Laminitis - how to recognize and early intervention

Summary

A typical laminitis affected foot has non-parallel hoof wall growth rings converging dorsally and a convex (dropped) sole. Foot pain is bilateral. The horse adopts a typical laminitis stance and walks in a characteristic way. Radiographs are important to identify if the distal phalanx is dislocated relative to the hoof capsule. Divergence of the hoof capsule away from the distal phalanx and sinking and lysis of the distal phalanx signify severe, chronic laminitis.  Apart from pain relief nonsteroidal anti-inflammatory drugs have no proven therapeutic value.  The aim of support shoeing is to encourage healing of the more severely affected dorsal half of the foot by utilising (loading) the palmar foot for weight bearing. Distal limb cooling is effective at preventing acute laminitis and is the only laminitis preventive/treatment strategy, with proven efficacy. It directly inhibits epidermal inflammatory events thus protecting the lamellar epidermal basal cell cytoskeleton from disintegration. The critical factor causing pasture associated laminitis is hyperinsulinemia particularly in insulin dysregulated horses and ponies. Management requires blood insulin concentration assessment using the oral glucose test to measure the insulin response to glucose absorbed from the foregut. Increasing insulin corresponds to increasing laminitis risk.

Introduction

The disintegration of the suspensory apparatus of the distal phalanx (SADP) is initially invisible to the naked eye. Clinically however there is bilateral foot pain; shifting weight from one foot to the other (paddling) with the forefeet placed forward of the normal position. If forced to walk the horse will arch its back and place the hind limbs forward, under the abdomen, to shift as much weight as possible to the hindquarters. The horse half rears before stepping forward in front. As time passes hoof and bone changes occur as internal pathology alters growth patterns and distorts hoof shape.  If lameness persists and worsens there is likely deteriorating displacement of the distal phalanx (DP) relative to the hoof capsule. A lateral to medial foot radiograph shows the position of the DP within the hoof capsule and enables recognition of laminitis.  Normally the DP dorsal cortex and the outer hoof wall are parallel and the DP is in a fixed position relative to the hoof capsule. Divergence of the hoof capsule away from the DP and DP sinking and bone lysis are typical of severe, chronic laminitis. When the DP descends into the hoof capsule coronary band connective tissue is taken with it. As a consequence dorsal coronary wall growth is displaced inwards, instead of downwards, resulting in non-parallel growth rings converging dorsally. Additionally, under pressure from the dislocated DP, the sole may bulge downwards creating a convex instead of concave sole. Ultimately it is the strength of the laminitis affected SADP that determines prognosis.  Many horses relapse after the acute laminitis episode despite early signs of improvement. Premature resumption of athletic exercise and thus greater foot break-over strain, particularly in the fore feet, can rupture surviving lamellar attachments.

Interventions

No drug based therapeutic regimen can arrest or block laminitis. It is more the extent and severity of the initial lamellar pathology that influences the outcome for the horse, not the treatment itself. The administration of nonsteroidal anti-inflammatory drugs (NSAIDs) during the developmental/acute stages, ameliorates foot pain and creates a more comfortable-looking horse, but the disease continues unabated [1]. NSAIDs have prognostic value however; a favourable analgesic response indicates relatively mild laminitis whereas little or no response means a severe case and a poor prognosis [2].  Foot rehabilitation and support shoeing should aim to spare (unload) the more severely affected dorsal half of the foot, while it heals, and utilise (load) the palmar foot for weight bearing.

Distal limb cooling

Distal limb cooling (DLC) is effective at preventing acute laminitis in a single cooled limb [3], all four limbs [4] or after acute onset [1; 5]. DLC is the only laminitis preventive/treatment strategy, with proven efficacy. In horses hospitalised and treated for colitis the odds of developing laminitis (and thus euthanasia) are significantly reduced (10X less odds) if effective DLC is part of the treatment protocol [6].  In the equine distal limb the target organ (lamellar tissue) can be cooled selectively, in isolation from other tissues.  Profound cooling (3-5oC), without apparent side effects, and with excellent tolerance from the horse can be applied continuously, to all 4 legs, for 3-4 days without side effects.  The ice must always be suspended in water; ice cubes must NOT make direct prolonged contact with the skin. A range of boots and tubs have been developed to maintain distal limb cooling; those that circulate cold water directly on the skin from the carpus down, as opposed to gels, wraps and pads, are the most successful. DLC directly inhibits epidermal inflammatory events (i.e., IL6 and COX-2 expression) in animals developing laminitis [1]. Cellular trafficking and receptor activation (de-phosphorylation) is virtually zero at 4°C thus protecting the LEBC cytoskeleton from disintegration.

Pasture Associated Laminitis (PAL)

Grasses and legumes make up the diet of horses in their natural state. Horses evolved eating complex structural carbohydrates, in the form of cellulose, hemicellulose, and lignin, as well as non-structural carbohydrates (NSC) in the form of fructans, simple sugars and starch. Domestic horses and ponies sometimes ingest excessive quantities of fructan, starch and simple sugars when they consume pastures in a sugar-producing phase. The risk of PAL is high in insulin dysregulated (ID) individuals. There is a functional enteroinsulinar axis in ponies mediated via the gut incretin hormones (mainly glucagon-like peptide-1 or GLP-1). GLP-1 is released from the intestine following carbohydrate consumption and works in concert with glucose to augment pancreatic insulin release. Thus the critical factor causing PAL is hyperinsulinemia originating, not from a failure of peripheral glucose uptake (IR), but from other, primarily gastrointestinal, causes. Owners of at-risk ID horses and ponies should avoid feeding high NSC pasture and hays, soak high NSC hay to reduce the simple sugar and fructan content or to use grazing muzzles. ID can be reversed by weight reduction and regular aerobic exercise. To manage HI laminitis in the field the blood insulin concentration must be known; current best practice is the oral glucose test measuring the insulin response to glucose absorbed from the foregut [7]. If the post-glucose insulin is < 50 µIU/mL the pony is unlikely to be insulin dysregulated and develop laminitis; if insulin is 50 to 200 µIU/mL there is a moderate chance; if insulin is >200 µIU/mL the horse or pony is at high risk of developing laminitis. Increasing insulin corresponds to increasing laminitis risk.