• theequinedocumentalist

Laminitis-A Pictorial Review

Updated: Apr 16, 2020

Our understanding of laminitis is changing and developing but one thing is clear, it can be a debilitating disease and has long been recognised as a painful cause of lameness in equines, in both its acute and chronic phases. Commonly it can have deformative influences on hoof growth. We all know prevention is better than cure, Laminitis has long been recognised as being caused by a dietary carb overload, yes, fat ponies are predisposed! Horses were designed to eat roughage, overfeeding and rich grass with a high carb content can cause onset, especially in horses with genetic predisposition, there is research and articles widely available on preventative measures, Earing et al (2018) described the benefits of soaking hay to reduce the carb content and Jones (2019) quoted that weight gain doubles the risk of laminitis, to quote just two. Recently laminitis has been described as a systemic clinical syndrome, commonly endocrinopathic laminitis which can be present sub-clinically for lengths of time often evident by divergent growth rings, this sub-clinical phase could signal opportunity for preventative measures (Patterson-Kane et al 2018). Endocrines are glands that produce hormones, in two common causes of laminitis, Equine Metabolic Syndrome (EMS) and Pituitary Pars Intermedia Dysfunction (PPID), insulin levels are effected which are responsible for vascular, inflammatory and tissue remodelling mechanisms, the chemical processes of laminitis are complexed and have different pathogenic routes, carb overload and fructose overload have a similar pathophysiology causing separation of the laminal basement membrane and release of Matrix metalloproteinase (MMP’s) which break down the extracellular matrix (Li et al 2015) responsible for binding together cells and regulating cell function (Theocharis et al 2016), put simply, the bond between the pedal bone and the hoof wall is disrupted, to different levels of severity.

Schematic diagram of the bond between the sensitive and horny laminae, also known as the suspensory apparatus of the distal phalanx. The pedal bone is suspended in the hoof capsule, when this apparatus fails in laminitis the bone can become displaced.

There are different pathophysiologies of laminitis and these can be catagorised according to their mechanism; ischemic: enzymatic: endocrine (metabolic) and inflammatory injuries.

Ischemic theory involves vasoconstriction, causing blood pooling and subsequent tissue edema and necrosis, these mechanisms can be seen in venograms, however this theory has been challenged as a primary cause (Laskoski et al 2016).

Enzyme theory states pathophysiology caused by the MMP’s mentioned above, possibly initiated by bacterial/toxic infection.

Endocrine and metabolic mechanisms described previously, are associated with cushings syndrome, obesity and prolonged exposure to glucocorticoids (Laskoski et al 2016), these pre-cursers show hormone imbalances such as hyperglycemia, hyperinsulinemia and insulin resistance.

Inflammatory processes can be systemic or localised to the hoof with an increase uptake of macrophages and subsequent cytokines into the laminal tissues associated with changes to these structures, systemic inflammation can be caused by systemic infection and/or carb overload (Laskoski et al 2016).

All of this causes pain and often the horse/pony has difficulty standing squarely on its feet adopting a distinctive posture during the acute phase (Fig1.), most commonly the front feet are affected, but it can present on any, some, or all of the feet, usually a strong digital pulse and heat in the hoof are present. First aid at this point can be the deciding factor in the progression and is focused on supporting the bone column through frog pressure (Fig.2).

Fig.1 Laminitic stance. Pony tries to alleviate weight bearing.

Fig.2a/b The Author applying Beenie frog support laminitis first aid pad (top image). Applying Dental impression material and hoof cast or vet wrap to an abscessed sole (Bottom image). Providing this frog support in the early stages can help to mitigate any boney displacement.

Treatment should correspond to the timeline of the pathology (Fig.3), inflammation during the build up and acute phase can be addressed with anti-inflamatories and cryotherapy which has proven to be most effective (Van eps and Pollitt 2004) Laskoski et al (2016) outlines the various drugs and treatments at the different stages. Although laminitis is commonly a systemic disease it’s the effect on the hoof that is most evident, the hoof morphology and prognosis can differ depending on the severity and longevity of pathology (Fig.3)

Fig.3 Flow chart showing the different routes of laminitis expressing how important the first 48hours are.

In the acute phase of founder the changes within the foot are commonly a loss of solar depth (Fig.4)

Fig.4 Bone is visible through abscessed sole as a result of loss of solar depth.

rotation and/or sinking of the distal phalanx and solar bruising around the apex of the distal phalanx often visible on the solar surface, separation of the stratum internum and the laminal wedge begins to form (Fig 5), the mechanism for the formation of the laminal wedge and capsular rotation are still debated but it is widely documented as the toe growth being stunted by pinching of the coronary corium and the heels continue to grow “pushing” the toe up and away from the surface of the distal phalanx, creating the tell tale Alladins slipper effect (Fig.6).

Fig.5 shows rotation vs sinking. The formation of the laminal wedge as the bone rotates within the hoof and the structure of the stratum internum is disrupted.

Fig.6 Before and after trim on a chronic laminitic with tel tale Alladin’s slipper hoof morphology.

The different effects of laminitis can clearly be seen on radiographs, capsular rotation vs phalangeal rotation vs sinking and type 1 vs type 2 laminitis.

Fig.7 Shows an ideal relationship between the dorsal surface of P3 and the dorsal hoof wall for comparison with laminitic changes. The dorsal wall and dorsal surface of distal phalanx are parallel.