Page 304 - Feline Cardiology

312 Section H: Arterial Thromboembolism

Box 20.1. Treatment of life-threatening hyperkalemia (reperfusion injury)

Drug Dose Onset of action

10% calcium gluconate 0.5–1.5 ml/kg IV slowly over 5–10 minutes 3–5 minutes
Sodium bicarbonate 1–2 mEq/kg IV slowly over 15 minutes 15 minutes
25% dextrose 0.7–1 g/kg IV over 3–5 minutes <1 hour
25% dextrose with insulin Regular insulin at 0.5 U/kg IV with dextrose at 2 g/U of insulin administered 30 minutes

Modified from: Riordan LL, Schaer M. Potassium disorders. In: Small Animal Critical Care Medicine, Silverstein DS, Hopper K, eds. St. Louis, Saunders
Elsevier, 2009.

and acidosis. It is a life-threatening condition that ated to evaluate efficacy of t-PA in cats with ATE was
usually occurs hours to several days after the embolic terminated due to a high frequency of adverse outcomes
event due to systemic release of the metabolic byprod- (Welch et al. 2010). Adverse effects were seen in 100%
ucts associated with ischemia. Treatment should be of treated cats (11/11) including azotemia (n = 5), neu-
aggressive and immediate. Hyperkalemia can be
rological signs (n = 5), cardiac arrhythmias (n = 5),
Arterial Thromboembolism glucose to drive K+ intracellularly. If a secondary brady- death (n = 1). Twenty-seven percent (n = 3) of t-PA
addressed with calcium gluconate and/or insulin and
hyperkalemica (n = 4) acidosis (n = 2) and sudden
cardia is present, atropine may be indicated. Fluid
treated ATE cats in this study were ultimately discharged
therapy with sodium bicarbonate is warranted to address
from the hospital (Welch et al. 2010). Considering the
metabolic acidosis. Unfortunately, the prognosis in cats
expense involved with these therapies, their use at this
time is difficult to justify. Moreover, if thrombolytic
that develop reperfusion syndrome is poor, and many
cannot be rescued. See Box 20.1 for emergency therapy
toring for acute life-threatening reperfusion syndrome
for cats in a hyperkalemic crisis.
Thrombolytic therapy seems intuitive because rapid therapy is elected, cats require intensive 24-hour moni-
and their use should be avoided in cats with intracardiac
resolution of the arterial occlusion theoretically would thrombi due to risk of new embolic events as the clot
be beneficial for the patient. However, streptokinase and undergoes lysis.
urokinase act by generating the nonspecific proteolytic A case series described efficacy of a commercially
enzyme plasmin, which can lead to a generalized lytic available rheolytic thrombectomy system in 6 ATE cats
state with the hazard of bleeding complications. Tissue (Reimer et al. 2006). This intravascular system mechani-
plasminogen activator (t-PA) has a lower affinity for cally breaks down the embolus, and resulted in successful
circulating plasminogen and does not induce a systemic embolus dissolution in 5 of the 6 cats. However, despite
fibrinolytic state. Rather, t-PA initiates local fibrinolysis successful thromboembolectomy, only 3 cats survived to
with limited systemic proteolysis. No controlled clinical discharge and the remaining succumbed to systemic
trials have evaluated the use of thrombolytic agents in hypotension during or after the procedure. It is possible
cats with ATE. However, in the case series that have been that with more experience the procedure will result in
published so far, the approach (with any of these agents) improved success; however, at this time the expense of
does not appear to significantly alter case outcome. In a the procedure (similar to medical thrombolytic therapy)
series of 46 ATE cats that were treated with streptoki- is difficult to justify since a hospital discharge rate of
nase, 33% survived to discharge (Moore et al. 2000). 50% is similar to what is reported for cats treated con-
Although these results were better than the 0% survival servatively (Smith and Tobias 2004).
noted in an older report of 8 cats treated with high dose
streptokinase (Ramsey et al. 1996), it was still no better Anticoagulant Therapy
than conservative therapy. Indicators of poor outcome Anticoagulant therapy has no effect on established
were similar to other feline ATE studies (azotemia and thrombi; however, by retarding clotting factor synthesis,
hypothermia) while having one limb affected was asso- or accelerating its inactivation, thrombosis from acti-
ciated with better outcome (Moore et al. 2000). Similar vated blood-clotting pathways can be prevented. The
results were reported in an abstract describing the use theoretical aim of anticoagulant therapy in the acute
of t-PA in 6 ATE cats, with 3 cats surviving to discharge phase is to prevent or reduce thrombus extension.
from the hospital (Pion et al. 1987). Another study initi- Heparin binds to lysine sites on plasma antithrombin,