Page 460 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

448 FLUID THERAPY

lethargy, paresis, and tachycardia. Serum concentrations greater than 9.0 mmol/L. There were significant
of ionized calcium and parathyroid hormone also differences in posttreatment lactate concentration within
increased after treatment, and findings were thought to the group that had high initial lactate concentrations.
be consistent with secondary hypoparathyroidism Dogs with minimal change in serum lactate concentra-
attributable to hypomagnesemia. 16 Some dogs also may tion had lower survival rates. 137
benefit from 25-hydroxyvitamin D or calcitriol supple- Gastric decompression and fluid therapy are the most
mentation to prevent tetany due to severe ionized hypo- important emergency treatments for dogs with GDV.
calcemia. A calcitriol dosage of 50 ng/kg PO q24h has Fluid therapy has traditionally consisted of shock doses
been recommended, or alternatively 10 to 20 ng/kg (60 to 90 mL/kg/hr) of lactated Ringer’s solution given
PO q12h for 3 to 5 days followed by 5 ng/kg PO via large-gauge catheters into the cephalic or jugular
q12h may be used for maintenance until protein-losing veins. Experimental studies that have compared
enteropathy is under control. 76 crystalloids (60 mL/kg 0.9% NaCl followed by 20 mL/
kg/hr) with hypertonic saline (5 mL/kg 7% NaCl in
GASTRIC DILATATION AND 6% dextran followed by 0.9% NaCl 20 mL/kg/hr) in
VOLVULUS dogs with GDV-induced shock indicated that hypertonic
Gastric dilatation and gastric dilatation-volvulus (GDV) saline maintains better myocardial performance, higher
are life-threatening conditions that are frequently heart rate, and lower systemic vascular resistance than
2
accompanied by severe hypovolemic shock. Hypovolemic crystalloid alone. The resuscitative dose of hypertonic
shock arises as a consequence of impaired venous return saline was delivered in 5 to 10 minutes as compared with
caused by obstruction of the caudal vena cava by gastric 1 hour for the crystalloid. Potassium and bicarbonate are
distention. Devitalization of the gastric wall, splenic tor- best administered based on blood gas and electrolyte
sion, congestion of abdominal viscera, and endotoxic measurements.
shock further exacerbate the hypovolemic crisis.
A variety of acid-base and electrolyte disturbances have ACUTE PANCREATITIS
been observed in dogs with GDV. 83,133 Metabolic acido- Acute pancreatitis is a potentially life-threatening condi-
sis and hypokalemia were the most common tion affecting dogs and cats. 49,51,111,112,117 Clinical
abnormalities in one study, occurring in 15 of 57 and abnormalities are highly variable and in dogs range from
16 of 57 dogs, respectively. 83 Metabolic acidosis is prob- mild dehydration and vomiting to shock, hemorrhagic
ably caused by decreased tissue perfusion, anaerobic diathesis, and death. Anorexia, lethargy, and weight loss
metabolism, and accumulation of lactic acid. 83 Metabolic are the most common clinical signs in cats with pancrea-
alkalosis may also occur as a result of vomiting or seques- titis. The severity of clinical signs is thought to reflect the
tration of acid in the stomach. 83 Either respiratory acido- severity of pancreatitis (i.e., mild edematous versus severe
sis or respiratory alkalosis may be observed and reflect necrotizing or suppurative) and the presence of systemic
hypoventilation or hyperventilation, respectively. The complications such as shock, pancreatic infection and
variety of acid-base and electrolyte abnormalities in dogs necrosis, sepsis, and disseminated intravascular coagula-
with GDV dictates that fluid therapy be individualized tion. A clinical severity index (CSI) has been developed
based on blood gas analysis and serum electrolyte for dogs with acute pancreatitis. In this study, CSI
concentrations. predicted severity of disease and the need for aggressive
Plasma lactate concentration appears to be a good pre- treatment. However, it did not predict a positive or neg-
dictor of gastric necrosis and survival among dogs with ative outcome in days. 74 C-reactive protein concentration
GDV. 29 In this study, 69 of 70 (99%) dogs with plasma measured within 2 days after the onset of clinical signs
lactate concentrations less than 6.0 mmol/L survived, tended to be lower in survivors as compared with
74
whereas 18 of 31 (58%) dogs with plasma lactate nonsurvivors. C-reactive protein concentration has
concentrations more than 6.0 mmol/L did not. Gastric been shown to be increased in various diseases, including
necrosis was identified in 38 (37%) dogs. The median acute pancreatitis, hemangiosarcoma, and polyarthritis,
plasma lactate concentration in dogs with gastric necrosis and it has been shown to be a more sensitive marker of
(6.6 mmol/L) was significantly higher than that in dogs inflammation than white cell count. 86 However, the role
without gastric necrosis (3.3 mmol/L). The specificity of C-reactive protein concentration in acute pancreatitis
and sensitivity of plasma lactate concentration (with a cut- remains to be determined.
off of 6.0 mmol/L) for predicting which dogs had gastric The cause of acute pancreatitis in dogs and cats usually
necrosis were 88% and 61%, respectively. Sixty-two of 63 remains undetermined. In a retrospective case control
(98%) dogs without gastric necrosis survived compared study in dogs with acute pancreatitis, ingestion of unusual
with 25 of 38 (66%) dogs with gastric necrosis. In a simi- food (OR 6.1), ingestion of table scraps the week before
lar study, 36 of 40 (90%) dogs with an initial lactate con- diagnosis (OR 2.2) or throughout life (OR 2.2), getting
centration of 9.0 mmol/L survived compared with only into the trash (OR 13.2), being neutered (OR 3.6), and
13 of 24 (54%) dogs with an initial lactate concentration undergoing surgery other than neutering (OR 21.1)