• theequinedocumentalist

Laminitis-A Pictorial Review

Updated: Apr 16

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.

Fig.8 Shows phalangeal rotation, caused by the pull of the deep digital flexor tendon and the break down of the laminal bond between the distal phalanx and dorsal wall, but the dorsal wall has minimal distortion.

Fig.9 Shows capsular rotation caused by a differencial in wall growth between the toe and the heels, causing a “slippering” effect and tearing away of the wall at the toe. This x-ray also shows a type 2 laminitis where the distal border of the distal phalanx has started to remodel.

The difference between type 1 and type 2 laminitis is the presence of bone remodelling of the distal phalanx clearly seen in fig.10 as a flick at the toe.

Fig.10 Type 2 laminitis.

When a horse sinks rather than rotates there is total break down of the bond between the hoof and the dorsal wall, the hoof is essentially loose within the hoof capsule, there is commonly little evidence radiographically of any rotation, however the distance between the hair line at the coronet and the extensor process of the distal phalanx can inform on how much the bone has sunk, for an average horse the founder distance at which the prognosis rapidly becomes poor is 14mm (Fig.11).

Fig.11 Modern x-ray machines can be calibrated to take internal measurements, this pony has a founder distance of 23.6 mm this carries a poor prognosis. Radiograph taken from

Certain external markers can provide valuable information to farriers when there is not a calibrated radiograph available (Fig.12).

Fig.12 shows the markers that should ideally be applied when taking a laminitic radiograph. A marker of a known length on the dorsal wall and a marker on the apex of the frog. This radiograph also exhibits multiple laminitic changes as well as a large founder distance.

The marker on the dorsal wall should begin at the hair line, this enables comparison of the wall angle and angle of the dorsal wall of the distal phalanx and enables measurement of founder distance. The marker at the apex of the frog enables the farrier to work out where the tip of the distal phalanx is in relation to external reference points so he/she can correctly apply a remedial shoe.

Farriery treatment differs greatly, firstly it is important to appreciate that farriery intervention follows the treatment of the acute causes. Historically a heart bar was the farriery treatment of choice and is till used effectively in some cases (Fig.13), however it presents some limitations, one being the application of positive frog pressure, when a hoof is loaded through the dynamic phases of locomotion the frog is loaded and compressed temporarily and then allowed to release when the hoof is in flight, when a positive pressure heart bar is applied this doesn’t allow for thus release and this can have detrimental effects on blood flow.

Fig.13 Heart bar shoe fitted by the author to counteract the prolapse of the pedal bone.

Modern materials and techniques now provide alternatives that overcome this issue and provide added benefits. The use of frog support padding in its different forms allows frog pressure without constant loading, it can also increase the surface area of load (Fig.14).

Fig.14 Possible Pad systems for the treatment of laminitis. Formahoof has been widely used for the treatment of laminitis (Top right). Note the bottom right picture, often laminitics are painful around the distal border of P3 and need to have this area free of pressure.

Hydroplastic shoes allow a heart bar application with a more flexible material and without the need for nails (Fig.15).

Fig.15 Imprint Hydroplastic Shoes.

Clogs are widely used to treat laminitis, they are fitted so the ground surface correlates to the pedal bone and their bevel reduces leverage forces and aids in easy locomotion, commonly fitted with impression material to evenly load the structures behind the apex of the frog (Fig.16), radiographs are imperative for correct administration as the breakover point should correspond with the tip of the distal phalanx.

Fig.16 Fitted clog, as the hoof improves transition back into shoes can progress. Courtesy of J.Mather Bsc (hons).


Laminitis is an extremely complexed subject and this review only scratches the surface of the scientific research that has gone into its study, as further understand of its pathophysiology is uncovered, prevention and treatment can develop. Farriery intervention can mean the difference between life and death and radiographs provide vital information on necessary treatment. Some animals are genetically predisposed but as horse/pony owners, understanding the predispositions of the disease such as obesity and lush grass and taking preventative measures can mean you avoid this horrific pathology and if you are unlucky, knowing first aid and acting fast can vastly improve your horse/pony’s prognosis.


Earing et al 2018,

Jones, 2019

Xinran Li, Renli Jiang, Guanying Wang, Yue Li, Xiaojing Fan, Xu Liu, Jinglu Wang, Jialiang Pan, Li Gao

MMP-2 plays an important role during the early acute developmental phase of oligofructose-induced equine laminitis

Bull Vet Inst Pulawy 59, 149-153, 2015 DOI:10.1515/bvip-2015-0022

Achilleas D.Theocharis, aSpyros S.Skandalis, aChrysostomiGialeli, abNikos K.Karamanos, 2016, Extracellular matrix structure, Advanced Drug Delivery Reviews, Volume 97, Pages 4-27

Luciane Maria Laskoski, Carlos Augusto Araújo Valadão, Rosangela Locatelli Dittrich, Ivan Deconto, Rafael Resende Faleiros, 2016, An update on equine laminitis, Cienc. Rural vol.46 no.3 Santa Maria

VAN EPS, A.W.; POLLITT, C.C. Equine laminitis: cryotherapy reduces the severity of the acute lesion., Equine Veterinary Journal v.36, n.3, p.255-260, 2004.

Patterson-Kane et al, 2018, Paradigm shifts in understanding equine laminitis, The veterinary journal, vol 231, pg 33-40


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