The first image shows normal blood flow and then blood flow following arterial shunt at the coronary band which is common following a period of laminitis. The illustrations depict the finality of the sequence of events that at the onset is restricted to unnoticeable histological changes to the digital vasculature which some 4 hours or so later progresses to endotheliar cell swelling and mild oedema. The lack of inflammatory cell influx indicates no active inflammatory process is involved in the early stages of laminitis and the reasons for its induction is due to circulatory disturbance to the foot and resultant laminar ischemia (inadequate blood supply causing a shortage of oxygen and glucose). Progressive pathological changes now follow including laminar distortion, epithelial hyperplasia (sudden increase in cell numbers) generalised micro-vascular thrombosis and haemorrhage. Necrosis of the stratum spinosum (the prickle cell layer of the skin) and the primary dermal layers undergo death of most or all cells within 40 days.
There is no initial single reason why Laminitis should occur, just as research appears to favour a common denominator there are exceptions, it is generally accepted that Endotoxemia (cell wall remnants in the blood from the decomposing of gram negative bacteria) can be implicated in the onset of laminitis but conversely in many cases actual administration of endotoxins into healthy ponies has not always induced laminitis and many horses that develop laminitis never exhibit signs of Endotoxemia. Endotoxemia can be blamed on carbohydrate loading causing gram-negative bacteria devastation in the caecum which changes intra-caecal pH which in turn liberates endotoxins from the walls of the bacteria which then cause damage to mucosal barriers causing circulatory disturbance. Although a lot more owners and trainers these days are aware of the dangers of carbohydrate overload and take particular steps to avoid it happening incidences of laminitis do not go down. This is because laminitis is initiated by multiple disease processes and no single agent has been identified as the specific mediator for triggering the deterioration of the vital soft tissue that normally provides the digital cushion that withstands downward vertical load through the bony column and stops laminar detachment from the hoof wall. Initially total blood flow to the foot can be higher or lower than normal with carbohydrate overload induced laminitis. Total blood flow increases however where laminitis is induced by other causes such as food rancidity, moulds, stress catecholamines (venal restrictors), pollutants and concussion etc. The total blood flow usually decreases but within a short while the consequences are the same there is disturbance of vascular supply to the foot and if it is to be stopped or avoided then any such measures taken must be about supporting circulation in one way or another as soon as possible. A clue to how to proceed can be got from questioning why horses and ponies less than 3 years old do not get laminitis. They too can be overloaded with sugars and starches and are not immune to endotoxins and the damage they can cause. The answer can only be because they have new livers, good bile exchange and circulatory systems, we cannot turn the clock back but if we focus on the very real possibility that ‘if you can keep the lymphatic system running freely it is difficult for the horse to become ill’ we will provide most useful support. We do this with L94, if we can ‘clear and clean’ the circulatory system of lymphatic stagnation and if necessary provide some digital vasodilatory support as well, which we do in REXFLO, after the first 10 days we are in a much more favourable position of avoiding the likelihood of arterial shunt occurring in the next few weeks and on a prophylactic basis if we can avoid the onset of laminitis with P45 and EQUINOURISH so much the better as there is no truer statement than prevention is better than cure as far as laminitis is concerned.