FLUID THERAPY in Small Animal Practice- current concepts

Kallahalli Umesh, Kallahalli.umesh@effem.com

Fluid therapy in animals is both challenging and rewarding. The principles of therapy are relatively
simple; creative, resourceful practitioners can overcome the physical, logististical, and economic
restraints.
The largest single compartment of an animal is water. For E.g. In the case of cattle 95% of an embryo
shortly after conception is water where as at birth the percentage is 75 % or more, decreasing 40-60% at
maturity. Total body water in inversely related to body fat.
Fluid compartments in body is divided into
• Intracellular -- consists of approximately 60% of body weight or 50 of total body water and is largest.
• Extracelluar-- consists of approximately 30% of the body weight or 45% of total body water
And is further classified to
o Interstitial water 25% of BW or 37% of total body water (TBW)
o Intravascular 5% of BW or 8% of TBW
• Trancellular fluid –1-2 % of BW or 5% of TBW. Much smaller, found in joints, pleural and peritoneal
cavities, CSF and as secretion in GIT.
• 80% of a puppy’s body weight at birth is water; Obese animals have less TBW compare with lean
animals. Male animals have slightly more TBW than females.
• Cations—NA, K, H, Ca, Mg, Anions---Cl, HCO3, carbonates, PO4, Lactate and proteins
• Predominant extracellualr ions---Na and Cl
• Predominant intracellular ions ---K and PO4
• Intracellular fluid resembles plasma (plasma --5% of total body weight) except for absence of
significant amounts of proteins.

Approximate electrolyte composition of body water fluid in dogs (meq/L)

Electrolyte Plasma Interstitial fluid Intracelluar fluid
Cations
Na+ 140-150 145.1 12
+
K 3.5-5.5 4.4 140
Ca++ (total)* 2.5-2.9 -- 0.0001
Ca++ (ionized) 1.12-1.42
Mg++ (total) 0.83-1.83 ---- 58
Average Total 149.9 153
Anions
Cl- 105-115 117.4 4
HCO3_ 18-26 27.1 10
HPO4-- 0.97-1.94 2.3 75
Proteins 14
Average Total 149.9 153

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Electrolyte Canine normal Feline normal
Sodium (mEq/L)(mmol/L) 140.3–153.9 145.8–158.7
Chloride (mEq/L)(mmol/L) 102.1–117.4 107.5–129.6
Potassium (mEq/L)(mmol/L) 3.8–5.6 3.8–5.3
Total calcium (mg/dL) 8.7–11.8 7.9–10.9
(mmol/L) 2.2–3.0 2.0–2.7
Magnesium (mg/dL) 1.7–2.7 1.9–2.8
(mmol/L) 0.7–1.1 0.8–1.2
Phosphorus (mg/dL) 2.9–6.2 4.0–7.3
(mmol/L) 1.0–2.0 1.3–2.4

Sodium and its related anions are primarily responsible for osmotic attraction and retention of water in
ECF (Intravascular and interstitial). Endothelial cell membrane is freely permeable to these ions. Large
colloidal particles i.e., Albumin (up to 65%of osmotic activity) and globulins (15% osmotic activity) to
which endothelium is not readily permeable are responsible for osmotic attraction and retention of
water in Intravascular compartment.

Most of the cell membranes are permeable to water but not to most charged particles(ions). The
extravascular space between the tissue compartments and cells is the interstitial compartment. The
arteries, veins, and capillaries contain the fluid of the intravascular compartment. Lipid soluble
molecules such as oxygen and carbon diaoxide are freely permeable in and rapidly cross thru the
endothelial cells to the area of lower concentration. Non lipid soluble particles, including water, must
diffuse thru tight endothelial intercelluar clefts.

The size of particle determines whether or not that particle can move freely across this capillary
membrane(composed of endothelial cells and basement membrane). The interstitium is composed of
collagen fiber bundles (provides tensile strength of tissues), proteoglycan filaments (forms a fine
reticular network that contains most of interstitial fluid) , and lymphatics.( are scavengers that remove
excess fluid, protein molecules, debris and other matter from tissue spaces). The amount of free fluid
present is less than one percent.

Approximately 90 percent of volume of fluid that leaves the arterial capillary is taken at the venular end
of the capillary. The remaining 10% is deposited into lymphatics The details of this exchange of fluids
between compartments will be discussed during pathophysiology of oedama.

The starlings law of capillary (Hydrostatic pressure pushes water out of capillaries and oncotic pressure
pulls fluid into the intravascular compartment) is replaced by double layer barrier concept, where in
fluid can exit through entire length of capillary. Luminal surface of endothelial cells is lined with a
glycocalyx of membrane-bound macromolecules comprised of sulfated proteoglycans, hyaluronan,
glycoproteins, and plasma proteins – the endothelial glycocalyx (EG). Filtration across the vascular
barrier is largely independent of the bulk colloid concentration surrounding the vessel. In regions with
high intravascular pressure, the inwardly directed oncotic pressure gradient across the EG prevents
flooding of the interstitial space in conjunction with the high resistance to flow within the narrow strand
gaps of the endothelium. Within low-pressure sections free and easy access of plasma constituents
toward the parenchymal cells allows a highly effective exchange of nutrients and waste products.
Therefore, the fluid shift is modest if the endothelial surface layer is intact because of the low
hydrostatic and oncotic pressure gradients in these segments

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 The principle role of the EG is to maintain the vascular permeability barrier, shielding vascular
walls from direct exposure to blood flow and mediating shear-stress-dependent nitric oxide production
endothelium. The EG also promotes retention of vascular protective enzymes and helps preserve the
intravascular concentration of coagulation inhibition factors. The EG also helps modulate the
inflammatory response by preventing leukocyte adhesion and binding of chemokines, cytokines and
growth factors endothelium. An endothelial surface layer (ESL) determine fluid movement from the
vasculature and the development of interstitial edema. Endothelial surface layer (ESL) also called as
Glycocalyx is major determinant of fluid flux and is maintained by Albumin. Trauma,
inflammation/sepsis, hemorrhage, ischemia-reperfusion injury and hyperglycemia, fluid overload can
damage this ESL. Hypoalbuminemia is strongly associated with a poor outcome, therefore serum
albumin concentration should be maintained within normal limits
While Albumin, Fresh frozen plasma known to protect/repair/reduce shedding of EG, Crystalloids
themselves cannot restore or repair the EG. In experimental studies, HES was marginally more effective
than crystalloid at restoring the EG but can not be recommended considering lack of evidence and risks
associated with these colloids. Numerous other therapies including Heparin, sulfoxide, metformin and
N-acetylcysteine have been suggested to have beneficial effects on the EG, but none are currently in
clinical use for this purpose.

In healthy animals, fluid intake and excretion are kept in balance by sodium and chloride ion activity as
well as serum osmolality. Osmoreceptors in the hypothalamus sense the sodium and chloride
concentrations in the vascular space. As the serum sodium concentration rises because of increased
sodium intake or an increase in free water loss, serum osmolality rises.
An increase in serum osmolality stimulates the release of arginine vasopressin, or antidiuretic hormone,
from the hypothalamus. Antidiuretic hormone stimulates the opening of water channels in the collecting
ducts of the renal tubules, which stimulates water reabsorption. Once water is retained in the vascular
space, sodium, urea, and glucose—the major contributors to serum osmolality—are diluted, and serum
osmolality decreases. Hypothalamic secretion of antidiuretic hormone ceases once serum osmolality
returns to normal
Fluid and electrolyte and acid - base therapy is symptomatic and supportive and should be used in
conjunction with and not as substitute for more specific diagnostic and therapeutic procedures to
identify and correct the primary problem.
PCV/Hematocrit- studies have shown that PCV >60% can markedly increase blood viscosity and reduce
capillary perfusion, and that in fact a PCV of around 30% provided the most optimal oxygen delivery to
tissues; therefore, the faster we can get the PCV below 60% will can only help improve tissue perfusion.
Also, BP does not equal perfusion or volume- initially have a relatively normal BP as the body's
compensatory responses come into play, but still be in a state of inadequate volume and perfusion.
Perfusion relates to intravascular volume, while Hydration mainly pertains to interstitial fluids
volume.

The indication for administration of parenteral fluids include

➢ Expansion of Intravascular volume in conditions such as shock, hypovoolemia and severe
dehydration, where reduction in IV volume results in poor tissue perfusion and hypoxia
➢ Maintenance of oncotic pressure in hypoproteinemic and inflammatory states, where edema
and third space loss also results in poor tissue perfusion and hypoxia.
➢ Rehydration of interstial and intracelluar spaces to maintain normal hydration, euvolemia, and
normotension
➢ Correction of acid-base and electrolyte disorders (hypercalemia, hypernatreima etc)

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 ➢ Use as a carrier for various medications (constant rate infusions)
➢ Maintenance of IV access in potential emergency situations *epileptic pateient)
➢ Treatment of specific medical problems *diabetic ketoacidosis, Renal failure etc)
➢ Nutrtional support

Disorders of fluid and electrolyte balance can develop as result of

• Decreased or inadequate fluid intake (primary water depletion)—first affects ECF-hypertonic. Then
water from ECF-drawn-equilibrium-electrolytes excreted to maintain ECF tonicity initially but if
losses continues-in need to maintain ECF volume-results in oliguric urine of high specific gravity and
hemoconcentration. Death occurs if 40% of water is lost. Thirst is a marked feature and Mucous
membranes dry. Treat-as ECF is hypertonic- replace with water in excess of electrolytes i.e., N/59
(0.18%) saline or 4.5% dextrose etc
• Extracellular volume depletion or refer to as "interstitial dehydration - Excessive or abnormal losses
of secretion from GIT(vomiting/diarrhea), respiratory or urinary tract or losses in form of discharging
wound, burns extensive pleural or peritoneal effusions (Mixed water and electrolyte depletion)
water and electrolytes (mainly Na, Cl but also K and HCO3) are lost but if animal continues to drink--
plasma Na concentration tend to fall so that ECF becomes hypertonic—this provides diuresis and
also causes water to move into ICF in attempt to maintain ECF osmolarity. Extracellular
compartment water loss seen in conjunction with extracellular sodium loss or a state of isotonic
dehydration (because the fluid loss from the extracellular compartment is isotonic to the
intracellular fluid). This results in early decrease in ECF (therefore plasma volume)-signs of
circulatory failure-oliguria-looks like water intoxication or cellular overhydration—affects cerebral,
intestinal and renal functions. Animal becomes dull and weak. Thirst is not marked feature a s
plasma Na concentration is normal or decreased. Mucous membranes moist but saliva are often
viscous. Since the fluid loss is isotonic, no osmotic gradient between the intracellular and
extracellular compartments is created; therefore, no shift of intracellular water occurs and the
intracellular fluid osmolarity and volume remains intact. Extracellular volume depletion is treated
with an isotonic solution; however, in an extreme states of EC volume depletion involving
intravascular deficits (e.g.. hypovolemic shock) the combination of hypertonic saline and a colloid be
advocated to provide a more immediate, longer-acting intravascular volume expanding affect,
initially, as compared to an isotonic crystalloid alone. Loss of hypertonic fluid or isotonic fluid with
water replacement will result in hypotonic dehydration where in the remaining body fluids are
hypertonic.
• Pure water loss and hypotonic fluid loss— e.g., excessive panting, inadequate access to water-
Hypertonic dehydration with increase in tonicity of remaining body fluids. True dehydration is the
loss of water alone without solutes like sodium, which results in a primary hypertonic dehydration
and fluid losses from all compartments. This leaves a state of extracellular hypertonicity (hypertonic
dehydration) and an osmotic gradient that causes water to move from the intracellular space into
the extracellular space (3/4 interstitial and ¼ vascular) causing an intracellular water loss and
increased intracellularly osmolarity. With pure water loss, unless severe or acute, very seldom
causes a state of hypovolemia (intravascular deficit) due to the massive reserve of the intracellular
compartment and oncotic pull of the plasma proteins intravascularly. True dehydration usually
occurs over a prolonged duration of time and, in the simplest terms, and again is most commonly
detected clinically by hypernatremia, this situation is best treated slowly with pure water (e.g.,
D5W); in this situation an isotonic fluid may be used in conjunction for maintenance requirements.

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 • Solution containing approximately 300 mosm\L is isotonic with plasma e.g., 0.9% saline.
(ECF 300 and ICF 400 mosm/l) . Electrolyte and osmolal abnormalities are not possible to detect
based on clinical signs alone. Therefore therapy must be based laboratory determinations of serum
electrolytes compositions and osmolality.Osmol gap, which is, calculated difference between the
measured and calculated serum osmolality will aid in diagnosis and as guide to therapy.
• With isotonic dehydration (loss of both water and solute) - there is relatively no fluid shift between
the intracellular and extracellular compartments as no osmotic gradient exists; instead, fluid losses
primarily occur from the extracellular spaces. An extracellular volume depletion is assessed by
o A. interstitial deficit with parameters such as body weight, degree of skin turgor, dryness of
mucous membrane, and the position of the eyes in the orbits
o B. Intravascular deficit with perfusion parameters such as HR, MM color, CRT, mentation,
PQ, temperature, etc.

History
The most frequent indication of fluid therapy in pets is for diarrhea. Regardless of etiology, the
metabolic changes resulting from diarrhea are similar. This includes dehydration, acidosis, electrolyte
abnormalities and negative energy balance and/or hypoglycemia. Acidosis results from bicarbonate and
strong cation loss in the stool, lactic acid accumulation in tissue, decreased renal excretion of acid and
increased production of organic acid in the colon in malabsorbtive diarrheas.
Physical examination of the animal is the first step in establishing the therapeutic needs. Determine the
presence /absence of diarrhea, polyurea/polydypsia, anorexia etc and ask how long signs have been
present. Acidosis can be gauged from the pets drinking drive, the degree of weakness and age of the
pet. Bradycardia may indicate presence of hypothermia, hypoglycemia or hyperkalemia. Poor body
condition indicates chronic infection/disorder or poor feeding etc. it is important to test for intercurrent
infections. By knowing the type of infection/disorder/ system involved.

One could guess type of fluid lost from the body. Some examples are as follows
• Pyrexia, unable to drink/swallow : Primary water depletion
• Bile stained vomiting/diarrhea : loss of water, Cl,HCO3, Na (K-in chronic)
• Gastric vomiting : loss of water,Cl,HCO3, K -Mixed + M.Alkalosis
• Bowel obstruction : loss of water,Cl,HCO3, K -Mixed + M.Alkalosis
• Urethral obstruction/raptured urinary bladder: Accumulation of K and H-Metabolic acidosis
Acute renal failure/Uremia
• Heammorhage : hypovolumeic shock-provide blood/P.expanders
• Burns/peritonitis/pancreatitis : loss of plasma and ECF-hypovolumeic shock
• Prolonged Anorexia -lack of calories and proteins : provide 60-80Kcal/Kg/Day for maintenance and
3-5g Amino acids/Kg/Day
• CHF - Na retention, K loss with diuretics use : provide half strength saline (0.45%) and 5% dextrose.
• Shock, ketosis etc : Metabolic acidosis.
• Pyloric/Gastic outlet obstruction etc : Metabolic alkolosis

Practice Tip : Most common disorders in dogs are associates with metabolic acidosis exception like
chronic gastric out let obstruction, Hypokalemia , Furosemide , Hypermineralocorticism Excessive
alkalinization therapy, Compensation for respiratory acidosis

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 The clinical signs of Intravascualr volume deficit are those associated with normal
compensatory response to hypovolumeia i.e., Tachycardia and vasoconstriction (pale mucous
membrane, prolonged capillary refilling time, cool extremities), oliguria, high urine specific gravity, low
fractional excretion Na. Pulse-quality and amplitude will be low. Central venous pressure and arterial BP
low. This type clinical signs seen in all categories of fluid loss.
An interstitial fluid loss or deficit causes reduced skin turgor. A patient with reduced skin turgor is said to
be dehydrated and by definition hypovolumeic because electrolyte composition intravascular
compartment is identical to interstitial fluid compartment and two are in equilibrium. This type seen in
all categories of fluid loss except whole blood loss.
Diagnosis of intracellular fluid is based more on presence of hypernatremia or hyperosmolality than on
clinical signs. This type occurs when free water loss (insensible and urinary) is not matched by free water
intake

Physical examination
A rough estimate of degree of dehydration may be made by examining texture and elasticity of skin and
apperance of mucous membrane and eyeball

Neonates : Dehydration in Neonates is normally linked to prematurity, diarrhea, pneumonia, high

ambient temperature or inadequate nursing. A yellowish color indicates dehydration, while dilute, trans-
lucent urine is normal. Dehydrated animals may also have dry, pale oral mucosae. Skin turgor is not
reliable in neonates. Pale mucous membranes with slow capillary refill time indicate 12% to 15%
dehydration

Small Animals
<5 Not detectable
5-6 Subtle loss of skin elasticity
6-8 Definitive delay in return of skin to normal position, slight prolongation of
capillary refilling time( normal 2-3 seconds), Eyes possibly sunken in orbits,
possibly dry mm.
10-12 Tented skin stands in place, definitive prolongation of CRT, Eyes sunken in
orbits, dry mm, Possibly signs of shock (tachycardia, cool extremities, rapid and
weak pulse)
12-15 Definitive signs if shock, death imminent

Loss of one pound of body weight equals approximately 500 ml of fluid and anorexic animals may loose
0.1 to 0.3Kg bodyweight/day/1000 cal energy requirement.

Cachectic animals tend to loose skin elasticity fast and fat animals tend to retain skin elasticity even
when dehydrated. The more severe stages of dehydration are also accompanied by signs of hypovolemic
shock. Other factors, including hemorrhage and third spacing of body fluids, can also result in a decrease
in intravascular circulating volume, resulting in signs of hypovolemia.
Severe hypovolemia resulting in more than a 15% depletion of effective circulating volume leads to a
transcompartmental fluid shift from the interstitial to the intravascular compartments, which occurs
within one hour of fluid loss. When fluid loss is so severe that intravascular fluid volume is affected,
hypovolemia can result in tachycardia, prolonged capillary refill time, decreased urine output, and
hypotension.

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Practice Tips

➢ A 10% to 15% loss of blood is undetectable in animals and results in occult hypovolemia.
➢ Heart rate, arterial blood pressure, and central venous pressure are unreliable, inaccurate for
knowing blood volume status
➢ Clinical signs (capillary refill time, mucous membrane color) and pulse variability index (PVI) are
clinically useful noninvasive indicators of poor tissue perfusion and hypovolemia. while Lactate
and venous oxygen saturation are surrogate markers.
➢ Fluid loss due to Vomiting/diarrhea but no increase in skin tenting = 4% ??
➢ Dry MM = 5 % ??
➢ Reduced skin turgor = 6 to 8 %
➢ Mild hypo-perfusion(tachycardia)= 8 to 10 %
➢ Signs of IV volume depletion ?? (CRT, Tachycardia, poor PQ) = 10-12 %

Laboratory evaluation
Packed cell volume and total plasma proteins increase and interpretation depends on clinical condition.
For every 1% rise in PCV over normal PCV (for e.g., 45 in dogs) one can administer 10ml /kg of fluids.
Specific gravity of urine may be increased and oliguria may be seen severe dehydration. Animals with
hyperkalemia may have bradycardia, cardiac arrhythmias; ventricular fibrillation etc. measurement of
electrolytes may or may not help. Low concentration of Na, K, and Cl always indicate severe net water
deficit.

Table 1 : Dehydration vs Hypovolaemia Tips

Dehydration Hypovolaemia

Intravascular volume  

Interstitial volume   /No change
Intracellular volume  No change
Heart Rate No change 
CRT No change  Progress to 
Skin Turgor  No change
Pulse quality No change Obvious progress to weak and short
Total solids/PCV  No change/  TS

Urine output  

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Table 2 : Signs of hydration and over-hydration

Signs Dehydration Normal Over hydration

Skin elasticity Slow to return to stands Rapidly returns to Jelly like pitting edema
in a fold resting position

MM Dry Moist Moist

Weight change Decreased None Increased

Ins and outs Ins < outs Ins slightly > outs Ins > outs

Urine output <1 ml/Kg/Hour 1-2 ml/Kg/Hour >2 ml/Kg/Hour

Central vein size Small Normal Distended

Na High Normal Usually normal

PCV/TP High Anything May be low but

anything

Urine sp gravity >1030 1010 to 1030 1010

Urine Na meq/L < 10 40-120 Iso

Table 3 : Interpretation of PCV and Total solids (plasma proteins)

PCV Total PP Interpretation
Increased Dehydration
INCREASED Normal Spleen contraction
Decreased Hypoprotenemia with spleen contraction

Increased Anemia "masked" by dehydration, Globulin

NORMAL Normal Normal
Decreased Increased protein loss (GIT, Kidneys)

Increased Anemia with dehydration

DECREASED Normal Increased hemolysis, chronic Blood loss,
Decreased rbc production
Decreased Overhydration, External blood loss

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 How does one tell if it is hypotonic or isotonic fluid loss?

• With hypotonic fluid loss, the fluid remaining in the animal will be more concentrated, and the PCV
and total plasma protein concentration will increase.
• With isotonic loss, the PCV and plasma protein concentration initially will not change (and later
will decrease as fluid is drawn into the plasma from the interstitium).
• Evaluation is complicated by the fact that we usually do not know exactly what the patient’s PCV
and plasma protein concentration were before dehydration developed and must rely on relatively
broad normal ranges (i.e., PCV 37−55%, total proteins 6−8 g/dL) to draw conclusions.
• Underlying anemia or hypoproteinemia also will complicate interpretation.

Osmolaity : The plasma osmollaity is most imp parameter that reflects the effects of fluid shits in the
body. It is also helpful in in determining the cause of dehydration. The normal osmollaity is 290 to 310
mOsm/K. Most animals with primary polyuria will have increased osmolaity (.350)The valu less than 260
mOsm/Kg or above 360- Mosm/Kg requites fluid therapy. Osmolality is calculated by
2 [ (Na +K)] + BUN/2.8 + glucose/18 where Na and K is in meq/L and BUN and glucose is in mg/dl.

Anion Gap : Helpful in determining causes of metabolic acidosis. It is calculated by Na + K - (cl +

Bicarbonates) = Anion Gap. Normal is 12-125. > 25 indicates accumulation of unmeasured anions. The
“anion gap” simply is the difference between the “commonly measured” cations (sodium and
potassium) and the commonly measured anions (chloride and bicarbonate).: there are more
unmeasured anions (i.e., negative charges on proteins, phosphate, sulfate and lactate as well as other
organic anions) than unmeasured cations (i.e., only calcium and magnesium). High anion gap (AG)
metabolic acidosis can be identified by a decrease in pH, decrease in HCO3 or base excess, and an
increased AG.
The major anion represented by the anion gap as calculated is albumin, which, again, is commonly
measured but seldom included, but is a big player in the game. The idea of the anion gap calculation is
that some acids, e.g. lactic acid, will titrate the bicarbonate downward (bicarbonate being replaced by
lactate which was traditional unmeasured), increasing the apparent anion gap.

AG = (Na + K) – (Cl + HCO3)

Two types of AG
1. Highanion gap or “normochloremic” acidosis : Unmeasured anion increases in proportion to the
decrease in bicarbonate, and serum chloride concentration is unchanged. Fixed acids decrease
serum bicarbonate concentration, and the anions of these acids accumulate as unmeasured
anions. Examples -diabetic ketoacidosis (where organic ketoanions accumulate), ethylene glycol
poisoning (where organic anion metabolites of ethylene glycol accumulate), renal failure (where
phosphate accumulates), Lactic acidosis, intoxicant acidosis
2. Normal anion gap” or “hyperchloremic” acidosis : There is no accumulated unmeasured anion
and serum chloride concentration increases in proportion to the decrease in serum bicarbonate.
- example small-intestinal diarrhea - bicarbonate-rich fluid is lost - low serum bicarbonate
concentration - kidneys reabsorb more of the sodium with chloride, leading to hyperchloremia.
Other causes of hyperchloremic acidosis is renal tubular acidosis, diuretics
Decreased anion gap occurs in conditions like Hypocloremic state with - IgG myeloma

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 Central Venous pressure : can provide helpful information aboutpatient's hydration status. It is
measures afrter placement of large bore IV cathetaer into jugular vein. Place the animal in lateral
recubency and clip the hair over the jugularvein. Surgically prepare the site and make a pecutaneous
puncuture of the jugular vein with intracatheter needle (17-18G) , and advance the tip to approximately
the third intercostal space(tip of cather at right atrium). Fasten the catheter securely to the neck of
pateint by adhesive tape so that hub of the needle comes to lie at the base of the ear. Connect the three
way stopcock to the catheter. Connect an IV setup of isotonic saline to the one end of the stopcock, and
to the other end of the stocock attach a piece of IV tubing , which should be taped vertically to a pole
or a piece of doweling. The metric rule is plced so that 0 level is aligned with the midpoint of the trachea
at the thoracic inlet, and the rule is taped to the vertical pole. To fill the CVP manometer, turn the three
way stopcock so that fluid will flow from the bottle of saline into manometer and will excee the 15 cm
mark. Next, turn the stocock so thata column of fluid exists from thee superior venacava (jugular vein)
into the manometer. The fluid in the manometer will fall until it reflects the level of CVP. The CVP of the
normal dog is -1 to+5 cm water. Elevations of +5 to +10 are n borderline. > 10 indicate abnormall
expanded blood volume, > 15 indicate congestive heart failure. If CVP is between 10 and 15, pulmonary
pressure approaches 22mm Hg and additional fluid shuld not be administered.

Acid-base balance
H+ ions are produced from oxidation of food and tissues, during hypoxia, sulphur containing a.a and
hydrolysis of phosphoproteins/phospholipids etc – is buffered by Hemoglobin, plasma proteins, HCO3
and Kidney. This H+ ions are measured as pH. pH of ECF= 7.35-7.45. pH less than 6.8 or more than 7.8 is
incompatible to life. Accurate assessment depends on measurement of arterial/venous blood pH.
Bicarbonate concentration and CO2 tension(p CO2) using blood gas analyzer but in practice this is rarely
possible.

There are four primary acid base disorders

pH pCO2 H+ Primary Disturbance Compensatory response
[ 0.03 x pCO2]
Metabolic acidosis  -  [<20] HCO3  pCO2

Metabolic alkalosis  -  [>20]  HCO3  pCO2

Respiratory acidosis    [<20] pCO2  HCO3

Respiratory alkalosis    [>20]  pCO2  HCO3

Metabolic acidosis[bicarbonate deficit]—increase retention or production of acid metabolites---some

causes includes extreme diarrhea, renal insufficiency, ketosis, abomasal displacement, severe/acute
mastitis, lactic acidosis, conditions resulting in shock, hypoxia etc, administration of acidic solutions
(Nacl, Amm.chloride)
Signs –hyperpnea-rapid rate and increased depth of resp, depression of CNS, urine pH acidic, blood pH
below 7.35. plasma HCO3 and also low chloride level.

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 Metabolic alkalosis —uncommon. Some causes are condition causing K loss, steroids therapy,
loop diuretics(lasix), alkaline salt therapy
Signs—depressed breathing, excitability of CNS, tetanic convulsions, urine pH alkaline, blood pH above
7.45, increase bicarbonate, low chlorides and K.
Resp.acidosis—[carbonic acid excess, hypoventilation], causes includes pneumonia, emphysema,
occlusion of breathing passages etc.
Signs—respiratory embarrassment, depression of CNS, urine pH acidic, pH below 7.35, bicarbonates
and chlorides 
Treatment –donot use alkalizing solution instead correct respiratory rate.
Resp.alkalosis—[carbonic acid deficiency, hyperventilation] fever, hypoxia, resp centre stimulation,
drugs, hysteria, anxiety etc
Signs-deep rapid breathing, tetany, convulsions, urine pH alkaline, pH >7.45,  bicarbonates,  chlorides
Treatment-increase pCO2 in atmosphere
Alkaline urine + high plasma bicarbonates---M.alkalosis
Alkaline urine + low plasma bicarbonates --- Resp.alkalosis
Acid urine + low plasma bicarbonates --- M.acidosis
Acid urine + high plasma bicarbonates—Resp.acidosis
Further tests --- Temperature, Central venous pressure, Pulse, ECG, Urine analysis, Anion Gap, Osmolality
etc (refer practicals)

Treatment goals
• Correcting life threatening hypovolumia
• Restoration of accumulated deficit of fluids and correcting electrolyte and acid base deficits
• Providing sufficient fluids and electrolytes to meet continuing losses each day
• Meeting normal daily requirement
✓ Restoration of normal vital signs
✓ Normalization of abnormal mentation
✓ Restoration of normal blood pressure (systolic >80-90 mmHg)
✓ Normal serum lactate (<2.5 mmol/L)
✓ Central venous oxygen saturation (ScvO2) >70%
✓ Packed cell volume (PCV) >25%
✓ Urine output (UOP) >1 mL/kg/hr
✓ Pulse oximetry (SpO2) >93% @ FiO2 = 21%
✓ Central venous pressure (CVP) = 5-10 cm H20

WHAT TYPE OF FLUIDS SHOULD BE GIVEN

This entirely depends on nature of diseases and composition of fluid lost from the body (refer some
examples mentioned above). There are two major categories of fluids- A crystalloid is a water based
solution withn small molecules that are permeable to the capillary membrane. The sodium and Glucose
concentration of these fluids determine the osmolality and tonicity of the fluid and distribution between
the fluid compartments. Eg., saline, dextrose. A colloid fluid is a water based solution with both small
molecules that are permeable to the capillary membrane as well as large molecules that cannot cross
the capillary membrane. Negatively charged, large-molecular-weight Osmotically active, drawing
sodium around their core structures. Colloids replace intravascular fluid deficits only. So colloids are
always administered along with crystalloids to restore both intravascular and interstitial fluid volume.
Eg;' plasma proteins, dextran, oxypolygelatin, Hexastarch, Pentastarch etc

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 A variety of crystalloid and colloidal fluids are available, including isotonic, hypotonic, and
hypertonic solutions and natural and synthetic colloids.

Crystalloid fluids
A wide variety of crystalloid fluids are available. Crystalloid fluids contain crystals or salts that are
dissolved in solution. Specific crystalloid fluids are indicated for some diseases or conditions and may be
contraindicated in others. Basic categories of crystalloid fluids include isotonic, hypotonic, and
hypertonic solutions, depending on the concentration and type of solute it contains relative to normal
body plasma. They can be replacement or maintenance solutions

Replacement fluids are used to replace body water and electrolyte deficits. Their electrolyte balance is
similar to extracellular fluid – that is, sodium concentrations of approximately 145 mmol/litre and
potassium concentrations of approximately 5 mmol/litre. They have a similar osmolality to plasma (and
therefore all body compartments). It is important to remember that these fluids will equilibrate fairly
quickly with interstitial fluids and so only 15 to 25 per cent will be left in the intravascular space within
an hour of administration. Examples ; RL, Normal saline, DNS

A maintenance fluid contains electrolyte concentrations similar to serum, whereas replacement

solutions contain slightly higher concentrations of potassium and slightly lower concentrations of
sodium relative to serum. Maintenance fluids should only be considered once a patient has been
stabilized by volume resuscitation with a replacement fluid. Maintenance fluids are used to maintain a
patient in a normal state of hydration and euvolaemia. They are not suitable for volume replacement
because they contain less sodium (40 to 60 mmol/ litre) and more potassium (15 to 30 mmol/litre) than
plasma. They are ideal for the provision of the water and small amounts of electrolytes that constitute
normal losses in animals (eg, urine, faeces and panting). Example : D5, half strength saline. 5% Dextrose
is rarely used in small animal practice except for replacing pure water in conditions like heat stroke etc
Isotonic fluids : Isotonic fluids have tonicity, or solute relative to water, similar to that of serum.
Examples of isotonic fluids are 0.9% (normal) saline solution, lactated Ringer's solution, Isotonic fluids
are indicated to restore fluid deficits, correct electrolyte abnormalities, and provide maintenance fluid
requirements. Long-term use of isotonic fluids can lead to mild hypernatremia in some patients.

Hypotonic fluids :Hypotonic solutions have a tonicity less than that of serum. Examples of hypotonic
fluid solutions are 0.45% saline solution, 0.45% sodium chloride plus 2.5% dextrose solution, and 5%
dextrose solution in water. Dextrose-containing fluids are isotonic in the bag but become hypotonic
once the glucose is metabolized in the body. Essentially, free water is being administered without the
risk of causing iatrogenic hemolysis. Hypotonic fluids are indicated when treating patients with disease
processes that cause sodium and water retention, namely, congestive heart failure and hepatic disease.
Hypotonic fluid therapy is also indicated in patients with severe hypernatremia and allows you to slowly
correct a free water deficit. To calculate a patient's free water deficit, use the following formula :

Free water deficit (L) = 0.6 × lean body weightkg × [(patient serum sodium concentration/140) – 1]

Correct the free water deficit slowly to avoid iatrogenic cerebral edema. Ideally, the patient's serum
sodium concentration should not decrease by more than 15 mEq/L during a 24-hour period.

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 Hypertonic fluids : Hypertonic solutions draw fluid from the interstitial fluid compartment and
into the intravascular space to correct hypovolemia. Hypertonic fluid administration is absolutely
contraindicated if interstitial dehydration is present. Hypertonic solutions such as 3% or 7% saline
solution have solute in excess of fluid relative to serum. Administer hypertonic saline solution in bolus
increments of 3 to 7 ml/kg as a rapid infusion. The rapid rise in capillary hydrostatic pressure can force
sodium to flow down its concentration gradient into the interstitium. Administering a low-sodium
crystalloid fluid after a hypertonic saline solution can lead to interstitial edema. Therefore, always
administer hypertonic saline solution in combination with a colloid (10 ml/kg hetastarch or dextran 70)
to help retain fluid within the intravascular space, thus maintaining intravascular fluid volume and
avoiding the secondary complication of interstitial edema.

Table 5
Isotonic 0.9% (normal) saline solution, lactated Ringer's correct electrolyte abnormalities,
solution ( Replacement solution) and provide maintenance
Hypotonic 0.45% saline solution, 0.45% sodium chloride plus Na and water retention –CHF,
2.5% dextrose solution, and 5% dextrose solution ( Hepatic
Maintenance solution)
Hypertonic 3% or 7% saline Hypovolumeia, Always administer
with colloids, Not low sodium fluids

colloids- Blood, plasma, Hypovolumeia, Shock,

Hypoprotenemia
Hetastarch, Dextran 70, HSA

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Tonicity Examples Indications and Remarks
Isotonic Isotonic fluids have tonicity, or solute correct electrolyte abnormalities, and
relative to water, similar to that of provide maintenance. restore fluid deficits,
serum. correct electrolyte abnormalities, and
provide maintenance fluid requirements.
Examples of isotonic fluids are 0.9% Long-term use of isotonic fluids can lead to
(normal) saline solution, lactated Ringer's mild hypernatremia in some patients.
solution,
Hypotonic Hypotonic solutions have a tonicity less Dextrose-containing fluids are isotonic in the
than that of serum. bag but become hypotonic once the glucose
is metabolized in the body. Essentially, free
Examples of hypotonic fluid solutions are water is being administered without the risk
0.45% saline solution, 0.45% sodium of causing iatrogenic hemolysis.
chloride plus 2.5% dextrose solution, and
5% dextrose solution in water. Hypotonic fluids are indicated when treating
0.45% saline solution, 0.45% sodium patients with disease processes that cause
sodium and water retention, namely,
chloride plus 2.5% dextrose solution, and
congestive heart failure and hepatic disease.
5% dextrose solution ( Maintenance Hypotonic fluid therapy is also indicated in
solution) patients with severe hypernatremia and
allows you to slowly correct a free water
To calculate a patient's free water deficit, deficit.
use the following formula :
Correct the free water deficit slowly to avoid
Free water deficit (L) = 0.6 × lean body iatrogenic cerebral edema. Ideally, the
weightkg × [(patient serum sodium patient's serum sodium concentration
concentration/140) – 1] should not decrease by more than 15 mEq/L
during a 24-hour period.
Hypertonic Hypertonic solutions draw fluid from the Hypertonic fluid administration is absolutely
interstitial fluid compartment and into contraindicated if interstitial dehydration is
the intravascular space to correct present.
hypovolemia.
Administer hypertonic saline solution in
Hypertonic solutions such as 3% or 7% bolus increments of 3 to 7 ml/kg as a rapid
saline solution have solute in excess of infusion. The rapid rise in capillary
fluid relative to serum. hydrostatic pressure can force sodium to
Administering a low-sodium crystalloid flow down its concentration gradient into
the interstitium
fluid after a hypertonic saline solution
can lead to interstitial edema. Always administer hypertonic saline solution
in combination with a colloid (10 ml/kg
hetastarch or dextran 70) to help retain fluid
within the intravascular space, thus
maintaining intravascular fluid volume and
avoiding the secondary complication of
interstitial edema.

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Choosing a crystalloid solution

Carefully consider the pH, buffer content, and total electrolyte composition of each type of crystalloid
fluid when choosing a fluid that is appropriate for specific diseases. For example, if an animal is
hyponatremic, a low-sodium or no-sodium fluid such as 0.45% saline solution or 5% dextrose solution in
water would exacerbate the hyponatremia. Administering an isotonic or a hypertonic fluid such as
lactated Ringer's solution or 0.9% sodium chloride solution may be most appropriate to replenish
sodium. Also consider the animal's acid-base status. For example, if an animal has metabolic acidosis as
well as hyponatremia, then administering 0.9% sodium chloride solution, which does not contain any
buffers or bicarbonate precursors, could worsen the metabolic acidosis. Administering lactated Ringer's
solution, which contains lactate, or poly ions which contains acetate and gluconate, may be more
appropriate.
Ringers Lactate: It has less sodium, potassium, calcium and magnesium than plasma and is also slightly
hypotonic. The alkalinizing effect of RL solution makes it ideal for use in animals with metabolic acidosis.
Is lactate in LRS is bicarbonate substitute or precursor or an ideal organic anion to substitute for
bicarbonate ? - The role of lactate (like all organic anions) in LRS is to be rapidly metabolized (disappear),
thereby increasing SID (difference between strong cations and strong anions). LRS contains a racemic
mixture of D and L-lactate as an inorganic ion. D-lactate is proinflammatory and can cause CNS
depression. It is true that Sodium bicarbonate solution administration produces CNS and intracellular
acidosis but transient and related to dose and rate of administration.
Metabolic acidosis occurs in vomiting patients with intestinal losses or when secondary hypovolaemia
results in lactic acidosis (pure gastric vomiting may lead to metabolic alkalosis). Patients with diarrhoea,
renal insufficiency, gastric dilatation–volvulus (GDV) syndrome and hypovolaemic or distributive shock
may all have metabolic acidosis. RL solution is suitable for all of these patients. It is also appropriate for
patients with normal acid–base status. As most animals (90 to 95 per cent) requiring fluid therapy in
practice fall into one of these categories, RL is a common first choice. but mixing with other drugs and
blood products should be avoided due to the presence of calcium

Limitation/avoiding RL : Lactated Ringer’s in patients with liver disease - Remember, however, that the
lactate in LRS is the salt form of the compound and cannot by itself cause lactic acidosis. In most animals
with lactic acidosis, the cause is decreased tissue perfusion and improvement of tissue perfusion by fluid
therapy (regardless of the fluid used) helps resolve the lactic acidosis. Other tissues including skeletal
muscle convert Lactate and unlikely to cause acidosis. Lymphoma; A study indicated that these dogs had
higher blood lactate concentrations than control dogs. The lactate concentrations increased after LRS
infusion in the lymphoma dogs but returned to baseline after 2 hours. There was no evidence that these
dogs were harmed by the LRS infusion. Blood transfusion-overwhelm the chelating capacities of the
citrate in stored blood, resulting in clot formation? – however some studies evaluating this potential
risk, found that LRS containing calcium concentrations did not cause increased coagulation or clot
formation when concurrently in blood transfusions Therefore there are NO Limitations with current
knowledge on use of RL. Use when your are confused !! until you find the right choice

Sodium chloride solution (0.9%) is an excellent choice for promoting renal calcium and potassium
excretion. In addition, the fluid does not contain calcium or potassium, so it is useful in treating animals
with hypercalcemia and hyperkalemia. It has an acidic pH in vitro and is also an acidifying solution
because it lowers plasma bicarbonate levels. The acidifying effect of physiological saline administration
is tolerated by most animals, but if that patient is already acidotic, 0·9 per cent saline is not the fluid of

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 choice. Conversely, animals with metabolic alkalosis benefit from physiological saline
administration for its acidifying effects. Physiological saline contains no potassium, which should be
added if the patient is at risk of hypokalaemia (eg, animals with anorexia, vomiting or diarrhoea).
Physiological saline may be the fluid of choice in hyperkalaemic and hyponatraemic patients with
hypoadrenocorticism. It will increase the sodium levels and dilute the potassium levels. Physiological
saline is ideal for patients with hypochloraemia or hyponatraemia. Physiological saline is indicated for
hypercalcaemic animals as it promotes calciuresis by increasing renal calcium filtration while decreasing
calcium reabsorption by direct. In human and animal studies, higher concentrations of chloride induced
renal afferent vasoconstriction with decrease i glomerular filtration rate (GFR)- may increase the risk of
AKI in the critically ill. Remember, the concentration of chloride in 0.9% saline solution (154 mEq/L) is
higher than that of plasma in healthy animals (average: 110 mEq/L [dogs], 120 mEq/L [cats]). Many
suggest to avoid colloids and Saline in AKI cases. 0.9% saline effect on [H+] is usually negligible in normal
healthy animals unless large volumes (>30 mL/kg) are administered over a short period (<1 h) or
administered to animals that already have metabolic acidosis

• Replacement fluids- 20-25 % remain within IV one hour after infusion

• Maintenance fluids - only 10% remain IV one hour after infusion

Colloids

The oncotic pressure is the force that holds fluid within a compartment. Starling's forces, which dictate
the amount of fluid retention within the vascular space vs. transvascular fluid flux into the interstitium,
depend on many factors, including intravascular and interstitial hydrostatic pressure, interstitial and
intravascular oncotic pressure, and capillary pore size. As intravascular volume is replenished with a
crystalloid fluid, the intravascular hydrostatic pressure increases and causes a dilutional decrease in
oncotic pressure, which can result in the movement of osmotically active substances into the
interstitium. A colloidal solution contains negatively charged, large-molecular-weight particles that are
osmotically active, drawing sodium around theirore structures. Wherever sodium is, water follows. By
drawing sodium around the particle, water is held within the vascular space.

Colloids replace intravascular fluid deficits only. So colloids are always administered along with
crystalloids to restore both intravascular and interstitial fluid volume. Consider colloids whenever
hypoproteinemia, decreased oncotic pressure, and increased capillary pore size exist, as in conditions
associated with sepsis or systemic inflammatory response syndrome. Although some of the colloid
particles can potentially leak into the interstitial space, the net effect is to maintain fluid within the
intravascular space to avoid interstitial edema. Whenever a colloid is administered with a crystalloid,
reduce the calculated crystalloid fluid requirements by 25% to 50% to avoid volume overload.

Natural colloids

Natural colloid solutions include whole blood and plasma. Fresh whole blood is indicated when loss of
both red blood cells and plasma has occurred. The Rule of Ones states that 1 ml fresh blood infused per
1 lb body weight will increase a patient's packed cell volume (PCV) by 1%, provided no ongoing losses
are present. This rule is a simple method to calculate the amount of whole blood to administer to reach
a target hematocrit. When working in kilograms, the Rule of Ones can be extrapolated: 2.2 ml/kg whole
blood will increase an animal's PCV by 1%, provided the PCV of the transfused blood is 40%.

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 A more accurate method to determine the volume of whole blood to administer is as follows:

ml donor blood needed = [(Desired PCV – Actual Recipient PCV) ÷ Donor PCV] × ml recipient blood
volume

(Note: For recipient blood volume, use 90 ml/kg for dogs and 70 ml/kg for cats.)

Fresh frozen plasma can be administered at 10 to 20 ml/kg/day to replenish clotting factors and provide
antiproteinase activity in states of inflammation, such as pancreatitis, and provide small quantities of
albumin.6 Infuse 20 ml/kg plasma for every 0.5 g/dl increase in plasma albumin needed, provided no
ongoing losses are present. The goal of plasma administration is to raise a patient's serum albumin
concentration to 2 g/dl; once this goal is achieved, provide the remainder of colloidal support with
synthetic colloids.

Synthetic colloids ( references up on request)

Examples of artificial colloids include hetastarch, dextran 40, dextran 70, and polymerized bovine
hemoglobin glutamer-200 (Oxyglobin—Biopure). Hetastarch and dextrans are commonly used in
veterinary practice. Concentrated human serum albumin (HSA) (25% albumin) should be considered in
severe cases of hypoalbuminemia (albumin < 2 g/dl). Hydroxyethyl starches have been implicated in
causing higher mortality, acute kidney injury, and coagulation abnormalities in people. Likewsie,studies
in people have shown that colloids are not superior to crystalloids for intravascular fluid replacement in
critical illness. Studies evaluating risks of these products in veterinary patients are needed. Despite the
limited study in pets, use of synthetic colloids in veterinary practices showed that 70% of the survey
respondents have limited the use of these products because of safety concerns.
Benefits
• Volume expansion of between 100–172% of the infused volume
• Superior to crystalloid solutions for treating perioperative hypotension in dogs and in people
• Experimental in dogs -volume expansion, HES = 5% HSA & dextran 70 and superior to crystalloids,
plasma and whole blood.
• Much more effective for restoring cardiac output, tissue oxygen delivery, and normal blood pressure
than crystalloids
Limitations
• Assumed that 3 to 4 volumes of crystalloid solution achieve similar plasma volume expansion as 1
volume of colloid solution
• Cases where glycocalyx is affected ( sepsis etc) synthetic colloids such as HES cannot be relied upon
to maintain their superiority over crystalloids in terms of plasma volume expansion.
• Colloids impede primary hemostasis by osmotically shrinking platelets, increasing platelet
degradation, decreasing the availability of soluble fibrinogen ligand for activating platelets, and
decreasing von Willebrand factor concentration and activation. Secondary hemostasis is impeded by
prolongation of activated partial thromboplastin time (aPTT) and decreasing TEG clot firmness.
However study in dogs -HES administration does not cause relevant platelet dysfunction beyond
hemodilution.
• HES induced AKI is dose- and time-dependent and leads to potentially reversible cellular
vacuolization, cellular swelling, and inflammation. A retrospective cohort study found that critically
ill dogs receiving HES 250/0.5 had a higher incidence of AKI and non-survival to discharge compared
to a control group

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 Recommendations based on current knowledge in pets
• HES is a potent and efficient plasma volume expander in patients with an intact endothelial
glycocalyx
• This property may be lost in situations where the glycocalyx has been damaged. -trauma, sepsis, or
anaphylaxis. HES may worsen fluid extravasation due to increased vascular permeability.
• The use of HES in dogs may adversely affect both primary and secondary hemostasis, and although
no study has documented an increase in clinical bleeding associated with the use of HES, caution is
advised in all patients at risk of hemorrhage
• There is very good evidence in critically ill people that HES is associated with AKI and mortality. In
dogs, some data suggest HES may increase the risk of AKI and death, but the available studies are
clearly conflicting.
• HES may be a reasonable choice only in states of acute hypovolemia or peri-operative hypotension,
and at the lowest effective dose and over a short period of time.

Hetastarch. Hetastarch is a polymer of amylopectin suspended in a lactated Ringer's solution. The

average molecular weight of hetastarch is 69,000 daltons. The hetastarch particles are broken down by
serum amylase and last in circulation for about 36 hours. Because hetastarch can bind with von
Willebrand factor, a patient's activated partial thromboplastin time (APTT) and activated clotting time
(ACT) may become mildly prolonged, but this will not contribute to or cause bleeding.

Administer hetastarch in incremental boluses of 5 to 10 ml/kg in dogs and 5 ml/kg in cats. Because rapid
hetastarch administration can cause histamine release and vomiting in cats, administer the bolus slowly
over 15 to 20 minutes. Many authors recommend that the total daily dose of hetastarch should not
exceed 20 to 30 ml/kg/day.6 After administering the boluses, administer hetastarch as a constant-rate
infusion (20 to 30 ml/kg/day intravenously) until the patient is able to maintain its serum albumin
concentration and colloidal support on its own. During hypovolemic shock, 5 to 10 ml/kg can be given as
an intravenous bolus.

Dextran. Dextran solutions contain polymers of glucose with average molecular weights of 40 and 70
daltons. Most practitioners favor dextran 70 over dextran 40 because dextran 70's larger particles
contribute to the water-holding capacity of blood. The smaller particles of dextran 40 last about four
hours in circulation before being cleared by the kidneys. The larger particles of dextran 70 last about
nine hours in circulation.

Both dextran 40 and dextran 70 coat platelets and red blood cells and can impair coagulation and
interfere with cross-match procedures. For this reason, dextran 70 may be preferred over hetastarch in
conditions of hypercoagulability and thrombosis. Anaphylaxis and renal failure have been reported in
people that received dextran 40.6 The dose is 10 to 20 ml/kg/day given intravenously when
administered along with a crystalloid. During hypovolemic shock, 5 ml/kg can be administered as an
intravenous bolus to treat hypotension.

Polymerized bovine hemoglobin glutamer-200. This solution contains bovine stroma-free hemoglobin
that acts both as a potent colloid and as an oxygen carrier in the face of thrombosis or anemia.
Recommended doses are 20 to 30 ml/kg/day. Polymerized bovine hemoglobin glutamer-200 can be
administered as an intravenous bolus of 3 to 7 ml/kg. Use caution when infusing this solution in
normovolemic patients and in those with congestive heart failure because of the risk of causing
iatrogenic volume overload. Not available in india

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 HSA. Albumin contributes 80% of the oncotic pressure of blood and acts as a carrier for various
essential compounds in the body, including hormones, zinc, copper, and drugs. Albumin is also a
mediator of coagulation and a free-radical scavenger at sites of inflammation. Hypoalbuminemia
(albumin < 2 g/dl) has been associated with delayed wound healing and an overall increase in patient
mortality. Patients with conditions associated with increased capillary pore size, such as sepsis,
vasculitis, and systemic inflammatory response syndrome, can benefit from maintaining the serum
albumin concentration at or ideally above 2 g/dl.

As a general rule, the serum albumin concentration should be raised to at least 2 g/dl with fresh frozen
plasma or HSA. Administering fresh frozen plasma can help restore some of the intravascular albumin,
but it is largely inefficient on a ml/kg basis when compared with HSA. Plasma is better suited to
replenish clotting factors and antithrombin and should be used in conjunction with a synthetic colloid
such as hetastarch to maintain oncotic pressure. A volume of 20 ml/kg plasma will raise the serum
albumin concentration by 0.5 g/dl, provided no ongoing protein loss is present.

Chronic hypoalbuminemia results when the body's interstitial albumin pool becomes depleted and can
no longer maintain intravascular albumin concentrations and oncotic pressure. The albumin contained
in an infusion of fresh frozen plasma will replenish the interstitial albumin stores before an increase in
serum albumin is detected. But in many cases, this can be costly and can deplete a hospital's resources
of plasma. Instead, a more efficient means of restoring both interstitial and intravascular albumin is to
administer HSA.

HSA has been used with success in a variety of critically ill dogs. It is a potent colloid and is effective in
restoring serum and interstitial albumin in patients with acute or chronic hypoalbuminemia for the short
term, but in animals with chronic hypoalbuminemia, the underlying cause of decreased albumin
production or increased loss must also be addressed for the best long-term outcome.

HSA also helps retain fluid within the vascular space. Like other colloids, HSA can also pull fluid from the
interstitium into the vascular space, so it may be helpful in treating interstitial edema. Carefully monitor
the animal for signs of intravascular volume overload such as tachypnea, orthopnea, chemosis, or
fulminant pulmonary edema.

HSA has only 79.3% homology to canine albumin (Francis et al JAVMA 230:873–879, 2007) Pretreat
animals with 1 mg/kg intramuscular diphenhydramine, and then give 2 ml/kg HSA over four hours.
Monitor for clinical signs of a reaction, including urticaria, angioneurotic edema, hypotension, salivation,
and vomiting. Rare reports of delayed reactions and systemic vasculitis and polyarthritis have been
observed in dogs about 14 days after albumin infusion. All patients had clinical signs of gastrointestinal
inflammation or septic peritonitis at the time of albumin infusion. Treat vasculitis and polyarthritis with
1 mg/kg prednisone given orally twice a day for two weeks and then tapered over two additional weeks.
Although the potential for a reaction exists, the benefits of albumin supplementation can outweigh this
small risk and can improve overall outcome.
Dose in grams = 10 (desired [Alb g/dL] - patient [Alb g/dL]) x (patient weight in kg) x 0.3
25- kg dog's serum albumin from 1 to 2g/dL:
➢ Desired dose = 10 (2-1) x 25 kg x 0.3 = 75 g
A 25% HSA preparation = 250 mg/mL = 0.25 g/mL. = 75g / 0.25 g/mL= 300mL.
300mL of 25% HSA to raise its albumin by1g/dL

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 BY WHAT ROUTE SHOULD FLUIDS BE GIVEN

Oral route
Indications : For the anorectic patient that has a shorttermed illness, More cionducive for small animal
less than 20 Kg. Very conducive for neonates
Technique : Can use a stomach tube, Pharyngostomy tube, Small dosing syringe or a small baby bottle
and nipple, Warm fluids to body temp
Remarks : Aspiration pneumonia is possible, Not useful for hypovolemic shock, Shoul not be used in
vomiiting patient and aviod air administartion

Maintain strict aseptic placement and maintenance protocols to permit the extended use of the
catheter. Place the largest catheter that can be safely and comfortably used. Very small catheters (24
gauge) dramatically reduce flow. Flush the catheter q 4 hr unless continuous fluid administration is
being performed. Research suggests that normal saline is as effective as heparin solutions for this
purpose. To minimize the risk of nosocomial infection, the Centers for Disease Control recommend
that fluid administration lines be replaced no more than q 4 days

Subcutaneous route
For correction of mild to moderate dehydration, For maintenance in the not too severely ill patient and
not conducive for animal weighing > 10 Kg
Technique : Use isotonic fluids ONLY, Best to administer bygravity flow thrru 18-20 G needle, Do not
deposit more than 10-12 ml/Kg per injection site, Fluid should be deposited dorsally along the area
bordered by the scapulae anteriorly and the ileac crests posteriorly, The average 5-6 Kg animal can
receive 150-200 ml once or twice daily. Ringers and normal saline are well tolerated
Remarks : Avoid using hypertonic/Hypotonic fluids ( example dextrose 5%), Do not inject under
infected/devitalized skin, Not useful for hypovolemic shock and do not use irritating solutions.
Subcutaneous fluids are best used to prevent losses and are not adequate for replacement therapy in
anything other than very mild dehydration

Intraperitoneal route
When IV access not avialble, Providess a vehicle for delivering ample volume of fluid over a short time,
relatively rapid absorbtion
Technique : Use isotonic fluid, Use 16-20G needles, Preapre sterile injectin site just lateral to the midline
and midway between the umbilicus and pelvic brim
Remarks :
Hypertonic fluid will worsen the dehydration, Do not use in setting of abdominal sepsis, ascites or
peritonitis, Donot use with pending abdominal surgery

Intravenous route
Preferred route for severely dehydrated and hypovolemic patients, Best route for correcting
hypotension. Provides for rapid elivery at the most precise dosage, Most effective for medium and large
sized animals
Technique : Preapre a sterile site for needle or cannula, Amount and rate of fluid delivery depends on
patient;s status, Use isotonic fluid for volume repletion.
Remarks : Aviod IV ovreload caused by excess fluid delivery, Aviod catheter sepsis and phlebitis, Avoid
cathret displacement and inadverdent extravascular plcaemnt of fluid infusion

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 Intraosseous route
The Bone marrow of the femur and humerus is occasionally accessed than small collapsed veins in
neonates and pediatric small animals. The circulation to the bone marrow does not collapse in cases of
hypotension and shock. Strict aseptic technique is required.

RATE OF INFUSION
Depend on severity of dehydration, safe is 100ml/kg/hour
In severe hypovolumic patients 4ml/kg/min for first 20 minutes and 20ml/kg/hour there after.
If given over 24 hours period to meet requirement 5-10ml/kg/hour
Flow rate (ml/kg/hour)converted to rate of drops (drops/min) using following formula
= drops/ml delivered by infusion set x ml/kg/hour x body weight (kg)
60
• Most infusion sets (dripsets) deliver 10- 15 drops/min
• Most standard drip sets 1 ml = 10 drops
• Micro-drips 1 ml = 60 drops
o Example 700 ml / 4 hours
o 2.91 ml /Min = 29 drops /min

Type of catheters/infusion sets and complications ---refer practical aspect of fluid therapy

HOW MUCH FLUID SHOUD BE GIVEN

I. Replacement requirement = % dehydration x body weight in Kg

Maintaince (sensible and insensible loss) = 50ml/Kg/day
Dogs----40-60ml/kg/day—sensible 27-40ml/Kg/day and insensible (fecal,cutaneous,resp) 13-
20ml/Kg/day
If oral route is chosen allowance must be made for partial absorbtion of fluids (60-80%) The success of
therapy is monitored based on clinical signs and urine output.

II. Daily fluid requirements are based on the metabolic water requirements of a patient in a state of
equilibrium. During a state of equilibrium, a patient's daily water intake equals water loss, creating no
net loss or gain of fluid. For each kilocalorie of energy metabolized, 1 ml water is consumed. Metabolic
energy requirements are calculated based on the following linear formula1 : kcal/day = (30 × body
weightkg) + 70

• By substituting 1 ml water for 1 kcal, the following formula can be used to estimate a patient's
daily metabolic water requirements: ml/day = (30 × body weightkg) + 70

Recommended Maintenance Fluid Rates (mL/kg/hr)

• Cats : 80 X body weight (kg)0.75 : Rule of thumb: 2–3 mL/kg/hr

• Dogs : 132 X body weight (kg)0.75 : Rule of thumb: 2–6 mL/kg/hr

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 III. For every 1% rise in PCV over normal PCV (for e.g., 45 in dogs) one can administer
10ml /kg of fluids.
IV. Loss of 0.45 KG (one pound) body weight equals approximately 500 ml of fluid
V. Anorexic animals may loose 0.1 to 0.3Kg bodyweight/day/1000 cal energy requirement.
VI. Basic dehydration estimates can be calculated based on the fact that 1 ml water weighs about 1
g and by using the following formula: Body weight kg × estimated percent dehydration ×
1,000 ml/L . This formula helps you determine the amount of fluid deficit in liters
VII. If signs of overhydration are not present and oliguria persists after apparent rehydration.
Cautious fluid challenge may be administered (increase body wt by 3-5%) while monitoring
for evidence of fluid overload. Monitoring body weight, plasma total solids, hematocrit, and
central venous pressure will help protect against overhydration.

Cachectic animals tend to loose skin elasticity fast and fat animals tend to retain skin elasticity even
when dehydrated

Neonates Warmed isotonic dextrose solution through a stomach tube, then 1 to 2 ml 5% to 10% glucose
solution can be administered orally /tube. 20% dextrose, 0.25 ml/25 g IV or intraosseous, up to 11
ml/min. If a neonate is too weak to nurse or suckle, a mixture of a warmed, balanced crystalloid
(lactated ringer's solution or Normal saline) and 5% dextrose may be administered subcutaneously at a
dose of 1 ml per 30 g of body weight, until the pup can be fed or nurses. A balanced warmed nutrient-
electrolyte solution can be administered orally by stomach tube every 15-30 minutes until the neonate
is capable of suckling. 50% dextrose solution should only be applied to the mucous membranes because
of the potential for phlebitis if administered intravenously; however, circulation must be adequate for
absorption from the mucosa. Intra peritoneal not very useful.
• Bolus fluid for hypovolemia: 3 to 4 mL/100 g (pups); 2 to 3 mL/100 g (kittens)
• Bolus glucose for hypoglycemia: 1 mL to 3 mL of 12.5% dextrose (eg, 1:3 dilution of 50%
dextrose with sterile water)
• Bolus colloid for hypovolemia that is nonresponsive to multiple crystalloid boluses: 2
mL/kg to 5 mL/kg, followed by 1 mL/kg/h as needed
• Whole blood for anemia: 10 mL/kg to 20 mL/kg

Tips
About 80% of the volume of crystalloid fluid infused will re-equilibrate and leave the intravascular space
within one hour of administration. A constant-rate infusion of a crystalloid fluid is recommended to
provide continuous fluid support in patients that are dehydrated and have ongoing losses. In some
cases, the fluid required to restore intravascular and interstitial volume can cause hemodilution and
dilution of oncotically active plasma proteins, resulting in interstitial edema formation. In such cases, a
combination of a crystalloid fluid along with a colloid-containing fluid can help restore oncotic pressure
and prevent interstitial edema.
Once immediate life-threatening fluid deficits are replaced, provide additional fluid based on the
estimated percentage of dehydration and maintenance needs.

In general, the choice of fluid is less important than the fact that it is isotonic. Volume benefits the
patient much more than exact fluid composition. Isotonic fluids won’t have a severe negative impact on
most electrolyte imbalances, and their use will begin to bring the body’s fluid composition closer toward
normal pending laboratory results that will inform the clinician of more specific fluid therapy. LRS or
acetated Ringer’s solution may be used in liver disease. LRS contains both D- and L-lactate and is unlikely
to increase blood lactate level

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 Tips : How to Rehydrate Anemic dogs ?
Consider the oxygen-carrying capacity of the blood, which is related to the hemoglobin concentration
and hence PCV. Crystalloids and colloids will restore circulating volume, but they will tend to decrease
the PCV. Consideration both the acuteness and severity of the decrease in PCV (e.g., a PCV that has
decreased suddenly from 40% to 17% is likely more cause for concern than a PCV that has slowly
decreased from 40% to 12% over many months of illness). Anemia from hemorrhagic shock may require
hypertonic saline 4-5 ml per kg over 10 minutes or balanced electrolyte solution 10ml per kg over 10
minutes targeting BP. If hypotension persists- Blood transfusion

Guidelines for fluid therapy when treating hypoalbuminemia include the following:
· Nutritional support is critical to treatment of hypoalbuminemia.
· Plasma administration is often not effective for treatment of hypoalbuminemia due to the relatively
low albumin levels for the volume infused. Human serum albumin is costly and can cause serious
hypersensitivity reactions. Canine albumin is not readily available in most private practice settings but
may be the most efficient means of supplementation when available.
· Synthetic colloids (e.g., hydroxyethyl starch) are beneficial because they can increase oncotic pressure
in patients with symptomatic hypoalbuminemia to maintain fluid in the intravascular space; however,
synthetic colloids will not appreciably change total solids as measured by refractometry. Therefore,
patient assessment determines response. Use up to 20 mL/kg/day of hetastarch for dogs and 10–20
mL/kg/day for cats.

Monitoring Fluid Therapy

• Perfusion Parameters - HR, CRT, MM, pulse quality, Temp. Mentation, Lactate, BP, Lactate and Base
Deficit
• Clinical Hydration- Skin Turgor, MM Moisture, Globe Position, Corneal Moisture, PCV/TP USG
• Daily Body weight Q 6-24hrs - in the beginning every 4 - 6 hrs until weight stabilizes
• Urine output (at the same time as body weight)
• "Ins" vs "outs - Catheterization or weighing urine absorbent pads knowing 1 mL = 1 gm
• Periodic USG

ACID BASE disorders basics ----- therapy

What is more reliable to know the acid base status ? pH because it is a measured value whereas the
bicarbonate is calculated from the pH and pCO2 using the Henderson equation.

Serum bicarbonate concentration is the traditional indicator of metabolic acid base balance. It is most commonly
calculated from the measured pH and PCO2 by a blood gas machine, although some chemistry laboratories
measure it directly.
The bicarbonate concentration - not independent of changes in the PCO2. As PCO2 increases, the bicarbonate
concentration increases it is possible that an increased bicarbonate concentration could be mistaken for metabolic
alkalosis, when in fact it had occurred subsequent to respiratory acidosis
The SBE (standardized base excess) is calculated* from the pH, PCO2, and hemoglobin concentration
representing the quantity of acid or base that would need to be added to a liter of blood to normalize the pH with
a PCO2 of 40 mmHg.
A simple metabolic acidosis exists when there is a decrease in bicarbonate and a more negative SBE in conjunction
with a lower than normal pH.

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3 golden rules of therapy
➢ Change in pCO2 (arterial) either up or down of 10 torr is associated with increase or decrease in pH
of 0.08 units i.e., increase or decrease in carbonic acid
➢ PH change of 0.15 is the result of base change of 10 meq/L. thus if pH  by 0.15 there will be  in
HCO3 by 10 meq/L. A change in plasma pH produces inverse change of 0.4 to 0.6meq/L in serum K.
➢ HCO3 requirement = base deficit (meq/L) x body weight/3 ( or 6 if loss is more than 24hours) Or
HCO3 (mmol/L) = body wt in Kg x (30 -TCO2 ) x 0.6 OR base deficit x body weight x 0.6 =HCO3 in
meq.
Or following table can be used -Refer the Table 1

Bicarbonate therapy- some instructions

Start therapy if less than 12 meq/L or base deficit of –10meq/L or when pH is less than 7.2.

Bicarbonate has immediate effect but cannot be added to polyionic solutions (particularly Calcium) and
it cannot be autoclaved during manufacture. Therefore sodium lactate/citrate/gluconate/acetate(L-
form)is used for large amount, however these salts must be metabolized to HCO3 .
Lactate is slowly metabolized where as acetate other tissues also metabolize. Lactate is metabolized in
liver, where as acetate is metabolized in skeletal muscle. Gluconate is metabolized in Lactated ringers
solution is contraindicated for animals with hypercalcemia. Ringer acetate-gluconate is preferred to
Ringers lactate in treating animals with liver dysfunction ??. (Refer table for more info on
incompatibilities in fluid and drugs therapy).
Less than 20% of administered RL solution remain in intravascular compartment in 2 hours in
hypovolemic solution. In absence of analysis use 2meq/Kg in mild to 5 meq/Kg in severe M.acidosis

1g NaHCO3 = 12meq Na+ or HCO3 [available 10 and 20 ml, 7.5% (0.892 mEq/mL) 8.4% (1 mEq/mL) 5%
(0.595 mEq/mL), 4.2% (0.5 mEq/mL)

Excess HCO3 infusion can cause

• M.Alkalosis and Respiratory depression,
• Shift hemoglobin dissociation curve, so that ability of Hb to transfer oxygen to tissues is reduced.
• Shift K into cell-hypokalemia,
• Decrease ionized Calcium.
• Rapid correction of acidosis with HCO3 also cause paradoxical fall in CSF pH—very rare (CO2 diffuses
but not HCO3)

Potassium therapy—
Hypokalemia (< 3.5 meq/L)becomes a life threatening problem when seum values of less than 2.5
meq?L are associated with ECG changes(T wave depression, Prolonged QT interval, U waves, And St
segment depression). Severe weakness, or ventilatory compromise. K should be administered with IV
fluids at a rate of 0.5meq/kg/hr. Mild hypokalemia can be treated with diet rich in K
Some cause includes Decreased intake Anorexia , Fluid therapy using potassium-free fluids , Increased
loss, Gastrointestinal losses Urinary losses: CKD, Post obstructive diuresis Polyuria Renal tubular acidosis
Hyperadrenocorticism, Hyperaldosteronism, Hypomagnesaemia, Metabolic acidosis Drug therapy (loop
and thiazide diuretics) , Potassium redistribution - Alkalaemia , Elevated insulin levels , Beta-adrenergic
drugs , Hypothermia , Hypokalaemic myopathy of Burmese cats, Hyperthyroidism

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Kallahalli Umesh
Serum K(meq/L) K added to 500 ml Fluids (meq)
<2 40
2-2.5 30
2.5-3 20
3-3.5 14
>3.5 - <5 10
Do not infuse K+ not more than 35mmol/L, recommended is 3-5meq/Kg/Day
KCl Inj 10 ml ampoules - A 7.5% potassium solution contains 1 meq of K+/ml; a 10% solution contains
1.34 meq of K+/ml; a 11.2% solution contains 1.5 meq of K+/ml; a 15% solution contains 2 meq of K+/ml;
a 20% solution contains 2.68 meq of K+/ml.

Hyperkalemia (> 7 meq/L) – prolong repolarization and evntually depolraizationn.--life threatening-

cardiac arrest/fibrillation etc. ECG changes includes Bradycardia, Tall-spike T waves, Prolongation of PR
interval, Flattening of P wave, widening of the QRS complex. Acidosis will cause a 0.6 meq/L rise in
serum K for each 0.1 decrease in pH.
Some causes includes Laboratory or interpretive error ,Haemolysed blood sample ,Thrombocytosis
Leucocytosis , Akita dogs , From exogenous sources ,Intravenous fluid therapy , Increased dietary intake
or supplementation , Reduced potassium excretion ,Anuric or oliguric renal failure Urinary outflow
obstruction Urinary bladder rupture , Hypoadrenocorticism Hypoaldosteronism , Drug therapy
(spironolactone, ACE-inhibitors, non-steroidal antiinflammatory drugs (NSAIDS)), Potassium
redistribution , Metabolic acidosis , Hyperosmolality , Pseudohypoadrenocorticism ,Massive tissue
destruction

Treat hyperkalemia using

• Calcium gluconate 0.5-1ml of 10% solution/kg IV—antagonize the effect of K
• Glucose and insulin— 1-1.5g/kg as 10-20% dextrose with 0.5U insulin /g dextrose—pushes k into
cell, and reduces K in half an hour.
• HCO3 –1-2mmol/kg slow IV-pushes K into cell, or use dialysis

Sodium
Hyponatremia(<115meq/L) with neurological signs require Na supplementation.
1. Hypoosmolar hyponatremia
• Hypovolumic - GIT loss, addisons, Renal, Diuresis etc
• Normovolumic- ADH increase, Polydypsia, Severe hypothyriodism
• Hypervolumic - CHF, Liver/renal diseases, Nephrotic syndrome etc
2. Hyperosmolar Hyponatremia - Diabetes Mellitus, Mannitol therapy
3. Pseudo hypornatremia -- Hyperprotenimia, Lipemia

Effects : Shift of water from ECF to ICF- Cellular swelling--Cerebral edema Hypertonic saline(3-5%) can be
used. It is corrected over a period of 12- 24 hours. Na deficit is calculated as follows
(140-measured Na) X kg body wt X 0.3 = meq/L Na deficit.

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 Hypernatremia
(>155meq/L) Associated
with
• water loss -- Normal Na and ECF - Diabetes insipdus, Heat sroke,Fever, Burns
• Hypotonic water loss --Reduced Na and EF -- Diarrhoea, Vomitting, Osmotic diuresis, CRF,
Diabetesmellitus, Diuretics, GlucoseIV
• Hypervolumic -- High Na and ECF -- Salt , Sea water, Saline emesis, IV hypertonic fluids, HCO3 ,
Cushing, Increase Aldosterone

Effects : Hypertonic ECF--Water moves from ICF to ECF--Cellular dehydration--primarily effects Brain
Neurological signs.
Serum Osmolality is calculated as 2 [(Na) + (K )] + Glucose/18 + BUN/2.8

Hydration deficits should be replaced slowly over12-24 hours using ringer's, normal saline or half
strength saline once adequate perfusion has been restored. Once rehydrated, the Na is remeasured and
New Na value is determined to remaining ECF water deficit. (new Na-140/140) x kg body wt x 0.6 =
water deficit in liters.

ORAL REHYDRATION THERAPY

Advantages
• Economy of materials, time ,equipment.
• Carried and stored in dry form
• Mixed with tap water
• Administration by nursing bottle/stomach tube
• Delivery into abomasum
• More flexibility in formulation-greater concentration of K, or osmolality can be given

Numerous preparations are available which contain substantial amount of NA, Cl, and Glucose. Most
contain HCO3 as alkalizer. Many contain glycine/acetate or citrate to enhance Na and water absorbtion.
Addition such as mucopolysaccharides and pregelatinized starch are also included as antidiarrheal
agents. ORS should not be mixed with milk or milk replacers.

Evaluation and Monitoring Parameters that May Be Used for Patients Receiving Fluid Therapy

• Pulse rate and quality • Skin turgor

• Packed cell volume/total solids • Creatinine
• Capillary refill time • Body weight
• Total protein • Electrolytes
• Mucous membrane color • Urine output
• Serum lactate • BP
• Respiratory rate and effort • Mental status
• Urine specific gravity • Venous or arterial blood gases
• Lung sounds • Extremity temperature

• Blood urea nitrogen • O2 saturation

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Traditional static methods for monitoring fluid therapy, such as central venous pressure (CVP),
ventricular end diastolic pressure, and pulmonary capillary wedge pressure, have been shown to be
unreliable The plethysmographic variability index (PVI) measures the dynamic changes in perfusion
index (PI) over respiratory cycles. PVI is a noninvasive method to determine both the need for and the
response to fluid therapy. It is based on the pulse oximeter plethysmographic (pleth) pulse pressure
waveform. The Masimo pulse oximeter uses the pleth variability index (PVI) to monitor fluid
responsiveness during anesthesia. Clinical evaluation of PVI in dogs and cats suggests that PVI values above 20
indicate hypovolemia and a need for fluid replacement therapy.

An increase in body weight may be the most accurate method for determining excessive fluid administration

Parental Nutrition Practice Tips

Different formulas for calculating Metabolic energy requirement
1. 132*BW(kg)^0.75
2. 140*BW^0.73
3. Empirical 60 - 75 mL/kg/day for cats/small dogs and 40 - 50 mL/kg/day for larger dogs

For Basal Metabolic Energy rates:

1. 70 x (BWkg)^0.73
2. 97 x (BWkg)^0.655
3. [30*BW(kg) + 70] for patients 2 – 50 kg, and [BW(kg)^0.75]*70 for animals <2 kg or >50 kg

Working example
➢ 20 kg dog, RER = 70 x 200.75 = 662 kcal
➢ Protein 4 g/100 kcal = 26.5 grams per day

Volumes of nutrient solns required

➢ 7.5% aa to supply 26.5 g protein = 26.5/0.075 = 353 mls
➢ 20% lipid to supply 60% of RER 397/2 = 199 mls
➢ 50% dextrose to supply 40% RER = 265/1.7 = 155 mls
➢ Total TPN volume = 353 + 199 + 155 = 707 mls
➢ Administer at 28 mls/hr
➢ 1.4 mls/kgBW/hr

Dextrose 50 % = 170 Kcal per 100ml

Intralipid ( 10% or 20%) = 100kcal per 50 ml ( 20%)
Aminoacids avialble as 7.5 % ( Aminodrip)

Total osmolality
➢ 7.5% aa = 353 ml * 1.144 mOsm/ml = 403 mOsm
➢ 20% lipid = 199 ml * 0.26 mOsm/ml = 52 mOsm
➢ 50% dextrose = 155 ml * 2.525 mOsm/ml = 391 mOsm
= 403 + 52 + 391 = 846 mOsm
Total volume of TPN solution = 0.707 L
Osmolality = 800/0.707 = 1196 mOsm/L
Administer centrally- Jugular vein/central veins

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 Parvo Therapy Update
• Lack of cytopenia, specifically leukopenia (≥4,500/μL) or lymphopenia (≥1,000/μL), had a positive
predictive value of 100% for survival 24 hours post admission. Higher CRP serum cortisol and low
serum thyroxine associated with poor prognosis
• Buprenorphine is given at 0.02 mg/kg SQ as frequently as q 6–8 h. Dogs with uncontrolled nausea
should receive ondansetron at 0.5 mg/kg SQ TID.
• Colloids ( Hetastarch) may be indicated when TP is less than 3.5 or albumin less than 2.5 G/dl
• Early enteral nutrition via a naso-esophageal tube, compared with nil per os - earlier clinical
improvement, significant weight gain, and improved gut barrier function
• Ampicillin and cefoxitin as single-agent treatments or in combination with enrofloxacin are rational
empirical choices. Ampicillin, 20 mg/kg intravenously [IV] every 8 hours) or amoxicillin clavulanate,
20 mg/kg IV every 8 hours) with amikacin, 20 mg/kg IV, intramuscularly, or subcutaneously every 24
hours once the dog has been rehydrated; used for a maximum of 5 days will provide effective
coverage.
• Metronidazole (15–20 mg/kg by mouth every 12 hours for up to 10 days) is ONLY indicated in cases
where protozoa are found on fecal wet prep.
• Immune serum is derived from healthy individuals or from groups of animals that have recovered
from a specific disease. Hyperimmune serum comes from animals that have been repeatedly
vaccinated against specified infectious agents. Passive immunotherapy has shown efficacy in the
treatment of several diseases including tetanus and Clostridium difficile infection. 2 to 4 mL/kg Sc or
IP. Evidence – NO CLINCAL BENEFITS or NO change in outcome
• Human recombinant granulocyte colony stimulating factor (r Hu-GM CSF- Emgrast-M500ug,
Filgastim 1-5ug/kg for 3-5 days) to improve leucocyte count –no evidence of benefits
• Recombinant feline interferon-w (rFeIFN-w). clinical signs and mortality reduced significantly in
those treated with rFeIFN- ω (2.5 mU/kg, intravenously, daily for 3 days
• Oseltamivir (2 mg/kg, per os, for 5 days) improved body weight and hematological parameters) –
not conclusive and no evidence of benefits.
• Fecal Transplant : 10 g of feces from a healthy dog diluted in 10 mL of saline were administered
rectally 6-12 hours post-admission. Faster resolution of diarrhea and shorter hospitalization time
• Other proposed therapies have included equine LPS antitoxin, recombinant bacterial/permeability-
increasing protein.
• Basic inpatient Vs Out patient Therapy outcome - Basic Inpatient : interventions included
administration of IV fluids, administration of cefoxitin (22 mg/kg IV q 8 h), and maropitant (1 mg/kg
IV q 24 h). Basic outpatient interventions included administration of subcutaneous (SC) fluid (30
mL/kg q 6 h), administration of maropitant (1 mg/kg SC q 24 h) and cefovecin (8 mg/kg SC once).
Survival was 90% for the inpatient group compared to 80% for the outpatient group. 50% and 60%
of dogs required dextrose and potassium supplementation respectively in outpatient
Parental Nutrition in Parvo- Guidelines only
Requirement: (kg x 30 + 70) x 1.2 = kcal/day
Peripheral vein (<600 mOsm) Central vein (>600 mOsm)
Lipids 100 mL 20% 250 mL 20%
Amino Acids 200 mL 8.5% 500 mL 8.5%
Glucose 400 mL 10% 500 mL 50%
Electrolyte solution 300 mL none
Potassium add 20 meq/L add 20 meq/L
Energy 0.337 kcal/mL 1.2 kcal/mL

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Kallahalli Umesh
This notes is for education and internal use only, No part of this notes should be reproduced in any manner
Kallahalli Umesh