Page 462 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

450 FLUID THERAPY

ally consist of metabolic acidosis, but metabolic alkalosis to be more protracted. No treatment regimens for
may also be observed. 49 pancreatitis have been critically evaluated in dogs or cats
Medical management of acute pancreatitis is usually with naturally occurring pancreatitis.
initiated before the diagnosis is confirmed and is based Specific therapy in humans consists of preventing fur-
on presenting clinical findings and laboratory ther pancreatitis from developing and limiting the local
abnormalities (e.g., PCV, urinalysis, and total protein, and systemic consequences of pancreatitis. Therapy
blood urea nitrogen, glucose, sodium, and potassium aimed at inhibiting pancreatic secretion (e.g., glucagon,
concentrations). (See the Overview of Fluid Therapy somatostatin) or intracellular activation of proteases
for Vomiting and Diarrhea section). Hypovolemia and (e.g., gabexate mesylate) that has been beneficial in
dehydration are evaluated and corrected by intravenous ameliorating experimental pancreatitis has shown little
administration of fluids. The type of fluid chosen should benefit in the treatment of clinical patients. This lack of
be based on serum electrolytes (e.g., sodium, potassium, success may be related to the timing of therapy in relation
chloride, total CO 2 ) to restore normal electrolyte and to the development of pancreatitis. Therapy in experi-
acid-base balance. Hypocalcemia usually is not associated mental pancreatitis is usually initiated before or shortly
with tetany or seizures, and the value of supplementing after induction of pancreatitis, whereas most clinical
calcium in patients with ionized hypocalcemia, especially patients are not presented until 24 to 48 hours after
cats in which hypocalcemia has been associated with the onset of pancreatitis. These findings have led to more
prognosis, remains to be determined. If hypoglycemia therapeutic emphasis on limitation of damage, including
is present, dextrose (2.5% to 5%) is added to the fluids. limiting the effects of inflammatory mediators or pancre-
Insulin therapy is initiated if hyperglycemia, glucosuria, atic enzymes and maintaining pancreatic perfusion.
and ketonuria are present. Stress hyperglycemia should The systemic effects of pancreatitis may be ameliorated
be ruled out when ketonuria is absent. in experimental animals by maintaining adequate
Other symptomatic treatments initially considered pancreatic microcirculation and protease-antiprotease
include enteral feeding and antacids or antiemetics when balance. The pancreatic microcirculation in dogs with
vomiting or nausea is persistent. Centrally acting experimental pancreatitis was maintained more effectively
antiemeticssuchasmetoclopramide,maropitant,orpheno- by use of dextran-containing solutions than by use of
thiazine derivatives are indicated for patients with intracta- crystalloids. 53,63 The pancreatic microcirculation of cats
ble vomiting. Maropitant has been considered a superior with experimental pancreatitis was maintained by low-
antiemetic for both centrally and peripherally induced dose dopamine infusion (5 mg/kg/min). 58 Fresh frozen
vomiting. 26,27,50,109,128 Anecdotally, maropitant has had plasma (FFP) has been advocated as a treatment for
limited effectiveness against nausea. However, one study pancreatitis to replenish antiproteases, primarily
showedthatadministrationofmaropitantdecreasedavisual a-macroglobulins, that are lost during the inflammatory
analogscorefornauseacausedbyadministrationofcisplatin process. 71,84 However, a recent retrospective case series
in dogs when compared with saline alone. 27 Antiemetics showed lack of benefit and higher mortality in dogs with
should be chosen based on the drug’s mechanism of action acute pancreatitis that received FFP. 131 Due to the
as well as the nature of the disease process itself (see retrospective study design, severity of illness scores were
Figure 18-8). Prophylactic use of antibiotics (i.e., difficult to assign, but preexisting illness, evidence of
cephalosporins or ampicillin alone or in combination with systemic inflammatory response syndrome, and presence
enrofloxacin or amikacin) may be warranted for patients of coagulopathy were not significantly different between
with shock, fever, diabetes mellitus, or hemorrhagic diar- the groups that did and did not receive FFP. 131 Adminis-
rhea or vomitus. Analgesia can be provided using opioids tration of FFP also may be beneficial for management of
(e.g., buprenorphine at 10 to 20 mg/kg intramuscularly). disseminated intravascular coagulation or other
After a diagnosis of pancreatitis is confirmed, fluid coagulopathies. Heparin administration (75 to
therapy is continued, and more specific therapy may be 150 U/kg subcutaneously every 8 hours) may be
used. The majority of dogs with acute pancreatitis warranted in the early stages of acute pancreatitis to delay
respond to fluid therapy and nothing by mouth for 48 development of disseminated intravascular coagulation.
hours. More specific therapy is usually reserved for dogs Heparin administration (1 unit/kg/hour IV) activates
that do not respond to fluid therapy or that have signs of lipoprotein lipase and decreases lipemia, a frequent
disseminated intravascular coagulation. Surgical inter- finding in acute pancreatitis. Clearing of lipemia decreases
vention and aggressive postoperative care may be neces- the risk of thromboembolic events secondary to hypertri-
sary in some dogs with extrahepatic biliary obstruction glyceridemia, and facilitates performance and interpreta-
secondary to acute pancreatitis or pancreatic abscessation. tion of serum biochemistry tests. Oral pancreatic enzyme
Patients with pancreatic abscesses have a more guarded extracts have been reported to reduce pain in humans
prognosis. 125 In contrast to dogs, cats with acute pancre- with chronic pancreatitis but are less likely to be effective
atitis are more commonly presented with anorexia than in dogs because dogs do not appear to have a protease-
vomiting, but episodes of pancreatic inflammation appear mediated negative feedback system.