Thrombosis and Embolism: Pathophysiology and Consequences

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Key Takeaways

• Virchow's triad (endothelial injury, altered blood flow, hypercoagulability) is the foundational framework for identifying thrombotic risk, with clinical thrombosis often involving multiple components.
• Thrombus composition varies with hemodynamic conditions: venous thrombi are typically fibrin-rich with trapped erythrocytes, while arterial thrombi are platelet-dominant due to higher shear rates.
• Neutrophil extracellular traps (NETs) are implicated in thrombus stabilization and organization during the inflammatory phase of venous thromboembolism, suggesting a role for ongoing inflammation in thrombus maturation.
• Pulmonary embolism acutely increases pulmonary artery pressure, leading to right heart strain and ventilation-perfusion mismatch, with D-dimer elevation serving as an early marker of fibrinolysis.
• Fat embolism involves lipid droplets occluding capillaries, causing time-dependent ultrastructural injury to cells like type II pneumocytes, particularly following trauma or intravascular lipid administration.
• Diagnostic approaches integrate signalment, history, physical examination, and targeted investigations such as CT angiography for intravascular filling defects and echocardiography for cardiac assessment and right heart strain.

Thrombosis and embolism represent a continuum of vascular pathology in which a solid mass forms within the circulatory system and, in the case of embolism, travels to occlude a distant vessel. This article examines the cellular and molecular mechanisms of thrombus formation, the factors that predispose patients to pathologic clotting, and the tissue consequences of embolic occlusion. It is written for veterinary students and practitioners who require a working understanding of these processes across species, with emphasis on the shared pathophysiology that underlies venous thromboembolism, arterial occlusion, and microvascular thrombosis.

The clinical relevance of this topic extends beyond the thrombus itself. The sequelae of thromboembolic disease, including pulmonary hypertension, ischemic tissue injury, and consumptive coagulopathy, often dominate the patient's presentation and determine outcome. Understanding the mechanisms by which thrombi form and emboli cause damage therefore informs diagnostic reasoning, risk assessment, and monitoring strategies in clinical practice. This first section establishes the conceptual foundation: the normal hemostatic balance, the pathophysiologic triad that permits thrombosis, and the structural features of thrombi that determine their behavior.

At a Glance

Hemostatic Balance and the Pathogenesis of Thrombosis

Normal hemostasis maintains blood in a fluid state while permitting rapid, localized clot formation at sites of vascular injury. This balance depends on the endothelium, which constitutively expresses anticoagulant and antiplatelet mediators, and on circulating coagulation factors that remain inactive until triggered. Disruption of this equilibrium shifts the system toward pathologic thrombosis.

The conceptual framework for understanding thrombotic risk remains Virchow's triad: alterations in blood flow, endothelial injury, and hypercoagulability. These three elements interact, and clinical thrombosis typically involves more than one. Venous thromboembolism, for example, is associated with risk factors that increase inflammation and coagulability, increase venous resistance, and damage the endothelial lining, as described in a recent review of venous thromboembolism biology and clinical challenges (Watson et al., institutional publication). Venous valves have been identified as likely sites of initial clot formation, although the precise sequence of events in this environment remains incompletely understood.

Endothelial Injury and Platelet Activation

Endothelial disruption exposes subendothelial collagen and von Willebrand factor, which support platelet adhesion, activation, and aggregation. Activated platelets release granular contents that recruit additional platelets and expose phosphatidylserine on their surface, providing a scaffold for assembly of coagulation factor complexes. The resulting platelet plug is reinforced by fibrin, which cross-links the growing mass.

Endothelial injury also removes the natural anticoagulant surface of the vessel wall. Healthy endothelium produces prostacyclin, nitric oxide, thrombomodulin, and heparan sulfate proteoglycans, all of which suppress platelet activation and thrombin generation. Loss of these mechanisms at sites of injury permits uncontrolled propagation of the thrombus.

Hemodynamic Factors and Thrombus Architecture

Blood flow velocity and shear rate shape both the likelihood of thrombosis and the structure of the thrombus that forms. In the venous circulation, where flow is slow and shear rates are low, thrombi are predominantly fibrin-rich with trapped erythrocytes, producing the characteriztic red thrombus. In the arterial circulation, higher shear rates favor platelet-dominant white thrombi. These distinctions matter clinically because they influence the expected response to therapeutic interventions and the pattern of downstream embolic injury.

Stasis promotes thrombosis by allowing coagulation factors to accumulate locally and by delaying washout of activated clotting intermediates. Venous dilation, immobility, and increased venous resistance all reduce flow velocity and increase thrombotic risk. The relationship between hemodynamics and thrombus formation has been studied extensively in computational models, though a fully satisfactory model of venous thrombosis has yet to be developed (Watson et al., institutional publication).

Inflammation and Neutrophil Extracellular Traps

Inflammation and coagulation are intimately linked. Inflammatory cytokines upregulate tissue factor expression on monocytes and endothelial cells, while activated platelets and coagulation proteases amplify inflammatory signaling. Neutrophils contribute to thrombus formation through the release of neutrophil extracellular traps (NETs), web-like structures composed of DNA, histones, and antimicrobial proteins.

The role of NETs in human venous thromboembolism has been examined in thrombus specimens obtained at surgery or autopsy. Histomorphologic analysis classified thrombus regions as unorganized, organizing, or organized, and NETs, identified by citrullinated histone H3 positivity with associated myeloperoxidase and DNA, localized predominantly during the organizing phase (Savchenko et al., institutional publication). This finding suggests that NETs contribute to thrombus stabilization and organization instead of solely to initiation, and it implicates ongoing inflammation in the maturation of venous thrombi.

Embolism and Target Organ Injury

Embolism occurs when a thrombus or part of a thrombus detaches and travels through the circulation until it lodges in a vessel too small to permit passage. The consequences depend on the size and composition of the embolus, the site of impaction, and the adequacy of collateral circulation.

Pulmonary embolism is the most consequential form of venous thromboembolism. Experimental models in dogs have demonstrated that acute multiple pulmonary microthromboembolism causes an immediate increase in pulmonary artery pressure, followed by partial resolution within one hour, with pulmonary hemorrhage, consolidation, and microembolism observed histologically (Wu et al., institutional publication). D-dimer levels rose early in the course, supporting its use as an early marker of thromboembolic events. Ventilation was not significantly affected in this model, indicating that the primary physiologic disturbance was hemodynamic instead of ventilatory.

Fat embolism represents a distinct form of embolic disease in which lipid droplets occlude the microvasculature. Ultrastructural studies in rabbits have shown time-dependent changes in type II alveolar cells and associated organelles following fat intravascular injection, with lipid droplets and inflammatory cells absent in control animals (Chen and Jiao, institutional publication). These findings provide a basis for understanding fat embolism syndrome in forensic and clinical contexts.

Iatrogenic embolism is also recognized. Experimental administration of polidocanol, a sclerosing agent, via the femoral vein in rabbits produced pulmonary vascular congestion, emphysematous changes, and intra-alveolar hemorrhage at higher doses, demonstrating that endovascular treatments can cause pulmonary complications beyond the intended target site (Zorlu et al., institutional publication).

Diagnostic Approach to Suspected Thromboembolism

Clinical recognition of thromboembolic disease begins with signalment, history, and physical examination findings that reflect acute target organ dysfunction. The diagnostic sequence is dictated by the organ system involved and the hemodynamic stability of the patient. In companion animals, the most commonly recognized presentations include pulmonary thromboembolism with acute dyspnea and collapse, aortic thromboembolism with ischemic neuromyopathy, and cerebral infarction with peracute onset of focal neurologic deficits. In large animals, jugular vein thrombosis and verminous cranial mesenteric arteritis in horses represent important clinical entities.

The diagnostic workup proceeds along three parallel tracks: confirmation of thrombosis, identification of the underlying cause, and assessment of end-organ damage. Thoracic radiography in suspected pulmonary thromboembolism may reveal regional oligemia, blunted pulmonary arteries, or alveolar infiltrates, but normal radiographs do not exclude the diagnosis. Advanced imaging, particularly CT angiography, offers superior sensitivity for intravascular filling defects. Echocardiography provides rapid assessment of right heart strain and can identify intracardiac thrombi or heartworm disease as a source of embolism.

Laboratory evaluation supports the diagnosis but rarely confirms it in isolation. D-dimer measurement offers high negative predictive value in dogs, though positive results are nonspecific. Acute multiple pulmonary microthromboembolism in a canine model produced early elevation of D-dimer, supporting its utility as an early marker of fibrinolysis. Antithrombin III, protein C, and protein S measurements may identify deficiencies that predispose to thrombosis, though interpretation requires species-specific reference intervals and awareness that consumption during acute thrombosis lowers measured values.

The diagnostic plan changes substantially with patient stability. A recumbent, dyspneic cat with absent femoral pulses and cold, cyanotic hindlimbs warrants immediate supportive care and presumptive aortic thromboembolism management instead of extensive imaging. A stable dog with suspected pulmonary thromboembolism can undergo CT angiography and comprehensive thrombophilia screening before treatment decisions are finalized.

Virchow's Triad as a Diagnostic Framework

The clinical assessment of any thromboembolic event should systematically address each component of Virchow's triad. This framework ensures that no predisposing factor is overlooked and directs the diagnostic search toward correctable causes.

The triad components interact multiplicatively instead of additively. A patient with mild hypercoagulability from hyperadrenocorticism may remain asymptomatic until prolonged recumbency during hospitalization adds venous stasis, at which point thrombosis develops rapidly. Venous thromboembolism risk increases with factors that amplify inflammation and coagulability, raise venous resistance, and damage the endothelium. The diagnostic workup must therefore consider recent historical events, also static patient characteriztics.

Thromboembolic Syndromes by Vascular Territory

Pulmonary Thromboembolism

Pulmonary thromboembolism arises from venous thrombi that dislodge and lodge in the pulmonary arterial tree. The clinical consequences depend on the aggregate cross-sectional area of occluded vessels and the premorbid cardiopulmonary reserve. Acute obstruction increases pulmonary vascular resistance, right ventricular afterload, and ventilation-perfusion mismatch. Experimental canine studies demonstrate that acute multiple pulmonary microthromboembolism raises pulmonary artery pressure immediately after embolization, with subsequent decline over one hour. The same studies documented pulmonary hemorrhage, consolidation, and microembolism on histologic examination, indicating that even small emboli cause measurable lung injury.

Diagnostic confirmation relies on CT angiography or pulmonary angiography. Echocardiography may show right atrial and ventricular enlargement, pulmonary hypertension, and occasionally visible thrombi in the main pulmonary artery. Treatment decisions hinge on hemodynamic stability, with unstable patients requiring more aggressive intervention.

Arterial Thromboembolism

Arterial thromboembolism in cats most commonly originates from left atrial thrombi associated with hypertrophic cardiomyopathy. The thrombus lodges at the aortic bifurcation, producing the classic clinical picture of hindlimb paralysis, absent femoral pulses, and firm, painful gastrocnemius muscles. The ischemic neuromyopathy that follows results from both ischemic nerve injury and reperfusion injury upon spontaneous or therapeutic recanalization.

Experimental branch retinal artery occlusion models demonstrate that focal arterial ischemia triggers local inflammatory responses, with immune cell recruitment to the ischemic territory. This principle extends to other arterial beds: cerebral infarction, renal infarction, and mesenteric ischemia all share a common pathophysiology of ischemic cell death followed by inflammation and reperfusion injury.

Fat Embolism Syndrome

Fat embolism syndrome occurs when fat globules enter the venous circulation and lodge in pulmonary capillaries. The condition is most frequently associated with long bone fractures, orthopedic surgery, or severe soft tissue trauma. Ultrastructural studies in rabbits demonstrate that fat embolism produces time-dependent changes in type II alveolar cells and related organelles, with lipid droplets and inflammatory cells absent in control animals. The pulmonary changes progress over days, and the clinical syndrome of respiratory distress, neurologic signs, and petechiation reflects both mechanical obstruction and biochemical injury from free fatty acids.

Venous Thrombosis

Venous thrombosis in veterinary patients most commonly affects the jugular vein, particularly in horses and cattle following venipuncture or catheterization. The thrombus may remain localized or embolize to the pulmonary circulation. Human venous thrombi demonstrate that neutrophil extracellular traps accumulate predominantly during the organizing phase of thrombus development, suggesting that inflammation contributes to thrombus maturation and stability. This observation has relevance for veterinary patients, as it implies that early anticoagulant intervention may be more effective than delayed treatment once thrombus organization is established.

Monitoring Parameters and Response Assessment

Serial monitoring serves three purposes: detecting thrombus progression or embolization, assessing end-organ recovery, and identifying complications of therapy. The specific parameters depend on the affected vascular territory and the treatment modality employed.

The monitoring intensity must be matched to the clinical setting. A referral hospital with 24-hour critical care can implement continuous electrocardiographic and pulse oximetry monitoring, while a general practice managing an outpatient with mild venous thrombosis relies on owner observation and scheduled rechecks. The correct approach depends on available equipment, staffing, and the patient's trajectory.

Documentation and Case Recording

Thromboembolic events require meticulous documentation for continuity of care, medicolegal protection, and outcome assessment. The medical record should include the time of onset, the duration of signs before presentation, the vascular territory involved, and the diagnostic tests performed with their results. Serial examinations should document objective parameters such as limb circumference, pulse quality scores, and respiratory rate instead of subjective descriptions.

Photographic documentation of visible lesions, such as ischemic extremities or jugular vein thickening, provides valuable baseline and follow-up information. Imaging studies should be archived with clear labeling of the findings that supported the diagnosis. The treatment plan should specify the drug, dose, route, frequency, and monitoring schedule, with explicit instructions for dose adjustment based on laboratory parameters.

Species differences affect documentation requirements. In food animals, treatment records must comply with applicable drug residue regulations, and the World Organization for Animal Health terrestrial animal health standards provide international guidance on disease reporting and surveillance obligations. In horses, the competitive status of the patient may impose additional medication restrictions that must be documented in the record.

Recognized Complications and Early Detection

Thromboembolic disease fails through several recognizable pathways. Recurrent thrombosis at the original site occurs when the underlying prothrombotic stimulus persists or when recanalisation exposes residual thrombus to renewed flow. Early detection relies on serial monitoring of the affected vascular territory, with deterioration in perfusion parameters or recurrence of clinical signs prompting re-evaluation. In experimental canine models of acute multiple pulmonary microthromboembolism, D-dimer elevation occurs at an early stage and pulmonary artery pressure rises immediately after embolisation before declining within one hour, findings that support using these parameters for early detection of recurrent embolic events (cardio-pulmonary functional changes in acute multiple pulmonary microthromboembolism in a canine model).

Post-thrombotic syndrome represents a second failure mode. Venous valvular damage and perivascular fibrosis follow organization of deep vein thrombi, producing chronic venous insufficiency, limb edema, and skin ulceration. Detection requires serial physical examination and, where available, ultrasonographic assessment of venous valve competence. The organizing phase of venous thrombi is also when neutrophil extracellular traps accumulate most prominently, suggesting that the inflammatory response during organization contributes to venous wall damage and subsequent valvular dysfunction (neutrophil extracellular traps in the organizing stage of venous thromboembolism).

Hemorrhagic complications arise from therapeutic anticoagulation or from consumptive coagulopathy. Petechiation, ecchymoses, or bleeding from venipuncture sites warrant immediate coagulation testing. Paradoxical worsening of perfusion can indicate thrombus extension instead of embolic fragmentation, and imaging is required to distinguish these possibilities.

Common Errors and Corrective Actions

Less experienced clinicians frequently misattribute thromboembolic signs to primary organ failure. A cat with aortic thromboembolism may be presented for acute pelvic limb paralysis, and the diagnosis is missed if pulse palpation and hindlimb temperature assessment are omitted. The corrective action is systematic vascular examination in any acute neurologic presentation.

A second error involves interpreting a single negative D-dimer result as excluding thromboembolism. D-dimer has high negative predictive value but is time-dependent, and sampling after fibrinolysis has subsided can produce false reassurance. Serial sampling and integration with imaging findings are required.

A third error is failing to identify the underlying cause. Thromboembolism is a complication, not a primary diagnosis. Hyperadrenocorticism, neoplasia, cardiac disease, sepsis, and protein-losing nephropathy all predispose to thrombosis, and the diagnostic workup must pursue these conditions. The MSD Veterinary Manual provides species-specific guidance on the differential diagnoses that should be considered when thromboembolism is confirmed.

Limitations of Current Evidence

The pathophysiology of venous thromboembolism remains incompletely defined. Venous valves are recognized as likely sites of initial clot formation, but the exact pathway by which thrombosis occurs in this environment is not entirely clear, and current models have not fully reproduced the hemodynamic and rheologic conditions of the venous system (review of venous thromboembolism biology and modeling). In silico models of venous hemodynamics have advanced considerably but do not yet capture the full complexity of thrombus growth and embolisation.

Species differences further limit extrapolation. Much of the experimental work on thromboembolism derives from rodent, rabbit, and canine models, and the translation of these findings to cats, horses, and production animals requires caution. The ultrastructural changes observed in experimental pulmonary fat embolism in rabbits, including time-dependent alterations in type II alveolar cells, provide a useful framework but may not fully represent the clinical syndrome in other species (ultra-structural pathological study of pulmonary fat embolism in rabbits).

Expert opinion still differs on the threshold for initiating prophylactic anticoagulation in hospitalized animals, on the duration of therapy after a first thromboembolic event, and on the role of thrombolytic agents versus surgical intervention in arterial thrombosis. These questions lack definitive trial data in veterinary medicine, and clinical decisions must be individualised.

Referral, Consultation, and Reporting

Referral is warranted when advanced imaging is required to confirm or exclude thromboembolism, when interventional procedures such as thrombectomy or catheter-directed thrombolysis are considered, or when a patient deteriorates despite appropriate medical management. Specialist consultation with a veterinary cardiologist, neurologist, or criticalist is appropriate for arterial thromboembolism, cerebral thromboembolism, and hemodynamically significant pulmonary embolism.

Laboratory involvement extends beyond routine coagulation testing. Thromboelastography or rotational thromboelastometry may characterize hypercoagulability, and specialised testing for antithrombin III, protein C, and protein S activity can identify inherited or acquired thrombophilia. The Davis-Thompson Foundation offers diagnostic pathology resources that support postmortem confirmation of thromboembolic disease and identification of underlying causes.

Regulatory reporting obligations vary by jurisdiction and species. Reportable diseases that may present with thromboembolic complications, such as certain viral hemorrhagic diseases, must be notified according to local requirements. The World Organization for Animal Health terrestrial animal health standards describe international notification obligations for listed diseases, and the American Veterinary Medical Association practice resources provide guidance on professional responsibilities in the United States. Clinicians should consult their regional veterinary authority for applicable reporting requirements.

Frequently Asked Questions

How Do I Distinguish a Postmortem Clot from an Antemortem Thrombus at Necropsy?

Postmortem clots are typically dark red, gelatinous, and often have a two-layered appearance with a yellow chicken-fat component. They are not adherent to the vessel wall and slide out easily. Antemortem thrombi are firmer, pale or mottled, and adhere to the endothelium. The surface is often dull and may show lines of Zahn, alternating pale and dark bands representing platelet and fibrin layers with trapped erythrocytes. When uncertainty remains, histology is definitive. Antemortem thrombi show endothelial attachment, organization with fibroblast ingrowth, and inflammatory cell infiltration. Postmortem clots lack these features. The distinction matters for interpreting whether a thromboembolic event contributed to death, particularly in medicolegal cases. The Davis-Thompson Foundation veterinary pathology resources provide case material that illustrates these gross and histologic differences.

What Can I Do When Advanced Imaging Is Unavailable?

When CT angiography or ultrasonography is not accessible, diagnostic decisions rest on physical examination, serial monitoring, and response to supportive care. Jugular venous distension, dyspnea with normal lung auscultation, or acute pelvic limb paresis with cold extremities and absent pulses support a thromboembolic diagnosis. Point-of-care coagulation testing, including D-dimer measurement, can provide adjunctive evidence. In a canine model of acute multiple pulmonary microthromboembolism, D-dimer elevation occurred at an early stage, supporting its use as a screening tool when imaging is unavailable. The pathology of and the cardio-pulmonary functional changes in acute multiple pulmonary microthromboembolism in a canine model documents this temporal relationship. Serial examinations documenting progression or stabilization are essential. If the patient deteriorates despite supportive care, referral for advanced imaging should be reconsidered.

How Does the Approach Differ in Small Animals Compared with Large Animals?

The clinical presentation and diagnostic feasibility differ substantially. In dogs and cats, arterial thromboembolism is more commonly recognized, particularly aortic thrombosis in cats with cardiac disease. Venous thromboembolism is diagnosed less frequently but occurs. In horses, jugular vein thrombosis is a well-recognized complication of intravenous catheterization and venipuncture. In cattle, caudal vena cava thrombosis with pulmonary embolism is an important sequela of hepatic abscessation. Diagnostic options vary with body size and temperament. Ultrasonography is feasible in most species but requires sedation in some. Advanced imaging in large animals often requires general anesthesia, which carries additional risk. Prognostic expectations also differ. The MSD Veterinary Manual provides species-specific guidance on clinical presentation and management of thrombotic disorders across domestic species.

What Are the Resource Considerations for Monitoring a Patient with Suspected Thromboembolism?

Serial monitoring of coagulation parameters, including D-dimer, antithrombin, and platelet counts, requires laboratory capacity that may not exist in all practices. In-house analyzers can measure some parameters but may not detect all abnormalities. When laboratory monitoring is limited, clinical parameters take priority. Respiratory rate, effort, mucous membrane color, pulse quality, and urine output should be recorded at regular intervals. The frequency of monitoring depends on stability. A stable patient may require assessment every four to six hours, while a deteriorating patient needs continuous observation. Staff time is a real cost. Discuss the monitoring plan with the owner early, including the financial implications of intensive care. The AVMA practice resources offer guidance on structuring client communications around treatment costs and care planning.

How Should I Explain Thromboembolism to an Owner?

Use a clear analogy. A thrombus is a clot that forms inside a blood vessel, and an embolism occurs when a piece of that clot breaks off and travels to block a smaller vessel elsewhere. Explain that the underlying disease, such as heart disease, neoplasia, or sepsis, creates conditions that make clotting more likely. Describe the diagnostic plan in terms of what each test will tell you. If imaging is unavailable, explain that you will monitor clinical signs and response to treatment. Be honest about prognosis. Pulmonary thromboembolism carries a guarded prognosis, and arterial thromboembolism in cats often has a poor outcome. The MSD Veterinary Manual provides reliable background information that owners can be directed to for further reading. Document the conversation in the medical record, including the owner's understanding and consent for the proposed plan.

When Should I Refer a Case and What Should I Send with the Patient?

Refer when the patient requires intensive monitoring or interventions beyond your practice capacity, when the diagnosis is uncertain despite initial investigation, or when the owner requests a second opinion. Before referral, stabilize the patient as far as possible. Send a complete summary that includes signalment, history, physical examination findings, laboratory results, imaging studies, treatments administered with times and doses, and the patient's response. Include a list of differential diagnoses considered and your primary suspicion. Contact the receiving clinician directly to discuss the case. This verbal handoff is as important as the written record. The WOAH terrestrial animal health standards remind us that clear documentation and communication underpin professional practice, and this principle applies equally to clinical referrals.

Related Clinical & Scientific Guides

• Hypersensitivity Reactions: Types and Mechanisms
• Therapeutic Decision-Making for Respiratory Infections in Cattle
• Monitoring Fluid Therapy in Critically Ill Veterinary Patients

References and Further Reading

• Venous Thromboembolism: Review of Clinical Challenges, Biology, Assessment, Treatment, and Modeling.. 2024.
• Establishment of the reproducible branch retinal artery occlusion mouse model and intravital longitudinal imaging of the retinal CX3CR1-GFP⁺ cells after spontaneous arterial recanalization.. 2022.
• [[Ultra-structural pathological study of pulmonary fat embolism in rabbits].](https://pubmed.ncbi.nlm.nih.gov/21899005/). 2011.
• Neutrophil extracellular traps form predominantly during the organizing stage of human venous thromboembolism development.. 2014.
• Investigation of the sclerosing effect of increasing doses of polidocanol on pulmonary vessels: Experimental study.. 2025.
• [[The pathology of and the cardio-pulmonary functional changes in acute multiple pulmonary microthromboembolism in a canine model].](https://pubmed.ncbi.nlm.nih.gov/12133329/). 2002.
• Davis-Thompson Foundation Veterinary Pathology Resources. Davis-Thompson Foundation.
• MSD Veterinary Manual, Professional Edition. MSD Veterinary Manual.
• American Veterinary Medical Association Practice Resources. American Veterinary Medical Association.

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This article is educational professional reference material for veterinary audiences. It is not a substitute for veterinary diagnosis, individual clinical judgment, current product labeling, or applicable regulatory requirements.