Module 3 Electrolytes Flashcards
List the main serum electrolytes which need to be monitored and clinically managed
Na. K, Cl, Ca, Phos
Recall the common causes of derangements in main electrolytes
SODIUM
Common causes of Hypernatraemia;
diuresis (frusemide, steroids, diabetes mellitus), post obstructive diueresis (low urine sg), v+/d+ (high urine sg), acute or chronic renal failure, burns, pancreatitis, diabetes insipidus, panting, exercise, reduced water intake, primary hyperaldosteronism, excessive i/v fluids containing sodium, sodium bicarb therapy, sodium phosphate enemas, high salt food intake.
Common causes of hyponatraemia;
hypoadrenocorticism, excessive free water drinking, whipworm,
v+/d+, renal failure, overhydration with i/v fluids, heart failure, effusions,
artificial lab low sodium reading due to hyperlipidaemia, hyperproteinaemia or hyperglycaemia.
POTASSIUM
Causes of Hyperkalaemia;
obstructive/ruptured uropathy, renal failure, hypoadrenocorticism, crush injury, metabolic acidosis, ACE inhibitor, trimeth sulpha, spironolactone.
Lab artefact ; haemolysed sample, very high white cell count or thrombocytosis.
Causes of Hypokalaemia;
d+/v+. diuresis, renal failure, chronic anorexia, Burmese polymyopathy, metabolic alkalosis,
CHLORIDE;
Causes of hyperchloraemia;
Hypoalbuminaemia, renal tubular acidosis, chronic respiratory alkalosis, ketoacidosis, iatrogenic from i/v fluids or i/v nutrition.
Lab artefact; Potassium bromide, bromide.
Causes of hypochloraemia;
vomitting or upper gi obstruction or stasis, compensation for chronic respiratory acidosis, diuretics (frusemide or thiazide), corticosteroids or hyperadrenocorticism.
Lab artefact: marked lipaemia or hyperproteinaemia.
CALCIUM;
Causes of hypercalcaemia;
Neoplasia, hyperparathyroidism, hyperalbuminaemia (eg dehydration), bone dz, hypoA, vitamine D toxicity (eg older rodenticides), idiopathic hypercalcaemia of cats, lab error.
Causes of hypocalcaemia:
hypoalbuminaemia, alkalosis, milk fever, hyperphosphataemia, hypoparathyroidism, chronic renal failure, acute pancreatitis, phosphate retention enema, oxalate toxicity, ethylene glycol, diet, vitamin d toxicity.
PHOSPHATE
Causes of hyperphosphataemia;
acute/chronic renal failure, uroabdomen/urethral obstruction, hypoparathyroidism, hyperthyroidism, tumour lysis, tissue trauma, metabolic acidosis, phosphate enemas, vitamin D toxicity, iatrogenic via i/v phosphate, youngsters, lab error (lipaemia, hyperproteinaemia).
Causes of hypophosphataemia;
insulin, i/v dextrose, alkalosis (met or resp), refeeding syndrome (overfeeding as compensation for previous starvation), hypothermia, hyperparathyroidism, renal tubule disorders, eclampsia, phosphate binders, vitamin D deficiency, diet, malabsorbtion, lab error.
Describe the common clinicopathological changes seen with common electrolyte derangements
HYPERNATRAEMIA;
Acute or chronic. Acute causes cell shrinkage (esp brain) and cerebral haemorrhage.
Chronic (24-48 hours) causes the formation of idiogenic osmoles. (these are intracellular molecules which are a semi-protective mechanism. Basically means the cell can be more concentrated with these molecules, without ill effect. It is possible that these are the reason that it is dangerous to recorrect states such as hypernatraemia too rapidly. Rapid rehydration of a hypernatraemic patient causes rapid decrease in sodium, therefore water into cells and cells swell, causing cerebral oedema.
Clinical signs: weakness, lethargy, ataxia, seizures, coma.
HYPONATRAEMIA;
brain swelling, neuro signs (lethargy, seizures, coma).
CHLORIDE
linked with sodium balance and oppositely with bicarb. May be increased with hyperosmolality or metabolic acidosis. May be decreased in hypoosmolarity or metabolic alkalosis (clini signs include muscle twitching which is usually ascribed to the accompanying reduced calcium).
POTASSIUM
Hyperkalaemia clinical signs: weakness, collapse, flaccid paralysis, bradycardia, arrythmia (loss of p wave, tall t wave, increased Q-R interval).
Hypokalaemia clinical signs: weakness, lethargy, ventroflexion, crouched gait, muscle cramps, anorexia, v+, pu/pd.
CALCIUM
Hypercalcaemia: weakness, pu/pd, v+/d+/ twitching, constipation,
seizures.
Hypocalcaemia: muscle tremors, fasciculation seizures, increased temp.
PHOSPHATE
Mild hypophosphataemia: weakness, tremors, muscle pain, nausea, ileus.
Severe hypophosphataemia: haemolysis, rhabdomyolysis, seizures, coma, resp failure.
Hyperphosphataemia (ca may be reduced or elevated); weakness, seizure, renal failure, tissue mineralisation, dysrhythmia.
List the appropriate management and treatment for common electrolyte disturbances
Common electrolyte disturbances:
1. Hypocalcaemia of lactating bitch:
i/v calcium gluconate 10% 0.5-1ml/kg slow i/v 15 min to effect. Monitor heart. Also use i/v valium. Wean pups. Supplement bitch with oral calcium. Note early weaning increases risk of mastitis. Subc calcium NOT recommended as risk of calcinosis cutis.
Note that correcting metabolic acidosis may turn slight hypocalcaemia into overt. If treating hypocalcaemia due to hypoparathyroidism, vitamin D is also required.
2. Feline idiopathic hypercalcaemia:
note that this is the most cause of hypercalcaemia in cats. Clinical signs of hypercalcaemia tend to be much more severe however with acute causes such as vitamin D toxicity.
Treat with 0.9% normal saline if indicated. Once rehydrated, judicious use of diuretics if indicated depending on cause and patient type. Corticosteroids used for cats with idiopathic hypercalcaemia BUT only after definitive dx. If in life threatening state, as well as fluids, also adding bicarb (1mEq/kg or 1ml/kg of an 8.4% solution) slowly i/v over 20min. Ideally this is only done if also has profound metabolic acidosis.
3. Diabetic ketoacidosis;
severe ones may require potassium, and sometimes also phosphate. The need for these is likely greater if on higher rates of cri insulin.
Potassium SHOULD be administered at <0.5mEq/kg/hr i/v. (occasionally higher rate for super super severe….)
4.Urinary obstruction hyperkalaemia;
If mild (serum potassium 5.5-6.5mmol/L) do isotonic crystalloid. If severe hyperkalaemia, cardiotoxic effects or severe metabolic acidosis, do i/v crystalloid to restore volume deficit, plus 10% calcium gluconate 0.5-1.5ml/kg slow i/v 10min (protects heart within 10 min but does not alter hyperkalaemia so also then do insulin+dextrose or just dextrose). Also, calcium gluconate causes nausea, therefore also use cerenia. Insulin is 0.25-0.5 IU/KG SHORT ACTING I/V PLUS 4ml of 50% dextrose per unit of insulin i/v or 40ml of 5% dextrose per unit of insulin THEN CRI of 1.25-2.5% glucose at maintenance rates for 6-8 hours.
5. Hypoadrenocorticism-may have hyperkalaemia-treat as above if appropriate. Consider basal cortisol (normal can rule out addisons but if low, would still later need acth stim test).
6. Chronic kidney failure
7. Acute kidney failure
Discuss hypernatraemia and hyponatraemia in terms of volume status
sodium is the biggest contributor to osmolarity of the extra cellular fluid. It is important not to think of sodium level and fluid volume levels as always being in sync. There may be hypernatraemia with hypo/normo/hypervolaemia or hyponatraemia with hypo/normo/hypervolaemia. Sodium levels are influenced by dietary intake, adh release and drinking of water.
Recall the specific calculations used in the management and treatment of sodium disorders
HYPERVOLAEMIC HYPERNATRAEMIA;
eg caused by iatrogenic fluids, salty food, renal failure, conn’s syndrome.
clin signs distended jugulars, pulmonary oedema,
Tx; part a) 5% dextrose for any fluid deficits
part b) loop diuretics to reduce sodium reabsorbtion eg furosemide 2mg/kg i/v
Serum sodium changes can be more rapid if salt intake eg was very rapid but if hypernatraemia occurred more chronically, aim to change sodium by <0.5mmol/L per hour.Otherwise will cause brain issues.
NORMOVOLAEMIC HYPERNATRAEMIA;
Free water loss without dehydration, eg from diabetes insipidus, hyposipidus.
Tx: part a)ideally oral fluid replacement but not all patients will drink
part b) calculate free water deficit;
FreeWaterDeficit=(([current Na])/([desired Na])-1)) x(0.6xbodyweight)
Then NumberofHours to reduce sodium by 0.5mmol/hr=
([current Na]-[desired Na])/0.5
Then FreeWaterDeficit/NumberofHours=ml of 5%dextrose per hour required.
OR can do 4ml/kg/hour of 5%dextrose.
part c) use another isotonic crystalloid to deliver any other ongoing fluid losses
part d) check electrolytes 4 hourly.
part e) if cerebral signs occur, use mannitol 0.5-1.5g/kg i/v slow 20min OR hypertonic 7% saline at 1-2ml/kg i/v 20min.
HYPOVOLAEMIC HYPERNATRAEMIA
renal or gi loss. dehydrated.
Tx; crystalloid solution supplemented with hypertonic saline of 7%
VolumeofHypertonicSalinetoaddto1litreFluidBag=
([currentNa]-[desiredNa])x1000 /
([desiredNa]-[hypertonicNa]).
If after a period, hypernatraemia not improving, switch to 5%dextrose as above
Note that once volume deficits have improved, the kidneys should start helping to shed some of the hypernatraemia.
HYPONATRAEMIA
Again, rate of increasing serum [Na] should not exceed 0.5mEqmol/hour ( note for Na 1mEqmol=1mmol/L)
HYPOVOLAEMIC HYPONATRAEMIA
There is dehydration and low sodium, usually from Addisons. ie dehydration has released ADH which has resulted in increased thirst and water resorbtion but reduced aldosterone (eg addisons) has meant there is very little sodium retention.
Tx;
part a) volume resuscitation with a fluid which has a [Na] within 5-10mEq/L of the patient’s [Na]. Use a mix of isotonic crystalloids and 5%dextrose in water to make the i/v solution.
part b) if sodium concentration does not rise, do maintenance fluids with added hypertonic saline;
VolumehypertonicsalinetobeAdded=
([currentfluidNa]-[desiredivFluidNa]) x 1000/
([desiredivNa]-[supplementalivNa])
HYPERVOLAEMIC HYPONATRAEMIA;
Retention of free water eg oedema/ascites/pleural effusion.
Treat withWater restriction treatment for adh inappropriate secretion or primary polydipsia 9BOTH ARE VERY RARE)
In congestive heart failure, the body interprets low cardiac output as reduced circulating volume, thus releases renin angiotensin, leading to release of ADH and aldosterone leading to increased thirst and ultimately increased free water.
In either advanced cirrhosis or nephrotic syndrome, significant reduction in albumin can lead in increased fluid in interstitium, reducing effective circulating volume and again triggering renin angiotensin, ADH and aldosterone.
Tx is to manage underlying disease and is not usually managed with fluids.
