PHARMACOLOGY
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treated with dexamethasone, neither omeprazole
nor misoprostol was effective in healing or preventing the further development of gastric ulcers.13
In dogs undergoing spinal surgery that received
methylprednisolone sodium succinate, neither cimetidine, sucralfate, nor misoprostol reduced postoperative GI bleeding.3,4
Treatment of Complications
Treatment of GI toxicity is intensive and mainly symptomatic. Anorexia and/or vomiting are frequently the first
indication of GI ulceration and perforation. Any dog or
cat that becomes anorectic or vomits while on combination NSAID and corticosteroid therapy should be
promptly evaluated by a veterinarian.
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•
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omiting & Diarrhoea: Fluid and electrolyte losses
V
from vomiting or diarrhea are managed with commercially available intravenous fluids.
Haemostasis Complications: Blood transfusions are
necessary in patients with haemostatic complications.
Hypoproteinaemia: Hypoproteinaemia that results
from loss of plasma proteins into the ulcerated GI
tract can be corrected with intravenous infusions of
plasma.
Renal Failure: The general principles of managing drug-induced renal failure include treatment of
life-threatening features, such as shock, respiratory
failure, hyperkalaemia, pulmonary oedema, metabolic acidosis, and sepsis. Further administration of
nephrotoxic drugs should be avoided and drug dosages should be adjusted as appropriate for the patient’s GFR.
Peritonitis & Bacterial Septicaemia: Broadspectrum
antimicrobials are indicated when there is evidence
of peritonitis or bacterial septicaemia.
Pain: Pain must be managed with opioid analgesics.
GI Perforation: If GI perforation is suspected or diagnosed based on abdominal fluid cytology, abdominal radiography or ultrasound, or endoscopy,
prompt surgical exploration and correction are necessary. Open abdominal drainage may be necessary
as well.7 Even with prompt surgical correction, GI
perforation has a high mortality rate.
vet360
Issue 05 | DECEMBER 2015 | 38
Article sponsored by Petcam®
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I Ulcers: Antiulcer medications may be beneficial
G
and speed healing of GI ulcers.
• The clinical “efficacy” of antiulcer drugs is typically
evaluated by comparing endoscopically detectable mucosal damage and ulcers in treated patients
control animals. However, a true ulcer is deep
enough to reach or penetrate the muscularis mucosa, which cannot be measured endoscopically.
• The NSAID-induced endoscopic “ulcers” seen in
these studies may not be relevant, as clinically significant GI hemorrhage is rarely seen in humans or
dogs with these lesions.14
• Currently, there are limited efficacy data on these
drugs in dogs and none of the antiulcer drugs has
been evaluated in cats.
• In humans, proton pump inhibitors are preferred
for healing and prevention of GI ulcers in patients
taking both traditional NSAIDs and selective coxibs, and who have risk factors associated with
more frequent or severe GI complications, including patients with previous ulcers, the elderly, and
those receiving concomitant corticosteroids or
anticoagulants.15
• Omeprazole, sucralfate, and misoprostol are limited to oral formulations, which are not feasible
in actively vomiting patients or if GI perforation is
likely.
• H2-blockers and pantoprazole are available in injectable formulations.
Summary
It is very difficult to predict which corticosteroid/NSAID
combinations (drug formulation, dose, dosing frequency, treatment duration) will result in adverse effects in
any individual patient. Therefore, concurrent therapy
should only be done when medically necessary and with
close and careful patient monitoring. Further evaluation
in dogs and cats is needed, but proton pump inhibitor
drugs, such as omeprazole, appear to be the best choice
for pharmacotherapy of GI ulceration because their effects are therapeutic as well as prophylactic. Management of adverse haemostatic and renal effects is mainly
supportive.
REFERENCES - available on www.vet360.vetlink.co.za