Should FIP Itself Be Treated as a Thrombotic Risk Factor?

A question for specialists, on positioning antithrombotic prophylaxis as a response to FIP itself rather than to its complications, with one case

A note on who is writing.
The author is the owner of a cat treated for FIP and a supporter of a rescue organisation. He is not a veterinarian. What follows is assembled from clinical records, laboratory reports and published literature, and its veterinary interpretation has limits. Corrections are welcome.
This article neither recommends nor argues against any specific treatment. Antithrombotic drugs carry bleeding risk and are not something to start or stop without veterinary direction.

Summary

The question. FIP is, at its core, a monocyte-driven vasculitis, and the endothelium is activated systemically. If that is the case, thrombotic risk is not an increment added when IMHA or cardiomyopathy supervenes. It is intrinsic to the diagnosis itself. Should it not be treated as such?

The current position. The ABCD 2026 FIP treatment guidelines mention prophylactic antithrombotic therapy exactly once — in the paragraph on myocarditis. The immediately preceding paragraph, which instructs the clinician to give glucocorticoids for FIP-associated IMHA, says nothing about thrombosis. The guideline does not fail to recognise thrombotic risk; it recognises it only by way of the heart. The feline antithrombotic consensus (CURATIVE 2022) classifies feline IMHA as low risk, and FIP does not appear among the conditions evaluated at all. In the largest cohort of FIP-associated IMHA (45 cats, Černá et al. 2025), thrombotic events were not an outcome measure, and the 27% mortality was not analysed by cause.

The case. A cat on FIP treatment developed immune-mediated hemolysis, received 34 days of steroids, and then deteriorated acutely with radiographic cardiomegaly. Five layers of thrombotic risk factor had accumulated. An antithrombotic was given only after collapse. There is no imaging confirmation of a clot.

What is being asked for. The view of specialists on this question. If prophylaxis is warranted, then the practical knowledge behind it: in whom, with what, from when, until when, and monitored how.

1. The structure of the question

Read through Virchow’s triad, FIP supplies all three elements without waiting for a complication.

Yet in current treatment guidance there is only one route to antithrombotic prophylaxis. ABCD 2026 raises it solely in the myocarditis paragraph. Neither the vasculitis itself, nor hemolysis, nor concurrent steroids acts as a trigger for the recommendation (§3.1).

In other words: the pathology literature describes FIP as a disease that makes clots, and the therapeutics literature receives that only as cardiac disease. What this article asks is whether a second route should be opened.

2. The pathological basis — FIP is described as a thrombogenic disease

2.1 The mechanism of the vasculitis (Kipar & Meli 2014)

The morphological signature of FIP is a granulomatous phlebitis and periphlebitis mediated by highly activated monocytes. Those monocytes strongly express TNF-α, IL-1β and the adhesion molecule CD18, and interact directly with activated endothelium. Endothelial cells are activated systemically; the restriction of lesions to the venous system of particular organs is attributed to selectivity in endothelial reactivity rather than to where the stimulus is.

Morphologically, this vasculitis is distinguished from immune-complex vasculitis (a type III hypersensitivity contribution is suggested in the necrotising lesions of fulminant cases, but it is not the principal mechanism). The argument here does not depend on an immune-complex mechanism. Systemic endothelial activation alone satisfies the first element of the triad.

2.2 Coagulopathy and thrombosis (Weiss 1980; Peterson 1995)

In experimental FIP infection, thrombocytopenia, hyperfibrinogenemia and raised FDPs develop after onset, together with reduced activity of factors VII, VIII, IX, X, XI and XII and prolongation of PT and aPTT — and, pathologically, widespread phlebitis with thrombosis. This is DIC in completed form.

In a retrospective study of hemostatic profiles in 101 cats at Ohio State University, the three conditions most often associated with an abnormal profile were hepatic disease, neoplasia and FIP (Peterson et al. 1995). A note on sourcing: what can be verified from the abstract is that 69% of the 101 cats had an abnormal profile, and that a mixed defect compatible with DIC, thrombocytopenia and prolonged APTT predominated. The ranking of the three conditions rests on the full text.

The Merck Veterinary Manual lists FIP explicitly among the risk factors for pulmonary thromboembolism in cats.

2.3 Extension to the heart — the myocardium is inflammatorily activated even without lesions

An antemortem diagnosis of FIP myocarditis has been reported (cardiac troponin I 1.31 ng/mL, left ventricular hypertrophy with left atrial enlargement, pleural effusion), in which cardiac remodelling reversed completely on GS-441524 (Korzybska et al. 2025). Myocarditis → chamber dilation → intracardiac stasis is the dominant route to arterial thromboembolism in cats.

Malbon et al. (Viruses 2019) compared myocardium from 18 cats with FIP against control cats and against cats with non-FIP systemic inflammatory disease. The findings were as follows.

• In FIP myocardium, mRNA transcription of IL-1β (p = 0.008) and of IL-6 and TNF-α (both p < 0.001) was significantly higher than in controls
• Transcription of all cytokines was likewise significantly raised in the liver, where the IL-12p40:IL-10 ratio was skewed toward inflammation (p = 0.047)
• None of the cats had FIP lesions in the heart, and no histopathological change was found in the myocardium
• That cardiomyocytes themselves are a source was shown by laser microdissection, but this was a proof of principle in a single animal and outside the statistical analysis (IL-6 immunostaining localised principally to cardiomyocytes)

The authors’ own qualification has to be stated alongside this. Malbon et al. describe the cardiac role as secondary and non-specific: comparable transcriptional upregulation was seen in non-FIP systemic inflammatory disease, with no significant difference between the two groups. Cardiomyocytes are positioned as bystander cells serving an amplification step.

One point nevertheless bears on the argument. Inflammatory activation of the myocardium occurs in animals with no cardiac lesion at all. The trigger that fires antithrombotic prophylaxis in ABCD 2026 is “myocarditis” — an entity defined by lesions. What Malbon et al. show is that cardiac involvement extends beyond the presence of lesions. The trigger may be drawn more narrowly than the underlying biology.

The same paper notes that TNF-α and IL-1β increase endothelial adhesion molecule expression and monocyte MMP secretion, contributing to destruction of the vascular basement membrane in FIP phlebitis — a cytokine-mediated path connecting the vasculitis mechanism of §2.1 directly to the coagulopathy of §2.2.

3. Guidelines and cohorts — why no answer exists

3.1 ABCD 2026 — prophylaxis is recommended, but only by way of the heart

In §4 (Supportive and Concurrent Disease Treatment) of the current ABCD FIP treatment guidelines (Tasker, Spiri et al., Viruses 2026;18:452), these two paragraphs sit adjacent to one another.

That is the only mention. Consequently:

• For the population in which thrombotic risk is most densely concentrated — hemolysis plus concurrent steroids — there is not a word about antithrombotic therapy
• The moment the text enters the cardiac paragraph, prophylaxis appears

Moreover the recommendation consists of the phrase “prophylactic antithrombotic treatment” and nothing else: no drug, no dose, no start point, no duration, no monitoring parameter. This contrasts with the antiviral table, which specifies formulation, dose, duration and adverse effects.

The author has not been able to verify every row of the supportive-care table. That does not change the fact that the mention in the body text runs through myocarditis alone.

The guideline does not fail to recognise thrombotic risk. It recognises it only by way of the heart. What this article asks is whether a second route should be opened.

3.2 CURATIVE 2022 (feline antithrombotic consensus)

Feline IMHA (guideline 1.3)

• Judged to be weakly associated with pulmonary thromboembolism (venous). Only one study suggests the association, in which 2 of 29 cats with PTE (7%) had IMHA. The 52 reports judged neutral include a total of 396 cats with IMHA of all forms, with no thrombosis reported
• There is no evidence that it is a risk factor for arterial thromboembolism — note the explicit separation of the venous and arterial systems
• However: “in the presence of other thrombotic risk factors, we suggest that antithrombotic therapy be considered”
• Why the thrombogenicity of IMHA differs between dogs and cats is flagged explicitly as an unresolved knowledge gap

Exogenous glucocorticoids (guideline 1.15)

• No evidence-based recommendation can be made; routine use is not recommended
• The basis: no thrombosis occurred among 25 cats receiving steroids; 2 of 6 cats with portal vein thrombosis were on prednisolone but all had concurrent hepatic disease; 2 of 44 cats with distal aortic thromboembolism had received steroids in the preceding weeks but had high-risk comorbidities
• However, in the retrospective series of 29 cats with PTE cited by the same review, 8 (27.6%) had recently received steroids. With no control group causation cannot be shown, but the figure is not negligible

Cardiac disease

• For cats judged to be at risk of ATE, antithrombotic therapy is recommended. Not “consideration suggested”
• But the criteria for that judgement are echocardiographic: moderate-to-severe left atrial enlargement, reduced left atrial fractional shortening, reduced left auricular flow velocity, spontaneous echo contrast. Radiographic cardiomegaly does not meet them

FIP is not among the conditions evaluated. The 2022 scope covers canine and feline dirofilariasis, feline IMHA, feline PLN, PLE, feline sepsis, feline hyperadrenocorticism, canine hepatic disease, portosystemic shunts, and catheters and devices. Cardiomyopathy and arrhythmia are handled separately.

The question here is whether FIP itself should count among CURATIVE’s “other thrombotic risk factors.” As long as FIP is outside the scope of evaluation, the guidance does not answer it.

And the handling of multiple sub-threshold factors in combination is nowhere defined. IMHA alone: insufficient. Steroids alone: insufficient. What, then, when both are present, along with FIP and radiographic cardiomegaly? No clause addresses it.

3.3 Černá et al. 2025 (45 cats with FIP-associated IMHA, Pathogens 14:660)

The largest cohort of FIP-associated IMHA. The salient points:

The largest dataset available cannot answer this question, because the question was never asked of it. How much of that 27% mortality was thromboembolic, nobody knows.

3.4 Pulmonary thromboembolism secondary to feline IMHA

A case of thrombus in the main pulmonary artery secondary to feline IMHA has been reported, confirmed echocardiographically and improved on dalteparin plus prednisolone (Yoshida et al. 2022). Rare, but hemolytic anemia in cats has been demonstrated to produce thrombosis.

4. The case (summary)

The cat died on the morning of 8 September. No necropsy was performed.
Nothing in the argument that follows depends on the outcome.

A note on the cardiomegaly of 7 September. The recommendation criteria for antithrombotic therapy in CURATIVE and in the ACVIM cardiomyopathy consensus are echocardiographic (left atrial enlargement, spontaneous echo contrast, reduced left auricular flow velocity). Radiographic cardiomegaly does not satisfy them.

In a cohort of rivaroxaban use in cats (Yarsley et al. 2025; 66 cats, 7 hospitals), cats without a complete echocardiogram were classified as carrying a major CURATIVE risk factor on the basis of cardiac findings including radiographic cardiomegaly and murmur. That operational rule, however, was applied to retrospectively classify cats who presented with ATE; it was not offered as a decision criterion for primary prophylaxis before an event. Whether it can be extrapolated to this case is itself a matter for examination (§7, question 4).

Echocardiography was attempted here but, given the equipment, neither left atrial dimension nor wall thickness nor spontaneous echo contrast could be assessed. NT-proBNP was likewise unavailable on the island.

Coinfection with FeLV and/or FIV is not held to affect response to GS-441524 (ABCD 2026), and FIV positivity is not considered to explain this cat’s course.

The accumulation of risk factors

1. ① FIP (monocytic vasculitis, systemic endothelial activation)the underlying disease itself
2. ② Immune-mediated hemolysismicroparticles, free hemoglobin, ADP
3. ③ Steroids for 34 days (2 mg/kg for 3 of them)weak feline evidence, but not excludable
4. ④ Cardiomegaly (myocarditis vs pericardial effusion unresolved)stasis
5. ⑤ Dehydration and recumbency (fluids 200 → 70 mL/day)hemoconcentration, stasis

Judging any one factor as “monitor and observe” is defensible. But when five layers stack in the same direction, there is no mechanism in current practice by which that judgement is automatically revisited. In this case thrombotic risk was raised three times over the course of treatment. Each time it went no further than “worth considering,” and never became a priority.

5. Objections and reservations — taken on directly

(a) The coagulopathy of FIP is consumptive (DIC-type); antithrombotics would promote bleeding.
Weiss 1980 showed prolonged PT and aPTT with factor consumption. In Černá 2025, 40% were thrombocytopenic. In this case the platelet count at presentation was 87,000/µL (feline clumping can produce spuriously low values). It may be that prophylaxis makes sense only in a hypercoagulable phase. That converts the question from “should prophylaxis be given” into “in which phase, in which subgroup, with which drug class.”

That said, the case for withholding on bleeding grounds is weak. The ACVIM consensus on canine IMHA sets a floor of 30,000/µL for antithrombotic administration and states that bleeding risk at recommended doses is low. The nadir here, 87,000/µL, was roughly three times that floor. There was no basis in this case for withholding an antithrombotic because of bleeding risk.

(b) The association between feline IMHA and thrombosis is weak (CURATIVE).
Correct. But CURATIVE’s evaluation centres on primary IMHA; IMHA whose underlying disease is a vasculitis has not been evaluated as a separate population.

(c) The thrombotic risk of steroids is poorly evidenced in cats.
Correct. The reliance on extrapolation from canine data is conceded.

(d) The clopidogrel evidence (FAT CAT) covers secondary prevention of cardiogenic ATE only.
Correct. There are no feline data on primary prophylaxis against vasculitis-driven or hemolysis-driven thrombosis.

(e) No thrombus was confirmed in this case.
Correct, and no necropsy was performed. The deterioration of 6–7 September is equally explicable by tamponade from FIP-related pericardial effusion (consistent with absent pulmonary edema plus cardiomegaly, and with cold hind limbs that were pink-padded and non-painful, as in low output), severe hypokalemia (last value 2.4 mmol/L, unmeasured for the following 34 days), or hypoglycemia (never measured). The same holds for the vocalisation and collapse on the morning of 6 September: ischemic pain from a visceral vascular thrombus is one strong explanation, but abdominal pain from pancreatitis, gastrointestinal obstruction or serositis, and syncope from arrhythmia or hypoglycemia, would also account for it (§6.4).

(f) The hemolysis may have been caused by GS-441524.
ABCD 2026 notes that very mild Heinz body hemolytic anemia was reported in 2 of 40 cats on GS-441524. A Hb of 3.7 g/dL with total bilirubin 4.6 mg/dL is of an entirely different order from “very mild,” and the hemolysis was steroid-responsive — but Heinz bodies were never assessed on a smear, so this cannot be excluded outright.

The argument of this article therefore does not depend on there having been a thrombus in this cat. It rests on three points: (1) FIP is described in the pathology literature as a thrombogenic disease; (2) clinical courses in which risk factors stack in layers do occur; (3) the only route to prophylaxis provided against them runs through cardiac disease.

6. A provisional framework from the author

Posing a question without a proposal does not start a discussion, so here is something to argue with. It comes from someone who is not a veterinarian, and it exists to be criticised.

The essential move is to stop listing the conditions as equals. A formulation of the type “when FIP + IMHA + steroids are all present” is not supported by the feline literature (as §3.2 sets out, IMHA alone and steroids alone were both judged sub-threshold). The starting point is not “have three conditions been met” but “what has been added to FIP.”

6.1 The framework

[Core] FIP

DIC, widespread phlebitis and thrombosis are experimentally demonstrated (Weiss 1980), and systemic endothelial activation from monocytic vasculitis sits at the centre of the pathology (Kipar & Meli 2014). The myocardium raises transcription of IL-1β, IL-6 and TNF-α irrespective of lesions (Malbon et al. 2019, with the authors’ own framing of this as a secondary, non-specific response). And yet FIP lies outside CURATIVE’s scope and has no position in the guidance at all.

[Contributing factors] each one lowers the threshold for prophylaxis

[Exclusions]

• Platelet count below 30,000/µL (adopting the floor from the ACVIM canine IMHA consensus)
• Active bleeding

The point of the framework is that none of ①–④ is on its own a basis for prophylaxis. CURATIVE states as much for each of them. But each also retains a clause about considering therapy in the presence of other risk factors. FIP is the strongest candidate for that role, and it has not been evaluated.

The practical form of the judgement is therefore:

In a cat with FIP, the moment any of ①–④ is present, assess the indication for antithrombotic prophylaxis on an individual basis, without waiting for laboratory trends.

Not “treat everyone.” “Count FIP explicitly as a risk factor, then assess individually.”

6.2 Applied to this case

②, ③ and ④ were in place by early August. ① was not assessed until radiographic cardiomegaly was found on 7 September.

And ① was never established. Echocardiography was performed, but the equipment did not permit assessment of left atrial dimension, wall thickness or spontaneous echo contrast, and NT-proBNP was unavailable on the island. As for the exclusions, the only measurable one — a platelet count of 87,000/µL — was about three times the floor and no barrier to treatment.

This is where the framework’s own defect becomes visible. The determination of ① presupposes echocardiography, and echocardiography presupposes access to secondary care. A decision rule that requires confirmation becomes, in an environment without the means of confirmation, indistinguishable from not deciding. What was absent in this case was not the risk factor. It was the means of confirming it.

Current guidance assumes access to referral practice. FIP is being treated, right now, in places where that assumption does not hold.

6.3 Limits of the framework

It combines mechanistic inference with the conditional clauses of existing guidance, and has not been validated against clinical data. What is unknown:

• The incidence of thrombosis in cats with FIP
• Whether prophylaxis improves outcome
• The bleeding risk associated with prophylactic dosing

The third cannot be waved away. The DIC picture in Weiss 1980 includes reduced factor activity with prolonged PT and APTT. In a disease state where thrombosis and bleeding can progress together, blanket prophylaxis carries danger. Whether it is adequate to set the exclusions at platelet count and active bleeding alone is also unvalidated.

6.4 The antecedent sign — the signal was there. The drug was not.

On the morning of 6 September, during a meal, a cat who does not vocalise cried out at length and then collapsed. This is something the owner recalled afterwards. For the roughly ten hours until third-eyelid protrusion was noticed at 18:40 and judged abnormal, the signal was received only as “an unusual way of crying.”

In feline thromboembolism, vocalisation from pain is a textbook finding. That the hind limbs were mobile, non-painful and pink-padded argues against a saddle thrombus, and onset after eating fits ischemic pain from increased intestinal blood demand. Third-eyelid protrusion is also a common finding with abdominal pain in cats.

Two reservations apply. First, sudden sustained vocalisation is not specific to thrombosis; pancreatitis, gastrointestinal obstruction and serositis produce it too. Second, if the thrombus is placed in an abdominal vessel, it does not connect with the course from the early hours of 7 September onward — frothing, incontinence, peripheral cooling beginning in the hind limbs — which suggests low output of a right-heart-failure type. One thrombus cannot account for both. Either there were separate thrombi, or the overnight deterioration was a cardiac problem unrelated to thrombosis (pericardial effusion, arrhythmia, anemic heart failure). This remains unresolved.

Whatever the mechanism, three things hold.

1. An observable antecedent sign existed roughly ten hours before anything was first recognised as abnormal
2. That sign — sustained vocalisation in a cat who does not vocalise — is detectable only by the person who provides daily care
3. Even had it been recognised as abnormal at the time, there was no means of obtaining an antithrombotic on the island. Forty minutes after the 18:40 recognition, a specialist opinion from Tokyo had arrived. The drug was nowhere on the island

The third point is the substantive one. A decision rule of the form “start when you observe X” does not execute if the only person who can observe X is an owner at home at night and the drug exists only at the clinic. Teaching observation and providing access to the drug do not work one without the other.

Two questions follow. First, should owners of cats under FIP treatment be told: if a cat who does not normally vocalise suddenly cries out and keeps crying, suspect thrombosis and make contact immediately? Second, in regions with neither referral nor after-hours care, could it be justified to dispense an antithrombotic in advance for the home, to be started by the owner on defined signs? The second is asked in full awareness that it departs from veterinary norms.

To be clear, the second point is a question, not a proposal, at this stage. Owner-initiated antithrombotic administration carries bleeding risk. It is restated here that it should not be carried out without veterinary direction.

7. Questions for specialists

1. In ABCD 2026 §4, the myocarditis paragraph carries prophylactic antithrombotic therapy and the immediately preceding FIP-associated IMHA paragraph does not. Is that distinction deliberate? If it is, the reasoning would be valuable — that the coagulopathy of FIP is predominantly consumptive and ill-suited to prophylaxis, that thrombotic deaths are in practice uncommon, or otherwise. If it is not, whether the recommendation should extend to the vasculitis itself, or to cases with concurrent IMHA, is the central question of this article.
2. Should FIP be added as a PECO question in the next revision of CURATIVE Domain 1? One of the feline infectious diseases with the best-demonstrated thrombogenicity is missing from the feline thromboprophylaxis consensus. CURATIVE also leaves undefined how to handle multiple risk factors that are individually sub-threshold. These two points are, separately from ABCD, matters for ACVECC.
3. If it should extend, to which subgroup rather than to all cases? Candidates: effusive form; myocarditis, radiographic cardiomegaly or raised NT-proBNP; concurrent IMHA; concurrent steroids; persistently raised AGP or SAA; the absence of thrombocytopenia.
4. May an operational rule designed for cats presenting with ATE be extrapolated to primary prophylaxis? Yarsley et al. 2025 counted radiographic cardiomegaly and murmur as major risk factors in cats without a complete echocardiogram. Can that be transferred to a pre-event prophylactic decision in a setting where echocardiography is unavailable? Views on the framework in §6 as a whole would also be welcome — the treatment of ①–④ as contributing factors, and the placement of the exclusions at 30,000/µL and active bleeding alone.
5. On teaching antecedent signs, and on positioning the drug in advance. The two questions in §6.4 — the soundness of teaching owners that sustained vocalisation is a thrombosis alarm, and the acceptability of dispensing an antithrombotic in advance to the home in regions with neither referral nor after-hours care.
6. On drug class. In a disease state with an underlying consumptive coagulopathy, which is the more coherent choice: an antiplatelet agent (clopidogrel) or an anticoagulant (dalteparin, rivaroxaban)? Or should the choice follow the phase?
7. On start and stop. Concurrent with the start of GS-441524? Only for the duration of steroid cover? Or until the serositis resolves (normalisation of AGP)?
8. On monitoring. In a general practice or an island clinic where neither TEG nor D-dimer is available, what is usable in practice — the platelet trend, PT/aPTT, or clinical signs alone?
9. On experience. Have you seen thromboembolism (ATE, PTE, cerebral) during FIP treatment? Among deaths on treatment, in how many was thrombosis suspected? If anyone knows the breakdown of causes behind the 27% mortality in the Černá cohort, that information would be valuable.

Comments are equally welcome — disagreement and corrections included.

8. References

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4. Weiss RC, Dodds WJ, Scott FW. Disseminated intravascular coagulation in experimentally induced feline infectious peritonitis. Am J Vet Res. 1980;41(5):663–671. PMID 6250426
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10. Černá P, Knies M, Assink M, et al. Immune-mediated hemolytic anemia in cats with feline infectious peritonitis. Pathogens. 2025;14(7):660. doi:10.3390/pathogens14070660
11. deLaforcade A, Bacek L, Blais MC, et al. 2022 Update of the Consensus on the Rational Use of Antithrombotics and Thrombolytics in Veterinary Critical Care (CURATIVE) Domain 1: Defining populations at risk. J Vet Emerg Crit Care. 2022;32(3):289–314. doi:10.1111/vec.13204
12. Hogan DF, Fox PR, Jacob K, et al. Secondary prevention of cardiogenic arterial thromboembolism in the cat: the double-blind, randomized, positive-controlled feline arterial thromboembolism; clopidogrel vs. aspirin trial (FAT CAT). J Vet Cardiol. 2015;17 Suppl 1:S306–S317.
13. Swann JW, Garden OA, Fellman CL, et al. ACVIM consensus statement on the treatment of immune-mediated hemolytic anemia in dogs. J Vet Intern Med. 2019;33(3):1141–1172.
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15. Yoshida T, Mandour AS, Sato M, et al. Pulmonary thromboembolism due to immune-mediated hemolytic anemia in a cat: a serial study of hematology and echocardiographic findings. Front Vet Sci. 2022;9:930210. doi:10.3389/fvets.2022.930210
16. Korzybska E, O’Halloran C, Culshaw G, Milevoj N, Fernandez-Gallego A, Oliveira MI. Successful treatment of feline infectious peritonitis-associated myocarditis in a cat. J Feline Med Surg Open Rep. 2025;11(2):20551169251366442. doi:10.1177/20551169251366442
17. Merck Veterinary Manual. Pulmonary thromboembolism in dogs and cats.

Disclaimer
This article is provided for information. It is not a substitute for veterinary diagnosis or treatment advice. FIP cannot be confirmed by any single test, and decisions about treatment belong with the attending veterinarian. No medication, antithrombotics included, should be started, altered or stopped on personal judgement. Nothing here is a reason to delay or interrupt treatment.
The figures in the case are transcribed from clinical records and may contain transcription errors or omitted dosing entries. This article was prepared by the owner’s side.