Laminitis
Recent posts on the subject of laminitis appear somewhat misleading and confusing.
In this post we set out the lamanitic time line and basic farriery treatment protocols based on the current understanding of the disease process.
Equine laminitis is a complex and severe condition affecting the hoof of horses, and it progresses through several stages, each with distinct clinical signs, treatment objectives, and methodologies. Below is a quantified clinical timeline, including acute onset, chronic stages 1 and 2, and sinker syndrome, supported by peer-reviewed research.
1. Acute Onset (0-72 hours)
Clinical Signs: The acute phase is characterized by the sudden onset of lameness, typically affecting the front limbs. The horse may exhibit a “sawhorse stance” (leaning back to take weight off the forelimbs), increased digital pulse, heat in the hooves, reluctance to move, and sensitivity to hoof testers, particularly over the toe region (Pollitt, 2004; Van Eps & Pollitt, 2006).
Treatment Objectives: The primary objective during the acute phase is to minimize further damage to the laminae by reducing inflammation and improving blood flow. Immediate intervention is crucial to prevent progression to chronic laminitis.
Treatment Methodologies:
Cryotherapy: Continuous icing of the distal limbs has been shown to be effective in reducing the severity of laminitis if applied early (Pollitt & Davies, 1998).
NSAIDs: Non-steroidal anti-inflammatory drugs like phenylbutazone are used to control pain and inflammation (Hood, 1999).
Supportive Therapy: Providing sole support (e.g., using Styrofoam pads) can help redistribute weight away from the laminae (Belknap et al., 2013).
2. Subacute/Transitional Phase (72 hours to 2 weeks)
Clinical Signs: If the acute phase is not adequately managed, laminitis can transition into a subacute phase, marked by persistent lameness, continued heat, and digital pulse in the hooves, with potential for mild rotation of the distal phalanx (Parks & O’Grady, 2003).
Treatment Objectives: The goal is to stabilize the hoof and prevent further laminar damage or progression to more severe chronic forms.
Treatment Methodologies:
Mechanical Support: Corrective trimming and shoeing (e.g., heart bar shoes) aim to redistribute load away from the affected laminae and reduce further mechanical stress (O’Grady, 2006).
Pharmacological Support: Continued use of NSAIDs or the addition of vasodilators like acepromazine to improve blood flow to the laminae (Peroni et al., 2006).
3. Chronic Laminitis Stage 1 (2 weeks to 6 months)
Clinical Signs: At this stage, the condition becomes chronic, characterized by the rotation of the distal phalanx. Clinical signs include a distorted hoof shape (e.g., “Aladdin slipper” appearance), increased hoof wall growth rate at the heels, and persistent lameness (Redden, 2003).
Treatment Objectives: The focus shifts to managing pain, preventing further rotation or sinking, and encouraging regrowth of healthy hoof tissue.
Treatment Methodologies:
Corrective Trimming: Regular trimming to realign the hoof-pastern axis and reduce leverage on the laminae is crucial (O’Grady, 2006).
Specialized Shoeing: Shoes that provide heel elevation (e.g., wedge pads) may be used to reduce tension on the deep digital flexor tendon (Eustace, 2010).
Pharmacological: Long-term pain management with NSAIDs and potential use of bisphosphonates to prevent further bone loss (Grosenbaugh et al., 2010).
4. Chronic Laminitis Stage 2 (6 months and beyond)
Clinical Signs: In this advanced chronic stage, horses may exhibit severe hoof deformity, recurrent abscessation, extensive hoof wall separation, and severe lameness. Radiographs often show significant distal phalanx rotation or sinking (Parks, 2011).
Treatment Objectives: The goals are to manage pain, maintain hoof integrity, and improve the quality of life. In severe cases, humane euthanasia may be considered if the horse’s quality of life is significantly compromised.
Treatment Methodologies:
Advanced Farriery: Customized shoeing solutions, such as rocker shoes or clogs, to protect the compromised structures and support the coffin bone (Kauffman & McKee, 2011).
Surgical Interventions: In some cases, a deep digital flexor tenotomy may be performed to reduce tension on the coffin bone and alleviate pain (Hunt, 2011).
Pain Management: Continued use of NSAIDs, gabapentin, or opioids for more severe pain control (van Eps & Pollitt, 2009).
5. Sinker Syndrome
Clinical Signs: Sinker syndrome is a severe form of laminitis where the entire hoof capsule detaches and sinks relative to the distal phalanx. This is often indicated by a marked depression around the coronary band and extreme lameness, potentially leading to euthanasia due to poor prognosis (Hood, 1999).
Treatment Objectives: If sinker syndrome is identified early, the primary objective is to stabilize the coffin bone and prevent further sinking, although the prognosis is often poor.
Treatment Methodologies:
Aggressive Supportive Care: Intensive care, including sling support to reduce weight-bearing, deep bedding, and mechanical stabilization with external devices, may be used to attempt stabilization (Hood, 1999).
Pharmacological: High-dose NSAIDs or corticosteroids in severe inflammation, though controversial due to potential side effects (Hunt, 2011).
Euthanasia: Due to the severe nature and poor prognosis of sinker syndrome, euthanasia is often considered the most humane option (Parks, 2011).
References
Belknap, J. K., Black, S. J., & Licka, T. F. (2013). The pathophysiology of sepsis-related laminitis. Equine Veterinary Journal, 45(5), 575-577.
Eustace, R. A. (2010). Laminitis: Pathophysiology and prognosis. Equine Veterinary Education, 22(9), 437-448.
Grosenbaugh, D. A., Reinemeyer, C. R., & Figueiredo, M. D. (2010). Pharmacology and therapeutics in equine practice. Veterinary Clinics of North America: Equine Practice, 26(1), 37-54.
Hood, D. M. (1999). Laminitis in the horse. Veterinary Clinics of North America: Equine Practice, 15(2), 287-294.
Hunt, R. J. (2011). Surgical management of chronic laminitis. Veterinary Clinics of North America: Equine Practice, 27(2), 451-459.
Kauffman, J. H., & McKee, S. L. (2011). Advanced farriery for the laminitic horse. Veterinary Clinics of North America: Equine Practice, 27(2), 409-419.
O’Grady, S. E. (2006). Farriery for the chronically laminitic horse. Veterinary Clinics of North America: Equine Practice, 22(2), 287-303.
Parks, A. H. (2011). Chronic laminitis: Clinical features and management. Equine Veterinary Journal, 43(1), 15-19.
Parks, A. H., & O’Grady, S. E. (2003). Chronic laminitis: Clinical signs and diagnosis. Veterinary Clinics of North America: Equine Practice, 19(2), 391-416.
Peroni, J. F., Furr, M. O., & Moore, R. M. (2006). Pharmacologic approaches to modulate laminar perfusion in horses with acute laminitis. Journal of Veterinary Internal Medicine, 20(3), 587-593.
Pollitt, C. C. (2004). Equine laminitis: Clinical and research update. Australian Veterinary Journal, 82(3), 131-138.
Pollitt, C. C., & Davies, C. T. (1998). Equine laminitis: Its development coincides with increased sublamellar blood flow. Equine Veterinary Journal, 30(2), 125-132.
Redden, R. F. (2003). Chronic laminitis: Strategies for successful rehabilitation. Veterinary Clinics of North America: Equine Practice, 19(2), 421-441.
Van Eps, A. W., & Pollitt, C. C. (2006). Equine laminitis induced with oligofructose. Equine Veterinary Journal, 38(3), 203-208.
Van Eps, A. W., & Pollitt, C. C. (2009). Equine laminitis: Cryotherapy reduces the severity of the acute lesion. Equine Veterinary Journal, 41(1), 87-92.
This quantified clinical timeline provides a detailed framework for understanding and treating laminitis from acute onset to chronic stages, including sinker syndrome, based on current evidence-based research.
For further information visit https://hoofflix.com/video-tag/laminitis/
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Q. What are the known Metabolic and Pharmacological Aspects of Laminitis
A. Laminitis is increasingly understood as a complex systemic condition often linked to metabolic disorders, particularly Equine Metabolic Syndrome (EMS) and Pituitary Pars Intermedia Dysfunction (PPID). These conditions predispose horses to laminitis through mechanisms involving insulin dysregulation, inflammation, and vascular dysfunction.
1. Metabolic Aspects
Insulin Dysregulation: Insulin resistance or hyperinsulinemia is a significant risk factor for laminitis, particularly in horses with EMS. High levels of insulin can lead to laminar failure through mechanisms that are not entirely understood, but they likely involve endothelial dysfunction and altered blood flow within the laminar tissues (Asplin et al., 2007; de Laat et al., 2012). The chronic hyperinsulinemic state may cause prolonged vasoconstriction, leading to ischemia and subsequent laminar damage.
Inflammation and Oxidative Stress: Inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α) have been implicated in the pathogenesis of laminitis, especially in cases associated with systemic inflammatory response syndrome (SIRS) or endotoxemia. Oxidative stress from excessive reactive oxygen species (ROS) can further damage the laminar tissues, compounding the effects of inflammation (Belknap et al., 2007).
2. Pharmacological Aspects
Anti-inflammatory Drugs: NSAIDs, such as phenylbutazone and flunixin meglumine, remain the cornerstone of laminitis treatment due to their ability to reduce pain and inflammation. However, concerns exist regarding their potential side effects, such as gastrointestinal ulcers, especially with prolonged use (Beretta et al., 2005).
Vasodilators: Drugs such as acepromazine are used to improve blood flow to the laminae by dilating peripheral blood vessels. This helps counteract the vasoconstriction that contributes to laminar ischemia (Peroni et al., 2006).
Insulin-Sensitizing Agents: Metformin and thiazolidinediones (e.g., pioglitazone) are used to manage insulin dysregulation in horses with EMS. These drugs help reduce insulin resistance, potentially lowering the risk of laminitis (Bertin & de Laat, 2017).
Cryotherapy: Although not a pharmacological intervention per se, cryotherapy is a critical early treatment modality that can be combined with pharmacological approaches. It has been shown to reduce the severity of laminitis by lowering tissue temperature and thus reducing metabolic activity and inflammation within the hoof (van Eps & Pollitt, 2009).
Q. Is Laminitis Considered a Clinical Emergency?
A. Yes, laminitis is considered a clinical emergency, particularly during the acute phase. Immediate intervention is crucial to minimize laminar damage and prevent the progression to chronic laminitis or the development of complications such as “sinker syndrome.” The acute phase of laminitis involves rapid laminar degeneration, leading to significant pain and potentially irreversible damage to the hoof structure if not treated promptly (Belknap & Black, 2012).
Recovery Rates and Prognosis
Recovery rates from laminitis vary significantly based on several factors, including the underlying cause, the severity of the disease at the time of diagnosis, the promptness and effectiveness of treatment, and the horse’s overall health. Generally, the prognosis is more favorable for horses with mild to moderate laminitis caught early in the disease process.
Mild to Moderate Laminitis: Recovery is possible, with some horses returning to full athletic function. However, long-term management, including dietary control and regular farriery, is often necessary to prevent recurrence (Wylie et al., 2013).
Severe or Chronic Laminitis: Horses with severe laminitis, particularly those with significant rotation or sinking of the distal phalanx, have a much poorer prognosis. Recovery rates in these cases are lower, and even if the horse survives, chronic pain and lameness are common. The need for ongoing medical and farriery interventions can be extensive (Katz & Bailey, 2012).
Sinker Syndrome: The prognosis for horses with sinker syndrome is generally poor, with many horses requiring euthanasia due to intractable pain and poor quality of life (Hunt, 2011).
Barriers to a Successful Outcome
Several barriers exist to achieving a successful outcome in cases of laminitis:
Delayed Diagnosis and Treatment: Early signs of laminitis can be subtle, and delays in diagnosis can allow the disease to progress to a more severe stage before treatment begins, reducing the likelihood of recovery.
Inadequate Pain Management: Insufficient control of pain can exacerbate stress and inflammation, complicating treatment and reducing the horse’s ability to bear weight properly, which can lead to further laminar damage.
Poor Farriery: Corrective trimming and shoeing are critical to managing chronic laminitis, but improper farriery can exacerbate hoof deformities and laminar strain, hindering recovery (O’Grady & Parks, 2012).
Metabolic Disorders: Underlying conditions like EMS or PPID must be managed effectively. Failure to control these conditions can lead to recurrent episodes of laminitis, further complicating recovery.
Owner Compliance: Managing laminitis often requires significant changes in horse management, including strict dietary controls and regular monitoring. Non-compliance with these measures can lead to poor outcomes.
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