FATEs Flashcards
Where do FATEs tend to originate in cats?
left auricular appendage
Which cardiac diseases are associated with FATEs?
All except ARVC
Includes secondary causes of myocardial disease including euthyroid treated hyperthyroid cats
How can you dx FATE from PE?
‘5 Ps’ of pain, paralysis, pulselessness, poikilothermy and pallor
Motor function is usually absent or reduced distal to the stifles, with skin sensation absent distal to the tarsus.
The combination of pelvic limb lower motor neuron signs with absent femoral pulses and cold extremities is pathognomonic for ATE.
cat is presented.
Rectal temperature is often reduced and is considered a poor prognostic sign.
It is important to recognise signs of CHF, as this confers a worse prognosis
half of cats will have a murmur, gallop or arrhythmia
What is often seen on biochem tests?
hyperglycaemia, and azotaemia and hyperphosphataemia are also common. Azotaemia
is usually prerenal, although can also be associated with thromboembolism of a renal artery
markedly high CK
Sometimes low Na or Ca
Although hyperkalaemia is an important and potentially
fatal complication of ATE, the rise in plasma potassium concentrations often occurs suddenly as perfusion is restored and some cats may actually be hypokalaemic on presentation.
Check T4 in older cats
What Ix should be performed in cats with FATEs?
Chest rads to check for pulmonary neoplasia and presence of CHF
BP to check if hypotensive and also to look for pulses
Check femoral pulses with hand
What are the risk factors for FATEs?
Previous one (even if mild/ transitory)
✜ Spontaneous echo contrast/ visible thrombus
✜ Left atrial enlargement
✜ Systolic dysfunction of the left atrium
✜ Systolic dysfunction of the left ventricle
Outline the initial approach to the FATE cat
Immediate - euthanise if going to as first 24 hours most painful
Then provide opiate pain relief
Oxygen should be administered to cats with respiratory distress.
Inspiratory crackles on auscultation are suggestive of pulmonary oedema.
Significant pleural effusion is less likely to develop acutely with ATE, although this can also be identified using physical examination
For tachypnoeic cats with normal breath sounds, thoracic radiographs should be obtained. If pulmonary oedema is suspected, then intravenous furosemide should be administered at 1–2 mg/kg. Furosemide
should be repeated to effect, at hourly intervals or more frequently depending on the severity of respiratory distress.
Deal with the clot
What is the recommended way of initally treating the actual thrombus?
The goal of antithrombotic therapy is to prevent extension of existing thrombus, and to prevent new thrombus formation, not to lyse existing thrombus.
The value of unfractionated heparin or LMWHs for this use has not been established in cats. An alternative
approach is to use oral agents such as aspirin
or clopidogrel from the start (or both)
What investigations should be done in the first 24 hours?
Once pain and CHF have been addressed
and antithrombotic treatment started only
Apart from monitoring vital signs, general demeanour and mobility, renal function and electrolytes should be monitored.
Echocardiography will help determine whether the underlying cause of ATE is cardiac disease.
What management may be needed in the first 24 hours?
IVFT if azotaemic
Although not authorised for use in cats, pimobendan (1.25 mg per cat q12h) may be helpful for cats with systolic dysfunction, and can be tried as long as there
is no murmur present. - Mostly given if hypotensive
physio if will tolerate it
Outline monitoring over the first few days
Pain usually decreases over the first 24–36 h. An
improvement in warmth, pulse quality and motor function of the affected limb(s) is an indication that limb perfusion is improving.
Pulse strength will often improve within 4–5 days, reflecting improved circulation
Where there is evidence of severe ischaemic nerve
damage, this may take weeks to improve.
Identifying the warning signs of adverse effects or complications is challenging. The main complications are CHF, reperfusion injury, azotaemia and the local
consequences of ischaemic tissue necrosis. As pulses return, reperfusion of ischaemic tissue can cause sudden life-threatening fluctuations in serum potassium concentrations and reactive oxygen species, as well as acid–base balance. Cats that are apparently making good progress can suddenly and dramatically deteriorate. This makes monitoring for such changes very difficult. Even with serum biochemistry testing q8h, critical electrolyte changes may develop between blood sampling periods
