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Fluid Therapy I. FLUID COMPARTMENTS/DISTRIBUTION OF BODY WATERA. Total Body Water (TBW) = 0.6 X Kg. Higher in neonates / Lower in elderly. Higher in animals of very lean mass. Affects drug distribution (greyhounds).B. CompartmentsTBW = ECF + ICF 1/3 2/3 ECF = Extracellular Fluid Compartment ICF = Intracellular Fluid Compartment ECF = Interstitial + Plasma ¾ ¼ (extravascular) (intravascular) C. Fluid spaces are iso-osmolar because water moves to equilibrate. II FLUID MOVEMENT A. Into and out of cells. Determined by concentration gradient in freely diffusible substances (ie: urea) 1. Tonicity dictates water movement in “nonpermeable” substances. (ie: Na/K, proteins) B. Between vascular and interstitial spaces C. Governed by starling forces D. Influenced by integrity of capillary endothelium (inflammation causes increased vascular permeability). E. Forces favoring fluid into vessel (reabsorbtion) 1. Tissue hydrostatic pressure 2. Plasma oncotic pressure F. Forces favoring fluid out of vessel (filtration) 1. Vascular hydrostatic pressure 2. Tissue oncotic pressure G. Net: Filtration at arteriolar end of capillary, reabsorption at venule end (also some fluid goes into lymphatic system). III FLUID RATES A. Maintenance rates (many) ml/day or kcal/day = 30 X Kg + 70 1 ml per lb. per hour 66 ml / kg / day for dogs 44 ml / kg / day for cats 30 ml / lb. / day Maintenance rates consider both sensible (urine, feces) and insensible loss. They do not take into account losses due to vomiting and diarrhea or PU/PD. Better to measure “ins and outs” and estimate volumes and then add 2 ml / kg / hour for insensible loss. Rates that are multiples of maintenance (ie: twice maintenance fluids) may be employed in specific disease situations (ie: diuresis in renal failure). Shock therapy is to rapidly replete intravascular volumes. Rates are up to 90 ml / kg in dogs and 45 ml / kg in cats as a bonus if given without hetastarch or other colloid. If colloids are given decrease crystalloid fluid volume by 30-40 %. Hypertonic saline may also allow decreased crystalloid fluid volume. B. Fluid deficits: 1. Deficits are typically replaced with isotonic balanced electrolyte solutions unless severe free water deficit exists. Unless life threatening, deficits are replaced over the first 24 hours by adding to maintenance fluid volumes. Too rapid replacement can result in cerebral edema since with prolonged volume contraction (dehydration) the brain may create “idiogenic osmoles” which will pull fluid into the brain if volume fluid is added too quickly. Fluid Deficit (ml) = % dehydration x kg x 1000 2. Sources of fluid loss: a. PUPD = urine production > 50 ml / kg / day Water consumption Urine loss is both ions and free water b. Vomiting: Two types very important in terms of electrolytes, loss of free water regardless. Ø Upper GI: Stomach contents only, ie: loss of HCI predominates therefore causes metabolic alkalosis and hypochloremia (because low Chloride limits NaHCO3 reabsorption in kidneys, this worsens alkalosis). Ø Vomiting of bile stained fluid: Here you lose NaHCO3 because vomitus is from past duodenal point where bile duct empties in, ie: pancreatic secretions lose HCO3, K+, causes metabolic acidosis and hypokalemia. This is why color of vomit is very important! c. Panting – loss of free water without ions. 3. Calculating daily fluid rate: Day 1 = maintenance + losses + deficit Subsequent days = maintenance + losses IV ELECTROLYTES AND ACID BASE A. Sodium - Most important extracellular cation - Major determinant of plasma “tonicity” - Low Na implies too much water in blood - High Na implies too little water - Must correct the deficits slowly so you do not shrink or swell the brain - Na metabolism / Water metabolism: · ADH released from post-pituitary causes water reabsorption in kidney (released in response to increased osmolarity of plasma). · Aldosterone – released from adrenal; causes Na and water reabsorption in the kidney (Renin Angiotensin Aldosterone System = RAAS). - Plasma Osmolality = 2 (Na + K) + BUN/18 + Glucose - Normal is 290 – 310mOsm/kg Free Water Deficit: Liters = 0.6 x kg x (1-142/patient Na Therapy for abnormal sodium depends on plasma osmolality ie: and may involve things other than fluids (eg: DDAVP furosemide). Clinical signs of high or low sodium are those of hypo or hypervolemia (follows later) neurologic or cardio. B. Potassim - Major intracellular cation - Na/k ATPase maintenance gradient - Like Na, important in action potentials neuro/muscle/cardio - Low K common with anorexia especially in cats - Maximum rate of administration is 0.5 Meq/kg/hr - Maintenance for normal animals is to use 20meq KCL/L fluids delivered at maintenance rate - Intracellular/extracellular movement can profoundly alter measured levels (acidosis causes movement out of cells, insulin “movement” into) - Serum levels do not adequately reflect body content/stores - Aldosterone promotes K+ excretion (and Na reabsorption) in the kidney - Hypomagnesimia promotes K+ excretion in kidney - Hyperkalemia – see weakness, spiked T waves, wide QRS, decreased P waves - Hypokalemia – weakness, “droopy” head, decreased T waves, long QT C. Magnesium - Low magnesium is common in ill animals, may be clinically silent but will make hypocalcemia and hypokalemia refractory to treatment - Most Mg is intracellular - Vitamin D is involved in / controls absorption - May see hyper Mg in renal failure - Normosol and Plasmalyte contain small amounts of Mg. Very low levels of serum Mg may require supplementation with MgSO4 IV. D. Chloride - Primary extracellular anion - Levels typically parallel Na - Hypochloremia is a serious problem due to inhibition of HCO3 reabsorption in the kidney as well as effects on volume E. Bicarbonate - Major buffer along with proteins, etc. - Determines the “metabolic” part of acid base status. - Cannot be added to calcium containing fluids (ie: LRS) will precipitate - Always undercorrect and then reassess as often correcting dehydration, and hypertension will correct the acidosis as organic acids are metabolized (ie: ketone bodies used for fuel) - Normals: pH~7.4 - HCO3~18-24 F. Phosphate - Hyperphosphatemia is common in chronic renal failure. Diuresis, phosphate binders (oral antacids which tie up PO4 and prevent absorption) and sometimes Calicitrol (1, 25 OHD3) are employed to manage. The long term consequences are soft tissue calcification if Ca x PO4 > 60. Also PO4 and parathyroid hormone are uremia toxins and promote CRF progression. - PO4 accumulates in CRF because of decreased GFR. The increased PO4 causes decrease of Ca. Ca levels are tightly regulated due to cardiac effects. Decreased Ca stimulated release of PTH which attempts to normalize (ie: increase Ca and decrease PO4 into normal ranges.) When GFR is low this is impossible since renal excretion is the main means of PO4 regulation. - Phosphate along with Ca levels can also be altered by primary disease of the parathyroid gland and by cancer (secretion of PTH like protein by tumor lysis syndrome). - Intracellular translocation and bone “sink” are important in maintaining levels of both Ca+PO4 - Hypophosphatemia is seen clinically in animals on phosphate binders and fluids, with parential nutrition, in feline hepatic lipidosis, in treated diabetic ketoacidosis (2-3 days after therapy starts) in alkalosis and in primary hyperparathyroidism. - Because PO4 is contained in many important biologically active molecules (ATP, 2, 3DPG, etc.) signs can be widespread. The most common are neurologic, cardiac and hemolysis - Water for hypercalcemia when PO4 is low - Therapy is with IV K2PO4 or in mild cases with oral supplements (cows milk) JoAnne
M. Roesner, DVM, DABVP |
