaemia
 HYPONATREMIA
• Hyponatraemia = serum Na < 135 mmol/L
• Types of hyponatremia include pseudohyponatremia, high osmolality
hyponatremia and true hyponatremia.
Pseudo hyponatremia
• Pseudohyponatremia is a falsely low sodium reading caused by the presence
of other osmolar particles in the serum
• Serum osmolality is normal and no shifts of water occur
• Seen in severe hypertriglyceridemia and hyperproteinemia (multiple
myeloma)
• Also caused by blood draw or laboratory errors
• Blood draw error occurs when blood sample is drawn near an infusion site
using 5% D 5 W.
High osmolality hyponatremia
• Dilutional hyponatremia caused by hyperglycemia
• Hyponatremia occur due to inward shift of water into the vascular space
through osmosis
True hyponatremia
• Classified as hypovolemic, euvolemic and hypervolemic
1. Hypovolemic hyponatremia
• ↓ total body water and sodium, with a relatively greater ↓ in sodium
Causes include,
• Body fluid losses: Sweating, vomiting, diarrhea.
• Third spacing: Bowel obstruction, burns, pancreatitis, rhabdomyolysis
• Renal causes: Diuretics, mineralocorticoid deficiency, osmotic diuresis,
renal tubular acidosis, salt-wasting nephropathies
2. Hypervolemic hyponatremia:
• ↑ total body sodium with a relatively greater ↑ in total body water
• Seen in Heart failure, Chronic renal failure and Hepatic failure or
cirrhosis (CCF, CKD, CLD)
3. Euvolemic Hyponatremia:
• ↑ total body water with nearly normal total body sodium
• Causes, abnormally high oral water intake (primary polydipsia)
• Result of medically infused fluids (IV dextrose)
• Absorption of sodium-free bladder irrigation fluid after
prostatectomy
• SIADH - endogenous source of vasopressin (either cerebral or
tumour-derived) promotes water retention by the kidney in the
absence of an appropriate physiological stimulus
Causes of SIADH
• Tumours
• Central nervous system disorders: stroke, trauma,
infection, psychosis, porphyria
• Pulmonary disorders: pneumonia, tuberculosis,
obstructive lung disease
• Drugs: anticonvulsants, psychotropics, antidepressants,
cytotoxics, oral hypoglycaemic agents, opiates
• Idiopathic
• Other non-osmotic stimuli that cause release of
vasopressin (pain, stress, nausea)
Clinical features
• Alteration in cerebral function,
manifesting as anorexia, nausea,
vomiting, delirium, lethargy,
seizures and coma
• Seen in rapid hyponatremia when
cerebral cells become swollen and
ischaemic
• When hyponatraemia develops
gradually, cerebral neurons have
time to respond by reducing
intracellular osmolality (may be
asymptomatic)
Clinical correlation
• Asymptomatic hyponatremia with
signs of hyperlipidaemia(xanthoma &
xanthelesma), possibly
pseudohyponatremia
• Hyponatremia with edema, raised JVP,
bibasilar crackles, hepatomegaly,
possibly hypervolemic hyponatremia
due to CCF, CKD OF CLD
• Signs of dehydration (↓ skin turgor,
dry mouth) - hypovolemic
hyponatremia
• Signs of raised ICP (headache, nausea,
vomiting, loss of consciousness) –
patient rapidly developed
hyponatremia
Investigations
Based on renal profile,
• Mild, 130–135 mmol/L
• Moderate, 125–
129 mmol/L
• Severe, < 124 mmol/L
 Management
Factors to consider when correcting hyponatremia
• Rate of development, severity, presence of symptoms and
underlying cause
• Developed rapidly (< 48 hours) with signs of cerebral oedema,
patient requires an infusion of hypertonic (3%) sodium
chloride given as an initial bolus of 150 mL over 20 minutes,
repeated once or twice depending on the observed
neurological response and rise in plasma sodium.
• Developed more slowly (> 48 hours), Rapid correction can be
hazardous (patient may develop central pontine myelinosis)
Management of underlying cause
• Hypovolaemic patients, this involves controlling the source of
sodium loss (e.g. vomiting/diarrhea), and administering intravenous
saline if clinically warranted
• Euvolaemic hyponatraemia generally respond to fluid restriction in
the range of 600–1000 mL/24 hrs
• Manage the cause of SIADH, (e.g. discontinue drugs causing SIADH)
• Vasopressin receptor antagonists tolvaptan may be used.
• Hypervolaemic patients with hyponatraemia need treatment of the
underlying condition (CCF, CKD, CLD) , accompanied by cautious use
of diuretics in conjunction with strict fluid restriction
• Potassium-sparing diuretics – promote sodium retention and reduce
fluid volume.
HYPERNATRAEMIA
LEESHANTI PATCHAIAPPAN
• serum Na is > 145 mmol/L.
 Causes
• Hypovolaemic
• Renal sodium losses:
– Diuretic therapy (especially osmotic diuretic, or loop diuretic during
water restriction)
– Glycosuria (hyperglycaemic hyperosmolar state)
• Gastrointestinal sodium losses:
– Colonic diarrhoea
• Skin sodium loss
– Excessive sweating
• Euvolaemic
– Diabetes insipidus
– Central :failure of the vasopressin system due to pituitary damage
– Nephrogenic : collecting duct cells are unable to respond to
circulating vasopressin
• Hypervolaemic
– Enteral or parenteral feeding
– Intravenous or oral salt administration
– Chronic kidney disease (during water restriction)
 CLINICAL FEATURES
• Symptoms of hypernatraemia are nonspecific.
• Vomiting
• Fever
• Confusion
• Polyuria Diabetes insipidus
• Polydipsia
• Thirst
• Convulsion (severe hypernatraemia)
 COMPLICATIONS
• brain hemorrhage
• subarachnoid or subdural hemorrhage
• due to rupture of bridging veins and dural sinus thrombosis.
• Hypernatremia is associated with a mortality rate as high as 15% to
20%.
 INVESTIGATION
• Serum electrolytes (Na+, K+, Ca2+)
• Glucose level
• Urea & creatinine
• Urine electrolytes (Na+, K+)
• Urine and plasma osmolality
• 24-hour urine volume
• Plasma arginine vasopressin (AVP) level
 MANAGEMENT
• Treat the underlying cause, e.g.
• In ADH deficiency, replace ADH in the form of desmopressin

• Severe hypernatraemia (>170mmol/L)

• 0.9% saline (150mmol/L) should be used initially
• Avoid too rapid a drop in serum sodium concentration ( aim is correction over 48h,
as over-rapid correction may lead to cerebral oedema)
• Less severe hypernatraemia (>150mmol/L)
• 5% glucose or 0.45% saline
• The latter is obviously preferable in hyperosmolar diabetic coma
• Very large volume (5L/day or more) may need to be given in diabetes insipidus
HYPOKALAEMIA
• serum potassium falls below 3.5 mmol/L.
 Causes
• Reduce intake
– Dietary deficiency
– Potassium-free intravenous fluids
• Redistribution into cells
– Alkalosis
– Insulin Caused by flux of K+ into
– Catecholamines cells
– β-adrenergic agonists
– Hypokalaemic periodic paralysis
• Increased urinary excretion
• Activation of mineralocorticoid receptor:
– Conn’s syndrome
– Cushing’s syndrome Associated with hypertension and
– Glucocorticoid excess alkalosis
– Carbenoxelone/liquorice
• Genetic disorders:
– Liddle’s syndrome
– Bartter’s syndrome
– Gitelman’s syndrome
• Renal tubular acidosis
– Type 1 (distal)
– Type 2 (proximal)
• Acetazolamide
• Diuresis:
– Loop diuretics
– Thiazides
– Recovery from acute tubular Increase sodium delivery to distal tubule
– necrosis
– Recovery from renal obstruction
• Increased gastrointestinal loss
• Upper gastrointestinal tract:
– Vomiting Loss of gastric acid
– Nasogastric aspiration Associated with metabolic alkalosis
• Lower gastrointestinal tract:
– Diarrhoea
– Laxative abuse
– Villous adenoma
– Bowel obstruction/fistula
– Ureterosigmoidostomy
 Clinical features
• mild hypokalaemia (plasma K+ 3.0–3.3 mmol/L) are generally asymptomatic
• muscular weakness and associated tiredness
• Ventricular ectopic beats or more serious arrhythmias
• ECG changes
– ST-segment depression
– Appearance of U waves
• Functional bowel obstruction may occur due to paralytic ileus.
• Long-standing hypokalaemia may cause hypokalaemic nephropathy
• interfere with the tubular response to vasopressin (acquired nephrogenic diabetes insipidus)
• resulting in polyuria and polydipsia.
 Investigations
 Measurement of plasma electrolyte
• Serum sodium
– serum Na - suggest that nephrogenic diabetes insipidus has occurred
secondary to hypokalemia.
• Serum bicarbonates
 Measurement of plasma renin
– primary hyperaldosteronism and other forms of mineralocorticoid excess
– raised in other causes of hypokalaemia.
 measurement of urinary potassium
– > 30 mmol/24 hrs
 ECG
 TREATMENT
• Treat the underlying cause
• slow-release potassium chloride tablets
• more acute circumstances intravenous potassium chloride
• alkaline salts of potassium
– potassium bicarbonate
• potassium-sparing diuretics
– amiloride
HYPERKALAEMIA
NURUL MARDHIYYAH MAFAUZY
 CAUSES
• Causes of hyperkalaemia :
Pseudohyperkalaemia
True hyperkalaemia
 CLINICAL FEATURES
Mild hyperkalaemia (plasma K+ 3.0–3.3 mmol/L)
 Generally asymptomatic
 Muscular weakness (reductions in plasma potassium) & tiredness.

 Severe hyperkalaemia (plasma K+ >7.0 mmol/L) is a medical

emergency
 Asymptomatic
 Muscle weakness
 Hypotension, bradycardia and eventual asystole
 COMPLICATIONS
• Cardiac arrest
• Ventricular ectopic beats
• Kussmaul respiration (metabolic acidosis)
• Functional bowel obstruction
• Hypokalaemic nephropathy (long-standing hypokalaemia)
 INVESTIGATION
• Measurement of serum potassium level
• Arterial blood gases (metabolic acidosis)
• Renal function test (Renal impairment)
• ECG (peak T wave, widening QRS complex)
• Blood glucose level (Hyperglycemia)
• In aldosterone deficiency - low plasma sodium concentration
 MANAGEMENT
 Patient with K+ concentration <6.5 mmol/L w/ absence of neuromuscular
symptoms or ECG changes
• Reduction of potassium intake
• Correction of predisposing factors

 Acute/ Severe hyperkalaemia :

• IV calcium gluconate (10 ml of 10% solution) – stabilise cell membrane potential
• Inhaled Beta2 adrenoceptor agonist
• IV glucose (50mL OF 50% solution) & Insulin (5 IU Actrapid) Shift K+ into cells
• IV sodium bicarbonate
• IV furosemide & normal saline
• Ion exchange resin (Resonium) Remove K+ from body
• Dialysis
HYPERCALCAEMIA
CAUSES
 CLINICAL FEATURES
 Mild hypercalcaemia (serum calcium <3 mmol/L) is frequently
asymptomatic

 Severe hypercalcaemia (serum calcium >3 mmol/L) - malignant disease,

hyperparathyroidism, chronic kidney disease or vitamin D therapy
• General - tiredness, malaise, dehydration and depression.
• Renal - renal colic , polyuria or nocturia, haematuria and hypertension
• Bones - bone pain.
• Abdomen - abdominal pain.
• Chondrocalcinosis and ectopic calcification (occasional features)
• Corneal calcification (marker of longstanding hypercalcaemia)
 INVESTIGATION
BIOCHEMISTRY
• Serum PTH – increase ( + hypophosphataemin) in primary
hyperparathyroidism
• If PTH undetectable
 Protein electrophoresis – myeloma
 Serum TSH – hyperparathyroidism
 9 hrs cortisol/ ACTH test – Addison’s disease
 Serum ACE – Sarcoidosis
 Hydrocortisone suppression test – Sarcoidosis, Vit D mediated
hypercalcaemia, Malignancies
• Hyperchloraemic acidosis (seen in mild)
• Renal function – usually normal
• 24-h urinary calcium – exclude familial hypocalciuric hypercalcaemia
• Elevated serum alkaline phosphatase – severe parathyroid disease

IMAGING
• Abdominal X-ray – renal calculi
• DXA bone density scan
• Ultrasound of parathyroid glands
• High resolution CT scan/ MRI
• Radioisotope scanning – detecting adenomas
 MANAGEMENT
Acute severe hypercalcaemia
• Rehydrate – 4-6 L of 0.9% saline of day 1 & 3-4 L for several days.
Monitor central venous pressure for hydration rate
• IV bisphosphonates – treatment of choice for hypercalcaemia of
malignancy/ undiagnosed cause. Pamidronate (60-90mg) IV infusion
in 0.9% saline or glucose over 2-4 hrs. Zoledronate is an alternative
• Predisolone (30-60 mg daily)
• Calcitonin (200 units IV 6 hourly)
• Oral phosphate (sodium cellulose phosphate 5g tds)

Treat the underlying disease