Equine Laminitis: Practical Clinical Considerations
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IN-DEPTH: LAMINITIS FOR THE PRACTITIONER Equine Laminitis: Practical Clinical Considerations Robert J. Hunt, DVM, MS, Diplomate ACVS Author’s address: Hagyard Equine Medical Institute, 4250 Ironworks Pike, Lexington, KY 40511; e-mail: [email protected]. © 2008 AAEP. 1. Introduction merous treatments have, therefore, phased in and out Over the past 20 yr, extensive research efforts as of vogue over the years with only a few, such as the well as clinical experience has greatly increased our non-steroidal anti-inflammatory drugs, withstanding knowledge base of equine laminitis. Our present the test of time. The objective of this discussion is to understanding of the disease is that there is failure review the salient features of laminitis and provide a of the lamellar attachment between the distal pha- realistic view point for the practitioner to consider lanx and hoof wall.1–7 This, in turn, initiates a when managing the patient and the client. sequence of events ranging from no permanent structural damage to loss of the hoof capsule. Af- 2. Overview fected individuals are often plagued with chronic The foot is a highly resilient and durable structure pain, and they may suffer chronic hoof abscessation able to tolerate extremes in load and concussion on a or abnormal hoof-wall development with recurring variety of surfaces under a variety of environmental bouts of laminitis. conditions, such as excessive moisture or dryness, The preponderance of laminitis research has been freezing temperatures, or extreme heat. It is well aimed at defining the events that occur systemically designed and able to withstand notable insult exter- and locally within the digit that result in clinical nally and internally. Considering the normal rig- laminitis. Although we have identified many early ors that the equine foot endures, it is almost events that occur, we have yet to determine a specific incomprehensible to think a variation in normal triggering mechanism that initiates the pathological physiology can result in such devastation as that sequence. Importantly, there is a disconnect between seen with laminitis. research and clinical medicine in that much of our Anatomy and physiology of the equine foot have acquired research information is not used clinically. received considerable attention.11–18 The most rel- This is partly because of the narrow time frame of the evant structures of the foot pertaining to laminitis prodromal and acute stage of laminitis compared with include the vascular architecture and the dermal the relatively late clinical presentation and relative epidermal interdigitation of the primary and second- long-standing nature of the disease. Also, because of ary lamella supporting the coffin bone to the hoof the variation in clinical case presentation and re- wall.11,12 The vascular supply to the digit and la- sponse, our treatments are anecdotal, based on clinical mellar bed is extensive and functions to provide signs, and in the long run, often ineffective.8–10 Nu- nutrition, structural support, and hydraulic damp- NOTES AAEP PROCEEDINGS ր Vol. 54 ր 2008 347 IN-DEPTH: LAMINITIS FOR THE PRACTITIONER ening against concussive shearing. The circumflex sis. One must ascertain if the horse does actually artery provides a large portion of the corium vascu- have laminitis and attempt to determine the under- lar supply through the laminar arteries coursing in lying cause. It cannot be overemphasized that this a distal to proximal direction. Venous drainage ac- is a dynamic disease that progresses at variable companies the arterial supply in a proximal to distal rates. Clinical laminitis is appropriately referred direction. The arteries of the digit are highly mus- to as a syndrome because of the differing presenta- cular, which likely function in the dampening mech- tions and stages. Managing an unstable acute anism as well as allow for little compliance. There sinker is vastly different than working with a horse are an abundance of arteriovenous shunts through- with a chronic stable laminitis that is able to per- out the vascular bed that allow bypass of the capil- form athletically. lary bed as well as rapid alterations in hoof Diagnostics remain basic for laminitis, but thor- temperature and capillary nutrition. oughness must be emphasized. The physical eval- Ultrastructurally, the hemidesmosome maintains uation and in particular, detailed evaluation of the the attachment between the secondary epidermal feet is mandatory. Assessment of the quality and lamella basal cell and its basement membrane. integrity of the feet, intensity of digital pulse, and The sequence of events that occur during experi- temperature should be made. The coronary band mental laminitis results in a disassociation of this should be assessed for the presence of edema (swell- junction beginning at the basement membrane level ing), depressed areas (sinking), or palpably tender of the secondary lamella from cleavage of the areas (possible abscess or separation of hoof wall). hemidesmosome.3 Irrespective of the initiating The shape and position of the sole is observed for cause, there seems to be some overlap in the patho- degree of concavity or protrusion, soft spots, or ex- genesis of the syndrome, because the end result is cessive thinning. The size, shape, and integrity of loss of mechanical support caused by laminar de- the feet are especially important when designing a tachment. Imposed biomechanical load on this podiatry program for the horse and for monitoring compromised junction causes further lamellar dis- change associated with the progression of the dis- ruption. Additionally, it results in additional phys- ease. The single evaluation provides limited infor- ical separation and displacement of the coffin bone mation relative to the long-term management of the from the hoof wall. patient with laminitis, and the clinician must look Several hypotheses have arisen from a sound body for trends in disease progression over time to guide of research to explain the pathophysiology of lami- appropriate therapy. nitis. Presently, it is not possible to apply a single In most instances, observation of the stance and theory to every case, and the pathogenic pathway gait are strong indicators of the presence of lamini- likely varies depending on the type and severity of tis. The characteristic stilted camped out front legs the inciting cause. The various hypotheses may be are believed to redistribute load to the hindlimbs.5 classified as vascular, metabolic/toxic, inflamma- Variations on this stance likely occur because of the tory, or traumatic (mechanical) in origin.7 There is presence of pain in the rear feet or variations in the likely some degree of interplay and overlap in the location of pain in the front feet. It is not often various mechanisms, but the connection has not necessary to perform diagnostic nerve blocks to di- been fully proven. It is beyond the scope of this agnose laminitis; instances of low-grade bilateral presentation to provide a detailed literature review pain associated with chronic laminitis can be an on these theories. From a pragmatic clinicians’ exception. perspective, it seems that a destructive endogenous There are three vital pieces of information to ob- agent (metalloprotease or others), vascular isch- tain when evaluating a patient and formulating a emia, or mechanical overload of tissue results in diagnostic, therapeutic, and prognostic plan. The separation at the basement membrane, loss of struc- clinician must determine the reason and source of tural integrity, and separation of the coffin bone pain, the location of pain, and the degree of insta- caused by mechanical load on the digit. We need to bility within the foot. It may take several visits be cognizant that data are lacking to support these and serial evaluations spread over days to weeks to theories on large groups of horses in a clinical set- accurately make this assessment. Ultimately, one ting, and because of the lack of reproducibility of this hopes to determine if the horse can continue to gen- syndrome, it remains difficult to prove. erate a viable and functional hoof capsule, and this is presumably correlated with the integrity of the 3. Clinical Presentation and Diagnosis germinal layers. Understanding the pathophysiology of laminitis is The source or cause of pain within the foot should important to the understanding of the disease; how- be determined, and differentiation should be made ever, it provides only a small piece of the puzzle between septic processes, non-septic processes, when managing a clinical case. Accurate assess- bruising, laminar shearing, ischemia, and bone pa- ment of the whole patient with consideration for thology. Digital sepsis or abscessation may occur signalment, occupation, and owner expectations without loss of structural integrity to the lamella. should be considered in every case when attempting Consideration of the etiology and stage of laminitis to provide appropriate treatment as well as progno- should be given when assessing the source of pain. 348 2008 ր Vol. 54 ր AAEP PROCEEDINGS IN-DEPTH: LAMINITIS FOR THE PRACTITIONER A horse with chronic laminitis with keratin hyper- tinely. Findings should be assessed in light of the plasia resulting in an overgrown foot with seedy toe rest of the clinical picture, which must consider the and prolapsed sole is more likely to have a subsolar stage of the disease and especially, the rate of change abscess contributing to the lameness than a horse of the position of the coffin bone within the hoof cap- with acute laminitis with radiographic evidence of sule. It is important to note that the radiographic sinking. With acute distal displacement, pain is study represents a static image of a dynamic model probably associated with laminar shearing, digital and disease. It is most useful when combined with collapse, and pressure on inflamed sensitive tissue. the clinical evaluation during serial sessions. In general, it is counterproductive to open the sole in Radiographic assessment has changed from only this situation.