Page 602 - Problem-Based Feline Medicine

594 PART 9 CAT WITH SIGNS OF GASTROINTESTINAL TRACT DISEASE

Treatment Cats are more susceptible to OP toxicity than dogs.
Poisoning often occurs following use of canine flea
Medical treatment:
products on cats.
● Control of esophagitis and clinical signs with
ranitidine (3.5 mg/kg PO q 12 h) or cimetidine Most cat poison cases are due to carbamates.
(5–10 mg/kg PO q12 h).
● Feed low-fat diet. Fat delays gastric emptying
Clinical signs
time and it is therefore desirable to feed low-fat
diets. Elevated feedings may help some cats Early signs include apprehension, increased swallow-
and should be trialled especially if megaesopha- ing, ptyalism, muscular twitching around the face
gus is present. and eyes. Miosis and bradycardia occur.
● If no response to medical therapy surgical
Muscular twitching progresses to whole-body muscle
repair is warranted.
fasciculations and generalized tetany causing a stiff-
Surgical repair involves anatomical replacement of legged gait progressing to a sawhorse stance (i.e. all
herniated organs, reduction in size of esophageal hia- four legs stiff and apart).
tus, phrenicoesophageal plexy and left-sided fundic
Abdominal pain, cramping diarrhea, vomiting and
gastropexy.
frequent urination occurs commonly and eventually
progresses to muscular weakness and paralysis.
Death can occur due to respiratory failure.
ORGANOPHOSPHATE AND CARBAMATE
TOXICITY Delayed neuropathy: certain OPs (e.g. fenthion) can
cause a delayed (usually 7–10 days) neuropathy caus-
Classical signs ing hindlimb weakness and characteristic ven-
troflexion of the neck. All the other signs of acute OP
● Ptyalism, lacrimation, vomiting, diarrhea,
poisoning are absent when delayed signs occur.
pollakiuria.
Delayed neuropathy may occur after minimal exposure
● Miosis, muscular tremors, seizures.
and there may be no history of acute signs in the pre-
● Dyspnea, respiratory failure.
ceding 7–10 days.
● Bradycardia, depression, death.
● Rapid onset of clinical signs.
Diagnosis
History of recent application of OP or carbamate and
Pathogenesis characteristic signs.
Organophosphates (OPs) and carbamates cause inhibi- Cholinesterase assay – whole blood, serum or plasma.
tion of acetylcholinesterase (AChE) and pseudo- Results should be interpreted in light of clinical signs
cholinesterase, which allows accumulation of and time of onset of signs.
acetylcholine (ACh) in RBCs and the post-synaptic
receptors of nervous tissue and muscle. Differential diagnosis
Accumulation of ACh results in marked excitation of
Pyrethrin toxicity – history of exposure.
all effector organs.
Quaternary ammonium toxicity – history of exposure
OPs are generally considered irreversible inhibitors of
and ptyalism with mouth ulcers rather than general-
AChE activity, while carbamates are slowly
ized parasympathetic signs as occur with OPs.
reversible inhibitors.
OPs are stored in fat and slowly released into the cir- Treatment
culation. Lean, long-haired breeds of cats are more
severely affected. Establish IV fluid line and (oxygen/ventilation if needed).