Page 587 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

574 FLUID THERAPY

especially those that exhibit vasodilatation and are GASTROINTESTINAL PROTECTANTS
refractory to catecholamine therapy, may therefore be
Stress related mucosal disease (SRMD), including both
beneficial. The drug also enhances sensitivity to
superficial and deep mucosal damage, is commonly
catecholamines and therefore may allow the dose of 136
recognized in people with critical illness such as shock.
concurrent catecholamine therapy to be lowered. Exper­
Hypoperfusion of the gastrointestinal tract is the most
imental studies in dogs have demonstrated an increase in
likely cause, although altered mucosal defenses, free radi­
blood pressure and cardiac output with minimal side
cal damage, and increased acid production in the stomach
effects. A clinical case series using vasopressin at 0.5 to
may also contribute. Although the incidence of SRMD in
4 mU/kg/min found an increase in blood pressure fol­
small animals with shock is unknown, the primary strat­
lowing vasopressin therapy as well. This drug will require
egy for prevention is to ensure adequate GI perfusion
further investigation, but may be considered in animals
and employ early enteral nutrition. High-risk patients
with catecholamine resistant vasodilatory shock, as is
may also benefit from pharmacologic prophylaxis for
commonly seen in animals with SIRS, MODS, and sepsis.
SRMD. Based on the currently available evidence in
human medicine, it appears that proton pump inhibitors
ANTIMICROBIAL THERAPY (PPI) are superior to histamine-2 receptor antagonists
The Surviving Sepsis campaign of 2008 recommended (H2RA), which are superior to sucralfate in the preven­
administration of broad-spectrum antibacterial therapy tion of SRMD in adult critical care patients. 97,138 Drugs
within 1 hour of diagnosing severe sepsis or septic available include omeprazole (PPI) 0.7 to 1.0 mg/kg PO
shock. 26 Delaying administration of antibacterials or q24h, pantoprazole (PPI) 0.7 to 1.0 mg/kg IV q24h,
withholding their use in a septic patient increases the famotidine (H2RA) 0.5 to 1.0 mg/kg IV q12 to 24h,
ability of the organisms to reproduce, spread, and induce ranitidine (H2RA) 0.5 to 4 mg/kg IV q8 to 12h, and
a greater inflammatory response. Timely localization of sucralfate (protectant) 0.25 to 1 g/25kg PO q6 to 8h.
the septic focus and procurement of infected tissue or Recent evidence suggests that ranitidine does not
fluid for bacterial identification and susceptibility testing decrease acid production in dogs at clinically
is of paramount importance in the treatment of a patient recommended doses. 8
with septic shock. However, sample collection may be
impossible in some patients due to cardiopulmonary CONTROVERSIAL THERAPIES
instability or the presence of a coagulopathy. Empiric
antimicrobial therapy should be selected based on the
following factors: antimicrobial characteristics (cidal GLUCOCORTICOIDS
versus static); most common bacterial flora in the affected Glucocorticoid therapy in shock has a long and contro­
tissue; ability of the antimicrobial to penetrate the infected versial history. The initial reasoning for steroid adminis­
tissue; history of recent antimicrobial use and potential tration to patients in shock was the mistaken belief
for resistance; safety profile of the drug(s); and source of shock was a form of an addisonian crisis. The indications
infection (whether nosocomial or community-acquired). and potential adverse effects of glucocorticoid therapy
Appropriate empirical antimicrobial therapy is vital for varies between different types of circulatory shock.
success. One canine study found that five dogs receiving
inappropriate empiric antibacterial therapy had a mortal­ Hemorrhagic Shock
ity rate of 80%. 75 Broad spectrum bactericidal antimicro­ There was a great deal of interest and research into the role
bial agents are typically administered to patients with of glucocorticoid therapy in hemorrhagic shock in the
septic shock via the intravenous route. Changes are made 1960s and 1970s. Although some initial experimental
based on the results of antibacterial susceptibility testing. studies were promising, they used models of high dose
Possible choices of four-quadrant, empiric therapy (i.e., steroids administered before the episode of hemorrhage
effective against many gram-positive and gram-negative and only evaluated short-term survival. 51,80 When
aerobes and anaerobes) include: ampicillin (22 mg/kg studies were performed with a more clinically relevant
IV q6 to 8h) and enrofloxacin (15 mg/kg IV q24h in design, high dose steroid therapy could not be shown to
dogs, 5 mg/kg IV q24h hours in cats), ampicillin and increase survival from hemorrhagic shock. 30,58,80 None
amikacin (15 mg/kg IV q24h), cefazolin (22 mg/kg IV of these experimental studies evaluated long-term survival
q8h) and amikacin, ampicillin, and ceftazidime (22 mg/ or the associated adverse effects of such large doses of
kg IV q8h), or clindamycin (10 mg/kg IV q8 to 12h) glucocorticoids. Given the lack of scientific evidence
and enrofloxacin. Single agents such as ticarcillin/ of any benefit of glucocorticoid therapy and our current
clavulanic acid (50 mg/kg IV q6h), cefoxitin (15 to understanding of the adverse effects of high dose steroids,
30 mg/kg IV q4 to 6h), or imipenem (5 to 10 mg/kg their routine use in patients with hemorrhagic shock, or
IV q6 to 8h, if bacterial resistance is suspected). other causes of hypovolemia, cannot be recommended.