Chapter 34 Laminitis
A tough, flexible, connective tissue suspensory apparatus suspends the distal phalanx (DP) to the inside of the hoof wall. The surface of the inner hoof wall is folded into leaflike lamellae (laminae) to increase the surface area of attachment between the hoof and the DP. A horse has laminitis when this attachment apparatus is compromised. Without the DP properly attached to the inside of the hoof, the weight of the horse and the forces of locomotion drive the DP down and away from the hoof wall. Arteries, veins, and nerves are sheared and crushed, and secondary to the lamellar pathology, the corium of the coronet and sole is damaged. Eventually even the DP itself may suffer deterioration and lysis of its dorsal margin. Unrelenting pain in the feet (bilateral forelimb usually) and a characteristic lameness occur. In acute laminitis the lamellar tissue suspending the DP from the inner hoof wall is affected at the junction between the connective tissue of the dermis or corium (the bone side) and the basal cell layer of the epidermal lamellae (the hoof side). This junction, the basement membrane zone or dermal/epidermal interface, appears to be the weak link in an otherwise robust and reliable structure. Wholesale epidermal cell detachment from and lysis of the lamellar basement membrane may occur,1,2 leading to disruption of lamellar anatomy and ultimately compromise (to varying degrees) of the suspensory attachment between the DP and hoof. Associated with basement membrane lysis and dysadhesion are changes to lamellar epidermal cell morphology that result in lamellar stretching and attenuation. Thus whether by loss of basement membrane attachment or by lamellar stretching (or both), the DP draws away from the inner hoof wall and sinks downward. The degree of separation and sinking varies between horses affected with laminitis, ranging from barely detectable (mild) to catastrophically severe (“sinkers”). Ponies and small horses are usually less severely affected than their heavier cousins. A good correlation exists between the severity, as seen with the microscope (histopathology), and the degree of lameness (using the Obel grading system3) shown by the horse.1 When a horse first shows laminitic pain, the anatomy of the hoof wall lamellae is already compromised. The higher the lameness grade, the more severe the microscopic damage. Any activity that places stress on an already weakened lamellar attachment apparatus (such as forced exercise) exacerbates damage and is contraindicated. The use of nerve blocks to eliminate pain encourages locomotion and does more damage. Favorable outcomes are associated with effective preventive and early therapeutic strategies.
Pathological deformation of the lamellar attachment apparatus begins during the developmental phase of laminitis. Tightly controlled metabolic processes are targeted, causing lamellar-specific pathology. One mechanism behind lamellar deformation involves lamellar enzymes. Enzymes are normal constituents of lamellar cells and respond to the stresses and strains of equine life and to constant growth. Sufficient enzyme is manufactured locally to release epidermal cell-to-cell and cell-to-basement membrane attachment as required, maintaining the correct shape and orientation of the lamellae. From time to time injury to the basement membrane requires its lysis and reconstruction. The controlled release of matrix metalloproteinases (MMPs) and specific tissue inhibitors of MMP (TIMPs) keeps repair and modeling in equilibrium.4,5 Normally the hoof lamellae slowly migrate distally past the stationary basement membrane that is firmly attached to the connective tissue covering the dorsal surface of the DP. Distal movement occurs because the hoof wall6 continually proliferates at the coronet and moves downward past the stationary DP by a process of controlled enzymatic modeling of the lamellar epidermis and the basement membrane zone. Accumulating evidence suggests that during developmental laminitis, compromise of the basement membrane zone occurs when production of constituent lamellar enzymes is increased and they are activated out of control. The enzymes known to be involved are metalloproteinase-2 (MMP-2), metalloproteinase-9 (MMP-9), membrane-type metalloproteinase (MMP-14), and aggrecanase (ADAMTS-4), and singly or together they destroy key components of the lamellar suspensory apparatus.7-10 A second, newly discovered lamellar deformation mechanism is seen in hyperinsulinemic horses. Experimental hyperinsulinemia is profoundly laminitogenic in ponies and horses, inducing clinical signs in 40 to 72 hours.11,12 Limited basement membrane dysadhesion occurred in insulin-affected horses but not to the extent seen in experimental carbohydrate-induced laminitis and was virtually absent in ponies. Mitosis, normally infrequent among lamellar epidermal cells, was a feature of hyperinsulinemic lamellar histopathology possibly contributing to lamellar lengthening.13 In laminitis induced by dosing horses with extract of Black walnut (Juglans nigra) heartwood, there was no evidence of basement membrane breakdown.14,15
Most descriptions of laminitis histopathology derive from laminitis induced experimentally with a single large dose of carbohydrate of either grain starch or oligofructose.3,16,17 The sequences of microscopic events that lead to clinical laminitis follow a consistent temporal pattern,18 and the stages of histological laminitis can be identified by the degree of severity of these changes. Making the lamellar basement membrane clearly visible is important and requires staining lamellar tissues with periodic acid–Schiff (PAS) stain or with immunohistochemical methods using basement membrane–specific antibodies.1,2
Fig. 34-1 Micrograph of normal hoof lamellae stained to highlight the basement membrane. The basement membrane (arrows) of each secondary epidermal lamella (SEL) is a magenta (black in the figure) line closely adherent to the SEL basal cells. At secondary dermal lamellae (SDL) tips, between the bases of each SEL, the basement membrane (BM) penetrates deeply (arrowheads) and is close to the anuclear, keratinized, primary epidermal lamella (PEL). The SEL tips are rounded (club-shaped). The basal cell nuclei are oval in shape (stars) and positioned away from the BM at the apex of each cell. The long axis of each basal cell nucleus is at right angles to the long axis of the SEL. The SDL are filled with connective tissue even at their very tips, between the SEL bases. These parameters of hoof lamellar anatomy form the basis of the histological grading system of laminitis histopathology. Stain, Periodic acid–Schiff; bar, 10 µm.
The earliest change attributable to laminitis is loss of shape and normal arrangement of the lamellar basal and parabasal cells. The basal cell nuclei become rounded instead of oval and take an abnormal position in the cytoplasm of the cell. The secondary epidermal lamellae become stretched, long, and thin, with tapering instead of club-shaped tips. These changes were present at 12 hours in serial lamellar biopsies taken after oligofructose dosing.18 First noticeable at the tips of the secondary epidermal lamellae, teat-shaped bubbles of loose basement membrane form. PAS staining shows this best (Figure 34-2).
Fig. 34-2 Grade 1 histological laminitis (periodic acid–Schiff stain). Micrograph showing hoof lamellar tissues stained to highlight the basement membrane. The basement membrane (arrows) is stained dark magenta (black in the figure). At the now-tapered tips of the secondary epidermal lamellae (SELs), the basement membrane has lifted away (stars) from the underlying basal cells. Between the SEL bases the basement membrane (BM) is in its normal position, close to the primary epidermal lamellae; bar, 10 µm.
Examination of laminitis tissues with the electron microscope confirms lysis and separation of the lamellar basement membrane.19 Importantly, the greater magnification shows widespread loss of basal cell adhesion plaques (hemidesmosomes) and contraction of the basal cell cytoskeleton away from the inner cell surface. Electron microscopy shows why the basement membrane separates from the feet of the basal cells. The filaments that anchor hemidesmosomes to the lamina densa of the basement membrane no longer bridge the dermal/epidermal interface (Figure 34-3).13
Fig. 34-3 Electron micrograph of hoof lamellar tip developing laminitis. The lamina densa (LD) of the basement membrane is separating from the plasmalemma of the lamellar basal cell (EBC). Some hemidesmosomes (black arrow) appear undamaged, but others (white arrow) have faded, are losing their anchoring filament attachments, and are drawing away from the basement membrane. Normally anchoring filaments (arrowhead) bridge the lamina densa firmly to the EBC. D, Dermis.
Because the basement membrane is no longer completely tethered to the basal cells, it slips farther away with each cycle of weight bearing by the horse. Portions of the lamellar basement membrane are lysed initially between the bases of the secondary epidermal lamellae (see Figure 34-2). The basement membrane retracts from the tips of secondary epidermal lamellae, taking the dermal connective tissue with it. The basement membrane–free epidermal cells appear not to be undergoing necrosis, at least initially, and clump together to form amorphous, basement membrane–free masses on either side of the lamellar axis.1
In laminitis the worst-case scenario is a rapid and near-total basement membrane separation from all the epidermal lamellae of the hoof toe, quarters, heel, and bars. Sheets of basement membrane peel away to form aggregations of loose, isolated basement membrane in the connective tissue adjoining the lamellae. The epidermal lamellar cells are left as isolated columns with little viable connection to the dermal connective tissue still attached to the DP. The hoof lamellar tips slide away from the basement membrane connective tissue attachments, at first microscopically, but as the degree of separation increases, the distance between hoof and DP becomes measurable in millimeters (Figure 34-4) and can be detected radiologically.20 This manifests clinically as a sinker. Because the basement membrane is the key structure bridging the epidermis of the hoof to the connective tissue of the DP, wholesale loss and disorganization of the lamellar basement membrane follow and inexorably lead to the pathology of hoof and bone that characterizes the chronic stage of laminitis.
Fig. 34-4 Grade 3 histological laminitis (immunostain). The basement membrane of a lamellar tip is highlighted by type IV collagen immunostaining. The tip of the primary epidermal lamella (PEL) has completely detached from its basement membrane. The PEL basal cells are now an unattached, amorphous mass. Collapsed tubes of basement membrane, now empty of epidermal cells, are still attached to connective tissue (arrowheads). The PEL has already moved 0.03 mm from its dermal compartment, and soon the distance will be measured, using a tape measure, on a radiograph. The inset shows a normal lamellar tip immunostained the same way. Type IV collagen immunostain; bars, 10 µm.
The laminitis process also affects the lamellar capillaries. As the basement membrane and the connective tissue between the secondary epidermal lamellae disappear, so do the capillaries. They become obliterated, compressed against the edges of the primary dermal lamellae. Without a full complement of capillaries in the lamellar circulation, blood probably bypasses the capillary bed through dilated arteriovenous shunts,21 changing the nature of the foot circulation. A bounding pulse becomes detectable by finger palpation of the digital arteries. Furthermore, epidermal cell necrosis, intravascular coagulation, and edema are not universally present in sections made from tissues in the early stages of laminitis. The vessels in the primary dermal lamella, even the smallest, are predominantly open, without evidence of microvascular thrombi. The gross anatomical appearance of freshly dissected laminitis tissue is dryness. Sometimes the lamellae just peel apart.
It is rare to detect leukocytes in the lamellar tissues of normal horses.14 However, extravasation of leukocytes into the perivascular lamellar dermis occurs in carbohydrate-,1 Black walnut extract–,14,22 and hyperinsulinemia-induced13 forms of laminitis. Because leukocytic infiltration of tissues is associated with inflammation, the discovery that leukocytic infiltration is common to most, if not all, forms of laminitis has reemphasized an inflammatory pathway to laminitis development. There is molecular evidence that inflammatory mediators may activate many of the processes known to damage the lamellar interface.23,24 Polymorphonuclear leukocytes are rich in MMP-9, and their presence within lamellar epidermal compartments in grade 3 histopathology1 suggests that this basement membrane–degrading enzyme may have a pathological role in disease development. Also neutrophils produce reactive oxygen species and proinflammatory cytokines that probably contribute to cellular damage within the lamellar milieu.15 Lamellar damage and leukocyte infiltration are readily detected by calprotectin immunostaining,14,25 and because leukocyte infiltration precedes the expression of calprotectin in the lamellar epidermis, a role for leukocytes in initiating lamellar pathology has been suggested.22,23 However, carbohydrate-induced laminitis studied at the 12-hour postdosing time point shows basement membrane degradation occurring in advance of leukocyte infiltration, thus downplaying an initiating role for leukocytes in lesion development.25
The enzymatic theory of laminitis, based on the triggering of lamellar MMP activity,26,27 challenged the alternative view that laminitis was caused by ischemia and ischemia/reperfusion injury damaging epidermal lamellae because blood flow was impeded.28 Evidence against ischemia/reperfusion involvement in Black walnut extract–induced laminitis came from studies measuring xanthine oxidase, a reactive oxygen intermediate that increases in tissues affected by ischemia and ischemia/reperfusion. Xanthine oxidase was absent in tissues with Black walnut extract–induced lamellar pathology, suggesting that a global lamellar hypoxic event had not occurred.29 Furthermore, there is evidence from three independent international laboratories that the foot circulation during the developmental phase of both carbohydrate- and hyperinsulinemia-induced laminitis is vasodilated.30-33 Laminitis did not occur if the foot was in a state of vasoconstriction during the developmental phase, suggesting that the trigger factors only cause laminitis if they reach the lamellar tissues at a high enough concentration and over a long enough time.30 In current laminitis therapy there is a consistent lack of efficacy of drugs addressing ischemia, suggesting other pathogenic processes, such as inflammation, may be more important.
The actual trigger factors of laminitis remain unidentified. Gram-negative bacterial endotoxin has been detected in the circulation of horses with carbohydrate-induced laminitis34 and is presumed to play a role in initiating lamellar pathology. Horses with colic, colitis, pleuropneumonia, and retained fetal membranes, the conditions often associated with laminitis development,35 develop pyrexia and appear “endotoxic,” but this is usually inferred from clinical signs rather than confirmed by endotoxin assay. Tumor necrosis factor and interleukin-6 (IL-6) along with other cytokines are expressed by mononuclear phagocytes within minutes of exposure to endotoxin.36-38 Decreases in digital blood flow and lamellar perfusion, secondary effects mediated by the platelet-derived vasoconstrictors 5-hydroxytryptamine and thromboxane, follow intravenous endotoxin administration.37 However, laminitis or even foot pain has never been elicited by the experimental administration of endotoxin into either the bloodstream or the peritoneal cavity.39,40 Gram-negative bacteria disappear early, before the onset of clinical signs, from hindgut samples taken from horses developing carbohydrate overload-induced laminitis, suggesting no role for endotoxin in laminitis pathogenesis.41 Instead a plethora of absorbed microbial toxins may affect lamellar compromise, including gram-positive exotoxins from the explosive proliferation of hindgut streptococci after carbohydrate overload.
Lamellar disintegration of laminitis occurs well before clinical signs. The molecular conformation of the lamellar basement membrane is altered 12 hours after dosing with oligofructose, and a major constituent of the basement membrane, collagen IV, begins to disappear. Previously, damage to the lamellar basement membrane was attributed to MMP release and activation, but new evidence places MMP activation many hours later than other molecular events.25 An enzyme capable of modifying the proteoglycan components of lamellar basement membrane is ADAMTS-4 (A Disintegrin And Metalloproteinase with ThromboSpondin motifs), the gene for which has the greatest fold increase of any thus far discovered in laminitis development.10,25,42 ADAMTS-4 gene expression occurs early in laminitis development, and the gene product may play a central role in the pathophysiology of the disease.
The activity of tissue MMPs correlates strongly with the degree of malignancy and invasiveness of lethal human tumors, such as malignant melanoma, breast cancer, and colon cancer.43 Research in this field has generated a wide range of chemical agents capable of inhibiting MMP activity in vitro and in vivo. BB-94 (Batimastat, British Biotech, Oxford, England) blocks the activity of the laminitis MMPs in vitro and has the potential to be a useful tool in preventing and managing acute laminitis. Whether MMP inhibitors can prevent or ameliorate naturally occurring laminitis has yet to be established.
To test the hypothesis that hyperinsulinemia triggers laminitis, normal, lean ponies with no previous history of insulin resistance or laminitis were subjected to prolonged hyperinsulinemia and euglycemia.44 All the ponies developed laminitis within 72 hours of hyperinsulinemia, a finding supporting the importance of insulin in the pathogenesis of endocrinopathic laminitis. Standardbred horses subjected to the same hyperinsulinemia/euglycemia clamp protocol also developed clinical laminitis but sooner (<48 hours) and with histopathology notable for lamellar basement membrane separation.33 Hyperinsulinemia causes profound changes in the peripheral microcirculation,45 and a vascular (ischemic) pathogenesis for laminitis has long been sought.46 However, hoof wall surface temperature, measured continuously in the hyperinsulinemic and control horses, showed hyperinsulinemia induced early-onset, prolonged vasodilation. Lamellar insulin receptors are located within blood vessels (but not elsewhere) and in the presence of insulin activate vascular nitric oxide synthase to produce the potent vasodilator nitric oxide. Perhaps unregulated vasodilation results in excessive cellular uptake of glucose, lamellar glucotoxicity, and oxidative stress similar to that involved in the pathogenesis of atherosclerosis and the associated up-regulated MMP-9 activity in human diabetes.47
Equine lamellae, cultured in vitro, have tested resistant to virtually all known cytokines, tissue factors, and prostaglandins. Gram-negative bacterial endotoxin, extract of Black walnut (J. nigra), and even anaerobic culture conditions fail to induce lamellar separation or significant MMP activation.48 Equine IL-6 added to cultured lamellar explants fails to activate lamellar MMPs or cause basement membrane disruption at the lamellar interface.25 Some notable exceptions occur, however. Factors present in the supernatant of cultures of Streptococcus bovis (S. bovis) isolated from the equine cecum activate equine hoof MMP-2 and cause lamellar separation.48 During carbohydrate overload, rapidly proliferating species of hindgut streptococci, predominantly S. bovis (now Streptococcus lutetiensis), ferment carbohydrate and produce large quantities of lactic acid.41,49,50 In the presence of virtually unlimited substrate, the population of S. bovis increases exponentially and then dies and lyses en masse. The liberated cellular components of lysed hindgut streptococci may cross the mucosal barrier of the damaged hindgut and reach the hoof lamellae hematogenously to initiate laminitis. Microbial and other factors probably associate with basement membranes throughout the body but probably only cause damage to lamellar basement membranes because of their uniquely equine involvement in weight bearing.
The term equine metabolic syndrome refers to horses with a history of laminitis, insulin resistance, cresty necks, and increased adipose tissue deposits in the withers, dorsal area of the back, and rump.51 Elevated serum insulin concentrations distinguish ponies that are susceptible to dietary pasture-associated laminitis.52-55 Furthermore, insulin concentrations are markedly elevated in ponies that develop laminitis after grazing high carbohydrate pasture, whereas glucose, free fatty acid, and cortisol concentrations remain normal.53,56 In contrast to people, insulin-resistant horses rarely develop pancreatic exhaustion and hyperglycemia and are capable of producing exceptionally high serum insulin concentrations.56,57 Insulin toxicity appears to be a key factor in triggering equine laminitis. The onset of laminitis is associated with plasma insulin that exceeds 100 µIU/mL (normal range = 8 to 30 µIU/mL).58
Horses and ponies at risk of laminitis should be blood tested for the early detection of hyperinsulinemia, and grain or other soluble carbohydrate should be withheld for 3 hours before testing. A single blood sample showing elevated insulin predicts that laminitis will occur or may become worse.58 Techniques should be used to lower insulin concentrations and restore insulin sensitivity. A weight-reducing diet with a low glycemic index and physical exercise reduce insulin resistance in horses.59 Insulin-sensitizing drugs of the type given to people with type 2 diabetes have been trialed in insulin-resistant horses. Metformin, at a higher dose than previously reported (15 mg/kg body weight per os [PO] every 12 hours), reversed insulin resistance during the first 6 to 14 days of treatment, but this effect diminished by 220 days.60 Pharmacokinetic and epidemiological studies and placebo-controlled trials may further define the potential applications of this drug in the treatment of insulin resistance and prevention of laminitis.
Older ponies and horses sometimes develop a problem with their pituitary gland, which enlarges, becomes dysfunctional, and results in the development of equine Cushing’s disease (ECD). Pituitary enlargement is sometimes described as a tumor (pituitary adenoma), but most affected horses have simply pituitary hyperplasia (an increase in size for unexplainable reasons). The region of the pituitary involved is the pars intermedia, giving the condition its common medical name: pituitary pars intermedia dysfunction (PPID). The dysfunctional pituitary produces an excess of hormones and peptides that control other hormones. A sign that horses are affected by PPID is hirsutism; the hair coat grows unnaturally long and is not shed at the usual times.
The hormone imbalance is associated with hyperinsulinemia that disturbs hoof lamellar metabolism, promoting an insidious, relentlessly developing, chronic laminitis. Affected horses and ponies often have higher than normal concentrations of glucose, adrenocorticotropic hormone (ACTH), cortisone, and insulin in their blood. The levels of these substances vary throughout the day (diurnal or circadian rhythm), and care has to be taken with the interpretation of blood analysis. The clinical signs of ECD are pot belly and wasted top line, bulging supraorbital fat, polyuria and polydipsia, susceptibility to infections, and laminitis. Insulin status is a powerful prognostic indicator in horses with ECD, and insulin-resistant animals with a basal serum insulin concentration of greater than 188 µIU/mL are much more likely to develop laminitis and survive less than 2 years after diagnosis.56 Laminitis that develops in association with ECD is usually refractory to treatment. However, promising results have been obtained after the administration of pergolide mesylate (Permax, Valeant Pharmaceuticals International, Costa Mesa, California, United States), a drug registered for use in people. Doses in the range of 1 to 2 mg/horse/day have been recommended. The drug mechanism is to reduce production in the pituitary gland of the hormone (ACTH) that controls cortisol production in the adrenal gland. With cortisol under control, insulin responsiveness in hoof lamellae returns, and the laminitis stabilizes. Using pergolide mesylate, the ACTH concentration in horses with ECD decreases within 1 week.58
Although not proven experimentally, an association was made between systemic or intraarticular administration of corticosteroids, including triamcinolone acetonide (TMC) and methylprednisolone acetate, and the development of laminitis in otherwise apparently healthy horses.61 A single dose of TMC (0.05 mg/kg) given intramuscularly was cleared slowly and induced hyperglycemia and hyperinsulinemia for at least 3 days.62 Larger intramuscular doses (0.2 mg/kg) prolonged this hyperinsulinemic effect, and serum insulin concentration of around 130 µIU/mL persisted for 6 days.62 However, none of the treated horses developed laminitis, although a “laminar” ring, coincident with the time of injection, grew down the hoof wall. In a retrospective clinical trial only 1 of 205 horses treated with TMC developed laminitis, and it had a previous episode of laminitis in its history.63 Nonetheless, clinicians must be aware of the risks associated with exogenously administered corticosteroids. As Bailey and Elliot61 warn, “Glucocorticoids might only increase the risk of developing laminitis when other causative factors are present, or when the lamellar tissues are somehow ‘primed’ to undergo changes leading to cell damage and dysfunction.” A risk factor may be the preexisting hyperinsulinemia associated with metabolic syndrome or ECD. Because hyperinsulinemia alone will precipitate clinical laminitis,11 injecting glucocorticoid into already insulin-resistant, hyperinsulinemic horses may elevate serum insulin concentrations into the laminitogenic range.
Laminitis in the lamellae of a single hoof can occur whenever a horse’s limb is forced to bear weight unilaterally for prolonged periods. This can occur when an injury (bone or joint fracture) or disease process (infectious arthritis) in the contralateral limb is so painful that weight bearing is impossible. After days to weeks of unrelieved weight bearing, the supporting limb develops lamellar pathology, often to a severe degree. Presumably the immobile limb lacks adequate lamellar perfusion and glucose delivery that eventually trigger a lamellar pathology indistinguishable from that initiated by other causes. Development of this form of laminitis may be delayed or prevented by supporting the limb by a firmly applied elastic support bandage and shoeing with an effective support shoe. The horse should be provided with a deep bed of wood shavings or sand so that it can lie down comfortably and allow blood to circulate through its feet. Deep, compliant bedding also allows the horse to find a foot position that promotes foot circulation. The injured limb should be treated promptly and fitted with a cast or splint so that it can begin to take its share of weight bearing. Pain should be controlled with analgesics for the same reason. An exercise regimen of walking every 6 hours to encourage circulation of the contralateral foot has reduced the incidence of supporting limb laminitis in an equine hospital, but this practice may not be possible or advisable in all horses.64
Laminitis is characterized by an acute-onset lameness of variable severity involving one or more feet. Most often both front feet are affected, with or without the hind feet, but unilateral laminitis does occur, usually caused by excessive load bearing because of severe contralateral limb lameness. Occasionally the hind feet are affected, without involvement of the front feet. The horse may be extremely reluctant to move and, if persuaded to move, tends to land heel first, with a short, pottery gait, with the hindlimbs placed unusually far underneath the body. There is a marked shortening of the caudal phase of the stride at the walk. Lameness may be accentuated as the horse turns. Lameness is worse on hard ground than on soft ground. Although many horses show severe lameness, in those with milder lameness the lameness may be less typical, although suggestive of foot pain. When standing still the horse may position the hindlimbs unusually far underneath the body and may constantly shift weight between the limbs. A horse with severe primary lameness that has developed laminitis in the contralateral limb may start to load the originally lame limb, shifting weight between the two limbs.
Usually, but not invariably, a clinically significant increase in digital pulse amplitude occurs; however, in a thick-skinned cob-type horse this may not be palpable. In the acute phase the affected feet may be hot. Pressure or percussion applied to the feet, especially in the toe region, usually causes pain, but if the horn is excessively hard, the horse may not react. Careful palpation around the coronary band may reveal an unusual depression associated with sinking of the distal phalanx (DP). An area of unusual softness may herald infection tracking proximally in association with laminitis complicated by submural abscessation.
Clinical signs are usually diagnostic, except in less severely affected horses or those with involvement of only the hind feet, when the characteristics of the lameness may suggest foot pain, but not necessarily pathognomonic for laminitis. The response to perineural analgesia varies and is not associated necessarily with the degree of pain and lameness. Apparent desensitization of the foot with palmar (abaxial sesamoid) nerve blocks may have absolutely no effect on the lameness in some horses, although some improvement may occur in others.
Because laminitis frequently develops secondarily to a primary disease process, it is critical to evaluate the entire horse and to identify any predisposing factors that require treatment, such as endotoxemia, septic metritis, equine metabolic syndrome, or equine Cushing’s disease. If equine metabolic syndrome is suspected, serum insulin concentrations and the response to an intravenous glucose tolerance test should be assessed. It has been suggested that the presence of three or more of the following may increase the risk of laminitis development tenfold: insulin resistance, compensatory β-cell response, hypertriglyceridemia, and obesity (body condition score, >6/9).1 Recent administration of corticosteroids may also be a risk factor; in a survey of 36 European sports horse practitioners, 12 had experienced the development of severe laminitis within 7 to 10 days of administration of corticosteroids in 22 horses.2 Corticosteroids incriminated included dexamethasone, triamcinolone, and betamethasone administered either systemically or intraarticularly for treatment of recurrent airway obstruction, joint disease, or back pain, at what would be considered to be normal dose rates. The majority, but not all, of the horses were considered overweight. Approximately 50% of affected horses were humanely destroyed because of uncontrollable sinking of the DPs.
Radiographic examination is critical for establishing a treatment protocol and prognosis. Although rotation of the DP often can be managed successfully, sinking warrants an extremely guarded prognosis. Lateromedial images help to determine whether the condition is acute or an exacerbation of a more chronic problem. Abnormal thickness of the dorsal hoof wall, with or without modeling of the toe of the DP, implies previous disease. Lateromedial images are also important to establish the baseline position of the DP within the hoof capsule. Dorsopalmar images may be useful for assessing mediolateral balance in horses with chronic, unstable laminitis and to delect radiolucent lines indicative of lamellar separation (Figure 34-6, B). If the foot is grossly misshapen, trimming it first is preferable; otherwise, a false impression of severe rotation of the DP, which merely reflects the abnormal hoof wall growth and the development of a lamellar wedge, may occur.