A single severe laminitic episode or repeated, less severe episodes can, depending upon the degree of separation of dermal and epidermal laminae, lead to either rotation or sinking of the pedal bone, both of which result in anatomical changes in the position of the coffin bone with visible separation of the laminae, colloquially known as founder. Rotation and distal displacement may occur in the same horse. Both forms of displacement may lead to the coffin bone penetrating the sole. Penetration of the sole is not inherently fatal; many horses have been returned to service by aggressive treatment by a veterinarian and farrier, but the treatment is time-consuming, difficult and expensive. Rotation is the most common form of displacement, and, in this case, the tip of the coffin bone rotates downward. The degree of rotation may be influenced by the severity of the initial attack and the time of initiation and aggressiveness of treatment. A combination of forces (e.g. the tension of the deep digital flexor tendon and the weight of the horse) result in the deep digital flexor tendon literally pulling the dorsal face of the coffin bone away from the inside of the hoof wall, which allows the coffin bone to rotate. Also, ligaments attaching the collateral cartilages to the digit, primarily in the palmar portion of the foot, possibly contribute to a difference in support from front to back. The body weight of the animal probably contributes to rotation of the coffin bone.
However, the continual shifting of weight required to balance in a moving vehicle may enhance blood circulation, so some horsemen recommend trailering as an initial step in rehabilitation of a horse after long confinement.Laminitis has been observed following an equine standing in extreme conditions of cold, especially in deep snow. Laminitis has also followed prolonged heating such as may be experienced from prolonged contact with extremely hot soil or from incorrectly applied hot-shoeing. Complex causes
Pituitary pars intermedia dysfunction, or Cushings disease, is common in older horses and ponies and causes an increased predisposition to laminitis. Equine metabolic syndrome is a subject of much new research and is increasingly believed to have a major role in laminitis. It involves many factors such as cortisol metabolism and insulin resistance. It has some similarities to type II diabetes in humans. In this syndrome, peripheral fat cells synthesise adipokines which are analogous to cortisol, resulting in Cushings-like symptoms. A retained placenta, if not passed completely after the birth of a foal, can cause mares to founder, whether through toxicity, bacterial fever, or both. Anecdotal reports of laminitis following the administration of drugs have been made, especially in the case of corticosteroids. The reaction may be an expression of idiosyncrasy in a particular patient, as many horses receive high dose glucocorticoid into their joints without showing any evidence of clinical laminitis. Even horses not considered to be susceptible to laminitis can become laminitic when exposed to certain agrichemicals. The most commonly experienced examples are certain herbicides and synthetic nitrate fertilizer.