Page 458 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
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446        FLUID THERAPY


            based on the patient’s hydration, tissue perfusion, and  The effect of vomiting and diarrhea on acid-base bal-
            electrolyte and acid-base status. The presence of anemia  ance is difficult to predict, and therapeutic intervention to
            or hypoalbuminemia and the potential for continuing  correct acid-base imbalance should be based on blood gas
            fluid loss through vomiting, diarrhea, fever, and compen-  analysis. Patients with normal acid-base status or mild
            satory hyperventilation associated with metabolic acidosis  metabolic acidosis may be given lactated Ringer’s solu-
            must also be taken into account. Minimal evaluation of  tion at a rate sufficient to correct fluid deficits and provide
            the patient with gastrointestinal disease should include  for maintenance and ongoing losses for a 24-hour period.
            determination of body temperature, heart rate, skin tur-  Potassium depletion may be a consequence of prolonged
            gor, capillary refill time, packed cell volume (PCV), total  diarrhea, vomiting, or anorexia, but most polyionic
            protein concentration, urine specific gravity, and urine  replacement fluids contain only small amounts of potas-
            pH, as well as serum concentrations of sodium, potas-  sium. Consequently, KCl is usually added to parenteral
            sium, chloride, total CO 2 , and glucose. Measurement  fluids  and  adjusted  based  on  serum  potassium
            of blood gases, blood pressure (central venous and   concentrations. When severe metabolic acidosis is present
            arterial), and urine output is required for optimal care  (pH <7.1; HCO 3    <10 mEq/L), sodium bicarbonate
            of patients with severe gastrointestinal disease.    (1 mEq/kg) can be given. Care should be taken to rule
               Oral fluid therapy may be useful for patients with diar-  out respiratory acidosis before administering sodium
            rhea that can tolerate oral intake. Subcutaneous adminis-  bicarbonate and to administer it slowly and in small
            tration of an isotonic balanced electrolyte solution may be  amounts (0.5 mEq/kg over 15 minutes) to prevent cere-
            sufficient to correct mild (5%) fluid deficits but is insuffi-  brospinal fluid acidosis, aggravation of hypokalemia, or
            cient for patients with moderate (5% to 10%) or severe  hypocalcemia. Additional bicarbonate supplementation
            (>10%) dehydration. For patients with moderate to    is based on repeated blood gas analyses. Metabolic alka-
            severe dehydration, inadequate oral intake, electrolyte  losis usually responds to correction of the volume, chlo-
            imbalance, or signs of hypovolemic or endotoxic shock,  ride,  and  potassium  deficits  with  0.9%  NaCl
            intravenous fluid administration is necessary.       supplemented with KCl administered intravenously.
               The rate of fluid administration depends on the pres-  Diagnostic investigations should initially focus on rul-
            ence or absence of shock, the extent of dehydration, and  ing out upper gastrointestinal obstruction. Administra-
            the presence of cardiac or renal disease that may predis-  tion of antisecretory drugs (e.g., H 2 antagonists) may
            pose the patient to volume overload. Patients with a  limit chloride efflux into gastric juice. When acid hyper-
            history of vomiting that are mildly dehydrated are usually  secretion is present or suspected, it is best managed by
            responsive to crystalloids (e.g., lactated Ringer’s solution  administration of a proton pump inhibitor (e.g., omepra-
            or 9% NaCl) at a rate that provides maintenance needs  zole at 0.7 to 1.0 mg/kg every 24 hours). Somatostatin
            and replaces existing deficits and ongoing losses over a  analogs may also be useful to control gastric acid
            24-hour period. Patients with signs of shock require more  hypersecretion (e.g., octreotide at 2 to 20 mg/kg subcu-
            aggressive support. The volume deficit can be replaced  taneously every 8 hours). 115
            with crystalloids at an initial rate of 60 (cat) to 90  Other symptomatic treatments considered initially in
            (dog) mL/kg/hr, which is then tailored to maintain tis-  patients with vomiting and diarrhea are antacids and
            sue perfusion and hydration. Central venous pressure  antiemetics when vomiting persists. Prophylactic use of
            monitoring and evaluation of urine output are necessary  antibiotics (e.g., cephalosporins, ampicillin) may be
            for patients with severe gastrointestinal disease, especially  warranted in animals with shock and suspected gastroin-
            those with third-space losses of fluid into the gut or  testinal barrier dysfunction. Analgesia can be provided
            peritoneum. Colloids and hypertonic solutions can    using opioids (e.g., buprenorphine at 10 to 20 mg/kg
            also be used to reduce the amount of crystalloid     intramuscularly).
            required (e.g., 5 mL/kg of 7% NaCl in 6% dextran intra-
            venously, 10 to 20 mL/kg/day of degraded gelatin     Oral Rehydration Solutions
            [Haemaccel] intravenously). Colloids are also useful in  The rationale for use of oral rehydration solutions (ORSs)
            hypoproteinemic patients. Endotoxic shock is a common  is the coupled transport of sodium with glucose or other
            complication of severe gastrointestinal disease. Warning  actively transported small organic molecules and hence
            signs of endotoxemic shock include fever or subnormal  the  promotion  of  water  absorption. 25,37  These
            body temperature, tachycardia, increased respiratory rate,  cotransport processes often remain relatively unaffected
            slow capillary refill time, hyperemic or pale mucous  in acute infectious (e.g., bacterial, viral) cases of diar-
            membranes, transient leukopenia followed by leukocyto-  rhea. 124  In secretory diarrhea, the epithelium maintains
            sis with a left shift and toxic neutrophils, low-normal cen-  its absorptive capacity and cotransport processes that
            tral venous pressure, and bounding pulses. Patients with  are important for the success of oral rehydration ther-
            endotoxic shock must be treated aggressively with fluid  apy. 124  With certain viral causes of diarrhea (e.g., rotaviral
            therapy, broad-spectrum antibiotics, glucocorticoids,  infection in children), patchy epithelial damage may allow
            oxygen, glucose, and bicarbonate as indicated. 47    oral rehydration to be of benefit. 106,107  A balanced ORS
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