Page 956 - Problem-Based Feline Medicine

948 PART 11 CAT WITH AN ABNORMAL GAIT

Diagnosis Diazepam should be avoided in these cats as it may
result in generalized muscle tremor, hypersalivation,
A presumptive diagnosis is based on the presence of
miotic pupils and vomiting similar to acute mus-
consistent signs and a history of exposure to an
carinic signs of organophosphate toxicosis.
organophosphate.
Concentration of serum cholinesterase activity may DIABETIC NEUROPATHY**
lend support to the diagnosis, but may be non-diagnostic
for chronic organophosphate toxicity. Values less
Classical signs
than 500 IU/L (normal 900–1200 IU/L) are considered
consistent with organophosphate toxicity. ● Subtle generalized weakness and reduced
activity, difficulty jumping.
Electromyographic changes are occasionally present
● Some cats have a classic plantigrade
and include fibrillation potentials, positive sharp waves
stance in the pelvic limbs.
and bizarre high-frequency discharges. A decremental
response to repetitive nerve stimulation may be present.
Pathogenesis
Beware that edrophonium (used to test for myasthe-
nia gravis) may produce an acute worsening of signs. The cause of the peripheral neuropathy is multifactor-
(Treatment with atropine (0.05 mg/kg IV) may help ial, including diabetes-associated metabolic changes in
the associated parasympathetic signs). the nerve metabolism and/or vascular abnormalities
resulting in nerve ischemia.
Differential diagnosis
Clinical signs
Rule out other diffuse causes of weakness. For the acute
form, other acute poisonings or toxicities such as snake Many diabetic cats prior to initiation of treatment, or if
bite (increased CK, prolonged clotting times) or poorly controlled, have subtle generalized weakness,
hypoglycemia (low plasma glucose usually in an insulin- usually evident as reduced activity, reluctance to move
treated diabetic cat) may appear similar. Differentials and difficulty jumping.
for the chronic form include thiamine deficiency
Some affected cats have a classic plantigrade stance
(response to therapy), polymyositis (increased CK,
in the pelvic limbs, suggesting sciatic (tibial) nerve
abnormal EMG and muscle biopsy), hypokalemic
dysfunction and tarsal extensor muscle weakness.
myopathy (low plasma potassium), hypernatremia (very
rare, hypernatremia), polyneuropathy (abnormal EMG
and decreased nerve conduction velocities), hyperthy- Diagnosis
roidism (other clinical signs and elevated plasma thyrox-
Clinical signs of polyuria, polydipsia, and weight
ine), and myasthenia gravis (IV edrophonium/Tensilon
loss, together with hyperglycemia (usually blood glu-
test, anti-acetylcholine receptor antibodies).
cose is > 17 mmol/L (309 mg/dl) and glucosuria, are
usually diagnostic for diabetes.
Treatment
Electromyographic abnormalities include evidence of
Treatment includes protopam chloride (2-PAM) (20 denervation (fibrillation potentials and positive sharp
mg/kg q 12 h IV) which reactivates cholinesterase and waves) and decreases in nerve conduction velocities.
diphehydramine (1–2 mg/kg PO q 8–12 h) which
Nerve biopsies may show axonal degeneration and/or
reduces muscle fasciculations.
demyelination. These changes, however, are not spe-
Atropine (0.2–0.4 mg/kg) can be given with acute toxi- cific for diabetic neuropathy.
city to decrease autonomic signs. Current recommen-
dations are that it only be used if marked bradycardia is Differential diagnosis
present, because it may precipitate respiratory arrest.
Salivation and defecation are not life threatening and Traumatic rupture of the gastrocnemius tendon may
generally do not require atropine. cause similar signs.