Page 86 - ONLINE PROCEEDING BOOK WSAVA 2017
P. 86

An Urban Experience
Hypokalaemia
Hypokalaemia can occur due to causes listed in table 3. Table 3. Causes of hypokalaemia
Causes of hypokalaemia
Decreased intake
Anorexia
Intracellular translocation
Alkalaemia
Insulin/glucose
Hypothermia
Hypokalaemic periodic paralysis in Burmese cats
Catecholamine release or administration
Refeeding syndrome
Hypomagnesaemia
Increased loss
Gastrointestinal
Urinary
Hyperadrenocorticism, hyperaldosteronism
Drugs (loop diuretics, thiazide diuretics, penicillins)
Chronic liver disease
Clinical signs of hypokalaemia are uncommon, but
can occur if potassium concentration is < 2.5 mmol/L. Potassium is necessary for maintenance of normal resting membrane potential. Therefore, one of the most common clinical sign of hypokalaemia is neuromuscular weakness, including a plantigrade stance, ventral  ection of the neck, wide based stance, stiff hind limbs and hypermetria of the fore limbs. Severe cases can result
in respiratory arrest from neuromuscular weakness. Myocardial cells are also affected, due to a high intracellular/extracellular potassium concentration ratio inducing a state of electrical hyperpolarisation leading
to prolongation of the action potential Thus, atrial and ventricular tachyarrhythmias, atrioventricular dissociation and ventricular  brillation can occur. Classical ECG signs can include peaked P-wave, prolonged PR interval, ST segment depression, decreased T wave amplitude and widening of QRS complex. Due to the change in action potential, hypokalaemia associated arrhythmias can
be resistant to type I antiarrhythmics (e.g. lidocaine). Metabolic consequences of hypokalaemia include glucose intolerance, where there is reduced release of insulin from the pancreas. Severe hypokalaemia can
also inhibit normal renal tubular function. And, metabolic alkalosis can occur due to intra- extracellular exchange of hydrogen ions.
Treatment involves intravenous administration of potassium chloride (KCl) (or potassium phosphate
if concurrent hypophosphataemia is also present). Intravenous KCl should not be administered at a rate greater than 0.5 mmol/kg/hr, due to adverse cardiac effects. Table 4 lists the recommended potassium concentration to be added to a 1L bag of  uids, and the maximum rate it can be administered at. In the rare
circumstance that the hypokalaemia is life threatening, potassium can be delivered at a faster rate with careful ECG monitoring. It’s worth noting that when adding potassium to a bag of  uids, the potassium should be mixed well to prevent large concentrations of potassium at the bottom of the bag. In addition, all  uid bags should be labelled to prevent accidental blousing of potassium containing  uids. Another important point
is that potassium is very hyperosmolar and can cause thrombophlebitis, therefore should not be administered through a peripheral catheter at concentrations greater than 60 mmol/L. If higher concentrations are required,
a long stay (e.g. jugular catheter) should be used; or another alternative is to have two IV catheters so each IV catheter is delivering half the concentration. If the patient can tolerate oral potassium supplementation, oral potassium supplementation can be given at 2 – 44 mmol per dog (depending on size) or 2 – 8 mEq per cat, divided over 24 hours.
Table 4. Potassium (K+) dosing for correction of hypokalaemia
References are available upon request.
Patient K+
K+ supplement per litre of  uids
Maximum rate of delivery (mL/ kg/hr)
<2
80
6
2.1 – 2.5
60
8
2.6 – 3
40
12
3.1 – 3.5
30
18
3.6 - 5
20
25
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42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS


































































































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