Veterinary Antithrombotic Calculator: When and Which to Use

Quick answer

• How to use
• Who needs antithrombotics
• Venous vs arterial
• Dose table
• Drugs in detail
• By condition
• ATE case
• Other emergencies
• Monitoring
• Stopping before surgery
• Common mistakes
• FAQs
• Glossary
• References

How to use this calculator

1. Choose a mode. Use Chronic to work out whether a patient with a prothrombotic condition needs an antithrombotic and which one, Acute for a cat or dog presenting with an arterial thromboembolism, a pulmonary thromboembolism, a portal vein thrombosis, a catheter or cranial vena cava thrombosis, or a left atrial thrombus found on echo (prognostic indicators from the published series, then a stepwise acute plan, species-specific), or Drug library to jump straight to any drug’s dose card.
2. Set species and weight. Pick dog or cat and enter the body weight in kg or lb. The decision logic works without a weight; the weight unlocks the calculated doses.
3. Tick conditions and risk factors. Select everything that applies. Dogs with IMHA, PLN or PLE, cats with cardiomyopathy plus a risk factor, and any patient with more than one risk factor are flagged as mandatory-therapy patients; the 2022 update's "consider only alongside another risk factor" and "not routinely" populations sit in their own groups and are scored as the update describes.
4. Add patient factors. Bleeding risks (active haemorrhage, coagulopathy, GI ulceration, NSAIDs) and planning flags (surgery, transient condition) adjust the warnings.
5. Read the plan. The verdict, thrombus type, first-line drugs and calculated doses appear with the working shown. Doses are in mg or units per dose, not mL, except where the source dose is itself a volume (the ATE rescue drugs) or a labelled practical aid – convert against your own product’s concentration.
6. Record it. Copy, print (with a signature line), email, download or share the plan as a link that restores the exact same inputs.

One deliberate design choice: results are in mg or units per dose, never mL. Injectable concentrations vary between products and countries, so the millilitre conversion belongs at the bench, against the vial in your hand. For CRI dilutions and mL/h, the dilution calculator does that step properly.

Which dogs and cats need antithrombotics?

The CURATIVE consensus splits patients into those in whom antithrombotic therapy is effectively mandatory and those less likely to need it.

The single-risk-factor group is where clinical judgment earns its keep. A dog with mild pancreatitis that is eating again tomorrow is a very different proposition from a dog with pancreatitis on a jugular catheter receiving glucocorticoids. Every additional prothrombotic hit moves the patient toward the mandatory group. The 2022 update added a second kind of entry: conditions that are a consideration only where another risk factor exists. The calculator scores those as the update describes, so a dog with atrial fibrillation alone reads "not routinely indicated", the same dog with pancreatitis reads "less likely to be needed" with two reasons rather than one, and the mandatory verdict is reserved for the populations the consensus actually names.

Venous vs arterial thrombosis: why the drug class changes

The drug choice follows the biology of the clot. Venous thromboembolism – the pattern behind pulmonary thromboembolism in IMHA and PLN – forms under low-shear conditions. These thrombi are fibrin rich and depend relatively little on platelet number or function, so anticoagulants (heparins, factor Xa inhibitors) are the convention.

Arterial thrombosis – the pattern behind aortic thromboembolism in feline cardiomyopathy – forms under high-shear conditions and is platelet rich, so drugs that stop platelets activating, aggregating and adhering are most effective: antiplatelets. Clopidogrel is recommended instead of aspirin in cats at ATE risk, and may be more effective than aspirin in dogs.

Patients with risk factors in both columns (a cat with cardiomyopathy that also has sepsis, say) sit in a mixed category where both classes come into play and combination therapy may be weighed against bleeding risk.

Antithrombotic dose table for dogs and cats

These are the doses from the CURATIVE guideline summary this calculator runs on. The calculator above multiplies them out for your patient’s weight and shows the working.

Antithrombotic drugs in detail

Every drug in the calculator, with its guideline dose, monitoring and stopping rules. Each section is deep-linkable, and the dose lines are checked at runtime against the calculator’s own data so this reference can never silently drift from what the tool computes.

Antithrombotics by condition

Blood thinners for dogs with IMHA

Immune-mediated haemolytic anaemia is the textbook mandatory indication. IMHA dogs die of pulmonary thromboembolism as often as they die of anaemia, and the CURATIVE consensus treats antithrombotic therapy as non-negotiable in this disease. The thrombi are venous-pattern – fibrin rich, formed under low shear – so the first-line choice is an anticoagulant, with LMWH (dalteparin or enoxaparin) preferred over UFH. In dogs at the highest VTE risk, adding an antiplatelet to the anticoagulant may be considered where clot risk is felt to outweigh the extra bleeding risk. Most IMHA dogs are also on glucocorticoids, which stack a further prothrombotic hit on top of the disease itself.

Antithrombotics for protein-losing nephropathy in dogs

PLN earns its mandatory status through a specific mechanism: the glomerulus that leaks albumin also leaks antithrombin, stripping out one of the blood’s main brakes on coagulation. The result is a venous-pattern hypercoagulable state, and the approach mirrors IMHA: an anticoagulant first, LMWH preferred, with anti-Xa monitoring where available. Because PLN is usually a chronic disease, discontinuation rarely arises – these patients tend to stay on therapy, and the stopping-before-surgery rules matter more than any endpoint.

Preventing arterial thromboembolism in cats with cardiomyopathy

Feline aortic thromboembolism – the “saddle thrombus” – is one of the most distressing emergencies in practice, and it is exactly the event this branch of the guideline exists to prevent. A cat with cardiomyopathy plus any associated risk factor (left atrial enlargement, spontaneous echo contrast, reduced left auricular flow velocity, a previous ATE, congestive heart failure) needs antithrombotic therapy. Because these are platelet-rich arterial clots, the drug is an antiplatelet: clopidogrel, 18.75 mg once daily, recommended instead of aspirin. Cardiomyopathy without any of those risk factors sits in the judgment zone – which is a reason to look for them on echo, not a reason to relax.

Pancreatitis, sepsis and stacking risk factors

Most antithrombotic decisions in general practice are not about IMHA – they are about the patient with two moderate problems at once. The guideline’s rule is clean: one risk factor alone means the patient is less likely to need therapy; more than one makes it mandatory, and pancreatitis with sepsis is the consensus’s own worked example. Neoplasia, hyperadrenocorticism, glucocorticoid therapy, protein-losing enteropathy and previous thromboembolism all count toward the tally. The counterweight is the transient-condition rule: a risk factor likely to resolve within days to weeks with treatment lowers the case for starting, and any therapy begun should be re-questioned as the underlying disease resolves.

Heartworm disease in dogs and cats

New in the 2022 CURATIVE update. Heartworm disease is associated with pulmonary artery thrombosis in dogs, with the risk rising with disease severity, and the panel recommends that antithrombotic therapy be considered, particularly in severe disease and in dogs undergoing adulticide treatment (statement 1.1). For cats the association is weaker and the suggestion is to consider therapy in severe disease or where other risk factors exist (1.2). Two honest caveats travel with the entry: the evidence behind it is old experimental work with antiplatelet drugs (aspirin, ticlopidine) rather than outcome data, and the American Heartworm Society does not currently recommend antithrombotics in heartworm management. The calculator therefore scores heartworm as a single risk factor (consider), follows the arterial pattern for the drug class, and prints the disagreement in the notes so the decision is made with eyes open.

Protein-losing enteropathy in dogs

Upgraded in 2022. PLE in dogs is moderately associated with thrombosis that can be venous or arterial (1.12a), and the panel recommends antithrombotic therapy for all dogs with PLE unless the risks, particularly gastrointestinal bleeding, are deemed to outweigh the potential benefit (1.12b). PLE therefore sits in the mandatory group beside IMHA and PLN, with the GI bleeding flag doing the work of the caveat: a dog with melaena gets a red warning before any dose. Cats with PLE are different: a weak association with pulmonary thromboembolism, no evidence of arterial risk, and therapy only where other risk factors exist (1.13).

Atrial fibrillation, liver disease and shunt surgery in dogs

Three more 2022 populations, each scored differently. Atrial fibrillation may be associated with arterial thrombosis, particularly where left atrial appendage flow velocity is reduced, and therapy should be considered where other risk factors exist (1.9b); for arrhythmias other than atrial fibrillation the panel recommends against therapy unless other risk factors exist (1.9c). Liver disease is associated with thrombosis in a small subset of dogs only, independent of the specific hepatic disease, and therapy is a consideration after an individual risk and benefit assessment or with other risk factors (1.5). Surgical correction of a congenital portosystemic shunt may be followed by postoperative thrombosis, so therapy is a consideration around surgery (1.7b), while routine therapy in unoperated shunt dogs is recommended against (1.7c). Portal vein thrombosis is the event these statements are guarding against, and the Acute tab has a case type for it.

The feline statements of the 2022 update

The update is more conservative for cats than the tool's original feline entries were. IMHA (1.3), PLN (1.4), PLE (1.13) and congenital portosystemic shunts (1.8) are each a consideration only where other risk factors exist, and each carries the note that there is no evidence of arterial risk. Sepsis is associated with thrombosis in a small subset of cats; the panel recommends against routine therapy and suggests it after an individual assessment or with other risk factors (1.11). For hyperadrenocorticism (1.14) and exogenous glucocorticoids (1.15) no evidence-based recommendation could be made and therapy should not be routinely used. The calculator's cat list now mirrors that: the four "with company only" conditions reach "less likely to be needed" when paired and "not routinely indicated" alone, sepsis keeps its single-risk-factor scoring with the statement printed beside it, and hyperadrenocorticism and glucocorticoids are recorded for the note without adding to the count. Arrhythmias in cats with structural cardiac disease went the other way: they are associated with arterial thromboembolism and the panel recommends antithrombotic therapy (1.10), so the entry sits with the cardiomyopathy risk factors.

Central venous catheters

The risk of thrombosis associated with IV catheters is unknown in both species, and the panel suggests antithrombotic therapy be considered only where other risk factors for thrombosis exist (1.16, 1.17). In the calculator a central line is a patient factor, not a condition: on its own it produces a note, alongside a risk factor it strengthens the case without changing the count. The practical advice comes from the caval thrombosis series (Palmer 1998): avoid central venous catheters in dogs with immune-mediated disease, sepsis, protein-losing nephropathy, neoplasia or cardiac disease where you can.

Arterial thromboembolism (ATE): managing the acute case in cats and dogs

Everything above this line is about stopping the clot from forming. This section is about the patient in whom it already has. The Acute tab of the calculator takes the species from the Patient card and changes its questions, its prognostic indicators and its plan accordingly, because the two diseases are not the same: in cats the clot is an embolus from a diseased left atrium and the emergency is hyperacute; in dogs it usually forms in place in the terminal aorta on a hypercoagulable background, and the onset is chronic in most cases (72 of 100 in Ruehl 2020, about half in Lake-Bakaar 2012). Cats first, dogs below.

Cats: the saddle thrombus (FATE)

FATE is what happens when the clot has already formed: a thrombus from the enlarged left atrium breaks free and lodges where the aorta splits, and a cat that was normal an hour ago is screaming, dragging both back legs, and cold from the stifles down. Around 90% of these cats have cardiomyopathy underneath, but only about one in five had a cardiac diagnosis before the event, and three quarters are male. Both pelvic limbs are affected in 70 to 75% of cases, a single pelvic limb in 10 to 15%, and a forelimb occasionally. For a cat, the mode takes the presentation you can see and measure in the first ten minutes and turns it into two things: an honest set of prognostic indicators for the owner conversation, and a stepwise acute plan with the doses worked out.

Recognising it: the five Ps

Pain (vocalising, often the presenting complaint), paralysis or paresis, pulselessness (no femoral pulse, no Doppler flow), pallor (pale, purple or cyanotic pads and nail beds) and poikilothermy (limbs cold to the touch). The gastrocnemius muscles become firm and painful within hours. A cat with the full set does not need much more to make the diagnosis; the bedside tests below are for the partial pictures and for documenting the case.

Confirming it at the bedside

Two drops of blood settle most doubts. Compare glucose in blood from an affected limb (a nail-bed prick or a distal vein) with a central sample from the jugular or an unaffected limb. A central minus limb difference of 30 mg/dL (1.7 mmol/L) or more was 100% sensitive and 90% specific for ATE in Klainbart’s 2014 series, and a 2024 multicentre study of 18 FATE cats and 41 controls found a 41 mg/dL (2.3 mmol/L) cut-off that was 100% sensitive and 100% specific. Lactate runs the other way: a limb minus central difference of 2.2 mmol/L or more was 100% sensitive and 95% specific in the same study. Neither differential predicted survival; they confirm the diagnosis, they do not grade it. Infrared thermography showing a 2.4°C difference between the affected and unaffected limbs had 80% sensitivity and 100% specificity, and a thrombus or spontaneous echo contrast in the left atrium on a quick echo closes the loop. Image the chest early, by POCUS if the cat is fragile: 50 to 70% of FATE cats are in congestive heart failure at presentation and it changes the fluid and diuretic plan from the first hour.

What the numbers say about prognosis

The published figures are sobering, and they are also more nuanced than the reflex “saddle thrombus, hopeless” suggests. The calculator’s prognosis panel uses the indicators in this table and never converts them into a single probability, because no validated score exists; it lays out the data so the conversation with the owner is honest in both directions.

The ACVIM 2020 consensus frames the decision plainly: treatment is reasonable in cats that are normothermic, have a single limb affected and are not in heart failure, and euthanasia can be considered in more severe presentations. Between those poles sits most of the caseload, and a committed owner with realistic expectations is entitled to try. What the numbers argue against is not treatment, it is treatment without the conversation.

Treatment, in the order it should happen

1. Analgesia before anything else. A full mu agonist, intravenous if a catheter is in and intramuscular if it is not: methadone 0.1 to 0.4 mg/kg, or fentanyl as a 2 µg/kg bolus followed by a 1 to 5 µg/kg/h infusion titrated to effect. Buprenorphine is a partial agonist and rarely enough for the first day; it earns its place as the step-down at 24 to 48 hours, alongside gabapentin 50 to 100 mg per cat once the cat is eating. No NSAIDs and no alpha-2 agonists.

2. Clopidogrel plus an anticoagulant. Neither drug dissolves the clot that is already there; they stop it propagating and stop the next one. The ACVIM consensus calls for anticoagulation with heparin or a factor Xa inhibitor in combination with clopidogrel, and CURATIVE names clopidogrel with LMWH as its preferred combination in cats at ATE risk. The calculator uses the CURATIVE cat doses from the registry above: clopidogrel 37.5 mg loading then 18.75 mg once daily, with dalteparin 75 U/kg SC every 6 hours or enoxaparin 0.75 to 1 mg/kg SC every 6 to 12 hours, and unfractionated heparin 250 U/kg SC every 6 hours as the fallback. Aspirin is off the list.

3. Thrombolysis: usually no. Covered in its own section below. The short version is that tPA reopens vessels more often than nature does and has not yet been shown to send more cats home.

4. Heart failure. Oxygen, minimal handling, thoracocentesis before radiographs if POCUS shows a large effusion, furosemide 2 mg/kg IV or IM then 1 to 2 mg/kg IM every 1 to 2 hours to effect, and no intravenous fluids while the cat is in failure. A cat on a full mu agonist rarely needs butorphanol on top, and butorphanol would partly reverse the analgesia.

5. The reperfusion watch. For the cat that is treated, the dangerous days are the reperfusion days. As collateral flow or lysis returns blood to ischaemic muscle, potassium, lactate and myoglobin flood back: hyperkalaemia, acidosis and acute kidney injury, typically at 24 to 72 hours but sometimes on the table. Potassium, creatinine and glucose every 6 to 12 hours for three days, an ECG whenever the potassium rises or the heart rate falls, and the hyperkalaemia rescue doses drawn up in your head before you need them: calcium gluconate for the myocardium, dextrose with or without insulin to shift potassium into cells.

6. Find the cause. Echocardiography once the cat is stable, for the cardiomyopathy that underlies about 90% of feline ATE and was undiagnosed in four out of five of these cats until the event; left atrial size and spontaneous echo contrast also set the prevention plan. Chest imaging for CHF, blood pressure, and thyroid testing in an older cat.

7. Supportive care. Rewarm the trunk, never the ischaemic limbs. Check the bladder at least twice daily. Feed from day one. Passive range of motion once pain is controlled, physiotherapy from 48 to 72 hours, and a watch for skin necrosis and self-trauma from day 3. Typical hospitalisation is 2 to 5 days; neuromuscular recovery, when it comes, takes 2 to 6 weeks.

8. Home on prevention. Clopidogrel for life, a conversation about adding rivaroxaban, cardiology follow-up, and a written list of the signs of recurrence for the owner.

Thrombolysis: what three studies actually showed

The intuition is obvious: the problem is a clot, so dissolve it. The evidence has not cooperated. Guillaumin’s 2019 retrospective series of 16 cats given tPA reported reperfusion or functional recovery in up to two thirds, and set up the question properly. The BLASTT trial (JFMS 2022) then randomised 40 cats with two or more limbs affected, presenting within 6 hours, to alteplase 1 mg/kg IV over an hour (10% as a bolus, maximum 6 mg) or placebo: 48-hour survival was 60% versus 40% and survival to discharge 45% versus 30%, neither statistically significant, with acute kidney injury in 22% versus 19% and reperfusion injury in 33% versus 19%. The MATTERS study (2026) looked back at 183 cats across two hospitals, comparing the 115 that were still being treated 6 hours after presentation: tPA more than doubled clinical reperfusion (54% versus 20%) and functional recovery (36% versus 14%), survival to discharge was identical (34% versus 35%), and sudden death was more frequent in the tPA group (46% versus 19%). Admission temperature, not treatment, was the consistent predictor of every outcome, with 35.9°C the best cut-off.

The guideline positions follow from that. The ACVIM 2020 consensus states that thrombolytics are not recommended. The 2022 CURATIVE update (Domain 6) allows that thrombolysis can be attempted in acute FATE, under 6 hours from onset, but endorses no protocol and notes that evidence-based recommendations are lacking. The calculator therefore shows the BLASTT and MATTERS protocol arithmetic only when you tell it the cat presented under 6 hours, labels it “for information”, and puts the reperfusion warnings next to it. Streptokinase belongs to history: 24% of 46 cats in an older series had severe haemorrhagic complications.

Preventing the next one

Recurrence is the enemy after discharge, and it is where the evidence is strongest. The FAT CAT trial (Hogan 2015) randomised 85 cats that had survived an ATE to clopidogrel 18.75 mg daily or aspirin 81 mg every 72 hours and analysed 75: recurrence was 49% on clopidogrel versus 75% on aspirin, and the median time to recurrence or cardiac death 346 versus 128 days. That trial is why clopidogrel is the floor. Lo and colleagues (2022) followed 32 cats on clopidogrel plus rivaroxaban 2.5 mg daily: median survival was 257 days for the whole group and 502 days for the cats whose indication was a FATE event, recurrence was 16.7%, and no cat started on dual therapy for a cardiac thrombus or smoke went on to have a first event, with bleeding-type adverse effects in 5 of 32. The SUPERCAT trial (JAVMA 2025) compared the two drugs head to head as monotherapy in 45 cats and found them equivalent: recurrence 39% on rivaroxaban versus 37% on clopidogrel, median time to recurrence 513 versus 663 days. A 2025 systematic review pulled it together: clopidogrel plus rivaroxaban or enoxaparin appears to be the most effective and best-tolerated strategy, with the caveat that most of the evidence is small series at moderate or serious risk of bias. In practice that means clopidogrel for every survivor, a real discussion about adding rivaroxaban, and echocardiography to size the left atrium and look for smoke.

Talking to the owner

Three things need saying in the first conversation, in plain words. First, what this is: a clot from the heart, not an injury, and the heart disease behind it is usually new news. Second, what the next three days involve: strong pain relief, blood thinners, blood tests every few hours for potassium, and a real risk of sudden deterioration as circulation returns. Third, the numbers, given as ranges with their sources, and the honest statement that for a cat with both legs paralysed, no movement and a low temperature, euthanasia is a reasonable choice and treatment is also a reasonable choice for a family that understands the odds. The calculator’s printout carries the indicators and figures so that the conversation is documented, and so that the same numbers are used by whoever picks the case up at handover.

Dogs: aortic thrombosis is a different disease

A dog with a thrombus in the terminal aorta is not a large cat. The thrombus usually forms in place rather than embolising from the heart; it is platelet rich, formed under high shear on a hypercoagulable background, and in the largest series it was partial or non-occlusive in 80 of the 90 dogs in whom that was assessed (Ruehl 2020). That is why the onset is chronic in most dogs (72 of 100 in Ruehl 2020, 15 of 31 in Lake-Bakaar 2012): weeks of exercise intolerance, a stiff or collapsing pelvic limb gait, intermittent claudication, cold feet. The acute presentations look more like FATE, with pain, bilateral paralysis and absent femoral pulses, and they carry a worse outlook. In Ruehl’s 100 dogs (Tufts and Ohio State, 1997 to 2014), 27 were acute (under 48 hours) and 72 chronic; acute dogs were more often non-ambulatory (63% versus 25%), painful (50% versus 26%) and bilateral (85% versus 39%). Labrador retrievers, Greyhounds and Shetland sheepdogs led the breed list, and the median age was 10 years.

The cause matters more in dogs than in cats because it is often treatable. Protein-losing nephropathy was the commonest association (32 of 100; severe proteinuria in 51% of the dogs tested, and lower antithrombin activity than in dogs without PLN, 64% versus 82%), then neoplasia (22), glucocorticoid administration (16), endocrine disease (13, of which hyperadrenocorticism 9), and infection including endocarditis (9). Seventy-seven dogs had at least one comorbidity (23 of them more than one) and 23 remained cryptogenic after work-up, with the same survival as the rest (60% versus 56%). Cardiac disease is a minority cause: 6 of 31 dogs in Lake-Bakaar 2012, and among the 35 dogs echoed in Ruehl 2020, suspected endocarditis in 4, a left ventricular thrombus in 3 and a cardiac mass in 3.

Diagnosis is by ultrasound of the terminal aorta, which confirmed 91 of the 100 cases and shows whether the occlusion is complete, partial or non-occlusive and whether it extends into the iliacs (54 of 100). The bedside glucose differential works in dogs as well as cats: in Klainbart 2014 a central minus affected-limb difference of 16 mg/dL (0.9 mmol/L) or more was 100% sensitive and specific in the 9 dogs with ATE, with a median difference of 46 mg/dL. No canine lactate cut-off has been validated. Raised CK (36 of 100), AST (50) and BUN (38) are common, and a prolonged prothrombin time is a marker worth taking seriously: of 11 such dogs, 2 survived and 9 did not.

Treatment follows the same eight steps, with canine doses. Analgesia first: methadone 0.1 to 0.2 mg/kg IV or 0.3 to 0.5 mg/kg IM every 2 to 4 hours, or fentanyl 2 to 5 µg/kg IV then 3 to 6 µg/kg/h (AVAAAP guidelines); buprenorphine 0.01 to 0.04 mg/kg for the claudication case or the step-down, gabapentin 10 to 15 mg/kg every 8 hours (WSAVA) for the neuropathic component once eating; no NSAIDs in a dog that may have PLN, azotaemia, glucocorticoid exposure or reperfusion ahead. Then clopidogrel plus an anticoagulant at the CURATIVE dog doses: clopidogrel 4 to 10 mg/kg loading then 1.1 to 3 mg/kg once daily, with dalteparin 100 to 175 U/kg SC every 8 hours or enoxaparin 0.8 mg/kg SC every 6 hours, or unfractionated heparin (100 U/kg IV then 20 to 37.5 U/kg/h) for a titratable infusion in the unstable dog, with rivaroxaban 1 to 2 mg/kg per day as the oral option once stable. CURATIVE notes that clopidogrel may be more effective than aspirin in dogs at ATE risk; in Ruehl 2020, 31 dogs received more than one agent, aspirin was used in 22 and warfarin in 8, and CURATIVE now advises against warfarin.

Thrombolysis and thrombectomy in dogs sit where the evidence is thinnest. The 2022 CURATIVE update found the canine literature mostly experimental and insufficient to say whether thrombolysis improves patient-centred outcomes, so no protocol is endorsed. In Ruehl 2020, 12 of 100 dogs were thrombolysed (systemic streptokinase 5, local tPA infusion 3, systemic tPA 2, urokinase 2), 9 had balloon-catheter thrombectomy, and 3 needed a pelvic limb amputation; no treatment variable was associated with survival in the regression, in which ambulation was the only predictor. Catheter-directed lysis or thrombectomy is a referral conversation for an acute, complete occlusion in a dog that is otherwise a candidate, and a prolonged prothrombin time is a contraindication until explained. The calculator therefore shows no canine tPA arithmetic.

Then find the cause, because the anticoagulant continues for as long as the driver does. Urinalysis and a urine protein:creatinine ratio, thoracic and abdominal imaging for neoplasia, a glucocorticoid history, adrenal and thyroid testing where the picture fits, echocardiography and blood cultures if there is a murmur or fever, PT and aPTT, and antithrombin activity or thromboelastography where available (11 of 21 dogs tested were hypercoagulable). Every survivor goes home on clopidogrel 1.1 to 3 mg/kg once daily with an anticoagulant alongside while the hypercoagulable state persists, a plan for the underlying disease, and a repeat aortic ultrasound in 2 to 4 weeks. For the owner: chronic-onset dogs that can still walk do best, with survival out to 959 days in Lake-Bakaar 2012; acute, non-ambulatory dogs carry the worst outlook, and 19 of 100 owners in the largest series chose euthanasia at admission.

Other thrombotic emergencies in the Acute tab

Aortic thromboembolism is the thrombosis with the best literature. The others are diagnosed less often, mostly because they are looked for less often, and the Acute tab now carries a case type for each. None has a consensus statement grading its prognosis, so the panels quote the series that exist, name their size, and stop there. Every dose comes from the CURATIVE registry or the ATE analgesia cards; the sequencing is the tool's, labelled practical where no source dictates it.

Pulmonary thromboembolism

The thrombosis that kills the IMHA dog. In the 29-dog necropsy series of Johnson, Lang and Wilkerson (1999) there were no pathognomonic findings; 12 of the 15 dogs with an arterial blood gas were hypoxaemic and all 15 had a widened alveolar to arterial gradient; the diagnosis was suspected in life in only 11 of 29; and neoplasia, systemic bacterial disease and IMHA were the diseases most often found, with 17 of 29 dogs carrying more than one disease process. Thoracic radiographs are normal in 9 to 27% of affected dogs and about 9% of cats, and CT angiography is the reference standard (Merck). D-dimer helps at the margins: above 500 ng/mL it was 100% sensitive and 70% specific for thromboembolism in 20 dogs (Nelson and Andreasen 2003), above 1,000 ng/mL 94% specific with 80% sensitivity, but in 10 necropsy-confirmed dogs a 250 ng/mL threshold caught only 80%, so a normal value does not exclude it (Epstein 2013). In cats the disease is a post-mortem diagnosis almost by definition: none of the 17 cats in Schermerhorn's 24-year series was recognised in life, and 16 had a concurrent disease, most often neoplasia, anaemia or pancreatitis. The tool's plan is oxygen and minimal handling, an anticoagulant as soon as the bleeding-risk flags are checked (venous disease, so LMWH or the UFH bolus plus CRI for the unstable dog), confirmation with echo, D-dimer, a blood gas and CT angiography when the patient can be moved, and a search for the cause across the CURATIVE populations. Thrombolysis gets a section that says no: the 2022 Domain 6 update found the canine literature mostly experimental and insufficient to show a patient benefit, and the feline evidence limited and often neutral.

Portal and splanchnic vein thrombosis in dogs

Respess and colleagues (2012) described 33 dogs: vomiting, diarrhoea, abdominal pain, ascites and hypovolaemic shock were the common signs; hepatic disease was the commonest association (14 of 33), then neoplasia (7), immune-mediated disease (5) and infectious disease (4); thrombocytopenia was present in 24, raised liver enzymes in 23 and hypoalbuminaemia in 20; 24 dogs were acute and 9 chronic; 19 survived to discharge. The predictors are the whole basis of the tool's panel: dogs treated with anticoagulants were more likely to survive, and dogs with acute portal vein thrombosis, multiple thromboses or SIRS were less likely. The plan is analgesia and fluids for shock, a tap of the effusion, an anticoagulant as soon as the bleeding-risk check allows, Doppler ultrasound of the portal system with CT angiography to map the extent, a search for the liver disease or whatever else lies underneath, and a standing watch for the abdomen turning surgical. The authors' own summary is the best screening rule: consider PVT in any dog with risk factors for venous thrombosis presenting with abdominal pain, ascites and thrombocytopenia.

Catheter-associated and cranial vena cava thrombosis

One series, 17 dogs (Palmer, King and Van Winkle 1998): 10 had cranial vena cava syndrome (swelling of the head, neck or forelimbs), 10 had a pleural effusion, 10 were dyspnoeic and 5 had a palpable jugular thrombus. Predisposing conditions were presumed immune-mediated haematologic disease with corticosteroids (6), sepsis (6), protein-losing nephropathy (2), neoplasia (2) and cardiac disease (1), and central venous catheterisation was implicated as a contributing cause. Thrombocytopenia was the most consistent laboratory finding and ultrasonography helped confirm the diagnosis. The outcome is the reason the panel is blunt: treatment varied, and 15 of the 17 dogs died or were euthanised within 20 days of the thrombus declaring itself, with thrombi also found in the right atrium, jugular veins and pulmonary arteries at necropsy. The plan removes or replaces the catheter, anticoagulates, drains the chest if needed and analyses the fluid for chyle, maps the thrombus by ultrasound and echo, and looks for the disease underneath. The authors' advice is written into the discharge section: avoid central venous catheters in dogs with the predisposing diseases.

The cat with a left atrial thrombus and no event yet

The ACVIM 2020 consensus lists an intracardiac thrombus with spontaneous echo contrast among the findings that make ATE a risk, and says that in cats believed to be at very high risk of ATE other antithrombotics can be considered in addition to clopidogrel: clopidogrel plus a PO factor Xa inhibitor, clopidogrel plus aspirin, or all three. The tool reads a visible thrombus as that group. The case type starts clopidogrel (with its loading dose) and an anticoagulant on the same day, LMWH for the first days and rivaroxaban 2.5 mg per cat once the cat is eating, treats heart failure if present, records the echo features that set the long-term plan (left atrial size, smoke, left atrial fractional shortening, auricular flow velocity), and briefs the owner on what an embolus looks like at 2 am. The numbers for that conversation come from cats after an event: recurrence 49% on clopidogrel versus 75% on aspirin (FAT CAT), 39% on rivaroxaban versus 37% on clopidogrel as single agents (SUPERCAT), and 16.7% on clopidogrel plus rivaroxaban in Lo's 32 cats (17 of them with an intracardiac thrombus and 16 with smoke), in which no cat newly developed an ATE while on dual therapy and bleeding-type adverse events occurred in 5 of 32. No study grades the risk for a cat with a thrombus and no event, and the panel says so.

Monitoring heparin therapy

Stopping antithrombotics before surgery

Discontinuation is a risk-level decision, not a drug habit. For antiplatelets: high-risk patients should generally not have them stopped; moderate-risk patients – consider stopping 5–7 days before surgery; low-risk patients – stop 5–7 days before. Unfractionated heparin must be tapered rather than stopped abruptly, whether given by CRI or SC injection, and surgery is best planned at the nadir of effect, roughly 6–8 hours after the last SC dose, with close attention to surgical haemostasis. LMWH needs no weaning but is stopped before procedures in low-to-moderate-risk patients. For rivaroxaban, weaning should be considered.

Common mistakes with antithrombotics in practice

The mistakes we see repeatedly: reaching for aspirin in cats when clopidogrel is the recommended antiplatelet; giving a cat an unfractionated heparin CRI when the feline evidence in the summary is for SC dosing; stopping a heparin CRI abruptly instead of weaning it; using warfarin at all; treating a fibrin-rich venous problem (IMHA) with an antiplatelet alone; forgetting that when two risk factors stack – pancreatitis plus sepsis, neoplasia plus glucocorticoids – prophylaxis stops being optional; and dosing enoxaparin once daily when the canine dose in the summary is every six hours. In the FATE cat, the recurring errors are different: delaying the opioid while the diagnostics happen, reaching for tPA by reflex, running intravenous fluids into a cat in heart failure, warming the ischaemic limbs directly, and missing the potassium rise at 24 to 72 hours because nobody was checking. In the dog, the classic error is the opposite one: treating a chronic claudication case as a spinal or orthopaedic problem for weeks, when a hand on the femoral pulses and an ultrasound of the terminal aorta would have found the thrombus, and then stopping at the thrombus without looking for the proteinuria, the adrenal disease or the tumour behind it.

Frequently asked questions

Glossary

ATE (arterial thromboembolism)

A clot forming in, or lodging in, an artery – classically the distal aortic 'saddle thrombus' of feline cardiomyopathy. Arterial thrombi form under high shear and are platelet rich, which is why antiplatelet drugs are the mainstay.

VTE (venous thromboembolism)

Clot formation on the venous side, including pulmonary thromboembolism. Venous thrombi form under low shear, are fibrin rich, and respond to anticoagulants rather than antiplatelet drugs alone.

IMHA

Immune-mediated haemolytic anaemia. Dogs with IMHA are at such high risk of thromboembolism that antithrombotic therapy is considered mandatory.

PLN (protein-losing nephropathy)

Renal protein loss that also loses antithrombin, tipping the coagulation balance toward clotting. The second canine condition in which antithrombotics are mandatory.

Spontaneous echo contrast (smoke)

Swirling echogenic blood seen in an enlarged left atrium on echocardiography – a marker of blood stasis and a recognised risk factor that makes antithrombotic therapy mandatory in a cat with cardiomyopathy.

Anti-Xa activity

The laboratory assay used to measure heparin effect. Targets: 0.35–0.7 U/mL for unfractionated heparin, 0.5–1.0 U/mL (2–4 h post-dose) for LMWH.

LMWH

Low molecular weight heparin – dalteparin or enoxaparin. Preferred over unfractionated heparin for its safety profile and more reliable bioavailability.

UFH

Unfractionated heparin. Titratable by IV CRI against anti-Xa, but must be tapered rather than stopped abruptly.

CRI

Constant rate infusion – continuous IV delivery, used for UFH in dogs at 20–37.5 U/kg/h after a 100 U/kg loading bolus.

Thromboprophylaxis

Antithrombotic therapy given to prevent a first clot in an at-risk patient, as opposed to treating an existing thrombus.

FATE (feline aortic thromboembolism)

The acute event: a left atrial thrombus embolises to the aortic trifurcation, classically paralysing both pelvic limbs. About 90% of cases sit on cardiomyopathy, most of it undiagnosed until that moment.

The five Ps

Pain, paralysis (or paresis), pulselessness, pallor and poikilothermy (cold limbs): the bedside signature of an arterial embolus.

Glucose differential

Central minus affected-limb blood glucose. A difference of 30 mg/dL (1.7 mmol/L) or more supports ATE (100% sensitivity, 90% specificity); 41 mg/dL (2.3 mmol/L) was 100% specific in a 2024 multicentre study. The lactate differential runs the other way: limb minus central of 2.2 mmol/L or more.

Reperfusion injury

What happens when blood returns to ischaemic muscle: potassium, acid and myoglobin wash back into the circulation, producing hyperkalaemia, acidosis and acute kidney injury, typically at 24 to 72 hours. It is a major cause of death in treated FATE cats and the reason for serial potassium checks and an ECG.

tPA (alteplase)

Tissue plasminogen activator, the thrombolytic used in the BLASTT and MATTERS studies. It improves reperfusion and limb function without a demonstrated survival benefit; not recommended by the ACVIM 2020 consensus, and permissible but unendorsed within 6 hours under the 2022 CURATIVE update.

Canine aortic thrombosis (ATh)

The dog version of the disease: a platelet-rich thrombus that usually forms in place in the terminal aorta on a hypercoagulable background (protein-losing nephropathy, neoplasia, glucocorticoids, endocrine disease, infection), rather than embolising from the heart. Onset was chronic in 72 of 100 dogs in the largest series, ambulation is the strongest prognostic variable, and survival to discharge runs at 50 to 60%.

References

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For CRI dilutions and mL/h from your heparin vial strength, use the dilution calculator. See also the emergency drug calculator, the anaesthetic drug calculator and the antibiotic calculator, or browse every tool on the vet tools hub.