Page 175 - Basic Monitoring in Canine and Feline Emergency Patients

Table 8.5. Continued.

VetBooks.ir Electrolyte Approach when hyper- Approach when hypo-
Typically when iCa <0.8–1.0 mmol/L
Typically when iCa >1.4 mmol/L
Calcium
Techniques to lower calcium levels while
2. If significant clinical signs (e.g. tetany/seizures/car-
treating the underlying cause: 1. Treat the underlying cause
diac arrhythmias):
1. Administer 0.9% saline fluid (Na in fluid ● Administer calcium (typically in the form of 10%
induces calciuresis in the renal tubules) calcium gluconate) IV slowly (over 5-10 min) or SQ
2. Furosemide (induces renal calciuresis) ● A continuous IV infusion of calcium gluconate may
3. Glucocorticoids (various mechanisms) be needed
4. Calcitonin (reduces osteoclast formation/ ● Start oral vitamin D therapy if the cause of
activity) hypocalcemia will be persistent
5. Bisphosphonates (e.g. pamidronate; ● Start oral calcium carbonate therapy chronically,
decrease osteoclast function/activity)
usually in concert with oral vitamin D therapy
3. If minimal to no clinical signs:
● Consider starting oral vitamin D and oral calcium
therapy without IV or SQ calcium gluconate
● It may take a long period of time to normalize calcium
unless the underlying disorder is rapidly corrected
Phosphorus Typically when [ PO ]> 7.0 mg/dL Typically when [ PO ] <1.5 mg/dL
3-
3-
4
4
In most cases, no specific therapy is required 1. Treat the underlying disease
to reduce phosphorus concentrations 2. Supplement phosphorus intake intravenously with
emergently phosphorus solution (often potassium phosphate
1. Treat the underlying disease solutions)
2. Administer fluid therapy to increase the 3. Recheck serum phosphorus levels every 6–12 hours
glomerular filtration rate and filter phosphorus 4. Monitor hematocrit tubing for signs of hemolysis/
in the kidney decreasing PCV
3. Administer oral phosphate binders (e.g.
aluminum hydroxide) to reduce dietary intake
of phosphorus once patient is eating
+
+
Potassium Typically when [K ]>7.5 mEq/L Typically when [K ]<2.5 mEq/L
Techniques to rapidly reduce potassium levels 1. Supplement potassium (usually potassium chloride
(while treating the underlying cause): solutions) intravenously. Usually added to intravenous
1. Administer crystalloid fluids with low to no crystalloid fluid bag for administration. Concentrations
+
K content (increase GFR and wasting of K [K ]>80 mEq/L should be given via central line to avoid
+
+
by the kidneys) phlebitis.
2. Furosemide therapy (stimulates potassium In order to avoid negative cardiac side effects from
wasting in the kidney) potassium, the maximum rate of potassium
3. Calcium gluconate (protects myocardium supplementation is 0.5 mEq/kg/h
from effects of hyperkalemia; does not reduce 2. Chronically, oral potassium supplements are
potassium levels) available (potassium gluconate)
4. Insulin and dextrose (insulin pushes
potassium into cells, dextrose prevents reflex
hypoglycemia)
5. Sodium bicarbonate (moves potassium
into cells in exchange for hydrogen ions)
iCa, ionized calcium; GFR, glomerular filtration rate; IV; intravenous; K , potassium, [K ], concentration of potassium in (mEq/L); Na,
+
+
sodium; [Na], concentration of sodium (mEq/L); [PO ], concentration of phosphorus (mg/dL); SQ, subcutaneous.
3 −
4
a Doses for specific medications are not included as the reader should reference other sources dedicated to treatment when faced with
a clinical case (see Further Readings for treatment-related references).
b When replacing water losses for CHRONIC hypernatremia (>24–48 hours), remember that sodium levels should not decrease
at a rate faster than 0.5–1.0 mEq/L/h to avoid rapid shifts of water into the brain cells causing cerebral edema. Therefore, chronic
hypernatremia should be corrected relatively slowly with frequent monitoring of sodium levels (usually every 4–6 hours) during
treatment to allow for adjustment of fluid rates. If the sodium levels are dropping too quickly with hypotonic fluids, fluids with a greater
Continued
Electrolyte Monitoring 167