Acute Laminitis: What the Research Says
Evidence from 53 peer-reviewed studies
2 Systematic Review
1 RCT
13 Cohort Study
10 Case Report
25 Expert Opinion
2 Thesis
What Professionals Should Know
- •CDH is evidence-supported for both prevention and early treatment of acute laminitis, with low risk of adverse effects, making it a valuable tool for at-risk horses
- •Current ice boot and ice bag methods work but are labor-intensive and impractical in many field settings—continue using them when feasible, but recognize the need for better solutions
- •Maintaining hoof temperature below 10°C is the target; monitor cooling effectiveness regularly as labor demands and ice availability may compromise compliance in long-term applications
- •Cryotherapy may reduce tissue damage in acute laminitis when applied early after clinical signs appear, but current evidence is weak and inconclusive
- •Consider cryotherapy as a complementary treatment option, but do not rely on it as a standalone intervention without other evidence-based laminitis management strategies
- •Additional quality research is needed before making strong recommendations; individual case assessment and owner communication remain essential
- •Cryotherapy applied to the hoof after lameness is detected in acute laminitis cases can significantly reduce lamellar tissue damage and prevent complete lamellar failure—it is not just a preventive tool
- •Early detection of lameness and immediate cooling intervention may be critical; the study initiated treatment within hours of lameness detection at walk
- •This provides strong scientific justification for recommending continuous digital hypothermia as a therapeutic treatment protocol in acute laminitis cases, not merely as prophylaxis
- •LLZ measurements offer a more reliable radiographic diagnostic tool for early laminitis than traditional distal phalanx displacement measurements based on outer hoof wall
- •Use the middle LLZ-to-cortical-length ratio (threshold >0.11) in practice as it provides superior diagnostic accuracy (95% sensitivity/specificity) and is robust to radiographic technique variations
- •These measurements can detect acute and subacute laminitis before obvious palmar rotation develops, enabling earlier intervention
- •Shoeing and support strategies for laminitic horses should prioritize support of the caudal and middle hoof regions to reduce peak pressure concentration in these areas during break-over
- •Recognizing the delayed peak loading in the toe during break-over in laminitic horses can guide farrier decisions about rocker placement and break-over location
- •Laminitic horses show consistent load redistribution patterns regardless of whether they are in acute recovery or chronic phase, suggesting therapeutic support strategies should remain consistent across both stages
- •Intrasynovial corticosteroid injections can be used to treat joint disease without fear of precipitating acute laminitis based on current evidence
- •The common perception that steroid injections are a major laminitis risk factor is not supported by this study, allowing more confident clinical decision-making regarding their use
- •Clinicians should continue to monitor injected horses for laminitis but need not avoid this treatment modality solely based on steroid-related laminitis concerns
- •This technique has adequate biomechanical strength to resist flexor tendon pull in normal horses, but further development is needed before clinical application in acute laminitis cases
- •Screw placement and removal were well tolerated procedurally, suggesting the technique itself is not harmful to normal foot tissues
- •The technique failed to prevent P3 rotation or improve pain in experimentally induced laminitis, indicating additional research on laminitis pathophysiology and screw positioning is necessary before recommending for field use
- •Endotoxemia may not be the primary driver of laminar tissue inflammation in laminitis—focus on controlling dietary carbohydrate intake and managing gastric dysbiosis in at-risk horses
- •Laminitis development involves local laminar tissue responses beyond systemic inflammation, suggesting that therapies targeting only circulating endotoxins may be insufficient
- •In hospitalized horses with gastrointestinal disease, consider that dietary management and carbohydrate fermentation may pose greater laminitis risk than endotoxin translocation alone
- •Prophylactic cooling of the digit during acute laminitis episodes reduces the inflammatory cascade at the cellular level, providing a mechanistic explanation for why ice therapy improves outcomes in clinical cases.
- •Early application of digital hypothermia (before lameness onset) may be particularly effective at preventing the inflammatory cascade; prompt cooling protocols are therapeutically justified.
- •These molecular findings support cryotherapy as a core intervention in acute laminitis management and suggest it should be initiated early in the disease process for maximum benefit.
- •Pasture-associated laminitis in first-opinion practice has a reasonably good prognosis overall (72% good outcomes), but large ponies and cobs have significantly worse outcomes than other types—adjust management expectations and client counselling accordingly.
- •Previous laminitis history is paradoxically protective against severe acute episodes but reduces return-to-work rates by half; these horses need different preventive strategies and realistic ridden exercise projections.
- •Weight management and body condition are critical modifiable factors—keeping affected animals at optimal weight rather than overweight significantly improves both survival and outcome, making this a primary intervention point in first-opinion practice.
- •Inflammatory cell infiltration (neutrophils/monocytes) and endogenous enzyme dysregulation may require different therapeutic targets, not a single anti-inflammatory approach
- •Variability in MMP profiles among laminitic horses could inform prognosis and treatment planning, potentially distinguishing different disease subtypes
- •Understanding that MMP dysregulation occurs independently of inflammation suggests some cases may benefit from enzyme-modulating therapies even when systemic inflammation is controlled
- •Monitor hospitalized horses for signs of endotoxemia, particularly those with gastrointestinal or respiratory disease, as early recognition and treatment may prevent secondary laminitis development.
- •Include laminitis prevention protocols when treating conditions associated with endotoxemia (diarrhea, colic surgery, pneumonia) in hospitalized horses.
- •Consider laminitis risk assessment as part of routine monitoring in hospitalized horses, especially those showing evidence of systemic inflammation or gastrointestinal compromise.
- •Acute laminitis involves systemic leukocyte activation and extravasation into laminar tissues; understanding this mechanism may improve therapeutic strategies targeting inflammatory cascade
- •Clinical laminitis cases secondary to systemic inflammatory diseases likely share common pathways of neutrophil and monocyte migration that could be potential intervention points
- •Early detection of systemic leukocyte changes and activation markers may provide prognostic indicators for laminitis development in at-risk horses
- •Heart rate variability analysis may provide objective assessment of pain response to treatment in laminitic horses, complementing clinical lameness scoring
- •The sympathetic-parasympathetic balance shift (declining LF/HF ratio) with NSAID treatment could help monitor analgesic efficacy when clinical signs are difficult to assess
- •Cortisol measurement alone is insufficient for pain monitoring in laminitis; HRV-based assessment may be more reliable than single hormone measurements
- •Coagulation/fibrinolysis testing is unlikely to be diagnostically useful for early laminitis detection, despite theoretical involvement in pathogenesis
- •Laminitis prevention and management should focus on other pathogenic mechanisms rather than anticoagulation strategies
- •Standard hemostasis panels do not show clinically useful changes in the prodromal stages of carbohydrate-induced laminitis
- •Lamellar tissue damage in acute laminitis is not primarily caused by lack of blood supply—other mechanisms (inflammatory, metabolic) should be investigated for treatment targets
- •The presence of increased blood flow to lamellae suggests hyperaemia and vascular shunting may play a role in laminitis pathophysiology, potentially guiding anti-inflammatory or vascular management strategies
- •Scintigraphic evaluation offers objective measurement of digital circulation patterns and can help differentiate between ischaemic and non-ischaemic causes of lameness in acute cases
- •Blood leukocyte and neutrophil counts can serve as diagnostic indicators for acute laminitis, reflecting the severity of inflammatory response
- •The marked elevation in white blood cells confirms laminitis is a systemic inflammatory disease, not merely a local hoof problem
- •Consider haematological findings alongside clinical signs when assessing laminitis severity and monitoring treatment response
- •Identify and eliminate modifiable risk factors—particularly excessive grain/lush pasture feeding, unnecessary corticosteroid use, and poor farriery—as these are common preventable causes of laminitis in working horses
- •Use Obel grading and clinical signs (digital pulse, hoof heat, lameness pattern) to assess severity; monitor vital signs and hoof condition closely as acute cases show marked systemic inflammation
- •Recognize that coagulation abnormalities occur in acute laminitis; combined with elevated inflammatory markers (haptoglobin, MMP-2), these suggest significant endothelial and systemic compromise requiring aggressive supportive care
- •Carbohydrate overload triggers specific MMP activation that progressively degrades the laminar attachment; this provides a mechanistic explanation for acute laminitis development and progression to severe lameness grades.
- •MMP-13 is a key enzyme involved in structural failure of the laminae, suggesting that therapeutic strategies targeting MMP activity or carbohydrate management timing could be critical for preventing progression from early to severe laminitis.
- •Understanding that laminar failure involves active enzymatic degradation of the extracellular matrix reinforces the importance of rapid intervention and dietary management in early laminitis cases before irreversible structural damage occurs.
- •Laminitis causes changes in keratinocyte differentiation in non-weight-bearing tissues, suggesting the disease involves systemic epidermal dysfunction rather than purely mechanical failure
- •The morphologic changes seen in chestnuts and periople during acute laminitis reflect primary cellular changes in keratinocyte maturation, which may help guide understanding of disease progression
- •Early assessment of tissue changes in non-weight-bearing areas may provide diagnostic insight into acute laminitis pathophysiology
- •Transdermal GTN patches applied to the pastern offer a non-invasive method to improve hoof perfusion and reduce lameness in acute laminitis cases
- •GTN treatment addresses the microvascular insufficiency underlying laminitis by enhancing nitric oxide-mediated blood flow
- •This approach may benefit both acutely laminitic and chronically affected horses and ponies as an adjunctive therapy
- •Thrombotic events occur very early in carbohydrate-induced laminitis (within 6 hours), suggesting early intervention may be critical to prevent vascular compromise
- •Vascular insufficiency and microthrombi in the hoof are key mechanisms in laminitis development, supporting the importance of therapies targeting blood flow and coagulation
- •Standard coagulation tests may not detect the localized prothrombotic changes occurring in the hoof during early laminitis stages
- •Venous congestion and impaired drainage from the digit appear to drive fluid accumulation in early laminitis, suggesting therapeutic strategies targeting venous return may be beneficial
- •The high interstitial fluid pressure measured explains the swelling and pain observed clinically during the prodromal phase of laminitis
- •Understanding these hemodynamic changes supports the rationale for therapies aimed at reducing digital swelling and improving microcirculation in at-risk horses
- •Blood work changes (PCV, leucocyte counts, glucose, protein) can indicate developing laminitis before clinical lameness becomes severe—use as early warning markers
- •Carbohydrate overload remains a critical trigger for acute laminitis; dietary management is essential preventive strategy
- •Platelet monitoring may be useful in assessing laminitis severity and progression in acute cases
- •Carbohydrate overload triggers rapid endotoxin release from the cecum, which may be a key mechanism in laminitis development—avoid grain overload in practice
- •Monitoring cecal lactate and pH changes may provide early indicators of laminitis risk before clinical signs appear
- •This mechanistic link suggests prevention of GI dysbiosis through careful feeding management is critical for laminitis prevention
- •Early hemodynamic compensation (increased cardiac output and contractility) occurs within hours of acute laminitis onset, before plasma volume depletion becomes clinically apparent
- •Monitoring heart rate and blood pressure changes in the first 24 hours after suspected carbohydrate overload or early lameness signs may help identify horses developing acute laminitis before severe clinical signs manifest
- •The delayed plasma volume decrease suggests laminitis pathophysiology involves initial cardiovascular compensation followed by systemic decompensation, relevant to understanding critical intervention windows
- •Hoof casts with heel wedges reduce breakover duration and decrease peak forces on the toe region during the critical breakover phase—key for acute laminitis management
- •This orthopaedic support works by increasing frog and sole weight-bearing contact, effectively offloading damaged lamellae and redistributing forces posteriorly
- •Kinetic data supports heel elevation as evidence-based supportive therapy; recommend continued use through acute phase rather than early removal to barefoot condition
- •Balance pain relief with the protective role of pain in acute laminitis—over-analgesia may increase lamellar damage through excessive movement
- •Use serial pain assessment methods to guide treatment decisions and recognize when euthanasia becomes the humane choice
- •Employ multimodal analgesia combining systemic medications with regional techniques for optimal pain control while preserving protective mechanisms
- •HGS offers a pain assessment tool for acute laminitis that does not require the horse to move, reducing iatrogenic pain compared to traditional Obel scoring during examination
- •You can assess HGS from brief visual observation in the stable without video recording, making it practical for clinical use alongside or potentially as an alternative to Obel grading
- •Good inter-observer reliability means different staff members can apply HGS consistently, though further validation studies are still needed before fully replacing movement-based assessments
- •Early recognition and intervention during the prodromal stage of laminitis is critical, as few current treatments can reliably prevent progression to severe complications
- •Understanding the multifactorial nature of laminitis (ischemic, enzymatic, metabolic, inflammatory) should inform your approach to prevention and management
- •Current therapeutic options are limited in controlling acute laminitis severity—focus on prevention and early detection strategies
- •Recognition that laminitis has multiple triggering mechanisms (metabolic vs. inflammatory) helps guide prevention strategies and dietary management specific to risk factors
- •Understanding experimental models of laminitis pathogenesis improves clinical diagnosis and treatment targeting based on suspected aetiology
- •Identifying which pathway (metabolic, inflammatory, or pasture-related) applies to individual cases may refine prognosis and therapeutic interventions
- •Treatment decisions for laminitis should be based on current scientific understanding of disease mechanisms rather than traditional or empirical approaches
- •Both developmental and acute laminitis presentations require pharmacologic consideration, likely with different therapeutic targets and timing
- •Understanding the pathophysiology underlying different laminitis cases can guide selection among available treatment options
- •Cryotherapy applied to the distal limb is an evidence-based intervention to prevent or reduce laminitis severity in at-risk horses
- •Continuous application protocols are recommended for clinical cases, suggesting this is a practical tool for acute laminitis management
- •Understanding the tissue effects of hypothermia helps justify early intervention with ice/cold therapy in suspected or confirmed laminitis cases
- •Understanding the lamellar failure site helps explain the biomechanics of laminitis but does not yet provide targets for preventing carbohydrate-induced cases
- •Histopathologic grading provides a standardized method to assess laminitis severity and progression, useful for research and prognostication
- •Until trigger factors are identified, dietary management remains the primary preventive strategy for carbohydrate-sensitive horses
- •Implement appropriate medical and supportive therapy protocols immediately upon acute laminitis diagnosis, as early intervention is critical to outcomes
- •Address the underlying primary condition while simultaneously managing the acute laminitic episode
- •Use current evidence-based guidelines to standardize your acute laminitis management approach for consistency and better prognosis
- •High-carbohydrate feeds causing rapid fermentation and pH drop in the cecum can trigger a cascade leading to laminitis within 20-30 hours; careful feed management is critical for at-risk horses
- •Platelet activation appears to be a key early event in carbohydrate-overload laminitis, occurring 12 hours post-insult before clinical lameness, suggesting antiplatelet or anti-inflammatory interventions during this window may be protective
- •Small quantities of endotoxin from the colon enter circulation during laminitis development but do not cause disease alone; the interaction with platelet activation is the likely pathogenic mechanism
- •Hindgut dysbiosis and bacterial amine production following carbohydrate overload may directly trigger the digital vasoconstriction seen in laminitis—managing hindgut health and preventing carbohydrate overload is critical
- •Digital blood flow reduction occurs selectively in the foot without systemic cardiovascular effects, explaining why laminitis can develop acutely without obvious signs of shock
- •Future laminitis treatments may target amine-mediated vasoconstriction or platelet 5-HT displacement as a novel therapeutic approach
- •Understanding that glucose deprivation and MMP activation trigger lamellar failure may inform emergency management strategies to preserve vascular perfusion and inhibit protease activity during acute laminitis
- •This research provides a laboratory model for testing potential therapeutic interventions targeting metabolic failure and enzymatic degradation in laminitis
- •Recognition of basement membrane zone vulnerability to metabolic and enzymatic stress supports the rationale for rapid treatment and aggressive systemic support in acute laminitis cases
- •Acute laminitis involves interconnected mechanisms (inflammation, circulatory changes, enzyme activity) rather than a single cause—treatment strategies should address multiple pathways
- •Understanding hindgut dysfunction as a precursor to laminitis may enable earlier intervention and prevention in at-risk horses
- •Emerging research on hoof tissue enzyme activation and inflammatory cascades may eventually enable more targeted and effective therapies beyond current supportive management
- •Single-target treatments addressing only vascular or enzymatic pathways are unlikely to be effective—clinicians should anticipate the need for combined therapeutic strategies in laminitis management
- •Contralateral limb laminitis in weight-bearing disease suggests systemic inflammatory activation rather than purely local vascular or mechanical mechanisms, supporting systemic anti-inflammatory protocols
- •The variable presentation and severity of naturally acquired laminitis across different predisposing conditions indicates that successful treatment will require individualized, multi-modal approaches tailored to the underlying cause
- •Understanding the four phases of laminitis progression helps determine appropriate timing for transitioning from acute to chronic management protocols
- •Chronic laminitis treatment strategies differ significantly from acute phase management, requiring a shift in therapeutic focus after the initial 2-4 week period
- •Early recognition of progression to chronic phase allows practitioners to implement longer-term treatment strategies appropriate for sustained hoof healing and support
- •Carbohydrate overload that triggers endotoxin release and dietary amines may elevate plasma 5-HT and contribute to laminitis pathogenesis through digital vasoconstriction
- •Managing hindgut fermentation and limiting dietary triggers is important in laminitis prevention since 5-HT-mediated vasoconstriction affects digital blood flow
- •This mechanistic research supports careful nutritional management during acute laminitis cases, as reducing endotoxin and dietary amine sources may help preserve digital perfusion
- •Improved understanding of laminitis mechanisms will lead to better preventive and therapeutic strategies, ultimately reducing laminitis impact
- •The asymptomatic developmental phase presents a significant clinical challenge—focus on risk factor management and monitoring in susceptible horses
- •Subacute and chronic laminitis management will remain problematic without earlier detection methods; long-term case management strategies are essential for practice planning
- •Early intervention with appropriate supportive therapy can salvage horses previously considered untreatable; assess degree of distal phalanx instability immediately upon diagnosis to guide treatment intensity
- •Biomechanical support and farriery management are critical components of treatment success—work closely with farriers to counter adverse forces and stabilize the distal phalanx
- •Prognosis remains unpredictable even with optimal treatment; manage owner expectations while remaining optimistic that previously hopeless cases may now have viable recovery pathways
- •Recognize acute laminitis early through clinical signs (severe lameness, digital pulse changes, toe pain) and confirm with radiographs to guide treatment decisions
- •Understand that corrective trimming and shoeing are essential components of laminitis management alongside medical therapies, not secondary measures
- •Accept that no single treatment regimen has proven superior—focus on assessing laminae damage severity to set realistic expectations for recovery and long-term soundness with owners
- •Microvascular thrombosis is a documented pathophysiological mechanism in acute laminitis, suggesting that anticoagulant or antiplatelet therapies may have therapeutic potential
- •Systemic coagulopathy changes occur before clinical lameness appears, indicating early intervention during the prodromal phase may be critical
- •Carbohydrate overload triggers measurable hemostatic alterations that precede and likely contribute to the thrombotic events causing laminar tissue damage
- •Alpha-adrenergic antagonists like prazosin may have therapeutic potential in early acute laminitis by preserving digital blood flow to critical laminar tissues
- •Black walnut extract causes measurable vascular changes in the foot within 12 hours; recognition of early clinical signs is critical for intervention
- •Laminar perfusion changes evolve over time, with some recovery evident by 84 hours even in untreated cases, suggesting potential window for therapeutic intervention
- •The heart bar shoe with dorsal hoof wall resection is a viable salvage treatment for severe laminitis cases with solar prolapse where the pedal bone tip penetrates the sole
- •This technique achieved return to work in 70% of cases, making it worth attempting before euthanasia in advanced laminitis
- •Expect variable outcomes: some horses resume full function while others may retain mild lameness or require euthanasia despite treatment
- •Understanding the vascular reactivity changes in laminitis may help identify therapeutic targets for managing acute laminitic episodes in clinical practice
- •The lack of endotoxin effect on baseline vascular reactivity suggests laminitis pathophysiology involves mechanisms beyond simple endotoxin-mediated vasoconstriction
- •Digital artery and vein reactivity patterns are consistent between limbs, indicating laminitis is a systemic vascular problem rather than localized to specific limbs
- •Acute laminitis treatment should focus on restoring microcirculation and preventing thrombosis in the foot corium to avoid chronic complications
- •Consider heparin anticoagulation therapy early in acute laminitis cases to manage corium thrombosis
- •Alpha-receptor blockers may help improve distal limb blood flow when used alongside conventional anti-inflammatory protocols in acute laminitis
- •Carbohydrate overloading triggers a predictable cascade of physiological changes leading to laminitis within ~40 hours; strict feed management is critical for prevention
- •Plasma volume depletion and electrolyte imbalances (particularly sodium and potassium) accompany acute laminitis development and may require fluid and electrolyte therapeutic support
- •Monitoring serum electrolytes and understanding the endocrine response (renin-aldosterone axis activation) can help guide clinical management during the acute phase
- •Gastrointestinal health management may be critical in laminitis prevention, as caecal dysbiosis producing excess amines could amplify serotonin-induced digital vasoconstriction
- •Acute laminitis episodes may be triggered or worsened by concurrent GI disturbances; managing gut health could reduce vascular crisis in susceptible horses
- •Understanding this 5-HT uptake mechanism provides a biological explanation for why some laminitis cases are preceded by colic or digestive upset
- •Elevated plasma 5-HT (particularly from platelet release) may contribute to pathological digital vasoconstriction during laminitis episodes through selective sensitivity of digital arteries
- •5-HT receptor antagonists could represent a potential therapeutic target to prevent or reduce digital vascular compromise in acute laminitis
- •Digital blood vessels appear uniquely sensitive to circulating 5-HT compared to other peripheral vessels, making them vulnerable during systemic platelet activation or endotoxemia
Key Research Findings
Continuous digital hypothermia modulates inflammatory response, produces profound vasoconstriction, and prevents tissue damage in lamellae
Nineteen publications evaluated CDH methods; twelve experimental studies found multiple positive effects on clinical improvement, immunological modulation, and histological protection
Optimal cooling temperature is below 10°C, but current methods face limitations including labor intensiveness, reliance on ice sources, and cost barriers to practical use
Despite clinical efficacy evidence, safer, more user-friendly, and effective cryotherapy methods are needed for both hospital and ambulatory settings
Cryotherapy of distal limbs reduced histological changes and lamellar injury in randomised controlled trials
Clinical severity of laminitis was reduced in horses treated with cryotherapy in retrospective cohort study
Overall strength of evidence is weak due to limited number and quality of studies available
Further randomised controlled trials are needed to establish definitive clinical efficacy
Continuous digital hypothermia initiated after lameness detection significantly reduced histological laminitis scores across all lamellar sections (proximal, middle, distal) compared to untreated contralateral limbs (P<0.05)
Complete dermoepidermal separation (lamellar structural failure) occurred in 4 of 8 non-treated feet but in zero cryotherapy-treated feet
Morphometric analysis showed significant differences in secondary epidermal lamellar length and width in distal sections favoring cryotherapy-treated limbs
This is the first experimental evidence that therapeutic digital hypothermia reduces lamellar injury severity when applied after onset of clinical lameness
Lamellar lucent zone (LLZ) measurements on lateromedial radiographs are significantly increased in acute and subacute laminitis compared to healthy controls across proximal, middle, and distal locations (p<0.001)
Middle LLZ measurement >7.5mm achieves 87% sensitivity and 91% specificity for acute laminitis diagnosis
LLZ ratio to distal phalanx cortical length (>0.11) achieves 95% sensitivity and 95% specificity, with the advantage that ratios are unaffected by magnification and obliquity
Evidence Base
Continuous digital hypothermia for prevention and treatment of equine acute laminitis: A practical review.
Lavado, Lewis, Montgomery (2023) — Veterinary journal (London, England : 1997)
Systematic Review
Cryotherapy of the distal limbs: an effective treatment for equine laminitis following onset of lameness?
Lucy Ryde (2021) — Veterinary Evidence
Systematic Review
Continuous digital hypothermia initiated after the onset of lameness prevents lamellar failure in the oligofructose laminitis model.
van Eps A W, Pollitt C C, Underwood C et al. (2014) — Equine veterinary journal
RCT
Evaluation of digital radiographic measurements for the diagnosis of acute laminitis.
Skelton Georgia, Acutt Elizabeth, Stefanovski Darko et al. (2025) — Equine veterinary journal
Cohort Study
Hoof kinetic patterns differ between sound and laminitic horses.
Al Naem Mohamad, Litzke Lutz-Ferdinand, Failing Klaus et al. (2021) — Equine veterinary journal
Cohort Study
Intrasynovial triamcinolone treatment is not associated with incidence of acute laminitis.
Haseler Callum J, Jarvis Gavin E, McGovern Kate F (2021) — Equine veterinary journal
Cohort Study
Novel technique for prevention of rotation of the distal phalanx relative to the hoof wall in horses with acute laminitis.
Carmalt, Carmalt, Henderson et al. (2019) — American journal of veterinary research
Cohort Study
Disparate effects of LPS infusion and carbohydrate overload on inflammatory gene expression in equine laminae.
Kwon, Moore, Robertson et al. (2014) — Veterinary immunology and immunopathology
Cohort Study
Digital hypothermia inhibits early lamellar inflammatory signalling in the oligofructose laminitis model.
van Eps A W, Leise B S, Watts M et al. (2012) — Equine veterinary journal
Cohort Study
Severity and outcome of equine pasture‐associated laminitis managed in first opinion practice in the UK
Menzies‐Gow N. J., Stevens K., Barr A. et al. (2010) — Veterinary Record
Cohort Study
Leukocyte-derived and endogenous matrix metalloproteinases in the lamellae of horses with naturally acquired and experimentally induced laminitis.
Loftus, Johnson, Belknap et al. (2009) — Veterinary immunology and immunopathology
Cohort Study
Risk factors for development of acute laminitis in horses during hospitalization: 73 cases (1997-2004).
Parsons, Orsini, Krafty et al. (2007) — Journal of the American Veterinary Medical Association
Cohort Study
Dynamic changes in circulating leukocytes during the induction of equine laminitis with black walnut extract.
Hurley, Parks, Reber et al. (2006) — Veterinary immunology and immunopathology
Cohort Study
The association between heart rate, heart rate variability, endocrine and behavioural pain measures in horses suffering from laminitis.
Rietmann, Stauffacher, Bernasconi et al. (2004) — Journal of veterinary medicine. A, Physiology, pathology, clinical medicine
Cohort Study
Evaluation of coagulation and fibrinolysis during the prodromal stages of carbohydrate-induced acute laminitis in horses.
Prasse, Allen, Moore et al. (1991) — American journal of veterinary research
Cohort Study
Scintigraphic evaluation of digital circulation during the developmental and acute phases of equine laminitis.
Trout, Hornof, Linford et al. (1991) — Equine veterinary journal
Cohort Study
Changes in the cellular composition of blood in horses in acute laminitis
A. Nefedov, Vladimir Lutsai, Svetlana Kontsevay et al. (2023) — Agrarian science
Case Report
Clinical, hemato-biochemical studies of equine laminitis in horses in Mosul
K. Alsaad, A. Abdul-Hameed (2020) — Iraqi journal of Veterinary Sciences
Case Report
Expression and activity of collagenases in the digital laminae of horses with carbohydrate overload-induced acute laminitis.
Wang L, Pawlak E A, Johnson P J et al. (2014) — Journal of veterinary internal medicine
Case Report
Cytokeratins of the matrices of the chestnut (torus carpeus) and periople in horses with acute laminitis.
Wattle (2001) — American journal of veterinary research
Case Report
Show 33 more references
Glyceryl trinitrate enhances nitric oxide mediated perfusion within the equine hoof.
Hinckley, Fearn, Howard et al. (1997) — The Journal of endocrinology
Case Report
Prothrombotic events in the prodromal stages of acute laminitis in horses.
Weiss, Trent, Johnston (1996) — American journal of veterinary research
Case Report
Evaluation of equine digital Starling forces and hemodynamics during early laminitis.
Allen, Clark, Moore et al. (1991) — American journal of veterinary research
Case Report
Haematological changes during development of acute laminitis hypertension.
Moore, Garner, Coffman (1982) — Equine veterinary journal
Case Report
Intracecal endotoxin and lactate during the onset of equine laminitis: a preliminary report.
Moore, Garner, Berg et al. (1979) — American journal of veterinary research
Case Report
Cardiac output, left ventricular ejection rate, plasma volume, and heart rate changes in equine laminitis-hypertension.
Garner, Hahn, Salem et al. (1977) — American journal of veterinary research
Case Report
Effect of heel elevation on breakover phase in horses with laminitis.
Al Naem, Litzke, Geburek et al. (2021) — BMC veterinary research
Expert Opinion
Pain management for laminitis in the horse
Hopster K., van Eps A. W. (2019) — Equine Veterinary Education
Expert Opinion
Using the Horse Grimace Scale (HGS) to Assess Pain Associated with Acute Laminitis in Horses (Equus caballus).
Dalla Costa Emanuela, Stucke Diana, Dai Francesca et al. (2016) — Animals : an open access journal from MDPI
Expert Opinion
An update on equine laminitis
L. M. Laskoski, C. A. A. Valadão, R. L. Dittrich et al. (2016) — Ciencia Rural
Expert Opinion
A review of recent advances and current hypotheses on the pathogenesis of acute laminitis.
Katz L M, Bailey S R (2012) — Equine veterinary journal
Expert Opinion
The pharmacologic basis for the treatment of developmental and acute laminitis.
Belknap (2010) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Therapeutic hypothermia (cryotherapy) to prevent and treat acute laminitis.
van Eps (2010) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Carbohydrate alimentary overload laminitis.
Pollitt, Visser (2010) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Acute laminitis: medical and supportive therapy.
van Eps (2010) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Plasma concentrations of endotoxin and platelet activation in the developmental stage of oligofructose-induced laminitis.
Bailey, Adair, Reinemeyer et al. (2009) — Veterinary immunology and immunopathology
Expert Opinion
The effects of vasoactive amines found in the equine hindgut on digital blood flow in the normal horse.
Bailey S R, Menzies-Gow N J, Marr C M et al. (2004) — Equine veterinary journal
Expert Opinion
Equine laminitis: glucose deprivation and MMP activation induce dermo-epidermal separation in vitro.
French K R, Pollitt C C (2004) — Equine veterinary journal
Expert Opinion
Current research and theories on the pathogenesis of acute laminitis in the horse.
Bailey Simon R, Marr Celia M, Elliott Jonathan (2004) — Veterinary journal (London, England : 1997)
Expert Opinion
Evidence for vascular and enzymatic events in the pathophysiology of acute laminitis: which pathway is responsible for initiation of this process in horses?
Moore, Eades, Stokes (2004) — Equine veterinary journal
Expert Opinion
Chronic laminitis: current treatment strategies.
Parks, O'Grady (2003) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Endotoxin and dietary amines may increase plasma 5-hydroxytryptamine in the horse.
Bailey S R, Cunningham F M, Elliott J (2000) — Equine veterinary journal
Expert Opinion
The pathophysiology of developmental and acute laminitis.
Hood (1999) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Treatment of acute laminitis. Supportive therapy.
Parks, Balch, Collier (1999) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Acute laminitis.
Baxter (1995) — The Veterinary clinics of North America. Equine practice
Expert Opinion
Microvascular thrombosis associated with onset of acute laminitis in ponies.
Weiss, Geor, Johnston et al. (1994) — American journal of veterinary research
Expert Opinion
Gamma scintigraphic analysis of the distribution of perfusion of blood in the equine foot during black walnut (Juglans nigra)-induced laminitis.
Galey, Twardock, Goetz et al. (1990) — American journal of veterinary research
Expert Opinion
Treatment of solar prolapse using the heart bar shoe and dorsal hoof wall resection technique.
Eustace, Caldwell (1989) — Equine veterinary journal
Expert Opinion
In vitro reactivity of digital arteries and veins to vasoconstrictive mediators in healthy horses and in horses with early laminitis.
Baxter, Laskey, Tackett et al. (1989) — American journal of veterinary research
Expert Opinion
[Pathogenesis and drug therapy of acute laminitis in horses: a literature review].
Boosman, Németh (1989) — Tijdschrift voor diergeneeskunde
Expert Opinion
Plasma volume, electrolyte, and endocrine changes during onset of laminitis hypertension in horses.
Clarke, Garner, Hatfield (1983) — American journal of veterinary research
Expert Opinion
Uptake of 5-hydroxytryptamine by equine digital vein endothelial cells: inhibition by amines found in the equine caecum.
Bailey S R, Wheeler-Jones C, Elliott J (2003) — Equine veterinary journal
Thesis
Plasma 5-hydroxytryptamine constricts equine digital blood vessels in vitro: implications for pathogenesis of acute laminitis.
Bailey, Elliott (1998) — Equine veterinary journal
Thesis