Pulmonary Thromboembolism

Pulmonary thromboembolism (PTE) is a life-threatening cardiovascular and respiratory disorder characterized by the lodgment of a thrombus (blood clot) or embolic material (e.g., fat, air, tumor cells, septic emboli) within the pulmonary arterial vasculature, leading to partial or complete obstruction of blood flow to a portion of the lung. This obstruction results in a spectrum of pathophysiological consequences, including ventilation-perfusion (V/Q) mismatch, increased pulmonary vascular resistance, pulmonary hypertension, right ventricular (RV) afterload elevation, and potentially acute cor pulmonale and death. PTE is often underdiagnosed in veterinary medicine due to its nonspecific clinical presentation and the limitations of diagnostic imaging. The disease can be classified based on the chronicity (acute, subacute, chronic) and the extent of vascular occlusion (massive, submassive, non-massive). In dogs and cats, PTE is typically a complication of an underlying hypercoagulable state, vascular endothelial injury, or venous stasis (Virchow's triad). The clinical severity ranges from asymptomatic incidental findings to fulminant respiratory failure and sudden death. Early recognition and aggressive management are critical to improve outcomes.

The etiology of pulmonary thromboembolism in veterinary patients is multifactorial, with most cases arising from a combination of risk factors that promote thrombus formation. The primary causes include: (1) Hypercoagulable states: Immune-mediated hemolytic anemia (IMHA) is the most common cause in dogs, where the release of pro-inflammatory cytokines and platelet activation leads to a prothrombotic state. Other causes include hyperadrenocorticism (Cushing's disease), protein-losing nephropathy (PLN) with loss of antithrombin III, protein-losing enteropathy (PLE), sepsis, disseminated intravascular coagulation (DIC), neoplasia (e.g., hemangiosarcoma, adenocarcinoma), and glucocorticoid administration. (2) Vascular endothelial injury: Trauma, surgery (especially orthopedic or abdominal), central venous catheterization, heartworm disease (Dirofilaria immitis) causing pulmonary arteritis, and vasculitis (e.g., immune-mediated, infectious). (3) Venous stasis: Prolonged recumbency, obesity, heart failure, and caval syndrome. (4) Embolic materials: Septic thrombi from bacterial endocarditis, tumor emboli, fat emboli from fractures, and air emboli from catheterization. In cats, causes include cardiomyopathy (especially hypertrophic cardiomyopathy), arterial thromboembolism (often referred to as 'saddle thrombus' but can also affect pulmonary arteries), and chronic kidney disease. Additionally, inherited or acquired thrombophilia (e.g., antithrombin III deficiency, protein C or S deficiency) may be identified in some cases, though these are rare in veterinary medicine.

Pulmonary thromboembolism is reported in both dogs and cats, with a higher incidence in dogs. The exact prevalence is unknown due to the difficulty in antemortem diagnosis, but postmortem studies suggest that PTE may be present in up to 5-10% of dogs with certain underlying diseases, particularly IMHA and neoplasia. There is no strong breed or sex predisposition, but breeds predisposed to immune-mediated diseases (e.g., Cocker Spaniels, Poodles, Old English Sheepdogs) may be at higher risk due to the association with IMHA. Age distribution reflects the underlying disease; for example, IMHA is more common in middle-aged dogs (median age 6-8 years). Cats with cardiomyopathy, especially males and those with congestive heart failure, are at increased risk. Geographic factors are relevant for heartworm disease, which is endemic in tropical and subtropical regions, and can lead to PTE as a consequence of pulmonary arterial thrombosis or embolization of adult worms after treatment. The condition is more likely to be diagnosed in tertiary referral centers, indicating a potential underdiagnosis in general practice. Mortality rates are high, with reported case fatality rates ranging from 30% to 60% in dogs with PTE, depending on the underlying cause and severity.

The pathophysiology of PTE involves a complex interplay between thrombus formation, pulmonary vascular obstruction, and the resulting cardiopulmonary consequences. The initial event is the formation of a thrombus, typically in the systemic venous circulation (e.g., deep veins of the hindlimbs, pelvic veins, or right atrium), which then embolizes to the pulmonary arteries. The thrombus lodges in a pulmonary artery, causing mechanical obstruction to blood flow. The severity of the obstruction determines the physiological impact: small peripheral emboli may be clinically silent, while large central emboli can obstruct >50% of the pulmonary vascular bed, leading to acute RV failure. The immediate consequence is an increase in pulmonary vascular resistance (PVR) due to both mechanical obstruction and reflex vasoconstriction mediated by hypoxia and the release of vasoactive substances (e.g., thromboxane A2, serotonin). This leads to pulmonary hypertension, increased RV afterload, and RV dilation. The RV may fail acutely, resulting in decreased left ventricular preload, reduced cardiac output, and systemic hypotension. Concurrently, the obstructed lung regions are ventilated but not perfused, creating a V/Q mismatch and hypoxemia. Hypoxemia is further exacerbated by right-to-left shunting through a patent foramen ovale in some cases. The release of inflammatory mediators from the thrombus and ischemic lung tissue can cause local inflammation, pulmonary edema, and bronchoconstriction. In chronic or recurrent PTE, pulmonary hypertension may become persistent, leading to right-sided congestive heart failure. Additionally, the underlying hypercoagulable state often persists, increasing the risk of recurrent thromboembolism.

Predisposing factors for PTE are numerous and often coexist, reflecting Virchow's triad: hypercoagulability, vascular endothelial injury, and venous stasis. Hypercoagulable states are the most common and include: (1) Immune-mediated hemolytic anemia (IMHA): The most significant risk factor in dogs, with up to 50% of dogs with IMHA developing thromboembolic complications. (2) Protein-losing nephropathy (PLN): Loss of antithrombin III in the urine leads to a hypercoagulable state. (3) Protein-losing enteropathy (PLE): Similar to PLN, with loss of antithrombin III and other anticoagulant proteins. (4) Hyperadrenocorticism: Glucocorticoid excess increases coagulation factor levels and platelet aggregation. (5) Neoplasia: Tumors can release procoagulant substances and cause vascular invasion. (6) Sepsis and systemic inflammatory response syndrome (SIRS): Inflammation activates coagulation and inhibits fibrinolysis. (7) Disseminated intravascular coagulation (DIC): A consumptive coagulopathy that paradoxically increases thrombotic risk. (8) Glucocorticoid therapy: Iatrogenic hypercoagulability. (9) Heartworm disease: Adult heartworms cause endothelial damage and inflammation in pulmonary arteries. (10) Trauma and surgery: Tissue injury and immobility promote thrombosis. (11) Central venous catheters: Direct endothelial injury and thrombus formation. (12) Obesity and recumbency: Venous stasis. (13) Cardiac disease: Especially in cats with cardiomyopathy, leading to arterial thromboembolism that can also affect pulmonary arteries. (14) Chronic kidney disease: Associated with endothelial dysfunction and hypercoagulability. (15) Pancreatitis: Inflammatory state. (16) Autoimmune diseases other than IMHA. (17) Genetic thrombophilia: Rare, but antithrombin III deficiency has been reported in some breeds.

Clinical signs of PTE are highly variable and often nonspecific, ranging from acute severe respiratory distress to sudden death. The classic presentation is peracute or acute onset of dyspnea, tachypnea, and cyanosis. Other common signs include: (1) Respiratory: Tachypnea, increased respiratory effort, coughing (often non-productive), hemoptysis (rare), and pleuritic chest pain (difficult to assess in animals). (2) Cardiovascular: Tachycardia, weak pulses, jugular venous distension, and syncope. In severe cases, signs of right-sided heart failure may develop, including ascites and peripheral edema. (3) Systemic: Fever, lethargy, anorexia, and anxiety. (4) In chronic cases, signs may be more insidious, with exercise intolerance and progressive dyspnea. Physical examination may reveal harsh lung sounds, crackles, or wheezes, but lung auscultation can be normal in many cases. In cats, signs may be more subtle, with lethargy and anorexia predominating. It is important to note that clinical signs are often overshadowed by the underlying disease (e.g., IMHA), so a high index of suspicion is required. In peracute massive PTE, animals may present with acute collapse, severe respiratory distress, and signs of cardiogenic shock, progressing rapidly to death.

The differential diagnoses for PTE include: (1) Acute respiratory distress syndrome (ARDS): Both present with acute respiratory distress and hypoxemia, but ARDS is characterized by bilateral pulmonary infiltrates on radiographs and a history of a triggering insult (e.g., sepsis, trauma). PTE may have normal radiographs or focal oligemia. (2) Pneumonia (bacterial, viral, fungal): Fever, cough, and pulmonary infiltrates are common; however, pneumonia typically has a more gradual onset and responds to antimicrobial therapy. Thoracic radiographs show alveolar or interstitial patterns, whereas PTE may show no significant changes. (3) Pulmonary edema (cardiogenic or non-cardiogenic): Cardiogenic edema is associated with left-sided heart failure, cardiomegaly, and pulmonary venous congestion. Non-cardiogenic edema (e.g., neurogenic, toxic) has a different history. PTE may cause localized edema due to ischemia, but it is not the primary pattern. (4) Bronchial disease (e.g., chronic bronchitis, asthma): Chronic cough and wheezing are typical, with a history of chronicity and response to bronchodilators/corticosteroids. (5) Pulmonary neoplasia: Primary or metastatic lung tumors can cause respiratory signs and may be visible on radiographs as nodules or masses. PTE may be a complication of neoplasia, so both can coexist. (6) Heart failure (congestive): Especially right-sided heart failure can cause dyspnea and ascites, but radiographs show cardiomegaly and pleural effusion. (7) Pneumothorax: Acute dyspnea with absent lung sounds in the affected hemithorax and radiographic evidence of free air. (8) Diaphragmatic hernia: History of trauma, abnormal lung sounds, and radiographic evidence of abdominal contents in the thorax. (9) Pulmonary hypertension (primary or secondary): Chronic PTE can cause pulmonary hypertension, but other causes (e.g., heartworm disease, interstitial lung disease) must be ruled out. (10) Foreign body aspiration: Acute onset after a choking episode, with localized radiographic changes. Definitive diagnosis of PTE requires advanced imaging (CT angiography) or postmortem examination.

The diagnostic approach to suspected PTE should be systematic and rapid, as the condition is life-threatening. Step 1: Clinical suspicion and initial stabilization. If the patient is unstable, provide oxygen supplementation, intravenous fluids (cautiously), and supportive care before proceeding with diagnostics. Step 2: Baseline bloodwork: Complete blood count (CBC), serum biochemistry profile, coagulation panel (PT, aPTT, D-dimer, antithrombin III, fibrinogen), and blood gas analysis. These tests help identify underlying diseases (e.g., IMHA, PLN) and may reveal abnormalities suggestive of hypercoagulability (e.g., thrombocytopenia, elevated D-dimer). Step 3: Thoracic radiographs: Obtain three-view radiographs (right lateral, left lateral, and ventrodorsal or dorsoventral). Findings may be normal or show nonspecific changes such as alveolar infiltrates, pleural effusion, or cardiomegaly. Classic signs like oligemia (Westernark sign) or a wedge-shaped opacity are rare. Step 4: If radiographs are inconclusive and PTE is still suspected, perform echocardiography to assess for right ventricular dilation, pulmonary hypertension, and to rule out cardiac disease. Echocardiography may also identify thrombi in the right heart or main pulmonary artery. Step 5: Advanced imaging: Computed tomography pulmonary angiography (CTPA) is the gold standard for antemortem diagnosis. It has high sensitivity and specificity for detecting filling defects in pulmonary arteries. If CTPA is unavailable, ventilation-perfusion (V/Q) scintigraphy can be used, but it is less specific. Step 6: D-dimer testing: A negative D-dimer (using a highly sensitive assay) can help rule out PTE, but a positive result is not confirmatory. Step 7: In cases where the patient is too unstable for advanced imaging, a presumptive diagnosis may be made based on risk factors, clinical signs, and supportive laboratory findings, and treatment should be initiated immediately. Step 8: Postmortem examination is often required for definitive confirmation in fatal cases.

Laboratory findings in PTE are often nonspecific but can support the diagnosis and identify underlying causes. Complete blood count (CBC): May show anemia (especially in IMHA), leukocytosis or leukopenia, and thrombocytopenia (due to consumption or underlying disease). In IMHA, there is often regenerative anemia with spherocytosis and a positive Coombs test. Serum biochemistry: May reveal hypoalbuminemia (PLN or PLE), hyperglobulinemia, elevated liver enzymes (if right-sided heart failure causes hepatic congestion), azotemia (renal disease), and hyperglycemia (stress or diabetes). Coagulation profile: Prolonged PT and aPTT may indicate DIC or liver disease. D-dimer levels are often elevated in PTE, but can also be elevated in other conditions (e.g., inflammation, neoplasia). Antithrombin III levels may be decreased in PLN or PLE. Fibrinogen may be elevated as an acute phase protein. Blood gas analysis: Typically shows hypoxemia (decreased PaO2) and respiratory alkalosis (decreased PaCO2) due to hyperventilation. The alveolar-arterial (A-a) gradient is often increased. In severe cases, metabolic acidosis may develop due to lactic acidosis. Biomarkers: Cardiac troponin I may be elevated due to myocardial damage from RV strain. NT-proBNP may be elevated in heart failure. In cats, if cardiomyopathy is suspected, NT-proBNP and troponin I can be measured. Urinalysis: Proteinuria may be present in PLN. Specific tests: Heartworm antigen and antibody tests should be performed in endemic areas. Serology for infectious diseases (e.g., ehrlichiosis, anaplasmosis) may be indicated if vasculitis is suspected.

Imaging plays a crucial role in the diagnosis of PTE. Thoracic radiography: Findings are often nonspecific and may be normal in up to 30% of cases. Possible abnormalities include: (1) Alveolar infiltrates (due to hemorrhage or edema) in the affected lung lobe, often peripheral and wedge-shaped. (2) Oligemia (reduced pulmonary vascularity) in the affected region (Westernark sign), though this is rare. (3) Enlargement of the main pulmonary artery segment (due to pulmonary hypertension). (4) Right-sided cardiomegaly (RV enlargement) in chronic cases. (5) Pleural effusion (especially in cats). (6) Atelectasis. Echocardiography: This is useful to assess for right ventricular dilation, right ventricular systolic dysfunction (decreased tricuspid annular plane systolic excursion, TAPSE), and pulmonary hypertension (estimated via tricuspid regurgitation velocity). It can also identify thrombi in the right atrium, right ventricle, or main pulmonary artery. In cats, echocardiography is essential to evaluate for cardiomyopathy. Computed tomography pulmonary angiography (CTPA): This is the gold standard. It involves rapid intravenous contrast injection and helical CT imaging. Findings include filling defects (partial or complete) within the pulmonary arteries, which may be central or peripheral. CTPA can also detect pulmonary infarction, consolidation, and pleural effusion. It is highly sensitive and specific. Ventilation-perfusion (V/Q) scintigraphy: This nuclear medicine technique compares ventilation and perfusion scans. In PTE, there are areas of normal ventilation but reduced perfusion (mismatch). It is less commonly used due to limited availability and lower specificity. Magnetic resonance imaging (MRI): Not routinely used for PTE but can detect thrombi in some cases. Fluoroscopy: Not typically used for PTE diagnosis.

Cytology and histopathology are not typically used for antemortem diagnosis of PTE, but they may be helpful in identifying underlying diseases. Fine needle aspiration (FNA) of lung lesions (if present) may reveal inflammatory cells, neoplastic cells, or hemorrhage. Thoracocentesis for pleural effusion: Fluid analysis can help differentiate transudate (e.g., right-sided heart failure) from exudate (e.g., infection, neoplasia). Histopathology: Postmortem examination is often the definitive diagnostic method. Gross findings include thromboemboli in the pulmonary arteries, often with associated pulmonary hemorrhage or infarction. Microscopic examination reveals organized thrombi with varying degrees of recanalization, endothelial injury, and inflammation. Special stains (e.g., Masson's trichrome) can help identify fibrin. In cases of septic emboli, bacterial colonies may be seen. Histopathology of other organs (e.g., kidney, adrenal) may reveal the underlying disease (e.g., PLN, hyperadrenocorticism).

Treatment of PTE is multifaceted and should address both the acute thromboembolic event and the underlying cause. Emergency stabilization: Provide oxygen supplementation (via nasal cannula, mask, or oxygen cage) to maintain SpO2 > 92%. In severe respiratory distress, mechanical ventilation may be necessary. Intravenous fluids should be administered cautiously, as excessive fluids can worsen right-sided heart failure. In cases of cardiogenic shock, vasopressors (e.g., norepinephrine) may be required. Anticoagulation: The mainstay of therapy is anticoagulation to prevent further thrombus formation and allow endogenous fibrinolysis. Unfractionated heparin (UFH) is commonly used: Loading dose of 200-300 IU/kg IV, followed by a constant rate infusion (CRI) of 15-50 IU/kg/h, titrated to maintain aPTT at 1.5-2.5 times baseline. Alternatively, low molecular weight heparins (LMWH) such as enoxaparin (1 mg/kg SC q12h) or dalteparin (100-150 IU/kg SC q12h) can be used, though they are more expensive. Warfarin (a vitamin K antagonist) can be used for long-term therapy, starting at 0.05-0.1 mg/kg PO q24h, with monitoring of PT (target INR 2-3). However, warfarin has a narrow therapeutic index and requires careful monitoring. Thrombolytic therapy: In severe, life-threatening PTE, thrombolytics such as tissue plasminogen activator (tPA) may be considered. Dosage: 0.25-1 mg/kg IV over 15-30 minutes, but this is associated with a high risk of bleeding and is rarely used in veterinary medicine. Surgical/interventional: In rare cases, surgical embolectomy or catheter-directed thrombolysis may be attempted, but these are not widely available. Treatment of underlying disease: This is crucial. For IMHA, immunosuppressive doses of glucocorticoids (e.g., prednisone 2 mg/kg/day) and other immunosuppressants (e.g., azathioprine, cyclosporine) are indicated. For PLN, management includes ACE inhibitors (e.g., enalapril 0.5 mg/kg q12h) and aspirin (0.5-1 mg/kg q24h) or clopidogrel (2-3 mg/kg q24h) for antiplatelet effects. For heartworm disease, adulticide therapy (melarsomine) is indicated, but must be done carefully to avoid embolic complications. Supportive care: Includes rest, nutritional support, and management of complications such as pulmonary hypertension (e.g., sildenafil 1-2 mg/kg PO q8-12h) or right-sided heart failure (diuretics, pimobendan).

The prognosis for PTE is guarded to poor, with a high mortality rate. Short-term survival depends on the severity of the embolic burden, the underlying disease, and the rapidity of intervention. In dogs with PTE, reported mortality rates range from 30% to 60%. Negative prognostic indicators include: (1) Severe hypoxemia (PaO2 < 60 mmHg on room air). (2) Hypotension and shock. (3) Right ventricular failure. (4) Underlying diseases with high mortality (e.g., IMHA, DIC). (5) Recurrent thromboembolism. (6) Delayed diagnosis and treatment. Medium-term prognosis is influenced by the ability to control the underlying disease. For example, dogs with IMHA that survive the initial episode may have a fair prognosis if immunosuppressive therapy is successful. Long-term prognosis is guarded due to the risk of recurrence and the progression of the underlying disease. In cats with cardiomyopathy and arterial thromboembolism, the prognosis is poor, with a high rate of recurrence and mortality. However, some animals may recover with aggressive treatment and have a good quality of life for months to years.

Follow-up care for PTE is essential to monitor for recurrence and manage the underlying disease. Initial follow-up: Recheck within 1-2 weeks after discharge. Assess clinical signs, oxygenation (pulse oximetry or blood gas), and coagulation parameters (if on anticoagulants). For heparin therapy, monitor aPTT every 4-6 hours until stable, then daily. For warfarin, monitor PT/INR every 2-3 days until stable, then weekly to monthly. Serial imaging: Repeat thoracic radiographs or echocardiography may be performed to assess resolution of pulmonary infiltrates, pleural effusion, or right heart changes. CTPA may be repeated if recurrence is suspected. Laboratory monitoring: Regular CBC, biochemistry, and urinalysis to monitor the underlying disease (e.g., IMHA, PLN). For IMHA, monitor PCV and reticulocyte count. For PLN, monitor UPC ratio and renal function. Long-term management: Continue anticoagulant therapy as indicated. For dogs with IMHA, taper immunosuppressive drugs slowly over months. For PLN, continue ACE inhibitors and antiplatelet therapy. For heartworm disease, follow the American Heartworm Society guidelines for adulticide therapy and retesting. Client education: Instruct owners to monitor for signs of recurrence (e.g., acute dyspnea, collapse) and to seek immediate veterinary care if they occur. Also, emphasize the importance of strict rest and compliance with medication administration.

Pearls: (1) Maintain a high index of suspicion for PTE in any patient with an underlying hypercoagulable disease (e.g., IMHA, PLN) that develops acute respiratory distress. (2) D-dimer is a useful rule-out test; a negative result (using a highly sensitive assay) makes PTE unlikely. (3) Thoracic radiographs are often normal; do not rule out PTE based on radiographs alone. (4) Echocardiography can rapidly assess for right heart strain and pulmonary hypertension, which are supportive of PTE. (5) CTPA is the gold standard; if available, perform it early in stable patients. (6) Anticoagulation should be started immediately if PTE is strongly suspected, even before definitive diagnosis. (7) In cats, always evaluate for cardiomyopathy when PTE is suspected. Pitfalls: (1) Failing to consider PTE in patients with respiratory distress, leading to delayed treatment. (2) Overinterpreting normal thoracic radiographs as excluding PTE. (3) Using D-dimer as a confirmatory test; it is not specific. (4) Administering excessive intravenous fluids, which can worsen right-sided heart failure. (5) Using heparin without monitoring aPTT, leading to inadequate or excessive anticoagulation. (6) Discontinuing anticoagulation too early, increasing the risk of recurrence. (7) Neglecting to treat the underlying disease, which is essential for long-term success.

Anticoagulants: (1) Unfractionated heparin (UFH): Dogs: 200-300 IU/kg IV loading dose, then 15-50 IU/kg/h CRI, titrated to aPTT 1.5-2.5x baseline. Cats: 200-300 IU/kg IV, then 15-30 IU/kg/h CRI. (2) Low molecular weight heparin (LMWH): Enoxaparin: Dogs: 1 mg/kg SC q12h; Cats: 1 mg/kg SC q12h. Dalteparin: Dogs: 100-150 IU/kg SC q12h; Cats: 150-200 IU/kg SC q12h. (3) Warfarin: Dogs: 0.05-0.1 mg/kg PO q24h, adjust to INR 2-3. Cats: 0.05-0.1 mg/kg PO q24h, adjust to INR 2-3. Thrombolytics: (1) Tissue plasminogen activator (tPA): Dogs: 0.25-1 mg/kg IV over 15-30 minutes; Cats: 0.25-1 mg/kg IV over 15-30 minutes. Use with extreme caution due to bleeding risk. Antiplatelet agents: (1) Clopidogrel: Dogs: 2-3 mg/kg PO q24h; Cats: 18.75 mg/cat PO q24h. (2) Aspirin: Dogs: 0.5-1 mg/kg PO q24h; Cats: 5 mg/cat PO q48-72h. Treatment of underlying disease: (1) IMHA: Prednisone 2 mg/kg/day PO, tapered over months; azathioprine 2 mg/kg PO q24h for 5-7 days, then q48h; cyclosporine 5-10 mg/kg PO q12h. (2) PLN: Enalapril 0.5 mg/kg PO q12h; benazepril 0.25-0.5 mg/kg PO q12h; clopidogrel or aspirin as above. (3) Hyperadrenocorticism: Trilostane 2-5 mg/kg PO q24h, adjust based on ACTH stimulation test. (4) Heartworm disease: Melarsomine 2.5 mg/kg IM, two injections 24 hours apart, followed by a third injection 1 month later; doxycycline 10 mg/kg PO q12h for 30 days; prednisone 0.5 mg/kg PO q12h tapering. (5) Pulmonary hypertension: Sildenafil 1-2 mg/kg PO q8-12h. (6) Right-sided heart failure: Furosemide 1-2 mg/kg IV/PO q8-12h; pimobendan 0.25-0.3 mg/kg PO q12h. Note: All dosages are based on Plumb's Veterinary Drug Handbook and should be adjusted based on renal/hepatic function and clinical response.

Evidence for the diagnosis and management of PTE in veterinary medicine is largely based on retrospective studies, case series, and expert consensus, as prospective randomized controlled trials are lacking. Key findings from the literature include: (1) IMHA is the most common underlying disease in dogs with PTE, with a high prevalence of thromboembolic complications (up to 50% in some studies). (2) D-dimer testing has high sensitivity but low specificity for PTE; a negative result can rule out PTE, but a positive result requires further imaging. (3) CTPA is the most accurate antemortem diagnostic tool, with a sensitivity and specificity exceeding 90% in humans and likely similar in animals. (4) Anticoagulation with heparin improves survival in experimental models and is recommended by consensus guidelines (e.g., ACVIM consensus on the treatment of IMHA). (5) Thrombolytic therapy is associated with a high risk of bleeding and is not routinely recommended. (6) The prognosis for PTE is poor, with mortality rates of 30-60% in dogs. (7) In cats, arterial thromboembolism is more common than PTE, but PTE can occur secondary to cardiomyopathy. (8) The use of antiplatelet agents (e.g., clopidogrel) is recommended for prevention of arterial thromboembolism in cats with cardiomyopathy, but their role in PTE is less clear. (9) Recent studies have evaluated the use of novel oral anticoagulants (e.g., rivaroxaban) in dogs, but data are limited. (10) The ACVIM consensus statement on the diagnosis and treatment of immune-mediated hemolytic anemia in dogs provides guidelines for anticoagulant therapy, recommending prophylactic heparin in all dogs with IMHA. Overall, the evidence base is growing, but many recommendations are extrapolated from human medicine. Further research is needed to establish standardized diagnostic and therapeutic protocols for PTE in veterinary patients.