Laminitis is frustrating for veterinarians because current knowledge and understanding of the pathophysiology and progression
of the disease are incomplete, limiting efforts to prevent and treat this devastating disease successfully. Scientific investigations
have shed light on the pathophysiologic events involved with laminitis; however, additional studies are needed to unravel
the remaining mysteries regarding the initiation and propagation of laminitis. Currently, numerous and varied therapies are
used to prevent and treat laminitis; however, clinicians' preferences and impressions regarding the most effective treatments
are based on an incomplete understanding of the initiating events in this disease. Because of the gaps in knowledge of the
pathophysiology of laminitis, the effectiveness of the currently used treatments is inconsistent at best. In some cases in
vogue therapies may actually be detrimental to laminar healing. Therefore developing a more thorough understanding of the
cascade of events involved with the onset and propagation of acute laminitis should help veterinarians develop more rational,
effective, and cost-efficient therapies.
Clinical Signs and Diagnosis
Laminitis is a disease that can affect all four feet; however, laminitis most commonly affects the forelimbs because they
bear approximately 60% of the mass of the horse.3 The increased load of the forelimbs compared with the hindlimbs is thought
to account for the increased occurrence of laminitis in the forelimbs. To define better the severity of clinical signs exhibited
by horses, Obel established a grading system in 1948. Grade 1 is the least severe and states that the horse alternately and
incessantly lifts the feet and that lameness is not evident at a walk but is evident at a trot as a short, stilted gait. Horses
that walk with a stilted gait but still have a foot lifted are classified as grade 2. Horses with grade 3 laminitis move reluctantly
and vigorously resist lifting of a foot. The most severe classification is grade 4, noted by the horse refusing to move unless
forced.11 Other clinical signs characteristic of laminitis are heat present over the dorsal surface of the hoof wall, bounding
of the digital pulse (increase in the difference between the systolic and diastolic digital arterial pressure), sensitivity
to hoof testers, swelling of the coronary band, and alteration of stance to redistribute weight to the hindlimbs (sawhorse
stance or rocking of weight to the hindlimbs) if laminitis is principally affecting the front limbs. More severe signs are
a dropped sole or palpation of a depression located at the level of the coronary band, both indications of rotation or distal
displacement (sinking) of the distal phalanx within the hoof wall.5,12 Lateral radiographs of the digit are indicated for
detection of rotation and distal displacement of the distal phalanx within the hoof capsule.
Following the onset of lameness, the initial histologic alteration occurs in the digital vasculature, including swelling of
the endothelial cells and mild edema formation.13 Laminar capillaries become obstructed with erythrocytes within 8 hours.
Within 6 to 12 hours, a perivascular leukocyte infiltration occurs that then dissipates as the inflammatory cells migrate
into the epidermal layer. Arteriolar endothelial cells become deformed because of cytoplasmic processes that extend into the
lumen. Microvascular thrombi and accompanying severe edema formation occur within 24 hours, and hemorrhage occurs within the
primary dermal laminae by 72 hours.
Primary histologic alterations of the laminae occur within 8 hours after lameness develops.13 Initially, thinning and lengthening
of the lamellar structures is accompanied by reduction, flattening, and displacement of epithelial cells. The secondary laminae
become redirected such that laminae nearer the base of the dermal lamina are directed toward the coffin bone and those nearer
the laminar tips are directed toward the hoof wall. Morphologic alterations following epithelial cell damage include swelling,
vacuolization, nuclear swelling and pyknosis, and leukocytic infiltration of the secondary epidermal lamina, which is observable
as early as 24 hours after the onset of lameness.
Development of acute laminitis often follows other primary diseases; therefore the mechanisms involved in the pathogenesis
of laminitis are most likely numerous and interrelated. Currently, inflammation, endothelial and vascular dysfunction, and
metabolic disease are considered pivotal events in the development of laminitis.