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. 2026 Apr 1;67(4):399–405.

Steroid-responsive meningitis-arteritis in a dog presented with marked cardiac dysfunction and a hypercoagulable state

Jessica Lam 1,✉, Daniel Moreno 1, Mathieu Paulin 1, Jasmine Gu 1, Anthony Carr 1, Susan Taylor 1
PMCID: PMC13040488  PMID: 41929721

Abstract

Canine steroid-responsive meningitis-arteritis (SRMA) is an immune-mediated inflammatory disorder targeting the leptomeninges and associated vasculature with systemic inflammation and occasionally with mild systolic dysfunction and cardiac arrhythmias. Hypercoagulability has not been previously documented in dogs with SRMA, despite increases in inflammatory markers. This case report describes a 6-month-old female Australian heeler dog with acute progressive pyrexia and cervical hyperesthesia. Notable findings included marked decreased cardiac contractility and hypercoagulability determined via viscoelastic coagulation monitor and rotational thromboelastographic analysis. The SRMA was diagnosed based on clinical findings, cerebrospinal fluid analysis, magnetic resonance imaging, elimination of infectious causes of meningitis, and resolution of abnormalities after treatment with immunosuppressive medications. This is the first report describing severe systolic dysfunction and hypercoagulability in a dog with SRMA. The findings support routinely evaluating cardiac function and coagulation in dogs with SRMA and considering treatment with antithrombotic drugs when warranted.

Key clinical message:

It is important to consider cardiovascular and coagulation complications in dogs with SRMA. Dogs exhibiting atypical findings, such as arrythmia or unexplained clinical deterioration, may require further diagnostic workup. Early identification of these complications could necessitate the use of antithrombotic drugs and prompt monitoring of cardiac function to optimize patient outcomes.

Canine steroid-responsive meningitis-arteritis (SRMA) is an immune-mediated disease causing systemic inflammation and leptomeningeal meningitis and arteritis, primarily affecting juvenile to young-adult dogs of medium to large breeds (1). Typical clinical manifestations include cervical rigidity and hyperesthesia, pyrexia, and stiff gait (1,2). Diagnosis relies on clinical findings, a non-degenerative neutrophilic pleocytosis in cerebrospinal fluid (CSF), negative infectious disease testing, and a rapid and complete response to immunosuppressive therapy (1–3). Delayed or inadequate treatment can lead to progressive ataxia, paresis, cranial nerve deficits, and other neurologic deficits, often due to meningeal vasculitis that can cause hemorrhage, fibrosis, or thrombosis (2–5).

Cardiac abnormalities identified in dogs with SRMA include arrhythmias, elevated cardiac troponin I concentrations, spontaneous echocardiographic contrast, pericardial effusion, and mildly decreased fractional shortening (5–8). These changes are usually mild and resolve with immunosuppressive treatment (5–8).

Biomarkers of inflammation such as plasma fibrinogen, serum haptoglobin, C-reactive protein (CRP), and neutrophil gelatinase-associated lipocalin are increased in most dogs with SRMA, but a disease-specific antemortem biomarker is not available (1–3,9,10). There is a paucity of data regarding assessment of coagulation parameters in these dogs. D-dimers are increased in CSF and serum of SRMA dogs with severe meningeal inflammation, suggesting increased fibrinolysis, but serum concentrations of D-dimer were reported to be higher in dogs with other systemic inflammatory disease than in dogs with SRMA (11). Local thrombosis of inflamed meningeal vessels and coronary arteries has been described in dogs with SRMA, but systemic hypercoagulability has not been documented (1,12–14).

This case represents the first reported instance of severe systolic dysfunction and hypercoagulability in a dog with SRMA. This is the first documentation of hypercoagulability in a dog with SRMA using a viscoelastic coagulation monitor (VCM) (VCM Vet; Entegrion, Durham, North Carolina, USA) and rotational thromboelastometry (ROTEM) (ROTEM Delta; Werfen GmbH, Munich, Germany). This case report aims to demonstrate the importance of evaluating cardiac function and coagulation in dogs with SRMA to enhance our understanding of SRMA and recognize potential therapeutic implications.

CASE DESCRIPTION

A 6-month-old intact female Australian red heeler dog weighing 13.3 kg was referred to the emergency department at the Western College of Veterinary Medicine (WCVM), University of Saskatchewan (Saskatoon, Saskatchewan), for investigation of an acute onset of cervical pain, transient paraparesis, and elevated rectal temperature (39.8°C).

The owners reported that the dog had shown lethargy and left pelvic limb lameness 1 mo before referral, which was empirically treated with a 10-day course of oral meloxicam. The dog’s lethargy had resolved, but an intermittent left pelvic limb lameness persisted. The dog had been primarily fed a grain-free commercial diet and was up to date for core vaccines (excluding rabies) but had not received parasite prophylaxis.

One day before referral, the dog began dragging both pelvic limbs and was evaluated by the primary care veterinarian. The dog was pyrexic (39.8°C) and had mild cervical discomfort and ambulatory paraparesis with strong synchronous femoral pulses. Neurologic examination revealed pelvic limb weakness, diminished withdrawal and sciatic reflexes, and patellar hyperreflexia. The referring veterinarian initiated fluid therapy with Ringer’s lactate solution (41 mL/h for 7 h, IV), hydromorphone (0.05 mg/kg, q4h, IV), and meloxicam (0.1 mg/kg, q24h, PO). The paraparesis resolved overnight and the dog was fully ambulatory. Survey radiographs of the thorax and the vertebral column were unremarkable. An irregular cardiac rhythm was detected, with pulse deficits, characterized on ECG as ventricular tachycardia (heart rate: 210 bpm) with a left bundle morphology. The arrhythmia persisted despite 2 lidocaine boluses (3 mg/kg, IV), prompting referral to the WCVM.

On admission (Day 1), physical examination showed cervical rigidity; low head carriage; generalized hyperesthesia on palpation and manipulation of the neck, back, tail, and all 4 limbs; and kyphosis. Auscultation revealed a heart rate of 130 bpm and an arrhythmia with pulse deficits. Rectal temperature was 39.2°C. The remainder of the physical and neurologic examinations were unremarkable. An emergency panel (packed cell volume, serum total solids, blood urea nitrogen, and glucose concentrations) and point-of-care ultrasound scan of the thorax and abdomen were unremarkable. A 3-lead ECG indicated a heart rate of 128 bpm with right ventricular premature complexes. The dog was hospitalized and received fluid therapy (21 mL/h, IV) to correct 5% dehydration and hydromorphone (0.05 mg/kg, q4h, IV).

The dog was transferred to the small animal internal medicine department on Day 2. The arrhythmia persisted and pain was still elicited on cervical manipulation. A CBC revealed nonregenerative anemia [hematocrit: 0.37, reference interval (RI): 0.39 to 0.56], neutrophilia (20.16 × 109/L, RI: 3 to 10 × 109/L), and thrombocytosis (303 × 109/L, RI: 117 to 418 × 109/L). Serum biochemistry profile revealed elevation of alanine aminotransferase activity (66 U/L, RI: 19 to 59 U/L), hypoalbuminemia (2.8 g/dL, RI: 3.2 to 4.2 g/dL), and normoglobulinemia (2.4 g/dL, RI: 20 to 24 g/L).

Echocardiographic measurements revealed marked decreases in fractional shortening (8.3%, RI: 33 to 46%) and ejection fraction (19.1%, RI: 40.7 to 72.7%), enlarged left atrial diameter (2.30 cm, RI: 0.63 to 0.96 cm), and an increase in left ventricular (LV) internal diameter during systole (2.99 cm, RI: 0.71 to 1.26 cm), indicating marked LV systolic dysfunction with mild mitral and tricuspid insufficiency (Figure 1) (15,16). Serum cardiac troponin I concentration was elevated (58.6 ng/mL, RI: < 0.2 ng/mL).

FIGURE 1.

FIGURE 1

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M-mode echocardiograms from an affected dog, demonstrating changes in left ventricular fractional shortening (FS), left ventricular internal diameter during systole (LVIDs) on Day 2 (A) and Day 9 (B).

Cervical magnetic resonance imaging (MRI) with contrast was done using a 1.5 Tesla closed-magnet MRI scanner (GE HealthCare, Mississauga, Ontario), and the following sequences were obtained: T2-weighted (T2W) in sagittal and transverse planes; T1-weighted (T1W) in transverse plane; T2W fluid-attenuated inversion recovery transverse images; T1W images in transverse, sagittal, and coronal planes immediately after IV administration of gadolinium (Omniscan, 287 mg/mL; GE HealthCare). Cervical MRI (Figure 2) revealed mild, patchy, intramedullary contrast enhancement between C3–C6 vertebral bodies; moderate diffuse meningeal enhancement; and marked bilateral asymmetrical T2W hyperintensity and contrast enhancement of C2–C8 nerve roots and musculature of the neck.

FIGURE 2.

FIGURE 2

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Transverse T2-weighted (T2W) (A), T1-weighted (T1W) (B), and T1W post-contrast fat saturation (C) magnetic resonance images at the level of C2 to C3 intervertebral foramen. Note the thickened and markedly contrast-enhancing left C3 nerve (smaller arrows in C) and patchy T2W hyperintensity and enhancement of the paravertebral muscles (larger arrows in A and C).

Examination of CSF collected from the cisterna magna revealed a mild neutrophilic pleocytosis (7.7 cells/μL, RI: < 5 cells/μL), increased total protein concentration (1.28 g/L, RI: 25 to 30 g/L), and moderate hemodilution (red blood cell count: 9600 cells/μL). The results of a 100-cell differential cell count showed 89% neutrophils and 11% small mononuclear cells. Microscopic examination identified a few possible bacteria in the CSF; however, aerobic and anaerobic bacterial enrichment cultures of urine and CSF were negative.

Results of PCR testing were negative for the pathogens Bartonella spp., Blastomyces dermatitidis, Coccidiodes spp., Cryptoccocus spp., Histoplasma capsulatum, canine distemper virus, Borrelia burgdorferi, Neospora spp., Toxoplasma gondii (Neurologic RealPCR Panel (standard)-canine; IDEXX Laboratories, Westbrook, Maine, USA); for antibodies against Borrelia burgdorferi, Anaplasma phagocytophilum, Anaplasma platys, Ehrlichia canis, Ehrlichia ewingii; and for antigen against Dirofilaria immitis (4DX SNAP; IDEXX Laboratories). The Lyme Quant C6 antibody ELISA (IDEXX Laboratories) was negative (< 10 u/mL, RI: 0 to 30 u/mL). Arthrocentesis of both tarsi, carpi, and stifles yielded clear viscous synovial fluid. Cytology revealed mild neutrophilic inflammation in the L carpus (20% neutrophils), R carpus (12% neutrophils), L stifle (8%) and R tarsus (9%).

Serum CRP concentration (IDEXX Laboratories) was elevated (11.2 mg/dL, RI: 0 to 1.0 mg/dL). Serum IgA and IgG concentrations were unremarkable, but serum IgM was elevated (310 mg/dL, RI: 70 to 270 mg/dL) (IgA, IgG, IgM; Antech Diagnostics Canada, Mississauga, Ontario). Plasma fibrinogen concentration was elevated (4.03 g/L, RI: 1.5 to 4.0 g/L). Viscoelastic coagulation testing results on both VCM Vet (Figure 3) and ROTEM (Figures 4, 5 A) (Table 1) were consistent with a hypercoagulable state characterized by low clotting time and increased clot firmness.

FIGURE 3.

FIGURE 3

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Viscoelastic coagulation testing on the VCM Vet analyzer (Entegrion) on admission (Day 1). Values in the right-hand column are reference intervals.

CT — Clotting times; CFT — Clot formation time; MCF — Maximum clot firmness.

FIGURE 4.

FIGURE 4

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EXTEM (A) and INTEM (B) tracings on rotational thromboelastometry (ROTEM) before glucocorticoid treatment (Day 2).

FIGURE 5.

FIGURE 5

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FIBTEM tracings on rotational thromboelastometry (ROTEM) before glucocorticoid treatment (Day 2) (A) and after 7 d of glucocorticoid treatment (Day 9) (B).

TABLE 1.

Tracing on rotational thromboelastometry (ROTEM) (EXTEM, INTEM, and FIBTEM) values before initiation of treatment (Day 2) and after 7 d of prednisone therapy (Day 9).

Profile Parameter Reference interval (26,27) Day 2 Day 9
EXTEM CT (s) 23 to 87 50 49
CFT (s) 85 to 375 46 (Low) 45 (Low)
α- (°) 42 to 77 81 (High) 81 (High)
A5 (mm) 15 to 45 65 (High) 61 (High)
MCF (mm) 32 to 65 77 (High) 74 (High)
MCE 45 to 142 343 (High) 285 (High)
ML (%) 0 to 12 2 3
INTEM CT (s) 133 to 210 196 139
CFT (s) 59 to 201 48 (Low) 46 (Low)
α- (°) 25 to 51 80 (High) 81 (High)
MCF (mm) 52 to 71 75 (High) 76 (High)
MCE 108 to 242 294 (High) 316 (High)
ML (%) 0 to 3 2 1
FIBTEM CT (s) 21 to 112 34 31
CFT (s) NA 42 —
MCF (mm) 2 to 9 36 (High) 17 (High)
ML (%) 1 to 99 13 18
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EXTEM — Rotational thromboelastometry with added aprotinin for inhibition of fibrinolysis; INTEM — Rotational thromboelastometry activated by propriety ellagic acid; FIBTEM — EXTEM with added cytochalasin D for inhibition of thrombocytes; CT — Clotting times; CFT — Clot formation time; A5 — Amplitude at 5 min; MCF — Maximum clot firmness; MCE — Maximum clot elasticity; ML — Maximum lysis; NA — Not available.

The dog was treated with clindamycin (10 mg/kg, PO, q12h) and dexamethasone (0.1 mg/kg, IV, q24h) in the hospital for presumptive SRMA while awaiting results of the infectious disease tests.

On Day 4, the dog had a normal posture and was more comfortable on palpation and manipulation of the neck and back. Serial ECGs showed sinus rhythm (80 bpm), except for a single right ventricular premature complex. The dog was discharged from the hospital on Day 5 and was prescribed oral pimobendan, prednisone and azathioprine, clopidogrel, and trazodone. Clindamycin, enrofloxacin, and amoxicillin-clavulanate were administered while awaiting final CSF bacterial culture and infectious disease screening results; antibiotics were discontinued on Day 11. Omeprazole was administered because a proper washout period between the previous meloxicam therapy and initiation of prednisone was not feasible. Switching to a balanced commercial diet that was not grain-free was recommended to the owners, but no change was made until Day 7.

On Day 9, the dog had a normal posture and gait and no pain on spinal palpation or manipulation. The cardiac auscultation and femoral arterial pulses were normal. A 60-second ECG revealed normal sinus rhythm. Repeat echocardiogram indicated improvement in fractional shortening (23.4 versus 8.2%, RI: 33 to 46.0%) and ejection fraction (47.8 versus 19.1%, RI: 40.7 to 72.7%). Left atrial diameter was 2.83 versus 2.30 cm (RI: 0.63 to 0.96 cm), La:Ao was 1.66 versus 1.45 cm (RI: 0.83 to 1.13 cm), and improved size of LV internal diameter was (2.62 versus 2.99 cm; RI: 0.71 to 1.26 cm) (15,16). There was persistent moderate homogenous hyperechogenicity of the myocardium of the left intraventricular septum and LV papillary muscles, along with unchanged mitral valve insufficiency. Repeat ROTEM showed dramatic improvement in maximum clot firmness (Figure 5 B).

On Day 55, the dog remained asymptomatic. Repeat CBC was unremarkable. Serum troponin I concentration had returned to normal (< 0.2 ng/mL, RI: < 0.2 ng/mL). On Day 114, repeat echocardiography showed continued improvement, with fractional shortening of 23.9 versus 23.4%; (RI: 30 to 46%), ejection fraction of 53.7 versus 47.8% (RI: 40.7 to 72.7%), left atrial size of 2.1 versus 2.83 cm (RI: 0.63 to 0.96 cm), and static LV internal diameter of 2.7 versus 2.62 cm (RI: 0.71 to 1.26 cm). The immunosuppressive course of prednisone was weaned as follows: 1 mg/kg, PO, q24h for 6 wk; 1 mg/kg, PO, q48h for 4 to 6 wk; and 0.5 mg/kg, q24h for 8 wk; and then discontinued. At the time of writing (Day 1032), the dog remained asymptomatic, with no apparent relapse.

DISCUSSION

This case report describes a unique presentation of SRMA in a 6-month-old intact female Australian red heeler dog. Acute SRMA typically manifests as cervical pain, stiffness, and fever (1–3). This dog exhibited pyrexia and cervical hyperesthesia alongside laboratory evidence of systemic and CSF inflammation. Severe cardiac dysfunction and hypercoagulability were also documented.

Diagnosis of SRMA was based on signalment, clinical findings of cervical hyperesthesia and historical fever; laboratory evidence of systemic inflammation, neutrophilic meningitis, and exclusion of infectious causes of meningeal inflammation; and rapid clinical improvement following immunosuppressive therapy (1–3,17). In this case, an initial microscopic examination of CSF revealed a few Gram-positive and Gram-negative rods, as well as Gram-positive cocci; however, subsequent cultures were negative. These bacteria were attributed to skin contamination during the collection process. Diagnosing bacterial meningitis can be challenging, with CSF cultures having a diagnostic yield of only 38% (18). Typically, bacterial meningitis in dogs arises from a nidus of infection, such as otitis media or interna, which was not observed on MRI in this case. A bacterial cause of meningitis was considered unlikely based on negative CSF cultures after aerobic and anaerobic enrichment, no apparent focal nidus of infection on MRI, and the rapid and durable response to therapy. Fibrinogen was mildly increased, and CRP was dramatically increased, consistent with systemic inflammation. Serum IgA concentration was normal, which is a finding in only 10% of SRMA cases (19,20).

Cervical MRI demonstrated contrast enhancement of the C2–C8 nerve roots and neck musculature, along with moderate diffuse meningeal enhancement, all consistent with a diagnosis of SRMA (12,21). Mild, patchy, intramedullary contrast enhancement was noted in this case, potentially due to hemorrhage or to microthrombi causing ischemia in that area (12,21,22).

Cardiac abnormalities such as slight decreases in fractional shortening (20 to 22%, RI: 30 to 46%) have been reported in dogs with SRMA (8). This dog exhibited significant LV systolic dysfunction, with a fractional shortening of only 8.3% (RI: 30 to 46%). Given this dog’s history of a nontraditional diet, the possibility of diet-associated dilated cardiomyopathy was considered; however, the rapid, marked improvement observed following immunosuppressive treatment before modifying the diet made diet-associated dilated cardiomyopathy unlikely. Cardiac manifestations of SRMA may be the result of systemic inflammation and myocarditis caused by circulating inflammatory mediators (6,8). Inflammatory cytokines can also cause systolic dysfunction without damaging heart muscle, but dramatic increases in cardiac troponin I in this case and others support actual cardiac myocyte damage (5–8). Another possible cause of myocardial damage is arteritis or thrombosis directly affecting the small- to medium-sized cardiac arteries, as has been documented in dogs with SRMA (6,8,13,14). Spontaneous echocardiographic contrast is the most common echocardiographic finding in dogs with SRMA and was not seen in this case (6,8).

A hypercoagulable state was supported in this case based on increased plasma fibrinogen concentration and VCM and ROTEM findings. The ROTEM revealed both elevated fibrinogen and increased clot firmness, which indicated a heightened risk of thromboembolic complications (23,24). Systemic thromboembolic disease is not common in dogs with SRMA, but pathological studies demonstrated widespread thrombosis in inflamed meningeal and coronary vessels (3,14,17). D-dimers have also been noted to be increased in CSF and serum, which may indicate recent hypercoagulation and hyperfibrinolysis (11,22). Due to concerns about the availability of D-dimer testing and receiving results in a timely manner, D-dimer was not measured in this case. Several reports have documented parenchymal or extramedullary hemorrhage in dogs with SRMA hypothesized to be secondary to thrombosis or rupture of severely inflamed vessels (12,24,25).

Although coagulation abnormalities have not been widely investigated in SRMA, this case represents the first reported instance of hypercoagulability in a dog with SRMA documented using ROTEM. Given these findings, the use of medications that enhance fibrinolysis or decrease platelet function, such as rivaroxaban or clopidogrel, may be considered in dogs with SRMA — especially those with cardiac dysfunction, neurologic deficits, or evidence of hypercoagulability. Perhaps measuring D-dimer and VCM in SRMA cases could provide information useful for guiding initiation of medications such as rivaroxaban or clopidogrel, especially when prioritizing this assessment for dogs with severe neurologic symptoms, persistent inflammation, or unexplained clinical deterioration.

In conclusion, this case report emphasizes the importance of investigating cardiac involvement and hypercoagulability in all dogs with SRMA. Specific therapy may be warranted to manage cardiac dysfunction and prevent thromboembolic complications of this very inflammatory disease. CVJ

Footnotes

Copyright is held by the Canadian Veterinary Medical Association. Individuals interested in obtaining reproductions of this article or permission to use this material elsewhere should contact permissions@cvma-acmv.org.

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