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Feline Aortic Thromboembolism

🐾 Comprehensive Information on Feline Aortic Thromboembolism (FATE / CATE) for NAVLE Preparation 🐾 Feline Aortic Thromboembolism (FATE), also known as Cardiogenic Arterial Thromboembolism (CATE) or “saddle thrombus,” is a life-threatening condition in cats characterized by the embolization of a cardiac thrombus—most often originating in a dilated left atrium—into systemic arteries, especially the terminal aorta. It is most commonly associated with underlying cardiomyopathies, particularly Hypertrophic Cardiomyopathy (HCM). Affected cats present acutely with hindlimb paralysis, pain, absent pulses, and hypothermia due to ischemic neuromyopathy. This condition is a true emergency requiring rapid diagnosis, stabilization, and aggressive multimodal treatment to reduce morbidity and mortality. This note provides a detailed and clinically focused overview of the etiology, pathophysiology, clinical signs, diagnostic approach, treatment options (including anticoagulation and thrombolysis), prognosis, and preventive strategies. It is intended to prepare veterinary professionals for recognizing and managing FATE with confidence during the NAVLE and in clinical practice.


🐱 Comprehensive Information on Feline Aortic Thromboembolism (FATE / CATE) for NAVLE Preparation

🔍 Definition and Overview

Feline Aortic Thromboembolism (FATE), also referred to as Cardiogenic Arterial Thromboembolism (CATE) or "saddle thrombus," is a life-threatening condition characterized by the embolization of a cardiac thrombus—most commonly from the left atrium—to the distal aortic trifurcation. It results in acute ischemia of the pelvic limbs and, less commonly, other systemic arteries.

  • Prevalence:

    • ~1 in 175 cases in US tertiary centers

    • ~1 in 379 in UK general practices

  • Primary cause: Cardiomyopathy in ~90% of cases

    • Most common: Hypertrophic Cardiomyopathy (HCM)

    • Others: Dilated Cardiomyopathy (DCM), Restrictive Cardiomyopathy (RCM), Unclassified Cardiomyopathies


⚙️ Pathophysiology

FATE results from Virchow’s triad:

  1. Blood stasis: Due to poor left ventricular filling, leading to left atrial dilation and stagnation.

  2. Endothelial injury: Damage to atrial endocardium promotes platelet activation and adhesion.

  3. Hypercoagulable state: Includes:

    • ↑ Platelet hypersensitivity

    • ↓ Antithrombin and Protein C

    • ↑ Factor VIII and fibrinogen


🧬 Thrombus Formation:

  • Platelet-rich → fibrin-rich thrombus within left atrium

  • Embolizes to:

    • Aortic trifurcation (70–75%) → Bilateral hindlimb infarction

    • Unilateral pelvic limb (10–15%)

    • Brachial arteries (~10%)

    • Less common: renal, cerebral, mesenteric arteries


🚨 Clinical Signs

Classic “5 Ps” of acute limb ischemia:

  1. Paresis/paralysis

  2. Pulselessness

  3. Pallor (cyanotic nail beds)

  4. Pain

  5. Polar (cold limbs)


🩺 Other signs:

  • Hindlimb rigidity, absent reflexes, firm painful musculature

  • Hypothermia

  • Respiratory distress (from CHF or cardiomyopathy)

  • Signs of underlying heart disease (dyspnea, gallop rhythm, murmurs)

  • Neurologic deficits (if emboli affect CNS)

  • Acute renal failure (renal infarction)


🧪 Diagnostics

Clinical Examination:

  • Sudden onset of hindlimb paresis/paralysis

  • Cyanotic, cold limbs

  • Absent femoral pulses

  • Pain response in affected limb


Point-of-Care Ultrasound (C-POCUS):

  • Enlarged left atrium

  • Visualization of intra-atrial thrombi

  • Identification of underlying cardiomyopathy


Imaging:

  • Thoracic radiographs: Evaluate pulmonary edema or CHF

  • Echocardiography: Assess atrial size, myocardial structure


Laboratory Findings:

  • ↑ CK, AST, ALT (muscle enzymes)

  • Azotemia (pre-renal or renal)

  • Hyperkalemia, hyperglycemia, metabolic acidosis

  • Elevated lactate in affected limbs (especially >11.5 mmol/L = poor prognosis)

  • Hypocalcemia, hypercholesterolemia


💊 Treatment

1. Acute Emergency Management

Analgesia:

  • Methadone, fentanyl CRI, buprenorphine, oxymorphone

Cardiopulmonary Stabilization:

  • Oxygen supplementation

  • Furosemide if pulmonary edema is present


Thromboprophylaxis:

Anticoagulants:

  • Unfractionated Heparin (UFH):

    • 250–375 IU/kg IV loading dose

    • 150–250 IU/kg SC q6–8h

  • Low Molecular Weight Heparins (LMWH):

    • Dalteparin: 100 IU/kg SC q12h

    • Enoxaparin: 1.0–1.5 mg/kg SC q12h

Thrombolytics (controversial):

  • Tissue Plasminogen Activator (t-PA):

    • 0.25–1 mg/kg/hr IV infusion

    • Total dose 1–10 mg/kg

    • High risk of bleeding; no definitive survival benefit

Reperfusion Injury Monitoring:

  • Hyperkalemia

  • Acidosis

  • Bradyarrhythmias → ECG monitoring critical


2. Chronic Management & Prevention of Recurrence

Antiplatelet Therapy:

  • Clopidogrel: 18.75 mg PO q24h (first-line)

  • Aspirin: 5 mg/cat PO q48h (less effective)

Oral Anticoagulants:

  • Rivaroxaban: 0.5–1 mg/kg PO q24h

  • Apixaban: Alternative, dose varies

Dual Therapy:

  • Clopidogrel + Rivaroxaban offers best protection against recurrence

Warfarin:

  • 0.06–0.09 mg/kg PO q24h

  • Requires close INR monitoring (target: 2–3)


Supportive Care:

  • Nutritional support

  • Passive range-of-motion physiotherapy

  • Management of concurrent CHF or cardiomyopathy


📊 Prognosis

  • Variable; depends on:

    • Number of limbs affected

    • Initial motor function

    • Rectal temp <37°C = poor outcome

    • Limb lactate >11.5 mmol/L = grave prognosis

  • Survival to discharge (bilateral): ~37.5%

  • Median survival post-discharge: 350–500 days


⚠️ Complications

  • Reperfusion injury: Hyperkalemia, acidosis, arrhythmias

  • Chronic ischemia: Risk of muscle necrosis, contracture, limb amputation

  • Acute kidney injury (from myoglobinuria or hypotension)


✅ Key Takeaways for NAVLE

  • FATE is often the first clinical manifestation of cardiomyopathy in cats.

  • Left atrial thrombus is the origin in >90% of cases.

  • Classic “5 Ps” help identify ischemic neuromyopathy.

  • First-line treatment includes clopidogrel; dual therapy is best for recurrence prevention.

  • Acute management must include analgesia, anticoagulation, and CHF stabilization.

  • Prognosis is guarded to poor, especially with bilateral involvement and hypothermia.


📚 References

  • Guillaumin, Julien. Feline aortic thromboembolism: recent advances and future prospects. Journal of Feline Medicine and Surgery. 2024.

  • Kittleson, M. D., & Côté, E. (2021). The feline cardiomyopathies II: Hypertrophic cardiomyopathy. Journal of Veterinary Cardiology.

  • Merck Veterinary Manual. Heart Disease and Thromboembolism in Cats.


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