Laminitis Flashcards
What are the layers of the hoof wall?
Stratum externum (periople) Stratum medium (horn tubules and intertubular horn) Stratum internum (interdigitations of corial and epidermal laminae)
Define laminitis
Laminar degeneration or breakdown of the interdigitations of the primary and secondary epidermal and dermal laminae of the foot
Specifically, dysadhesion occurs between the epidermal basal cells and the basement membrane
Pathophysiology of laminitis
Separation of dermal and epidermal laminae and pull of DDFT lead to movement of P3 relative to hoof capsule
Predisposing/risk factors
Mechanical: road founder, supporting limb with severe lameness
Toxic/infectious: Severe infections of GI, lung, or uterus
Nutritional: grass founder, carb overload
Endocrine: pituitary pars intermedia dysfunction, equine metabolic syndrome
Pathogenesis of laminitis
Vascular Ischemia hypothesis
- Laminitis develops because of laminar hypoperfusion/ischemia
- Angiographic studies have demonstrated a reduction of laminar corium circulation in horses with laminitis
Toxic/Metabolic Hypothesis
- Excessive enzymatic degredation of lamellar attachments, caused by hematogenous “laminitis trigger factors” delivered to the foot
Systemic/Digital Inflammation Hypothesis
- Inflammation results in intravascular coagulation and microthrombi formation in the digital vasculature
Vascular Ischemia Hypothesis
Digital venoconstriction (endothelial damage leads to decrease in nitric oxide) -> increased postcapillary resistance -> increased capillary pressure -> movement of fluid into the interstitium -> increased tissue pressure (edema) -> decreased microcirculatory perfusion -> opening of arteriovenous shunts -> ischemia/hypoxia
Toxic/Metabolic Hypothesis
Destruction of the epidermal/basement membrane construct by excessive enzymatic degredation leading to separation of the epidermis and the dermis
Increased activated MMPs in hoof tissues of horses with laminitis is caused by unknown “laminitis trigger factors” delivered to the foot
Decreased glucose uptake by dermis and epidermis of the foot
- Cell death
- Decreased production of nitric oxide
Increased digital blood flow precedes the development of carbohydrate laminitis
- Enhances delivery of “trigger factors?”
Activation of MMPs is hypothesized to be induced by the exotoxin from Strep species which are typically found in the cecal lumen
Distal limb cryotherapy prevented development of acute laminitis
T/F: Cells of foot need blood supply and nutrient delivery or they will separate
True
Toxic/Metabolic Hypothesis Summary
Acute metabolic stress syndrome (colitis, metritis, sepsis, carb overload) results -> Increased cortisol, epinephrine: reduction of glucose consumption by peripheral tissues -> Hemidesmosome dissolution and down regulation
Primary pars intermedia dysfunction
Increased adrenocorticotropic hormon production by pituitary gland -> Increased serum levels of cortisone and insulin -> Peripheral insulin resistance -> Decreased glucose uptake
Systemic/Digital Inflammation Hypothesis
Systemic inflammation (carb overload, sepsis, endotoxemia) alters homeostasis within various organ systems - Fluid imbalance, coagulopathy, and increased circulating inflammatory mediators
Intravascular coagulation and thrombi within the digital vasculature leads to decreased blood flow and development of laminitis
Support limb laminitis
Excessive unilateral weight bearing
Overload of soft tissue structures of the foot
Decreased perfusion in the laminae dt constant tension on the dorsal laminar attachments of the coffin bone
Compression of vessels delivering blood to the dorsal laminae
What are the phases of laminitis?
Developmental: period between exposure to causative agent to first sign of lameness
Acute: Period between first signs of lameness to rotation or sinking
Subacute: Mild lameness without mechanical failure
Chronic: Mechanical failure
- Early chronic: first several months
- Chronic active: recurrence after improvement
- Chronic stable: stable coffin bone with improvement in hoof
Refractory: minimally responsive over first 7-10d
CS of acute dz
Increased digital pulse amplitude Elevated hoof temperature Positive pain response to solar pressure Lameness: - Treading - Camped out in front/under behind - Land heel to toe - May not allow foot to be lifted from the ground
CS of chronic dz
Acute phase signs may be present
Chronic dz specific signs: Abnormal hoof growth, recurrent foot abscesses, coronary band depression
